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Chapter 3 Doctors Need to “Unlearn” Nutrition

Chapter 4

Dietitians Lost Their Mind

Dietitians and Math

Decades ago, the ability to dispense nutritional advice was “claimed” by dietitians. The field of modern dietetics was borne out of two concepts, both of which turned out to be false. The first is the idea that a “calorie is a calorie,” which was espoused by the Atwater system, developed by agriculturist Wilbur Olin Atwater in 1916. His claim to fame was that he standardized how much heat energy (i.e., how many kilocalories, or kcal) three specific macronutrients would liberate when burned in a bomb calorimeter (a device that measures heat release of organic substances), and he calculated the ratios, which computes the number of kcal in a given food by its protein (4 kcal/gm), carbohydrate (4 kcal/gm), and fat (9 kcal/gm) content. As fat was the most calorie-dense, Atwater thought it was the most egregious in terms of weight gain.

Since then, dieticians have clung to the idea that a patient’s food plate can be calculated using this arithmetic. The problem is that our bodies are a bit more complicated. The Atwater equation neglected to account for the intestinal microbiome and its inherent metabolism of approximately 25 to 30 percent of everything you eat, as well as the role of fiber in altering that percentage (see Chapter 12). Since fiber doesn’t contribute any calories to your total but alters the percentage of the total that you absorb, the number of calories you eat versus how many you metabolize are completely disparate. Nowhere is this more true than for nuts such as almonds, where the amount of calories absorbed is a full 30 percent less than those generated from a bomb calorimeter; in fact, some manufacturers are now ratcheting down the labeling of caloric content of their products specifically to reflect this fact. But, of course, we didn’t know the intestinal microbiome even existed back in 1916. We do now, but the dietitians have not changed their math, methodology, or message.

The modern dietetics movement began in 1917, with the founding of the American Dietetic Association, rebranded in 2012 as the Academy of Nutrition and Dietetics (AND). The AND has always argued that obesity, and indeed all of nutrition, can be determined with some simple math. Just add up what’s in the food versus what you need, and you have all the evidence you need to determine nutrient deficiency or excess. They say that chronic disease is caused by excess calories, and therefore obesity—thus giving rise to the partnerships between the Big Food companies and the AND, as exemplified by their motto “Eat Right” and exercise. In the process, we were offered such subterfuges as Smart Choices (a food industry coalition), NuVal (David Katz), and the Global Energy Balance Network (both Coca-Cola); fortunately, all of these are debunked and relegated to the dustbin of history. Nonetheless, the beat goes on. Coca-Cola sponsors the nonprofit Exercise is Medicine, to get people to focus on exercise, not diet.

Corporate dietitians have continued to exonerate processed food over the decades, as has the AND. They do this for three reasons. The first is that they espouse calories, and virtually all food has calories, so what makes an individual food a problem? The Atwater system was, is, and always will be defective. Where those food calories come from determines where they go. It’s not physics, it’s nutritional biochemistry. My hope is that you will see past this fallacy, and that this book will finally kill the calorie, a stake right through the heart of the myth, once and for all. They also claim it’s what’s in the food that matters—this is clear from their support of the Nutrition Facts label. Except that it’s not what’s in the food, it’s what’s been done to the food, which doesn’t appear on the food label (see Chapter 17). They’ve missed the mark on both counts.

And, last, 90 percent of their operating budget comes from Big Food, as documented by public health lawyer Michele Simon. They exonerate dietary sugar even to this day because they can’t possibly kill the goose that lays the golden eggs. This was proven to me personally, when I was attacked by a Dallas dietitian, Neva Cochran, RD, while I was a guest on the Diane Rehm Show in 2013, for arguing that a calorie is not a calorie. Despite the evidence, Ms. Cochran later lashed out on YouTube, saying a calorie IS a calorie. Why was Ms. Cochran so vehement? Because she represents the processed food industry. Calories are the industry’s shield; it’s how they hide from culpability. It’s Ms. Cochran’s job to discredit me, and anyone else who gets in the way of processed food.

Dietitians Need a Schooling

Since dietitians (either actively or passively) took over nutritional counseling back in the 1960s, our health has steadily gotten worse. Maybe that’s correlation rather than causation, but the one thing we can say is that despite the abject deterioration of American health, dieticians haven’t altered their advice; they’re still stuck on calories. Current modeling suggests that virtually half of all Americans will be obese by 2030. Patients remain ill, because processed foods are addictive, doctors are ambivalent, confused, or just plain ignorant, and dietitians are complicit with Big Food.

Ultimately, you can be part of the problem, or you can be part of the solution. To be sure, many dietitians are attempting to change the profession from the inside, and they are to be applauded and supported. But the core of the profession must abide by the AND and its corporate sponsorship in order to receive and maintain certification.

How can you tell which side a dietitian is on? One question: ask them if you need sugar to live.

Dietetics Is a Protection Racket

Dietitians around the country are indemnified from lawsuits by an entity known as the Commission on Dietetic Registration (CDR). Their mission statement is: “To administer valid, reliable, and rigorous credentialing processes to protect the public and meet the needs of CDR credentialed practitioners, employers and consumers.”

Note: “protect the public”

Currently, 104,000 dietitians and nutritionists are registered with the CDR. Legislation exists in forty-seven states (Arizona, Michigan, and New Jersey are not included) to protect dietitians registered with the CDR. This has created a monopoly position on giving out dietary advice. Their only responsibility: conform to the policies of the AND—including those about processed food. Well, where does the AND get its marching orders? Here is the list of funders and sponsors for 2019: Abbott; American Pistachio Growers; a2 Milk Company; BENEO Institute; Campbell Soup Company; Conagra Brands; DanoneWave; Egg Nutrition Center; Florida Department of Citrus; FMC (a chemical producer); Ingredion; Lentils.org; National Cattlemen’s Beef Association; National Dairy Council; Nestlé USA; Premier Protein; Quaker Tropical Gatorade; Splenda sweetener; Sunsweet Growers; and The Wonderful Company. Some Real Food companies, to be sure, but a whole lot of processed ones as well.

Dietitians and the Battle for the “Soul” of the Profession

Lenna Cooper and Lulu Graves cofounded the AND in 1917, in response to dietary needs of soldiers in World War I.

Graves was a home economist who was trained and certified as a hospital dietitian. She had plenty of experience dealing with hospitalized diabetic patients and knew that high-protein and high-fat diets were the only effective therapies against hyperglycemia at the time. She even sponsored a 1921 treatise in Modern Hospital called “A high-fat diet for diabetic patients.” Indeed, up to that point, a high-fat diet was the only rational treatment for diabetics; Dr. Frederick Allen, the successor to Dr. Elliott Joslin at the Joslin Diabetes Center at Harvard, argued in 1919 that a 70 percent fat, 8 percent carbohydrate diet was optimal for diabetics. But 1921 was a watershed year for diabetes with the discovery of insulin. And insulin meant that carbohydrate was back on the menu for diabetics, and treatment was now easier to institute than prevention. The high-fat paradigm for treatment of diabetes was destined for the trash heap (at least until ninety years later). Cooper and Kellogg won out, and the low-protein, high-carb diet became codified into dietetic lore.

Nutrition and Religion

Adventist physicians currently embedded in the AMA. Except for one thing—there is no science. And the reason is because “God is the author of science.” Therefore, how could there be science, because that would put the “created” over the “Creator.”

There’s just as much medical evidence for the benefits of the low-carb high-fat (LCHF) or ketogenic diet as there is for the vegan diet. The reasons both work, when they work, is because they: 1) protect the liver, 2) feed the gut (see Chapter 11). Either diet is a choice, not a mandate. Either diet can be easily co-opted by charlatans and bad influencers. The two factions could learn a lot from each other, because there’s valid science on both sides. But one faction doesn’t talk to the other, in part out of religious fervor.

Chapter 5

Dentists Lost Their Way

Dentists Were the Original Anti-Sugar Advocates, So Why Do They Give Out Lollipops?

In the beginning, there was the barber surgeon, who yanked out the offending tooth right after giving you a haircut and a close shave. It wasn’t until the early twentieth century that Ohio dentist Weston Price (1870–1948) made oral health the purview of dentistry. In fact, dentists knew the true cause of dental caries (the disease that causes cavities) because of Weston Price. Price was arguably the most important and influential dentist in the history of dentistry, but today he’s a (mostly) forgotten man—and not because he was proved wrong. Because he was proved right.

The disease is called Mountain Dew mouth. It’s the scourge of Appalachia, all the way through Nashville, Tennessee, where Mountain Dew was invented, and beyond. Dental caries is the number one cause of chronic pain worldwide, as well as tooth loss, a chronic condition experienced by children, cause of outpatient anesthesia, and source of income for practicing dentists in the US. And it’s getting worse, not better. It’s the bane (or boon, depending on the dental professional’s point of view, as cavities are good for business) of dentists’ existence.

Dental caries is a modern phenomenon. Our ancestors didn’t brush their teeth, and they also didn’t have appreciable dental caries. Analysis of fossils dating back to the Paleolithic era demonstrates bad tooth mineralization and only occasionally poor dental alignment, but little in the way of dental caries. Even starting with recorded history (3000 BCE and forward), the prevalence of dental caries among European populations was at a relatively low 1 to 5 percent, and it stayed that way, until the early to mid– Industrial Revolution. Then there was a huge jump in prevalence to 25 percent in a very short period of time. How come?

Nowhere was this epidemic more noticeable than in England.

Great Britain of the 1800s was the test kitchen for processed food; white flour and sugar were mixed with everything. Working long hours in the mills and mines, British workers didn’t get time for a proper meal, but were afforded a biscuit (often laced with sugar). They also drank tea imported from India with at least one lump of sugar, if not two. As a result, the prevalence of dental caries increased markedly.

The Beginnings of Nutritional Dentistry

Weston Price watched the rise in prevalence of dental caries in his Cleveland practice. His assessment that the reason was the “displacing foods of modern commerce” was accurate. The culprits were and are white flour and rice, packaged pastries and baked goods, refined sugar and jams, canned and chemically preserved goods, and processed vegetable oils. Price abandoned his lucrative practice to travel the world—he spent the decade 1925 to 1935 visiting primitive cultures and industrializing countries, in order to understand the anthropology of tooth decay, heart disease, and cancer. Irrespective of the race of the isolated groups that he studied—be they Inuit, Swiss or Peruvian Indian mountaineers, Australian Aborigines, Kenyan Watusi or Maasai—Price found that they universally maintained near-perfectly aligned teeth and jaws, as well as no dental caries, as long as they followed their traditional diets. Conversely, every country that migrated to the processed food diet saw an exorbitant rise in dental disrepair. He labeled this process modern degeneration, and authored his now classic volume, Nutrition and Physical Degeneration (1939). By examining isolated populations south of the US, Price came to this simple conclusion—it’s all about the diet. His teachings were seminal to the foundations of the burgeoning field of nutritional anthropology.

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On March 27, 1934, perhaps the most consequential debate in the history of dentistry took place at the Hotel Pennsylvania across from Penn Station in New York. In front of an audience of 1,500 health professionals, the dentists duked it out over what causes dental caries. In one corner was Team Bacterial: Dr. Thaddeus P. Hyatt of Metropolitan Life and New York University; Dr. Alfred Walker of New York University; and Dr. Maurice William of the Oral Hygiene Committee of Greater New York. They came armed with the evidence that clean teeth don’t decay. Brush them often enough and everything will be fine. In the other corner were the members of Team Nutritional: Dr. Elmer V. McCollum of Johns Hopkins University; Dr. Arthur H. Merritt of the American Academy of Periodontology; and, of course, Weston Price. They were armed with the evidence that other countries brushed less than we did and still didn’t experience decay.

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On the bacterial front, we know that the flora of the mouth and gut have changed considerably over human evolution. Our ancestors’ native oral bacterial flora are no longer native, at least not in the oral cavity; there’s been a mass migration of bacteria to different ends of the gut. When an environment becomes inhospitable, it’s time for those denizens to up and move somewhere else or die in the process. For example, by examining the DNA in ancient calculus deposits of the teeth, we know that one particular bacteria type, Proteobacteria, was rare in the mouth among our hunter-gatherer ancestors, but as biological and cultural evolution changed over time, they came to dominate it. Conversely, another type of bacteria, Firmicutes, was prevalent in the mouth of our ancestors, but has since migrated and taken up residence in our lower gut, where it’s now causing all sorts of ruckus (see Chapter 19). In fact, there used to be numerous types of bacterial species in the mouth contributing to bacterial diversity, but with the advent of the Industrial Revolution, that diversity has dwindled, and new previously “alien” bacteria have colonized the oral neighborhood. In its place we have this new squatter in the mouth, a particularly onerous species of bacteria called Streptococcus mutans, which have been shown to be a major producer of lactic acid and demineralize (burn holes in) teeth. While this bacterium isn’t the sole perpetrator of dental caries and subsequent tooth rot, it is the prime suspect.

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What could account for this wholesale microbial cleansing and bacterial migration? In the early 1910s, the dental biofilm was discovered and shown to harbor various bacteria. Despite evidence at the time to the contrary, the biofilm was considered by many dentists to be the source of caries, and therefore frequent brushing was espoused as the method to rid the teeth of unwanted bacteria.

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Some believe that the toothpaste industry was responsible for this stance, as Pepsodent advocated this policy as early as 1919, before there was any data in either direction (Big Business strikes again). But even though debunked, it’s one of the reasons that dentists promote the concept of frequent brushing as a preventative for dental caries, a notion that remains with us today. Maybe there is something to it—for instance, frequent brushing was recently shown to be associated with reduced risks for heart failure, just not for dental caries. You would have to brush within ten minutes of eating saltwater taffy in order to remove the lactic acid fast enough to prevent caries just from brushing; this is untenable as a strategy.

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On the nutritional front, it’s generally assumed, even by dentists, that carbohydrates are a primary driver of dental caries (cavities). This is technically true but misleading, and actually misses the point. After all, as stated earlier, our foraging/gatherer ancestors ate tons of carbohydrates and didn’t develop caries.

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There are three different forms of digestible carbohydrate: 1) monosaccharides (one sugar molecule—glucose or fructose or galactose; high-fructose corn syrup is an example of two monosaccharides at once); 2) disaccharides (two sugar molecules bound together; maltose (e.g., beer) is glucose-glucose, sucrose (e.g., fruit) is glucose-fructose, and lactose (e.g., milk) is glucose-galactose); and 3) starch, which is a string of glucose molecules polymerized together. But only the first two, monosaccharides and disaccharides, can cause dental caries. The reason is that the oral bacteria can only metabolize carbohydrates that are “fermentable”; that is, single free molecules. This is particularly true in sugared beverages, since the glucose and fructose are not bound, and they aren’t trapped within a food matrix, giving the bacteria immediate access. Starch, because it’s polymerized, isn’t immediately fermentable by bacteria; rather, it is actually protective against dental caries because it contributes to the biofilm surrounding the tooth. However, Streptococcus mutans, the most cariogenic bacterium in the mouth, has a neat trick; it possesses an enzyme called fructanase that can cleave the glucose-fructose bond of sucrose in about a nanosecond, making Streptococcus mutans a champion cavity-maker.

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The relationship between the sucrose molecule and dental caries goes back to 1954, with the seminal Vipeholm study—436 individuals observed for five years showed that increased frequency of sugar consumption between meals resulted in a marked increase in caries, while withdrawal of sugar halted their progression. Shortly thereafter, caries incidence was directly tied to sugar consumption in children and adults. Even getting rid of the sugar in the school cafeteria reduced caries rates in New Zealand children.

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The Dentists Got It …

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Price’s admonitions seemed to carry weight back in the 1930s. His colleague McCollum wrote, “It seems that were we to turn to a low sugar, high fat type of diet, such as is prescribed for diabetic patients, we might expect a prompt and marked reduction in caries susceptibility. This type of diet is practicable in many countries, but fats are in many regions considerably more expensive to produce than are starches and sugars.” Another colleague, William Davis, summed up the conundrum quite nicely: “Most people would prefer some decay rather than to eliminate the sweets … let us hope our research workers discover a more practical means of controlling or preventing dental decay.”

Note: enabling addicts

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… But Then They Lost It—Because of Fluoride

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Davis’s prayers were answered in 1945, as a third hypothesis of dental caries entered the fray. Team Tooth took over, and forever changed dentistry. It was discovered that a simple compound, sodium fluoride, at a low concentration of 0.1 parts per million, could inhibit dental caries formation. It did this in two ways: it reduced the amount of time that the pH of the saliva was low, thus reducing the time of burning a hole in the tooth; and it bound to the calcium hydroxyapatite crystals in the enamel itself, rendering them harder to dissolve in response to a low pH. Fluoride was on its way to overtaking modern dentistry. Dental researcher Frank McClure said, “In 1945, Grand Rapids became the first city in the world to fluoridate its drinking water… . During the 15-year project, researchers monitored the rate of tooth decay among Grand Rapids’ almost 30,000 schoolchildren. After just 11 years, [Dr. H. Trendley] Dean—who was now director of the NIDR (National Institute of Dental Research)—announced an amazing finding. The caries rate among Grand Rapids children born after fluoride was added to the water supply dropped more than 60 percent.” Consequently, the government got involved; fluoride started to be added to drinking water around the world, and the prevalence rate of dental caries was cut in half. It was a major public health win.

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But, similar to Kellogg’s thumb on the scale of nutrition research, the ostensibly positive triumph of fluoride has a darker side, and likely shields an industrial conspiracy driven by politics and profit. The story of fluoride’s transition from industrial contaminant to public health panacea has been the fodder of countless treatises on environmental health over the decades. The original discovery of the “magic” of fluoride was quite serendipitous, first pointed out by dentist Frederick McKay, who noted in 1909 that despite the fact that seven out of eight children residing in Colorado Springs manifested brown indelible stains on their teeth, they nonetheless appeared to be protected from dental caries. McKay isolated the reason to the fluoride in the water supply.

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In 1927, McKay implored the U.S. Public Health Service (at that time a division of the U.S. Department of the Treasury) to assist. Simultaneously, the same brown dental stains became manifest in the residents of Bauxite, Arkansas (named for its high aluminum content), following the drilling of three water wells by the Aluminum Company of America (ALCOA) corporation. These two isolated dental oddities independently rose to the notice of none other than Andrew W. Mellon (of Carnegie Mellon), who just happened to be both the U.S. Secretary of the Treasury (1921–1932) and the cofounder of ALCOA.

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Up to that point, fluoride was considered to be a toxic waste product of the aluminum and phosphate mining industries, and a chief contributor to environmental pollution. Clearly, aluminum needed a shiny new façade. Mellon made three quick calculations. First, in 1930 he assigned dentist Gerald Cox at the newly founded Mellon Institute at the University of Pittsburgh to investigate the effects of fluoride in dental caries prevention; his work paved the way for community water fluoridation. Second, in 1930 he assigned ALCOA chemist Henry Churchill to work with the Kettering Laboratory at the University of Cincinnati to find the “sweet spot” where fluoride could prevent dental caries without producing brown dental stains like those seen in Colorado Springs and Bauxite. They arrived at a dose of one part per million. Last, in 1931 Mellon reassigned dentist H. Trendley Dean from a U.S. Marine Corps hospital to the NIH—specifically to carry the positive message of fluoride back to the dental community. Dean had no formal research training, but it didn’t matter for the purpose. In 1932 Dean reported to the U.S. Surgeon General that the brown stain, termed dental fluorosis, was really the entrée to combatting dental caries. Dean spent the rest of his career advancing fluoride as a dental panacea. Dean got his reward—he was appointed the first director of the National Institute of Dental Research in 1948.

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Fluoride in the public drinking water and toothpaste appeared to be a magic bullet, touted as the “end of dental caries.” Or was it? Between 1971 and 1988, caries rates in the US dropped from 25 percent to 19 percent in toddlers, and from 55 percent to 24 percent in six-to-nine-year-old children. Definitely an improvement—but despite dentistry’s best efforts, they never got lower than that. They tried everything: standard fluoride toothpaste (1,500 ppm), which led to a 30 percent reduction in adult caries prevalence; yet increasing the fluoride to 5,000 ppm only led to a 40 percent reduction. They never even broke 50 percent. Hardly a miracle.

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Moreover, the dentists started to lament—“If we somehow got rid of dental caries, who will fill our chairs?” Caries prevention may be a public health issue for countries, but caries promotion is an economic issue for dentists and Big Business, pushing a myriad of toothpastes, mouthwashes, dental x-rays, and sealants. Slowly but surely, rank-and-file dentists backed away from Weston Price and their original anti-sugar stance,

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The Failures of Fluoride

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The dental profession bet a lot on fluoride, and they’re not going to give that up easily. But there’s been a recent wave of public dissent and distrust around the country about fluoride. In fact, Portland, Oregon, has banned public fluoridation since 1956. If you’ve seen Portlandia, you might chuckle to yourself about their residents’ granola personae. But now seventy-four cities around the country have followed Portland’s lead and also banned fluoride. Do they know something you don’t?

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there were the conspiracy theorists who were convinced it was a Soviet plot for mind control (in Dr. Strangelove [1964], General Jack D. Ripper says, “Fluoridation is the most monstrously conceived and dangerous communist plot we have ever had to face!”).

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New data also shows a small but statistically significant negative correlation between fluoride exposure and childhood IQ, which appears to be exacerbated when fluoridated water is used to mix infant formula.

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Now, to be honest, the effect is small, and correlation is not causation. I’m not a fluoride expert by any means; I’m agnostic on the issue. Here’s what I do know: fluoride is a tried and true adjunct to prevention, but it’s not a primary prevention in and of itself. If it were, the dental profession would have done better than a 50 percent reduction in caries. My take on this is very simple. Do that which works. What does the science say?

Sugar restriction is the most effective way of reducing and preventing the modern scourge of dental caries. Based on UK dental epidemiologist Aubrey Sheiham’s estimates, a reduction of dietary sugar to less than 5 percent of calories would reduce the prevalence of caries significantly; this method is nontoxic, and it wouldn’t cost anything. Then, maybe we wouldn’t even need fluoride.

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This isn’t rocket science. It’s barely even dental science. Without sugar, caries would be negligible. The profession knows the score, but the professional doesn’t seem to. The American Dental Association issued its guidelines for caries, and sugar restriction isn’t even mentioned as an option. They list eight nonsurgical therapies to treat dental caries. Nutrition is not even mentioned as a prevention.

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Conversely, the World Dental Federation (FDI)—composed of two hundred member organizations—has no choice but to prevent dental caries, especially in the most impoverished countries of South America and Asia. There just aren’t enough dentists to drill all the fillings, and there certainly isn’t enough money to pay them. In the FDI’s White Paper, sugar restriction is the #1 strategy to deal with dental caries. This should be a slam dunk worldwide, but it’s not. Because of the money.

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Chapter 10

Foodable, Not Druggable

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There are three commonalities to all the diseases that we call metabolic syndrome: 1) despite all efforts, these diseases are all increasing in incidence, prevalence, and severity at a faster rate than obesity; 2) they’re all exacerbated by obesity, although not specifically caused by it; and 3) while there are drugs to treat the symptoms of each one (including obesity), there are no drugs to either treat, cure, or prevent the diseases themselves. Further, as explained in Chapter 2, physicians treat the symptoms of each of these diseases with drugs, in order to prevent other disastrous sequelae like stroke, heart attack, amputation, or dialysis. And that’s because each of these diseases is due to problems inside the cell—and we don’t have medicines to treat them. Therefore, none of these diseases will remit, no matter the drug. The patient will continue their inexorable slide to oblivion, whether it be diabetes or cirrhosis or dementia—and if they don’t die of one of those diseases, then they’ll most assuredly develop another because the subcellular pathologies are still there. The three enzyme checkpoints (Chapter 8) are still dyssynchronized.

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A Bitter Pill to Swallow

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However, every single one of these pathologies can be prevented, mitigated, and in many cases reversed, by changes in diet. And none of these changes in diet have anything to do with calorie restriction. In most cases, reversal can be accomplished just by removing processed food and substituting Real Food

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Let’s take mitochondria as an example. While lots of research on treating mitochondrial disease is underway, no drug has yet made it to market. People will try to sell you stuff that purports to be a mitochondrial tonic, a wonder drug—just check out Amazon. There’s a lot of charlatanism in this space. For instance, coenzyme Q10 has been shown to be ineffective against the diseases of metabolic syndrome, with the exception of heart failure (which isn’t a disease of metabolic syndrome). These supplements don’t get where they need to go in the cell to be effective, but because they are nutraceuticals (a food with purported health properties), the FDA can’t regulate them (see Chapter 24).

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There’s a reason that drugs and nutraceuticals don’t work for metabolic syndrome. If you look at those eight subcellular pathologies at the biochemical level and 1) examine their transcription factors (the proteins that turn them on); 2) their co-activators and co-repressors (the proteins that bind to the DNA to amplify or inhibit them); and 3) their second messengers (proteins that mediate the effects within the cell), our drugs don’t touch them. None of the underlying causes are responsive to medicines in our current drug armamentarium (see Chapter 14). Treating the symptom doesn’t treat the problem.

However, all of them are driven by, and therefore responsive to, specific components of food, because Real Food gets where it needs to inside the cell. People think processed food is food, because it’s calories and macronutrients, but in fact processed food gets in and poisons those pathways instead.

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People think supplements are the antidote for bad food. They’re not. Rather, Real Food is the treatment, while bad food is the poison. In particular, we’ve learned that sugar, the main component of processed food, is the primary driver of four chronic diseases. It’s also a likely candidate for another five, listed in order below. These nine diseases together total about 75 percent of the healthcare burden in the US, and 60 percent globally. Processed food is behind them all, sugar makes them worse, and there’s no drug that prevents or reverses any of them. Below is a comparison of how well drugs versus food work to ameliorate these nine different chronic diseases.

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Diabetes—the Modern Scourge

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To this day, the American Diabetes Association continues to tout drug therapy to reduce blood glucose levels as the prime directive of diabetes therapy. They also promote weight loss as the primary strategy for prevention. While it’s true that a 10 percent weight loss over one year can reverse type 2 diabetes, only 30 percent of the subjects were able to achieve it, leaving most people out in the cold. The ADA doesn’t own up to the fact that diabetes can be reversed by dietary changes apart from weight loss, and their own dietary recommendations fall short on many counts.

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Changes in food composition instead of quantity accomplishes the same result, which is exactly what Virta Health attempted to do. Using a ketogenic diet (see Chapter 14) for two years without caloric restriction, they reversed diabetes in 80 percent of their patients, were able to discontinue insulin in 94 percent of their patients who were injecting, and induced a twenty-nine-pound weight loss as well.

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It’s the consumption of refined carbohydrate that’s associated with type 2 diabetes. In particular, dietary sugar, even more than starch, drives the metabolic reactions that lead to type 2 diabetes, especially because of effects in the mitochondria. The glucose in the dietary sugar drives the insulin release, which drives the weight gain, while the fructose drives the liver fat accumulation that drives the insulin resistance. Processed food is the primary vehicle.

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While drugs can lower the plasma glucose, they can’t reverse the insulin secretion driving the weight gain, or the insulin resistance at the core of the disease. Furthermore, mitochondria generate more oxygen radicals with processed food than with Real Food. New studies from the UK and Europe demonstrate that it’s the degree of food processing that predicts diabetes (see Chapter 17). Food can either prevent, cause, or reverse diabetes. Drugs may lower the blood glucose, but they can’t fix the diabetes.

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Heart Disease—Don’t Have a Coronary …

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In Chapter 2, we saw that statins lower LDL-C, but don’t reduce risk of heart attack (except in those who’ve already had one). One scientific study argued that triglyceride-lowering agents, such as fenofibrate, could prevent deaths from coronary events. But then the authors of that report issued a correction that amended the finding to total nonfatal events, so it’s not as clear what fibrates really do. On the other hand, fish oil, a dietary supplement, reduced incidence of heart attack by 8 percent—as well if not better than statins—because most of us are omega-3 deficient to start with (see Chapter 19).

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It’s processed food that foments heart disease risk. The relationship between food and heart disease is somewhat more complex than that of diabetes. The first issue is the role of omega-3 fatty acids (see Chapter 19), which act in two ways: by reducing general levels of inflammation, risks for heart disease are lower; and by reducing serum triglyceride levels, there’s less chance of plaque buildup. The second issue is insulin, because insulin increases coronary artery smooth muscle proliferation, making it more likely to get a clot. And the third issue is sugar—the percent of calories in the diet as added sugar predicts risk for dying of a heart attack, exclusive of calories or obesity. Conversely, removing added sugar from the diet removes the atherogenic particles (the small dense LDL), lowers triglycerides, and raises HDL—all protective against heart disease.

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Nonalcoholic Fatty Liver Disease (NAFLD)—Human Foie Gras

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NAFLD is now the leading cause of liver transplant in the US. It was unheard of prior to 1980, and now affects 25 percent of the world’s population, and 40 percent of the adult US population. Every pharmaceutical company is looking for the magic bullet to treat or reverse it. Scientists have tried novel drugs with funny-sounding names (obeticholic acid, selonsertib, elafibranor, cenicriviroc), but the best of them demonstrated only a 10 to 30 percent success rate. Noticing a common theme here? Drugs don’t do it. But diet does.

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While many things in the environment can damage the liver, there are two stages of fatty liver disease both driven at least in part by processed food and drinks. And guess what? Alcohol and soda have the same detrimental effects. The first stage is the deposition of liver fat, and the second is inflammation. If you eat a processed food diet, you’re vulnerable at both stages. The high fructose content in sugar-sweetened beverages and the high trans-fat content in highly processed and fried food (even though trans-fats have been removed by the FDA from processed food, the heat of frying can create them anyway; see Chapter 18) are damaging at both stages. In fact, sugar-sweetened beverage consumption has been shown to be an independent predictor of NAFLD.

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Tooth Decay and Periodontitis—Oral Hazard

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The primary role of sugar in dental caries is and has been quite clear for at least a century (see Chapter 5). But what hasn’t been discussed is the relationship between caries and other metabolic syndrome diseases. Doctors don’t think about the mouth, because we’re not trained to. Dentists don’t think about the heart or liver, because they’re not trained to. But the same processes are going on everywhere, and there’s a strong association between the rotting of your teeth and your liver. Dental caries are associated with NAFLD, whether separately or linked is undetermined, but the instigator of both is sugar.

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There’s an even more pernicious disease process going on in the mouth—periodontitis, which affects half of all Americans. There’s no question that periodontitis is associated with heart disease; there are defined mechanisms linking the two. But that’s not even the big kahuna. How about oral disease and dementia? Another oral bacterium, Porphyromonas gingivalis, has been associated with the development of Alzheimer’s, and researchers have found DNA for P. gingivalis in the brains of people who died from it. How did it get from the mouth to the brain? And what is it doing there? We don’t know yet, but we know it’s concerning.

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Cancer—the Emperor of All Maladies

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Like diabetes and heart disease, the degree of food processing has been shown to increase risk for cancer, regardless of calories or obesity. Chapter 8 explained why; if you stimulate PI3-kinase, block AMP-kinase, and disinhibit mTOR, you’re going to drive cell growth and risk for cancer. Sugar does the same thing. In fact, sugar consumption has been implicated in many cancers of endodermal (the inner lining of the embryo) origin, including breast, lung, bladder, ovarian, and pancreatic cancer. It also increases risk for cancer recurrence. But sugar is just one reason as to why processed food drives cancer.

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Refined carbohydrate is its own driver, by increasing insulin release. Processed meats are laden with nitrates, known to cause colon cancer and breast cancer. And fiber has been known to prevent colon cancer for decades, but did you know that fiber can also prevent breast cancer? Processed food is dangerous because of the lack of fiber—thus flooding the liver and starving the gut (see Chapter 11). This is why cancer centers like Memorial Sloan Kettering in New York and MD Anderson in Houston are experimenting with fiber-rich and low-carb diets in many cancer treatment plans.

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Dementia—Brain Drain

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Given the $290 billion annual cost of dementia in the US and that there’ve been 146 failed trials, it’s almost laughable that we keep trying to develop a drug. The fact of the matter is, diabetics are four times more likely to develop dementia than the general population. Furthermore, both forms (Alzheimer’s disease and vascular dementia) are increased in people with diabetes—because insulin resistance affects the brain.

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New research shows that sugar consumption is associated with the development of Alzheimer’s disease. It appears that fructose alters mitochondrial function in the brain, reducing energy generation, which puts the identified neuronal proteins amyloid and tau at risk for clumping, forming the classic neurofibrillary tangles of Alzheimer’s. A processed food eating pattern has been shown to be predictive of future Alzheimer’s disease, although no one has yet demonstrated that switching to Real Food lessens one’s risk.

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Obstructive Sleep Apnea (OSA)—Not a Snoozer

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OSA has many causes, many unrelated to body weight (see Chapter 16). But obesity of the neck can reduce the diameter of the airway, cutting down on oxygen delivery to the lungs, which causes fitful and restless sleep. The sympathetic nervous system and stress hormones get kicked up when you don’t sleep, and the cortisol spikes drive insulin resistance. Lack of sleep also increases the hormone ghrelin, which makes you eat more, driving weight gain. But there’s a reciprocal relationship between OSA and metabolic disease—the lack of oxygen to the liver likely inhibits AMP-kinase, causing the liver to turn more sugar into fat, thus increasing the amount of triglyceride and fomenting more obesity, inflammation, and heart disease.

Although OSA is clearly linked to obesity, which increases the risk of diabetes, there’s also evidence that OSA can cause diabetes independent of obesity. Indeed, OSA, processed food, and metabolic syndrome travel together. One may lead to another and they often coexist.

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Autoimmune Disease—the “Leak” in Your Gut

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Autoimmune diseases are a disaster and there are no good medicines available (steroids work, but the treatment is worse than the disease). They’ve been around for centuries, but there’s been a clear uptick in the last fifty years. Why? Two hypotheses have been proffered to explain it: the barrier hypothesis (our skin or lungs are letting in antigens) and the hygiene hypothesis (we don’t eat dirt and are too hygienic). But in fact, in the gut, they’re the same thing; because the gut is the dirtiest place in the world—one hundred trillion bacteria to have to fend off at all times—you don’t need an intestine, you need a fortress. We’ve known for a while that leaky gut is akin to chinks in the walls of that fortress. Antigens, like enemy soldiers, escape through those chinks into the bloodstream, where T cells and antibodies react against them. But in a case of mistaken identity, these immune cells then accidentally identify parts of your body as foreign invaders and generate an immune response to kill them off, a process termed molecular mimicry.

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Then there are two new twists. First, it appears that one autoimmune disease, called ankylosing spondylitis, produces antibodies to a gut bacterium called Klebsiella pneumoniae. Conversely, a different autoimmune disease called rheumatoid arthritis produces antibodies to a second gut bacterium called Proteus mirabilis. Now, this might not seem that earth-shattering, but recent work has shown that the refined carbohydrates in processed food feed those two bacteria in particular, and that carbohydrate restriction improves both of these diseases. Indeed, a low-sugar, high-fiber Mediterranean diet has been shown to be efficacious at prevention and treatment of rheumatoid arthritis. Furthermore, introduction of fiber to the diet appears to improve asthma (frequently an autoimmune disease), likely by improving gut function and reducing inflammation.

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Depression—the Moody Blues

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Insulin resistance has been shown to be a primary cause of clinical depression in humans. Sugar is a specific driver of insulin resistance, and one cause of depression in both rats and humans. So it should be no surprise to anyone that two studies, one in Europe and one in China, showed that ultra-processed food consumption is associated with depression in people.

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The foods that drive metabolic syndrome are those that are most clearly associated with the foods that people binge on—refined carbs and sugar. The question is, does the depression drive the food choices, which then drive the metabolic syndrome; or do the food choices drive the metabolic syndrome, which then drives the depression? Which is cause and which is effect? We still don’t know. But what we do know is that many people can eat their way both out of their metabolic disease and out of the depression by switching to a Mediterranean diet. The fact that your food choices can lift your mood certainly argues that the food is one driver, though many changes in our society are associated with depression and other mood disorders.

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You Can’t Outrun a Bad Diet

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Inquiring minds want to know: can’t I just exercise past my bad diet? Won’t an extra ten minutes on the elliptical trainer solve everything? Amateur Finnish triathlete Sami Inkinen tried and failed. Sami was one of the original founders of Nokia, sold his share early, and moved to the US to attend Stanford Business School. There he started the real estate website Trulia, which was bought by Zillow for $2.5 billion. In other words, Sami had more money than God—and he exercised five hours per day.

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Nevertheless, by age thirty-eight, his performance was down. His glucose tolerance test revealed that he was a prediabetic. He didn’t get it—how can a triathlete be a prediabetic? He consulted UC Davis professor and low-carb physician Dr. Stephen Phinney, who had the answer: it was the sports drinks. Caffeine has its own effect on insulin resistance separate from fructose, and together they can cause their own brand of insulin resistance and glucose intolerance, ratcheting down some of the beneficial effects of exercise.

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Point being, exercise without dietary change can help to affect five of the eight subcellular pathologies (see Chapter 7): mitochondrial dysfunction by generating newer and fresher mitochondria; insulin resistance by reducing skeletal muscle and liver fat; improvement of propensities toward autophagy and reduce inflammatory markers; and maybe even epigenetics, although this effect appears to be mediated through exercise’s suppression of inflammation. However, exercise alone won’t improve glycation, oxidative stress (exercise actually makes this worse), or membrane integrity and fluidity. In other words, you can stop some of the aftermath of bad food by engaging in exercise, but exercise can’t undo it all.

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Recognizing the limitations of exercise on health improvement, Sami, Steve, and low-carb physiologist Jeff Volek went on to found Virta Health, a ketogenic diet start-up that proves diet matters more than exercise in reversing type 2 diabetes. The results have been impressive, so much so that the former chief medical officer of the American Diabetes Association, Dr. Robert Ratner, signed on to be their chief executive officer after having previously eschewed the low-carb diet.

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Chapter 11

What Does “Healthy” Really Mean?

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Chapter 7

The “Diseases” That Aren’t Diseases

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Diseases tend to have difficult medical-technical names that no mere mortal can pronounce, so they’re often assigned more manageable monikers, based on the name of the doctor who first described it (e.g., Alzheimer’s disease), or its most famous patient (e.g., Lou Gehrig’s disease). Sometimes it’s even based on the country of origin (e.g., Jamaican vomiting sickness), on the tissue of interest (e.g., foot-and-mouth disease, polycystic ovarian syndrome), or on the symptoms expressed (e.g., fibromyalgia). However, sometimes naming the disease after the symptom can be quite cryptic. For instance, “diabetes” is a Greek word that means siphon, because you’re in the bathroom peeing your brains out, but it doesn’t say anything about glucose, insulin, or the subcellular dysfunction that causes it. Cardiovascular disease localizes the problem to the heart and blood vessels, but doesn’t really say what’s happening there or how it got that way. Hypertension tells the patient there’s high blood pressure, but unless they have such high blood pressure that they get a headache or stroke, they don’t feel it, don’t know what it means, don’t know what to do about it, or whether they should even care. Many of them will make contractions of disease processes to take the onus off—for instance, “I got the high blood,” “I got the low blood,” “I got the sugar.” They might be tempted to think that the process is just a part of normal aging, or that since their parent had it as well that it might be genetic.

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In any case, the prevailing wisdom is that these diseases are inevitable. And doctors don’t do anything to alter that illusion. I can’t tell you how many patients I’ve seen who said, “Well my mother had diabetes, so I’m not surprised I got it.” These lay formulations couldn’t be further from the truth. But do you know of any doctors who disabuse their patients of these mythologies? That’s because they don’t understand them either.

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The US population, and indeed the populations of most developed and developing countries, is verifiably sick. While this metabolic dysfunction is exacerbated by body weight, it’s not even remotely dependent on it (remember “thin-sick” from Chapter 2). Yes, the adult American population is 67 percent overweight, but the data argues that 88 percent of the population exhibits some level of metabolic dysfunction. Is obesity the problem, or the symptom (see Chapter 2)? And what do the doctors tell the other 21 percent who aren’t obese but still metabolically ill? What disease do they have? After all, if doctors don’t know how to diagnose, treat, or prevent an unknown disease, why would they even bring it up?

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Sadly, you’re going to have to bring it up. And that means being facile with the science. I offer Part II so that you have the option of understanding the science, to take ownership over it. Unavoidably, I’m going to have to introduce some new concepts and biochemistry that address food, cancer, and aging. If the science is daunting, then just skip to Chapter 9, which will provide you with the do-it-yourself approach to your own personal health and well-being.

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Metabolic dysfunction is the “disease without a name.” The cells of the body, and often of the brain, are sick, due to eight—count ’em, eight—intracellular processes that have gone awry. These eight processes are not mutually exclusive—often if you have one going on, you likely have more than one. Also note that these eight processes, when working right, contribute to longevity; but when not working right underlie the various chronic diseases that result in mortality. They’re not considered diseases per se—as they don’t have an easy lab test or biomarker. They don’t have an ICD-11 code, so they aren’t reimbursable. They don’t have a drug target (see Chapter 10), so doctors don’t talk about any of them with their patients—because why would you want to bring up something you can’t solve? It recalls a saying I learned while I was a visiting professor in Paris, “If there is no solution, there is no problem.”

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But scientists who work in the field of chronic disease do know about them. Each of these eight processes can work for you, in which case you’ll live to be one hundred playing tennis—or against you, in which case you’ll be disabled, depressed, on dialysis, or dead before your time. Further, they’re not mutually exclusive—each interacts with the others, and so they tend to cluster together. They are the processes belying most, if not all, of the chronic diseases that are killing people and costing billions of dollars. And they are all exacerbated by processed food.

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Cell Bio 101

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To explain these eight subcellular pathologies, I first have to explain a cell and its contents. That means an ultra-short course in cell biology. For this exercise, I’ll limit the syllabus to energy metabolism only, which is the root of all eight subcellular pathways.

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The cell is nature’s basic building block of life. Each of us is composed of ten trillion cells, most of them specialized and residing in different organs. In order to stay alive, a cell has to burn energy. Any cell can (and normally does) burn glucose, a simple sugar and the building block of starch. The liver and adipose (fat) tissue need the hormone insulin (released from the pancreas) to open the metabolic door within the membrane, the bag that holds the cell together, to let the glucose enter the cell; however, other organs don’t need insulin for glucose entry. But if glucose is in short supply and insulin levels are low, then adipose tissue will give up some of its stored fatty acids to enter the bloodstream, and the liver will turn those fatty acids into ketones, which then seep back into the bloodstream, so that any cell can burn those ketones instead, even without insulin.

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Cells are magicians. They either make glucose disappear, or if there’s too much, then presto-change-o, they turn glucose into fat, which wreaks havoc on metabolism. But how and when is the key. Once inside the cell (Fig. 7–1), glucose undergoes breakdown through a series of metabolic steps called glycolysis to the intermediate pyruvic acid, releasing only a small amount of energy, which is captured within a molecule called adenosine triphosphate (ATP). From there, the pyruvic acid has one of two choices: 1) either enter the mitochondria (the energy-burning factories inside the cell), where the metabolic breakdown continues, a process called the Krebs cycle, to yield a lot more ATP (and making the waste product carbon dioxide, which you breathe out from the lungs); or 2) if the mitochondria are busy or dysfunctional, the pyruvic acid diverts to a process called de novo lipogenesis (new fat-making) to turn into a fatty acid called palmitic acid, which is then bound to a glycerol molecule and exported out of the liver cell as a triglyceride particle.

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Figure 7–1: Energy metabolism 101. The cell imports glucose and converts it into pyruvic acid (glycolysis, left side), yielding two ATPs. If the mitochondria are functioning, the pyruvic acid is metabolized by the Krebs cycle (right side), yielding twenty-eight ATPs and carbon dioxide.

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These two pathways of energy metabolism, especially within the mitochondria, consistently release toxic by-products inside the cell called oxygen radicals (kind of like what hydrogen peroxide does on a wound). If not detoxified, these can damage the cell, and even cause it to die. Therefore, the cell has another structure called a peroxisome, which is where various antioxidants are stored to neutralize the oxygen radicals.

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Glycation

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Why do we get cataracts and wrinkles as we get older? Each of these is an example of an undeniable and inevitable fact of life—the Maillard or glycation or browning or caramelization reaction. All four terms describe the same process, which is the primary process of aging. First described by Professor Louis Camille Maillard in 1912, this process occurs in all living cells. It doesn’t need any energy or enzymes or cofactors or other nutrients, it just happens. It’s a by-product of living, yet it’s the primary reason for dying. We’re all browning, all the time, and the only way to stop it is by dying. The faster the Maillard reaction occurs, the faster you age—you get wrinkles, your arteries become sclerotic, and you eventually reach the pearly gates. But you can slow this process down—and if you’re successful, you’ll be a lot healthier for a lot longer.

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The Maillard reaction only needs two molecules to occur: a carbohydrate (fructose or glucose), plus an amino acid (e.g., proteins). Put them together and the protein starts to “brown” and become less flexible. Ideally, these damaged proteins will be cleared away by cellular waste processing systems, but if the reaction occurs faster than the waste can be cleared, eventually the buildup of advanced glycation end products, or AGEs, will lead to cell, organ, and human dysfunction. The question is not if the Maillard reaction will occur, but rather how fast.

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And this is where the metabolic differences between glucose and fructose becomes important (see Chapters 2 and 12). One might think that glucose and fructose, both being molecules found in dietary sugar (sucrose, high-fructose corn syrup, honey, maple syrup, agave—they’re all metabolically the same; take your pick), would drive this reaction at the same rate. You would be very wrong. Yes, they’re both carbohydrates, and yes, they both bind to proteins, but that’s where their similarities end. Because glucose has a six-member-ring structure (see Fig. 7–2), it’s more stable and engages in the Maillard reaction relatively slowly. Conversely, fructose’s five-member ring is more easily broken apart, and engages in the Maillard reaction seven times faster than glucose. It also generates one hundred times the number of oxygen radicals (see Oxidative Stress). Furthermore, our research group has shown that a specific breakdown product of fructose, called methylglyoxal, drives the Maillard reaction 250 times faster than glucose.

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All in all, when it comes to aging, fructose is worse than glucose, and therefore sugar is worse than starch. That doesn’t make glucose “good”—it raises insulin and drives obesity—but compared to fructose, it’s a walk in the park.

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Oxidative Stress

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Oxygen (O2) is a peculiar molecule. Our brain is completely dependent on it; in fact, the brain dies in four minutes flat without oxygen, while the rest of your body can keep on living. However, many types of cells grow specifically when they’re deprived of oxygen; this is particularly true of cancer cells (see Chapter 8). Oxygen also has the unique capacity to create an inhospitable environment for foreign invaders (like bacteria), but also for our own cells.

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Figure 7–2: Structures of a) glucose and b) fructose, in the linear form and the ring form. This figure demonstrates that a sugar is not a sugar. Glucose is a six-membered ring and is more stable than the five-membered ring of fructose, which breaks down more easily to the linear form. Only the linear form can engage in the Maillard reaction. Therefore, fructose drives the Maillard reaction seven times faster than glucose, causing seven times the damage.

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Inside our white blood cells, oxygen undergoes a reaction catalyzed by an enzyme called superoxide dismutase (SOD), which turns O2 (the stuff we breathe) into O2—, an oxygen radical or reactive oxygen species, similar to how water (H20) can be turned into hydrogen peroxide (H2O2). When you put hydrogen peroxide on a wound, it bubbles and fizzes as the liberated oxygen radicals kill everything in sight. And that’s great if you’re cleaning a wound. But this process occurs in all of our cells all of the time. Oxygen radicals are a standard by-product of three normal reactions in the body: glycation; energy metabolism in our mitochondria; and iron metabolism (equivalent to rusting, which is constantly occurring in all of our cells). Furthermore, oxygen radicals are formed in response to anything that causes inflammation. Thus, each cell in our body ordinarily has to deal with an oxygen radical pool; if unleashed they would kill us pretty quickly.

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Each of our cells possesses specialized subcellular organelles called peroxisomes, which is where antioxidants lie in wait to quench incoming oxygen radicals and render them inert (see Chapter 19). But if there are more oxygen radicals than antioxidants (termed oxidative stress), it causes cellular dysfunction, structural damage to lipids, proteins, or DNA, and in the extreme, cell death. When this happens in the liver and the pancreas, you get diabetes. It’s also why we need to consume Real Food that has color, because color is an indication that these plants contain the antioxidants we can’t make on our own.

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Mitochondrial Dysfunction

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Imagine an old-style factory with a coal-burning furnace. The coal is transported on railroad cars, and there are able-bodied furnace stokers working in shifts to feed the furnace. As long as the rate of arrival of the coal and the offload by the stokers are matched, the factory runs at full capacity. Now imagine that many of the furnace stokers are old and infirm, or perhaps stricken ill at once. There just aren’t enough stokers for continual twenty-four-hour work. As a result, they’re not going to generate enough energy for the furnace to burn at full capacity, and the factory will not put out the best product. There’s also the scenario where the railroad cars filled with coal start arriving inside the factory walls faster than the furnace stokers can unload it—the cars build up, taking over the factory floor, and eventually the factory will be overwhelmed, will choke off, and shut down.

Now imagine both of these issues happening at the same time. That’s mitochondrial dysfunction. Chronic disease is mitochondrial dysfunction, and mitochondrial dysfunction is chronic disease. They are one and the same.

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Mitochondria are really bacteria that decided eons ago that they were happier living inside of animal-based cells than facing the cold, cruel world on their own. Bacteria were great at burning energy, while animal cells were great at fending off invaders—so they made a symbiotic decision to stick together. To this day, mitochondria have their own DNA and their own genetic program apart from the human DNA found in the nucleus of the cell. But like the shift workers, mitochondria tend to go defective with time and are prone to oxidative stress and damage. Mitochondria are finicky, lose capacity easily, and constantly need to be renewed and replenished. They need to divide, and the cell needs to clear the old ones out. The single best stimulus to make more and fresh mitochondria is exercise—but even your mitochondria can’t outrun a bad diet (see Chapter 10). Not surprisingly, the pharma industry has identified increasing mitochondria as a primary drug target for metabolic disease—yes, they believe you can market “exercise in a pill”—but there is no magic pill.

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When glucose and oxygen availability, as well as mitochondrial capacity, are all matched, everything goes smoothly. Using the coal factory analogy, when the glucose comes in faster than the mitochondria (stokers) process it, the excess chokes off the factory. The mitochondria have no choice but to divert the excess pyruvic acid into fat, a process called de novo lipogenesis (new fat-making). When this happens in the liver, you get fatty liver, which leads to liver insulin resistance (see Insulin Resistance). If instead this happens in the pancreas, you get fatty pancreas and insulin deficiency. And fructose (in processed food) makes twice as much liver fat as does glucose.

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The sicker your mitochondria, the earlier you die. The organs that need mitochondria and energy production the most are the brain and hormone-secreting organs—because neurotransmission and hormone secretion are energetically expensive. If the mitochondrial DNA is defective, you end up with a class of nasty diseases known as mitochondrial encephalomyopathies. I took care of one girl with a mitochondrial disease called Kearns-Sayre syndrome who came to my practice at age nine with seizures and droopy eyelids (keeping your eyes open is a high energy task!). Over the next ten years, she slowly developed diabetes, a heart rhythm disturbance, inability to walk, and finally went comatose at age twenty. She died at twenty-three, and there was nothing we could do for her. Mitochondria can be defective because of genetics, or because of the pathologies discussed in this chapter. Either way, the results are disastrous.

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Insulin Resistance

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As we’ve explored, most people think of insulin as the “anti-diabetes” hormone; it lowers the blood glucose, which prevents diabetic microvascular complications (eye, kidney, nerve disease) from occurring. This is only half of the story. Insulin’s main job is actually to store energy for a rainy day.

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Just two organs in your body need insulin to function: the liver and adipose tissue. Too much insulin can get in the way, forcing glucose clearance from the bloodstream into tissues. It can also lead to hypoglycemia (low blood glucose) and inadequate glucose delivery to the brain, which can make you dizzy or unconscious or seize or die, depending on its severity. The pancreas senses the drop in the blood glucose, and stops releasing insulin before you lose consciousness.

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But nowadays, more often than not, the opposite problem occurs; different types of cells are not responding to the insulin in the bloodstream. This is called insulin resistance. When glucose can’t get into certain cells, those cells starve, which leads to organ dysfunction. When the liver or muscles are resistant, glucose builds up in the blood, leading to diabetes. The fact of the matter is that insulin resistance isn’t due to low insulin levels, but rather high ones—because the cell isn’t responding to the insulin signal. Of course, genetics can play a role—but then again, genetics haven’t changed in fifty years, but the environment sure has.

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Various problems that can lead to defective insulin signaling are: obesity; chronic stress; environmental chemicals that drive weight gain (obesogens like estrogen, bisphenol A [BPA], phthalates, PBDE flame retardants); and, our favorite, processed food (see Chapters 18, 19, and 20). High insulin levels cause cellular dysfunction, which ultimately leads to chronic disease, morbidity, and early death. Insulin resistance is the central problem in metabolic syndrome, and different people can have different reasons for insulin resistance—but processed food is by far the biggest player. Even those who are overweight and those who are under stress don’t exhibit metabolic syndrome if their diet is unprocessed.

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Membrane Integrity

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Every cell has an outer membrane to protect and contain its contents. When membranes get damaged, cells spill their contents and all hell breaks loose, usually leading to cell dysfunction and death. Then the mop-up crew follows behind and does even more damage during the cleanup (see Inflammation).

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Membranes are composed of a lipid bilayer, like a sandwich; lipids on the inside facing the cellular contents, lipids on the outside of the cell facing the bloodstream, and proteins forming the filling of the sandwich. Membranes can be damaged through two mechanisms: the lipids themselves are damaged either from toxins or from oxidative stress (see Oxidative Stress); or the lipids are inflexible, like rubber tubing where cracks appear due to plastic that has gotten old and dried out. Membranes should be flexible and malleable like a balloon, called membrane fluidity—they should give somewhat when poked from one direction. When they don’t, they can burst.

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There are seven different types of fats in your diet, and all can impact your cell membranes in different ways. But for this exercise, we only need to consider three of them, as shown in Fig. 7–3.

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Figure 7–3: a-c) Structures of free fatty acids. a) palmitic acid (16-carbon saturated), b) trans-palmitoleic acid (16-carbon trans-unsaturated), and c) cis-palmitoleic acid (16-carbon cis-unsaturated). Note that the COOH carboxyl group (which is inflammatory) is free. d: Structure of a triglyceride, which is composed of three different free fatty acids (at least one of which must be unsaturated), linked to a glycerol backbone, so that the inflammatory COOH carboxyl groups are not free and available to do damage.

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Problems with lipids can damage outer membranes in one of two ways. First, saturated fatty acids (which are different from saturated fats; see Chapter 12) are completely flexible because they don’t have any double bonds, which normally apply a degree of inflexibility to a fat’s structure. This means that saturated fatty acids can conform in any shape, which normally is good for membrane integrity. However, new research suggests that because they’re so fluid, they can sometimes layer on top of each other and form a clump of lipid within a membrane, the subcellular version of cellulite, which reduces the cells’ overall fluidity.

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Unsaturated fats are almost always better for you than saturated ones, which themselves are none too problematic in regard to metabolic syndrome. Because of their cis-double bonds, unsaturated fatty acids have fixed angles built into them, which prevents them from layering. But there are two problems with unsaturated fats. First, those cis-double bonds are exactly where toxins and oxidative stress like to do their damage, by oxidizing that double bond. And when they do, they release an oxygen radical (see Oxidative Stress). Second, when an unsaturated fat is heated beyond its smoking point, the cis-double bond can “flip”—and now you’ve got a trans-fat, which is deadly to the cell (see Chapter 20). Even though the FDA finally got around to banning trans-fats in commercial foods, you can still accidentally make them on your own (see Chapter 18).

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Inflammation

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Foreign invaders (e.g., viruses and bacteria) can damage cells directly. Our body has developed an inflammatory response, which recruits various white blood cells to release toxins like oxygen radicals and cytokines (peptides with killing activity) to destroy the invaders. While we need an inflammatory response (or we would be eaten by the maggots), unfortunately there are four downsides.

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The process kills normal tissues, too, which can lead to long-standing damage after the invader is cleared (e.g., kidney disease after E. coli, coronary aneurysms after Kawasaki disease, and now we are learning about long-term damage with COVID-19).

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The inflammatory process can sometimes be triggered against a body tissue because a body tissue molecularly resembles a foreign invader, a phenomenon called molecular mimicry. This is why, for instance, some people develop rheumatic fever, kidney disease, and even psychiatric disease after a strep infection.

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Bad bacteria can proliferate in the gut in response to an aberrant environment (either the food itself or the antibiotics in the food; see Chapter 20), which can cause pathogenic bacteria to predominate, such as Streptococcus mutans in the mouth and dental caries. The inflammatory reaction will cause breaks in the intestinal barrier, allowing toxins and bacteria to pass across the intestinal wall into the bloodstream; they then head to the liver and cause insulin resistance, a process known as leaky gut. Leaky gut is one reason for the dramatic increase in food allergies and autoimmune disease in people (see Chapter 14).

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Body fat (subcutaneous or visceral fat) can release palmitate, an inflammatory lipid, which in turn drives up the inflammatory response. Palmitate can also be formed in the liver in response to excessive sugar intake, resulting in liver inflammation, which makes chronic disease even worse. In fact, palmitate is the real bad actor in the story of metabolic syndrome (see Chapter 12).

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There are connections between metabolism and inflammation in both directions. For instance, when fat cells get so large that they spill their grease, macrophages come into the fat depots to mop it up, and then release a set of cytokines that directly interfere with liver insulin signaling, driving chronic disease.

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There are also connections between specific foods and inflammation. For instance, increased dietary fructose reaching the liver spurs on an enzyme called c-Jun N-terminal kinase-1 (JNK1 for short), which inactivates the insulin signaling pathway as well.

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The key to the chronic disease kingdom is that there are not four separate problems (nutrition, metabolism, inflammation, immunity); there’s only one, and they are all related. Screw up one and you screw up the other three.

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Epigenetics

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Lots of effort has been placed on looking for genetic reasons behind metabolic syndrome, but the studies say only 15 percent is genetic—the rest is environmental. But environment can change genes as well, through a phenomenon called epigenetics. Epigenetics refers to changes in the areas around our genes that can cause them to be turned on or off, usually inappropriately, altering responses to these pathologies, and which over time can result in the development of various diseases.

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Think of it this way: epigenetics is the on-off switch attached to the dimmer on your living room chandelier. The gene is the lightbulb, the epigene is the light switch. If the lightbulb is defunct or the switch is frozen in the “off” position, the dimmer function is useless. Likewise, epigenes control the effect to which the gene turns on. Epigenetic modifications acting on various tissues typically only influence the physiology of the exposed individual, changing the risk of disease development later in life. This might partly explain the developmental origins of health and disease.

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In some cases, environmental factors alter the epigenetic programming of germ cells in the sperm or egg, and alterations in disease can appear in future generations without further direct exposure. This is known as transgenerational epigenetic inheritance. So far, it’s been shown to affect as many as four generations going into the future. So it’s not just what you ate; it’s what your mother ate. In fact, it’s what your great-great-grandmother ate. And as you can imagine, if each person has two offspring, these epigenetic changes can multiply across the population pretty fast. These changes might be a plausible partial explanation for the pandemic of obesity and related diseases that cannot be fully accounted for by genetic variations and lifestyle factors.

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Altered nutrition also appears to be a primary driver of altered epigenetics. For instance, take the vitamin folic acid, a necessary and limiting cofactor for the nuclear enzymes called DNA methyltransferases (DNMTs), which adds a methyl group to DNA to alter whether genes are being activated. Folic acid is so important to normal fetal development in order to prevent the occurrence of spina bifida that the FDA has remanded the baked goods industry to add it to grocery store– bought bread. In addition, folic acid is necessary to catalyze the breakdown of a metabolite called homocysteine (Hcy; see Chapter 9), which has been linked to one form of early heart disease, although its role in general heart disease remains controversial. Some people carry a mutation in the gene that activates folic acid; these people have higher Hcy levels and greater risk for heart disease, but supplementing their diet with extra folate can reduce some of their risk.

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Other nutrients such as vitamin B12 (cyanocobalamin), vitamin B6 (pyridoxine), vitamin B2 (riboflavin), methionine, choline, and betaine are also involved in epigenetics. And nutrients such as retinoic acid, resveratrol, curcumin, sulforaphane, and polyphenols can also modulate it (see Chapter 14 for more on supplements).

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Last, epigenetics has also been shown to be at work in the long-lasting effects of some endocrine-disrupting chemicals (EDCs), which mimic hormonal actions and alter long-term metabolism. Examples include elements that come in contact with our processed food supply, such as BPA and phthalates found in processed food cans and plastic bottles (see Chapter 20), both of which can lead to insulin resistance and obesity.

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Autophagy

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Clearing biological waste products is a process known as autophagy, and it plays a key role in healthy aging, especially in the brain. The brain uses more energy than any other organ, and so there are lots of mitochondria, oxygen radicals, and therefore lots of damage in it. Omega-3 fatty acids (see Chapter 19), which we need for healthy brain functioning, are particularly susceptible to damage—which equals lots of cleanup.

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And as you might imagine, there’s not a lot of extra room in the brain for this waste, so the brain has to be particularly adept and rapid at removing debris. That’s what sleep is for—our intracerebral pressure goes down during sleep, which opens small pores within the brain called glymphatics. An ebb tide fluid shifts slowly during sleep to remove damaged cellular components into the bloodstream for disposal. In other words, in the brain, every night is garbage night. And if you don’t get enough sleep, it’s like having your brain’s garbagemen on strike.

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But this isn’t just good for the brain—all organs do better with autophagy, which is an essential process that maintains healthy cells by removing damaged proteins and malfunctioning organelles, especially mitochondria. Old mitochondria make a lot of oxygen radicals. Therefore, to improve metabolism and slow aging, it’s essential to get rid of the old mitochondria by autophagy. In fact, people who clear their mitochondria more efficiently live longer.

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There’s also evidence to support that autophagy is under various nutritional controls. For instance, vitamin D deficiency is associated with cellular aging; and vitamin D appears to play an important role in promoting autophagy, by increasing calcium influx into old cells, which induces a cellular program to purposefully kill it. Paradoxically, vitamin B1 deficiency accelerates neurodegeneration, while supplementation appears to promote autophagy and slow neurodegeneration, by reducing oxygen radical formation. The biggest effect of nutrition on autophagy has to do with the metabolic improvements that can be seen with the now-popular maneuver of intermittent fasting, which lowers insulin and raises ketones, both of which promote autophagy (we’ll get into more detail in Chapter 14).

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The “Hateful Eight”? or the “Grateful Eight”?

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As you can see, none of these eight processes evoke disease outright. In fact, when they are working right, they contribute to longevity and good health. But, screw up a few, and you have the makings of a very short and miserable life. More important, all eight processes are related to chronic disease, and also related to each other and to food. See a pattern here? These are the true diseases of processed food; they’re just not called diseases or taught in medical school. But they should be taught before any mention of any drug, so that medical students can triangulate, “How does this drug impact these eight processes?” Only in this way can we unlearn doctors to focus on what’s important and patients to understand the limits of disease therapy. Otherwise, both Big Food and Big Pharma win again and again and again.

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Chapter 8

Checkpoints Alpha, Bravo, Charlie: Nutrient-Sensing and Chronic Disease

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Food drives both illness and wellness; it’s the poison and the antidote. Metabolic syndrome could colloquially be redefined as cells eating badly, as every one of the eight subcellular pathologies is made worse by providing the wrong food in the wrong place at the wrong time. In fact, there are really only two processes that handle energy properly—growing or burning. And there are two proper outcomes—living or dying. Every cell has to grow at one time in its life versus burn at another time—but never both at the same time. Similarly, every cell has to live and die, but clearly not both at the same time.

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What determines when a cell grows or burns, and what determines when a cell lives or dies? What if a cell is burning when it should be growing, and living when it should be dying, or vice versa? Any perturbation of the growing/burning or living/dying pattern will lead to disease. It’s through this lens where we find the clues to the real reasons for metabolic syndrome (spoiler alert: it’s processed food!), and also for both treatment and prevention. It’s complex science, so feel free to skip to Chapter 9, but it’s very cool; it’s Nobel Prize– winning work—twice.

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Oxygen Is So Overrated

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Does life need oxygen? Plant life clearly doesn’t. In fact, green plants need carbon dioxide for photosynthesis, making oxygen as the by-product. But does animal life need oxygen? The first clue to this puzzle came in 1924. German biochemist Otto Warburg made an astounding observation—cancer cells didn’t need oxygen to grow.

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So regular cells need oxygen, but cancerous ones don’t? Aren’t cancer cells just regular cells sped up? They divide way faster than normal, which is why some chemotherapies work—they poison the dividing process (called mitosis). But how can growing cells not need oxygen? Doesn’t every cell need oxygen?

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The answer is a resounding no. In fact, there’s very little oxygen in the gut. The intestinal microbiome has adapted to it; 99 percent of the bacteria in our intestine, called obligate anaerobes, don’t need oxygen. In fact, many bacteria grow just fine without it and don’t have mitochondria.

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But that’s all the bacteria in your gut do—they grow. They don’t burn. They generate a lot of lactic acid, because that’s the waste product of glucose metabolism without oxygen, but those bacteria stay (or, at least, are supposed to stay) in the gut. Your muscles can also produce lactic acid, which causes pain when you’ve run a marathon (so I’ve heard, but running a marathon is still on my bucket list). The bacteria in your gut don’t make or release stuff. They divide and increase in mass, just like cancer cells. Cancers double every fifty to two hundred days. And they make boatloads of lactic acid in the process.

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Any idea about what cells grow even faster than cancer cells? Fetal cells. A sperm and an egg meet, called fertilization, to make one cell called a zygote. That zygote doubles (divides in two) over and over to achieve 36 doublings (236 cells) over 270 days of pregnancy for a total of 68 billion cells at birth; that averages doubling about every 7.5 days. This growth happens in the lowest oxygen environment imaginable (the placenta delivers to the fetus a partial oxygen pressure of 30 millimeters of mercury (30 mm Hg), compared to the 100 mm Hg that the lungs deliver to adult cells). So how do fetal cells grow so fast with so little oxygen?

The discovery of the metabolic signal for this effect that drives cancer and fetal cells to grow without oxygen is so important the Nobel Prize was awarded to its discoverers (Gregg Semenza, William Kaelin Jr., and Peter Ratcliffe) in 2019.

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If you’re a cell in growth phase without oxygen—making structural components and the by-product lactic acid—do you even need mitochondria? Do you even want mitochondria? There are only four states of increased lactic acid production in humans: post-exercise, cancer, mitochondrial diseases like Kearns-Sayre syndrome (see Chapter 7), and metabolic syndrome—because that’s mitochondrial dysfunction as well. As cells divide, mitochondria have to divide, too (remember they have their own DNA); and they can’t divide fast enough to keep up with the cell’s growth, especially in cells that are growing rapidly—meaning mitochondria become an unwanted luxury for a rapidly growing and dividing cancer cell or fetal cell. However, these cells still need to generate ATP (the fuel of your cell) to power them.

How do they do that without mitochondria or oxygen? This conundrum perplexed scientists until recently.

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Blood Flow Restriction for Muscle Growth

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This phenomenon of growth without oxygen has recently been exploited to treat a common disease of aging, called sarcopenia, or loss of muscle mass. As people advance into their seventies, they can lose half their muscle mass, which renders them frail and susceptible to falling and fracture. To treat this, exercise physiologists have started putting tight bands around the patient’s arms and legs with low-intensity resistance and endurance training. Lo and behold, muscles increase in mass and strength—because depriving muscle cells of oxygen switched them from burning to growing.

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Two Metabolic Programs—One for Growth, One for Burning

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Growing cells need all sorts of structural components in order to divide and make new cells. They need lipids for membranes, ribose (a 5-membered monosaccharide) as the backbone for DNA and RNA, and amino acids for proteins. Where do all of these building blocks come from?

They’re not imported in the blood, but instead are created on-site from available materials. Imagine a piece of wood in your house. That wood could be used to make furniture, or it could instead be used for firewood, but not at the same time. It’s the same for glucose inside the cell. Will it be used for growth and structural components, or will it be burned? There are two linked metabolic pathways inside the cell; when the cell is burning, they run in tandem, but when the cell is growing, they can dissociate from each other (see Fig. 7–1).

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The first pathway is called glycolysis (see Chapter 7), which prepares glucose to be used for structural components, and pyruvic acid is the end product. If the pyruvic acid is not used for burning in the next stage, it can leave the cell as lactic acid. Glycolysis provides the added bonus of generating a grand total of two ATPs, all without needing oxygen.

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The second pathway is called the Krebs cycle (see Chapter 7). The pyruvic acid enters the mitochondria, where it burns all the way to completion, at the end of which you have twenty-eight ATPs and carbon dioxide. If the goal is burning (e.g., aerobic exercise), you need both glycolysis and the Krebs cycle working in tandem. If the goal is structural components for growth (e.g., blood flow restriction, or bodybuilders using high-intensity interval training to build muscle mass), then you only need glycolysis, and the pyruvic acid will be diverted for building muscle.

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Nutrient-Sensing, Kinases, and the Setup for Chronic Disease

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Both of these pathways, glycolysis for growth and the Krebs cycle for burning, are adaptive. Basically, they’re the superhighways of your cell. If they get blocked, then the detours can be highly excruciating, even killing you. Essentially, when energy metabolism goes awry, those eight subcellular pathologies of Chapter 7 become maladaptive. And this is where processed food becomes maladaptive.

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There are three protein checkpoints (like traffic lights) inside the cell called kinases that determine what happens to each molecule of glucose or fructose; these are turned on and off within seconds by the addition of a phosphate molecule generated from the food we eat. When the three checkpoints (which we’ll call Alpha, Bravo, Charlie) are coordinated in one direction, you get growth. When they are coordinated in the opposite direction, you get burning. But when they are uncoordinated, that’s when you get a traffic jam and chronic metabolic disease happens.

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Figure 8–1: The three enzymes that determine cell fate. PI3-kinase lets glucose into the cell; AMP-kinase directs that energy either to produce structural components for the cell or to enter the mitochondria to burn all the way to carbon dioxide; and mTOR determines whether the cell lives or dies.

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Checkpoint Alpha: Phosphatidylinositol-3-kinase (PI3-kinase)

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Glycolysis generates a total of two ATPs from a glucose molecule, hardly enough to power a cancer cell. But who said anything about just one glucose molecule? Cancer cells import two hundred times the amount of glucose than normal ones do—meaning they’re not making two ATPs, they’re making four hundred. Lewis Cantley of Weill Cornell Medical College in New York City showed that this first enzyme, called PI3-kinase, opens the glucose floodgates of the cell. Lots of glucose entry means that cell has lots of fuel to power itself, all without mitochondria or oxygen. No wonder cancer cells and fetal cells have high levels of PI3-kinase.

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So could blocking PI3-kinase stop cancer? Originally, drug trials of PI3-kinase inhibitors had been disappointing, until Cantley’s group showed that if you first cut down on insulin signaling by reducing the amount of dietary refined carbohydrate, then the PI3-kinase inhibitors became much more effective. Insulin drives cancer cell growth because it’s how the glucose gets into the cell in the first place; it’s the key to the door, and PI3-kinase determines how wide the door swings open. Insulin and PI3-kinase work together to flood the cell with glucose.

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Checkpoint Bravo: Adenosine Monophosphate-kinase (AMP-kinase)

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OK, the glucose is now inside—then where does it go? If the cell is low on energy, it needs to burn. The second checkpoint, AMP-kinase, is the cell’s fuel gauge. It knows the difference between full and empty. When a cell has used up its ATPs, the mitochondria need to burn pyruvic acid completely, to generate twenty-eight new ATPs to replete the cell’s energy stores (with the waste product of carbon dioxide). AMP-kinase has the added bonus of signaling the cell to make more mitochondria in order to burn more glucose to make even more ATP. Anything that gooses AMP-kinase, like exercise or the anti-diabetes drug metformin, will keep mitochondria functioning optimally and improve insulin sensitivity.

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But on the other hand, when a cell has too much ATP, AMP-kinase gets turned off. Mitochondria aren’t burning, and the cell will divert the pyruvic acid to make structural components. Anything that impairs AMP-kinase will drive fat synthesis and worsen insulin resistance. And what food impairs AMP-kinase the most? Sugar, of course.

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Checkpoint Charlie: Mammalian Target of Rapamycin (mTOR)

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If a cell has plenty of energy but limited oxygen or mitochondria, it may decide to divide; while if a cell has adequate oxygen and glucose, it may just hang out. Finally, if a cell has limited energy and is getting old, it may decide to die to make room for new ones (autophagy). What signals this three-path Rubicon of fate? That’s the job of the third checkpoint, mTOR, which determines a cell’s commitment to growth, quiescence, or death.

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The discovery of mTOR highlights its central role in cell fate. In the late 1970s, a soil sample from Rapa Nui (the native name for Easter Island) yielded a compound called rapamycin that had bizarre effects. Rapamycin turned out to be not just an immunosuppressant, or an anticancer drug, or a fungicide—but all three at once because it alters the growth phase of the cell. mTOR determines whether a cell lives or dies, so autophagy can clear out the debris. It’s the major regulator of growth in animals and the key link between what’s in the cell versus what happens to the cell. mTOR is the holy grail of cell fate, and the target of most current longevity drugs. However, because it’s so multifaceted, the medical establishment hasn’t yet figured out how to harness its power.

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As you might expect, mTOR is highly sensitive to diet. A high protein composition of your diet activates mTOR, thereby promoting cell division, development of lean body mass, insulin sensitivity, and bone and cardiovascular health. Conversely, caloric deprivation (see Chapter 14) leads to lowering of ATP levels, which reduces mTOR, making growth an impossibility. Also, activating AMP-kinase can shut down mTOR in its tracks because now you’re burning, not growing. So while mTOR is its own checkpoint for cell survival, it’s also dependent on the cell’s AMP-kinase status. This will become important when we see how dyssynchrony of these three checkpoints can cause chronic disease.

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Growth Versus Burning, and Everything in Between—the Eight Combinations

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These three enzyme checkpoints together explain how the cell metabolizes energy: PI3-kinase imports glucose into the cell; AMP-kinase directs the energy to mitochondria for burning; and mTOR determines whether a cell lives or dies. While cell metabolism has everything to do with energy, it has nothing to do with calories. It’s not calories that drive growth or burning, it’s what the chemicals that reach the cell, and especially the mitochondria, do to these three enzymes. And it is these three enzymes that show why everything we thought we knew about nutrition is wrong.

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Here’s why. Each of these three enzymes can exist in one of two states—on or off. Therefore any cell’s metabolic status can be described by one of a total of 2 x 2 x 2, or 8 different combinations of these three enzymes. I want to state that this is a hypothesis, not proven—but this is a new way to think about the role of diet and nutrition, and it fits the available scientific data of nutrients and their effects on growth, burning, and disease. One biochemical constraint on this hypothesis is that when AMP-kinase is turned on, it preempts mTOR, which turns off. These three enzymes explain health and longevity when they are working in harmony, but when dyssynchronous they explain the eight subcellular pathologies, metabolic syndrome, and even cancer.

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Table 8–1 numerically lists each of these eight combinations. The combinations of the three enzymes for normal growth are listed in column 1, and for normal burning in column 2; both of which are needed for the cell to survive, and programmed to occur at different times in your life. But when the combinations of those enzymes are dyssynchronous, which means energy is not being handled in a normal way, it sets you up long-term to develop a disease. The scenario for each combination and its metabolic result follows. For instance, neurons are supposed to burn, not grow—but if the combination is defective, they can turn into a neuroblastoma, a devastating pediatric tumor. Any of the other combinations (columns 3 to 8) occur due to an energy fork-in-the-road, and can lead to one or more chronic pathologies, which if unchecked could foment different types of NCDs. We don’t know that the last two combinations actually occur (because when AMP-kinase is turned on, it preempts mTOR), but they make sense to include for completeness. Each of these permutations are subject to dietary manipulation, either for good or for bad.

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PI3K +, AMPK–, mTOR +

This combination leads to growth and occurs in the absence of oxygen. When PI3-kinase and mTOR are turned on and AMP-kinase is turned off, cells will import lots of glucose, and use it to make lipids for membranes, amino acids for proteins, and ribose for DNA. It can also increase the risk for cancer; every time a cell divides there’s a chance that a mistake will be made in the DNA copying, which could lead to cancerous mutations.

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PI3K–, AMPK +, mTOR–

This combination leads to burning in the presence of oxygen. Because PI3-kinase is turned off, glucose will be in low supply, thus glycation and oxygen radical formation will be low. More AMP-kinase means healthier mitochondria. Since mTOR is turned off, old cells can be cleared. Risks for metabolic syndrome and cancer development are low.

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PI3K +, AMPK–, mTOR–

This combination leads to classic metabolic syndrome. Glucose enters the cell but mitochondria aren’t activated, so it has nowhere to go. Glycation, oxidative stress, and inflammation will increase. Even though mTOR is turned off, the high glucose supply will mean that the cell will likely not die of autophagy. Insulin will be high, driving production of lipids/fat, and eventually type 2 diabetes.

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PI3K–, AMPK–, mTOR +

This combination is likely to lead to early aging. Without glucose flooding the cell, glycation and oxidative stress is low and cell damage will be slow. Lack of AMP-kinase means mitochondria won’t be generating oxygen radicals. But because mTOR is turned on, there is no autophagy, and damage will accumulate slowly.

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PI3K–, AMPK–, mTOR–

This combination is likely to lead to early cell death. Less glucose is imported, but it’s not being burned; and there is also increased autophagy. The cell is likely to die more easily, allowing for quicker turnover, and very little risk for cancer; but excessive early death could lead to organ dysfunction.

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PI3K +, AMPK +, mTOR–

This combination is likely to lead to low-level inflammation. It is similar to (5), but with more autophagy, so there would be less long-term damage.

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PI3K +, AMPK +, mTOR + becomes–

This is similar to (6). This combination is likely to lead to high-level vascular injury and heart disease. Increased glucose entering the cell means glycation and oxidative stress. The glucose will be burned by mitochondria; as AMP-kinase partially inhibits mTOR, there will be some but not complete autophagy, and some clearing of dead cells. This could result in heart disease.

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PI3K–, AMPK +, mTOR + becomes–

This is similar to (2) and should lead to burning, occurring only in the presence of oxygen. Not much glucose, and the burning is aerobic, so not much oxidative stress, and mTOR reduced.

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As you can see, these eight combinations of three enzymes (on or off) will cause cells to grow, burn, or create disease. Does this hypothesis stack up with the data in the literature? One way to assess its veracity is to look at the effects of specific drugs utilizing these enzymes on the cell and the organism. We have data on PI3-kinase inhibitors, AMP-kinase stimulators, and mTOR inhibitors at our disposal, and they demonstrate reduced cancer growth and increased longevity, therefore supporting this hypothesis.

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Again, the scourges of chronic disease are all about how energy is handled at these three checkpoints. And each checkpoint is modulated by your diet. However, there’s currently no blood test to measure any of these checkpoints. So what can you or your doctor do to assess your health? Chapter 9 will show you how to use the information your doctor gleans from standard tests in order to diagnose yourself. It’s time to take charge of your own health, because no one else will.

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Kinase

PI3K

—

AMPK

—

mTOR

—

+ —> —

Normal Growth

Normal Burning

Metabolic Syndrome

Early Aging

Early Cell Death

Low-level Inflammation

Becomes #6

Becomes #2

Table 8–1: The activity of three enzymes (PI3-kinase, AMP-kinase, and mTOR), in two different states (on [+] or off [–]), leads to eight separate permutations. In any given cell at any given time, each enzyme can either be (+) or (–), although AMP-kinase (+) activation automatically results in mTOR (–) inactivation; thus combinations 7 and 8 are theoretical.

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Chapter 9

Assembling the Clues to Diagnose Yourself

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Nutrition vs. Nutritionism

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Nutrition is the most important and malleable factor influencing people’s life span (how long we live) and health span (how well we live). Studies on fraternal vs. identical twins show that genetics account for 25 to 30 percent of a person’s longevity. The other 70 to 75 percent proves that while favorable genetics clearly play a role, the environment, including a bad diet, can easily overcome those gifts, hence why the US has seen reduced life expectancy four years in a row. It’s impossible to specifically calculate what percentage of someone’s life span is attributable to nutrition, but given what’s happened to chronic disease incidence, prevalence, and severity statistics over the last fifty years, food plays a huge role. It always has.

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Since the publication of The Omnivore’s Dilemma (2006), food journalist Michael Pollan has made the point that nutrition is religion—because it requires believing without seeing. After all, nutrition must be all about what’s in the food. With the discovery of the first vitamin (B1, or thiamine) in 1912, scientists became convinced that there were chemicals in food that conferred health, so there must also be chemicals in food that conferred illness. This in turn has led to the concept of nutrients as being the lowest common denominator for any eating paradigm, giving rise to the religion of nutritionism. This is the procedure that the dietitians and the food industry have been promulgating for decades—just add up the good stuff and the bad stuff, and call it science! It’s how we got the FDA food label (see Chapter 24), which empowered the plethora of nutritional pundits on YouTube and Reddit and Medium. You don’t have to have an advanced degree to be a nutritionist. Which means that everyone is a nutritionist. And this has given rise to faith over science—because nutritionism is about zealotry.

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The Knights of the Dinner Table

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“Developed World” Kwashiorkor

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In order to understand how diet affects our eight pathologies and three enzymes, you need to understand the difference between nutrient deficiency and excess. If we feed a healthy individual with the “right” amount of calories per day—say 2,500 to 3,000—but provide only sugar as the food source (say 700 grams/day), that person will exhibit weight loss and not survive more than two to three weeks. In contrast, as we saw in the documentary Super Size Me (2004) by Morgan Spurlock, the same number of calories supplied as processed food rapidly devolves into massive weight gain with miserable and adverse health outcomes.

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It’s more than enough calories in both cases; one caused weight loss, and the other weight gain—but both put health at risk. As Mr. Spurlock developed nutrient excess (energy), he also became nutrient deficient (micronutrients). Nutrient deficiency diseases can bear striking resemblances to nutrient excess diseases.

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Recall two different diseases made known to the public in the 1960s as the US attempted to solve the malnutrition epidemic in Africa; marasmus and kwashiorkor. Marasmus babies are “skin and bones”; they don’t get enough to eat, and suffer from protein and calorie deficiency. This is what happens if you consume straight sugar for three weeks; sugar alone without any nutrients can’t even be absorbed from the intestine. Kwashiorkor is a different disease, resulting from protein deficiency without calorie deficiency. These babies have huge bellies because their livers are filled with fat—they’ve got nonalcoholic fatty liver disease (NAFLD). What caused the fatty liver? Cassava flour—a high-carbohydrate, low-fiber food, resulting in glycation, oxidative stress, mitochondrial dysfunction, insulin resistance, poor membrane integrity, and inflammation (see Chapter 7). In other words, they have “developing world” metabolic syndrome. Well, guess what? We have instead “developed world” kwashiorkor.

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People with metabolic syndrome are frequently both overnourished and undernourished. They consume plenty of calories, but they are also deficient in rare amino acids like tryptophan (needed to make serotonin) and methionine (needed to make glutathione, the liver antioxidant). They’re deficient in micronutrients once the grains have been stripped of their germ (location of the vitamins, polyphenols, and minerals).

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Another disease explains the dissociation of overnutrition and obesity with metabolic syndrome. This disease, called lipodystrophy, is a disorder of subcutaneous fat production. Because people with lipodystrophy don’t make fat cells, they are not obese; rather, any extra energy ends up as ectopic fat in the liver and muscle, which leads to all the diseases of metabolic syndrome.

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Whether people get lipodystrophy has nothing to do with calories. No surprise, whether people get metabolic syndrome has nothing to do with calories. In each case, it has to do with whether the liver mitochondria is working right to process the energy to keep itself healthy. And in kwashiorkor, lipodystrophy, and metabolic syndrome, those mitochondria are not working right, leading to those eight subcellular pathologies (see Chapter 7). That’s what chronic disease is really all about.

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Nutritional Naysayers

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There are several reasons why these truths took a back seat to mythology and why the science of nutrition took a wrong turn in favor of zealotry. First of all, most pundits in the field aren’t bench scientists or clinicians; they tend to be nutritional epidemiologists, and nutritional epidemiology has significant limitations.

Epidemiology means correlation, not causation. Like John Snow’s cholera/Broad Street pump exercise (see Chapter 2), nutritional epidemiology studies are discovery, and discovery can be very important in posing the questions that truly need answering. However, it almost never answers the questions by itself; you need to design a proper study to answer them (see below). Just because A is associated with B, does that mean that A causes B? Or could it be reverse causality (B causes A)? Or could it be intermediate causality (C causes A or B)? Could it be irrelevant (C is associated with B and D, and D causes A)? As an example, ice cream consumption correlates with frequency of drownings. Does that mean eating ice cream causes you to drown? Or do survivors of the drowned victim bury their sorrows in a baked Alaska? More likely we eat ice cream when it’s hot, we swim when it’s hot, and some unfortunate people drown when they swim. Correlation does not automatically imply a cause-and-effect relationship. But the media, in its effort to sell newspapers or snatch eyeballs, treats almost all epidemiological studies as causation. Therefore, the public doesn’t understand the difference either.

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Some investigators and news sources tout meta-analyses, an attempt to conglomerate multiple studies. It’s the gold standard to prove your point. And meta-analyses can do this well, when the individual studies are independent of industry and are also scientifically sound. But many such analyses are GIGO—“Garbage in garbage out”—as they are only as good as the data they are based on. And when the food industry is in charge, the results are suspect.

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Another reason why nutrition remains an academic backwater is because we don’t have good biomarkers (e.g., blood tests) that measure what people are actually eating. Most of the data in nutritional studies are obtained through memory recall to food questionnaires. You can see for yourself—try asking someone what they’ve eaten for the last three days. Most people can’t tell you what they’ve eaten in the last three hours. Which doesn’t even factor in that sometimes people lie, not always intentionally, but perhaps they put on rose-colored glasses when it comes to memory recall.

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For example, Leann Birch at Penn State University asked a group of eleven-year-old girls what they ate, and videotaped them while they ate it. She then divided up the group into weight tertiles—thin, normal weight, overweight—and showed that the thin and normal weight kids reported correctly, while the overweight kids underestimated the candy, soda, and desserts that they ate—except for one item. They reported their juice intake correctly because they thought juice was healthy (we’ll deal with juice more fully in Chapter 19).

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Dr. John Ioannidis, an internist and accomplished statistician from Stanford University, has proposed that we do away with nutritional epidemiology entirely, as the studies are impossible to control, the data is perennially abused, and the results are virtually guaranteed to be wrong. I disagree. There’s no doubt that people read too much into these studies, but they also need to be educated. No single nutrition epidemiology study is ever the final word, because they don’t rise to the level of causation. There are only two types of studies that can approach the rarified air of causation. One, called econometric analysis, looks at the natural history of both consumption and disease prevalence, but also accounts both for confounders and for time (time is essential to causation). Developed by iconic UK statistician-epidemiologist Austin Bradford Hill, this level of evidence provides what we call causal medical inference; the level of proof we have today for tobacco and lung cancer. The second is called randomized controlled trials (RCTs), where the investigator varies only the one nutrient under study. However, such studies must have a placebo control group to be able to rise to the level of proof.

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But, aside from study design, there’s yet another and more prescient reason why these epidemiologic studies, even those that purportedly assess causation, are suspect. They measure what goes in the mouth and assume it’s what’s absorbed in the intestine and ends up in our bloodstream—which isn’t true. Think of what really happens as analogous to eating for two. When pregnant, the mother’s intake is wildly increased over baseline. She gains weight, but we don’t care because we know about 30 percent of the energy is going to the growing fetus. Well, even without being pregnant, each of us is always eating for two, because we also have to feed our own intestinal microbiome, which receives and metabolizes about 30 percent of our ingested nutrients. If the nutrients didn’t enter our bloodstream, did we really get them?

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The discovery of our symbiotic relationship with our intestinal microbiome changed everything. We now know that we have to feed it to stay healthy. When we don’t feed it right (e.g., depriving it of dietary protein), those bacteria send blood-borne and neural signals that tell our brains to alter our behavior so that they can get the nutrition that they do need. Whether you like it or not, you’re eating for two—you’re in a symbiotic relationship with your gut, and if you hurt your gut, your gut will hurt you back.

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The argument I’ll make throughout the rest of this book is that it’s not what’s in the food, it’s what’s been done to the food that matters. Because the real nutritional question is: who and what are you feeding? Are you feeding the human? Or are you feeding the intestinal microbiome? And is your liver working right based on the share that you get? Based on our current eating paradigm and Nutrition Facts label, you can’t figure either of those two questions out.

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Who Decides What’s Healthy, and for Whom?

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In a population where 88 percent have some level of metabolic dysfunction, the entire concept of healthy has been obfuscated. And who obfuscated it? All the usual suspects, plus some. The American Heart Association demonized saturated fat; we took the fat out of milk and got cheese and chocolate milk instead—but they’re healthy, or so we’re told. The American Diabetes Association pushed whole grains, so we foisted whole-grain bread on the public, except that as soon as it’s milled, it’s not whole grain anymore (see Chapter 19). The Academy of Nutrition and Dietetics told people that eggs had cholesterol, so Americans opted for refined carbs like breakfast cereal. But my personal all-time favorite is the U.S. Institute of Medicine, which in 2004 codified an upper limit for added sugar at 25 percent of total calories. In what universe is 25 percent of calories as added sugar justifiable? This gave the food industry carte blanche to add as much as they possibly could, making us sicker and sicker.

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When it comes to food, the only labeling rule is for allergies like eggs, gluten, peanuts, shellfish, and the like—things that can kill people acutely. After that, anything goes (see Chapter 23). Most people trust and buy products based on the way they’re promoted on the package, rather than their actual nutritional value, which still means nothing—because it’s not what’s in the food, it’s what’s been done to the food that counts. But that’s nowhere to be found on the label.

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My Definition of “Healthy”

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The key to fending off chronic disease is to keep those eight subcellular pathways running right—and each and every one of them can be made to run right with two simple dictates:

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Protect the liver. You have to protect the liver from fructose, glucose, branched-chain amino acids, omega-6 fatty acids, iron, and other oxidative stresses—all of which end up causing fat accumulation and liver damage, and generate insulin resistance. This can be done by either reducing the dose of dietary liver stressors (e.g., a low-sugar diet) or their flux (e.g., a high-fiber diet, which blocks sugar absorption, thus reducing the rate by which fructose and branched-chain amino acids reach the liver).

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Feed the gut. If you don’t feed your microbiome, your microbiome will feed on you; it will literally chew up the mucin layer that protects your intestinal epithelial cells, which increases the risk for leaky gut, inflammation, and more insulin resistance. The goal is to deliver more nutrients farther down the intestine (e.g., a high-fiber diet).

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Fiber is an essential nutrient—not for only you, but also for your microbiome. The fiber in Real Food is of two kinds: soluble, which is globular, like what holds jelly together (e.g., psyllium, pectin, inulin); and insoluble, like the stringy stuff in celery (e.g., cellulose, chitin, peptidoglycan). You need both, as they do different jobs; and you also need the geometry in order to make fiber work for you.

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Here’s a thought experiment: imagine a spaghetti colander. You run the water, it goes right through the holes. Now throw a glob of petroleum jelly into the center of the colander. You run the water, it might bounce off the jelly, but it still runs right through the holes. Finally, take your finger and rub the petroleum jelly all throughout the inside of the colander. Now run the water—you have an impenetrable barrier. When fiber (soluble and insoluble) is consumed within food, the insoluble fiber (stringy) forms a latticework on the inside of the duodenum, while the soluble fiber (globular) plugs the holes in the lattice. Together, along with this geometry, they form an impermeable barrier along the duodenal wall, which has numerous biological benefits. It’s because of this geometry that dietary fiber, when occurring naturally in food and without adulteration, protects against metabolic syndrome—by protecting the liver and feeding the gut.

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Cellulose is an insoluble fiber. Alone it could form the latticework, but not plug the holes. Psyllium is a soluble fiber. It can swell and absorb water, but can’t lay down the scaffolding. To get the benefits on delay of absorption to protect the liver, you need both. Real Food has both. Could you put both into one pill? Perhaps. But the side effects would be highly problematic. Cellulose isn’t compressible, so in order to lay down the latticework, you would have to take a high dose of cellulose. On the other hand, psyllium swells with exposure to water and doesn’t release it, causing severe bloating, distress, and diarrhea. It also doesn’t absorb macronutrients, just water.

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On the other hand, intact fiber—found in Real Food—has many benefits, and not just short-chain fatty acids (SCFAs). In the processed food industry, the germ of the grain (the nucleic acids, flavonoids, polyphenols) is removed along with the fiber because they can go rancid (see Chapter 19). Protecting the liver means maintaining the fiber and keeping the germ intact as well.

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Two simple precepts—protect the liver, feed the gut. Real Food (low-sugar, high-fiber) does both. Processed food (high-sugar, low-fiber) does neither. Processed food is the primary suspect in our current health and healthcare debacle, because it doesn’t improve our eight subcellular pathologies, our three nutrient-sensing enzymes, and our two physiologic precepts.

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Chapter 12

Nutrition “Unwrapped”

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Politics is often spread through myths, which themselves are easily turned into propaganda, thus perpetuating the politics—a vicious cycle. These three are replete within nutrition, perhaps more so than any other medical discipline, because there are so many stakeholders with their own beliefs and agendas. That’s why we need the science; it’s the only way to debunk the myths. Then and only then can the propaganda be shattered, clearing the way for a new political landscape. The healthcare professionals didn’t create the myths or the propaganda, but they’ve bought them hook, line, and sinker. Let’s start with the myths surrounding terminology. Here are just three examples:

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The word “weight”—when did it become a synonym for health? When we decided that health was the new morality. Political correctness meant you couldn’t shame people for poverty or race—but fat-shaming continues to this day, because “it’s your fault you’re a glutton and a sloth.” But the data shows that it’s your liver and visceral fat that determines your health, not your weight or total body fat. Liver fat tops out at about one pound, and visceral fat at about six pounds. You can’t see that on the scale. Normal weight people have liver fat, too. It’s not the fat you can see, it’s the fat you can’t see that matters.

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The word “fat”—does it mean body fat or dietary fat? Or, as you will soon learn, fatty acid? Or, “do these pants make my butt look fat?” (Pro-tip: never answer this question.) Two-thirds of the US populace continue to believe and perpetuate the myth that “fat makes you fat.” While it’s true that dietary fat could become body fat, it does so only in response to insulin. And so weight isn’t driven by dietary fat, which doesn’t raise insulin, but rather by dietary refined carbohydrate

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The word “sugar”— does it mean blood sugar (glucose) or dietary sugar (glucose-fructose)? The food industry says “you need sugar to live”—but while you do need a blood glucose level to live, you don’t have to consume that glucose. In fact, your liver can make glucose from the glycerol (see Fig. 7–3d) released from the breakdown of triglycerides in either dietary fat or body fat, or from amino acids, a process called gluconeogenesis. Conversely, you don’t need fructose (the molecule that makes food sweet) to live at all. In fact, there’s no biochemical reaction in any animal cell on the planet that requires dietary fructose. Which means you may want dietary sugar, but you don’t actually need it.

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Nutrition myths die hard, kind of like Voldemort and vampires; they seem indestructible, especially when the Dark Forces of Industry (see Chapter 23) spend a lot of money to maintain and propagate them. What follows are my best efforts to drive a stake through the heart of each of these nutritional myths, so that you can “unlearn” what you’ve been taught.

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A Calorie Is Not a Calorie

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This myth is all that is left of the legacy of Wilbur Atwater. It argues that all calories possess the same heat generation, equivalent to 4,184 joules of energy. From a physics standpoint, a calorie is a calorie. But so what? This has nothing to do with what happens to those calories in the human body, because weight gain is only about how those calories are stored.

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The efficiency of capturing all those calories and transforming them into chemical energy in the human body is highly uneven. Understanding these various phenomena shows that in fact “a calorie is not a calorie,” and there’s an actual difference between eating a handful of almonds and a donut, even if their calorie count is the same.

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The “calorie is a calorie” myth can be disproven through five examples:

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Fiber. You eat 160 calories in almonds, but you only absorb 130. The other 30 are prevented from early absorption because the fiber in them prevents early absorption in the duodenum (early intestine), so the bacteria in the jejunum and ileum (middle and late intestine) will chew the 30 up for their own purposes. You ate them, so they’re considered “calories in,” but you didn’t get them (your bacteria did).

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Protein. If an amino acid is to be prepared for energy metabolism, the amino group must be removed by the liver to convert it into an organic acid (e.g., aspartate to oxaloacetate). It costs two ATPs to do this, as opposed to preparing carbohydrate, which costs one ATP. This is known as the thermic effect of food (TEF). Fats generate about 2 to 3 percent of TEF, carbohydrate about 6 to 8 percent, and protein about 25 to 30 percent—meaning it takes more energy to burn a protein than a carbohydrate. If a calorie isn’t recouped because it’s burned, it can’t be stored.

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Fat. All dietary fats would liberate 9 calories per gram if you burned them. But omega-3 fatty acids aren’t burned—they’re hoarded, as they’re needed for cell membranes and neurons in the brain (see Chapters 7 and 19). Furthermore, trans-fats can’t be burned, as humans don’t have the enzyme to cleave the trans-double bond. They instead will clog your arteries and kill you, unrelated to their calories. All in all, neither are burned, but one will save your life and the other will kill you.

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Sugar. Added sugar is made up of equal amounts of glucose and fructose. Both provide the same number of calories, but are metabolized differently in the liver and perform different jobs in the brain. Glucose can be metabolized by all of your body’s tissues and only 20 percent of a glucose load goes to your liver, and even then insulin tells the liver to turn it into glycogen (liver starch). On the other hand, fructose can only be metabolized by the liver, so the whole load goes to your liver, insulin doesn’t have an effect, the mitochondria are overwhelmed, and the rest is turned into liver fat, driving insulin resistance (see Fig. 2–1). And on the third hand, fructose drives glycation seven times faster than glucose (see Chapter 7), doesn’t shut off the hunger hormone ghrelin, and is addictive (see Chapter 21).

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Different fat depots. It’s not just if the calorie is stored, it’s where it’s stored. There are three fat depots, but they confer different risks for development of metabolic disease: 1) subcutaneous (butt) fat: you need about 22 pounds to worsen your health; 2) visceral (belly) fat: you need about 5 pounds to worsen your health; and 3) liver fat: you only need about 0.3 pounds to worsen your health. And almost all calories from added sugar are going to liver fat. If a calorie stored were a calorie stored, it wouldn’t matter which fat depot was doing the storage—but it does. Protecting the liver is the prime directive.

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But It’s Zero Calories … ?

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Sugar sweetened beverages (SSBs) are causative for at least three diseases of metabolic syndrome—type 2 diabetes, heart disease, and fatty liver disease—plus tooth decay. So, what about noncaloric diet sweeteners, for those with a “sweet tooth”? Stevia, sucralose, aspartame, acesulfame-K, allulose, xylitol, erythritol, and others would seem the obvious choices—no calories, so no heart disease, right? No fructose, so no liver fat or diabetes, right? Not so fast. Though the US has slowly turned to diet drinks because of the obesity epidemic—as of 2010, 42 percent of Coca-Cola sales in the US were of the no-sugar variety—33 percent of all sugar consumption is in drinks, and 42 percent of drinks are now no-sugar, so someone somewhere should be losing weight, right?

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Unfortunately, diet sweetener consumption is also correlated with metabolic syndrome. Studies of switching out sugar for diet sweeteners don’t show beneficial effects on weight loss. Rather, the data show that sugar is a direct cause of metabolic syndrome—though thus far we only have correlation with diet sweeteners. So, do diet sweeteners cause metabolic syndrome, or do people with metabolic syndrome consume more diet drinks? The question really is if the substitution of diet sweeteners for sugar actually reduces caloric intake, body fat, and metabolic disease. Here are five reasons to be concerned:

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There’s a difference between pharmacokinetics (what your body does to a drug) and pharmacodynamics (what a drug does to your body). We have pharmacokinetic data on diet sweeteners to determine acute safety, which is part of the FDA’s charter (see Chapter 24), but none of the pharmacodynamics. This has to do with chronic effects, which is not in the FDA’s charter. The fact of the matter is, we don’t know what any of these diet sweeteners do to your long-term food intake, weight, body fat, or metabolic status. The food industry doesn’t do these studies because such studies are expensive and could have detrimental effects on sales. The NIH won’t do them, saying it’s the food industry’s job. So the studies aren’t done.

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You drink a soda. The tongue sends a signal to the hypothalamus that says, “Hey, sugar is coming, get ready to metabolize it.” The hypothalamus then sends a signal along the vagus nerve to the pancreas, saying, “A sugar load is coming, get ready to release the insulin.” If the “sweet” signal is from a diet sweetener, the sugar never comes. What happens next? Does the pancreas say, “Oh, well … I’ll just chill until the next meal,” or does it say, “WTF? I’m all primed for the extra sugar. Let’s eat more to get it.”

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In one study, four groups of Danish men ate their normal diet for six months plus a liter of sugared soda per day, a liter of diet soda per day, a liter of milk per day, or a liter of water per day. No surprise, the sugared soda group gained 22 pounds. The diet soda group gained 3.5 pounds. The milk group stayed the same. The water group lost 4.5 pounds. Now, 3.5 is better than 22 pounds, but they still gained weight even without the calories. And the milk has as many calories as the sugared soda, so why didn’t that group gain weight? It all has to do with insulin—meaning the diet sweetener still caused insulin release, while the lactose and fat in the milk didn’t. Plus the fat was satiating, so people ate less.

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A second study took diet soda drinkers and switched them to water. They lost another 6 pounds. If there are no calories in either case, why did their weight change? Insulin again. Insulin response to oral glucose tolerance testing was performed in seventeen morbidly obese adults without diabetes, both with and without a diet sweetener pretreatment. After the diet soda, the insulin response was 20 percent higher than with the seltzer control. The sweet taste alone can both stimulate appetite and insulin release, which drives energy storage.

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Diet sweeteners might change the composition of intestinal bacteria, which could cause leaky gut, generate inflammation, increase deposition of visceral fat, and drive metabolic syndrome, unrelated to calories (see Chapter 7). The intestinal microbiome plays a role not only in what the tongue tastes, but also what the brain senses.

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Early studies suggest that certain diet sweeteners act directly on fat cells grown in a petri dish to promote energy transport inside the cell. In other words, diet sweeteners may have insulin-like properties of their own, but this has yet to be confirmed.

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We don’t know the role that diet sweeteners may play in sugar addiction (see Chapter 21), as this field is in its infancy. However, there are animal studies that suggest brain pathways react similarly to sucrose and diet sweeteners.

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Recent studies argue that artificially sweetened beverages are associated with diabetes, cardiovascular issues, and dementia. Thus far, all of these studies have been correlative—we don’t yet have causation. Nonetheless, quantitatively, the data suggests that the toxicity of two diet sodas is equivalent to one sugared soda, and that they’re way worse than water in terms of obesity and diabetes development. As an example, take the case of aspartame (NutraSweet), which in animal models affects three of our eight subcellular pathologies: oxidative stress, membrane integrity, and inflammation (see Chapter 7). These health concerns are just swept under the rug—a University of Sussex report looked at the original approval of aspartame by the European Food Safety Authority (EFSA). They documented that the EFSA discounted fully 100 percent of the seventy-three studies that showed aspartame caused harm, while accepting 84 percent of the studies that showed no harm.

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While none of this research closes the book on diet sweeteners in either direction, it should certainly give us pause. In the last fifteen years, American sugar consumption has dropped from 120 to 94 pounds per year, yet obesity and metabolic syndrome persist unabated. Could diet sweeteners be playing a role? The only surefire way to find out is for Americans to de-sweeten their food across the board—drinks, too. And don’t start thinking juice is the answer (see Chapter 19).

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Instead of worrying about calories, we should instead focus on the interaction between genetics and sugar consumption, as this determines insulin levels and where that fat will develop and deposit. Understanding the role of different foods in generating different insulin responses is paramount, and that includes diet sweeteners.

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A Fiber Is Not a Fiber

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As mentioned earlier, there are two types of fiber—soluble and insoluble—and you need both. The reason you hear doctors espousing a plant-based diet isn’t because of the plant origin per se; it’s because plants come with both types of fiber. Together, the two kinds of fiber form a gel on the inside of the duodenum, reducing intestinal absorption by 25 to 30 percent, thus protecting the liver. Reciprocally, a sizeable portion of what you eat stays in the intestine, where the bacteria can feast on it and grow, thus feeding the gut.

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As discussed in Chapter 11, the fiber in food is perhaps the most important nutrient for health, because it singlehandedly protects the liver and feeds the gut in six different ways:

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Both kinds of fiber together form a gel on the inside of the duodenum to reduce the rate of absorption of monosaccharides and disaccharides, as well as slow the breakdown of starches. Reduced absorption means reduced transport to the liver, thus preventing the liver from turning excess energy into fat—in turn preventing liver insulin resistance.

The reduction in the rate of absorption also reduces the glycemic excursion in the blood, keeping the insulin response down, and reducing energy deposition into fat tissue.

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There are two flavors of bacteria that live in your gut: the white hat and the black hat bacteria—and it’s a daily struggle to see which will prevail. The white hat bacteria (e.g., Bacteroides) need more energy to survive and grow in order to battle the black hat bacteria (e.g., Firmicutes). Thankfully, the good bacteria can proliferate and maintain a balanced intestinal ecosystem, but need a greater and more robust supply chain to ward off the bad guys. What’s that supply chain made of? Fiber—both types.

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The fiber transits the food through the intestine faster, generating the satiety signal (the gut hormone peptide YY3–36, which is released into the bloodstream and goes to the brain) sooner, thus reducing second portions.

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Soluble fiber is metabolized by gut bacteria into short-chain fatty acids like butyrate. They uniquely feed the microbiome of the colon (large intestine) and are absorbed into the bloodstream where they are anti-inflammatory as well as suppress insulin secretion from the pancreas.

Insoluble fiber acts as a mild abrasive in the lumen of the colon, which dislodges and sluffs old dead cells, thus reducing cancer risk.

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Be forewarned: the processed food industry will tout the benefits of “added fiber” to various products. But you can’t put the toothpaste back in the tube. Yes, they can add back some soluble fiber (e.g., the psyllium in Fiber One bars), but they can never recapitulate the insoluble fiber lost during processing.

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The same goes for whole grain. We’ve been taught that brown bread is better for you because it has more fiber. The Whole Grains Council says, “Whole grains or foods made from them contain all the essential parts and naturally-occurring nutrients of the entire grain seed in their original proportions. If the grain has been processed (e.g., cracked, crushed, rolled, extruded, and/or cooked), the food product should deliver the same rich balance of nutrients that are found in the original grain seed.” In other words, if it starts as whole grain, it remains whole grain. It’s not what’s in the food, it’s what’s been done to the food.

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Fig. 12–1 is a good example of the problem. The one-pound loaf of bread on the right is big and fluffy. If you threw it at someone’s head, it would bounce off. The slices are thick. The bread on the left is small and dense. If you threw it at someone’s head, it would knock them unconscious. The slices are thin, and they crumble easily. Which one makes a better sandwich? Which is healthier? The bread on the right has milled grain, and the starch and gluten are dissociated from the bran. It generates a rapid and high glucose and insulin response, but makes great avocado toast. The bread on the left still has its starch and gluten within the kernel, and crumbles easily, and it’s an “acquired taste.” Both have soluble fiber, but only the one on the left has structurally and functionally maintained its insoluble fiber.

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Figure 12–1: Two kinds of whole grain bread. Each weighs one pound. The one on the left is and remains whole grain, while the one on the right started as whole grain but was then milled and processed.

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A Carb Is Not a Carb

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For decades, the American Heart Association, American Diabetes Association, and American Medical Association advocated a low-fat diet. By definition that means a high-carbohydrate diet. Is that a good trade? Just like “a calorie is not a calorie” and “a fiber is not a fiber,” “a carb is not a carb.” There are three inherent myths about carbohydrates that play a role as to whether they’re causative of, or preventative against, NCDs:

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Sugar vs. starch. Sugars are monosaccharides and disaccharides (one or two molecules), while starch is a complex polymer (many molecules). Sugars either have one bond or no bonds to break, so they’re digested and absorbed quickly in the duodenum, especially when they’ve been liberated from a food matrix, as they often are (e.g., soda, fruit juice, alcohol). Starch has more bonds to break, and is digested and absorbed slower. All of this adds up to a more rapid and higher insulin response with sugar, which drives weight gain.

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Type of starch (the two “Amys”): But “a starch is not a starch.” There are two kinds of starch: amylose (brown foods including beans, lentils, and legumes; carbs that are digested and absorbed slowly) and amylopectin (white foods including wheat, pasta, rice, and potatoes; carbs that are digested and absorbed rapidly). Amylose is better for you, as it’s a string of glucoses with two ends; therefore, only two enzymes at a time can chew it up, resulting in slow digestion and absorption. Amylopectin is more like a tree of glucoses, with lots of branch points. Many more enzymes can chew it up at once, releasing glucose more rapidly, which is more likely to be absorbed early, flood the liver, and generate a bigger insulin response.

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Carbs are rarely ingested in isolation. A slice of white bread is straight glucose. But Real Food is glucose plus protein plus fat plus fiber. Those other macronutrients, or lack thereof, influence the glucose’s absorption in the intestine, the insulin response that follows, and risk for weight gain.

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Carbs and Glycemic Index (GI)

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Higher glucose spikes during eating are associated with more insulin, more inflammation, and higher mortality. Therefore, a primary goal of improving metabolic health is to get the insulin down. One way is to eat foods that don’t make your blood glucose rise too fast. This is where amylose—the “good Amy”—comes in. Thus was born the concept of the glycemic index (GI). Tables of specific foods and their inherent GI are readily available. Some claim that a low-GI diet will keep blood glucose down and help you lose weight. But does it work to keep insulin down? Is it the glucose spikes or the insulin spikes that do the damage?

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Unfortunately, GI isn’t the panacea that the zealots hype. GI is defined as: how high does your serum glucose rise in response to 50 grams of carbohydrate in a given food, as compared with the glucose response in 50 grams of straight starch (e.g., white bread). However, there are four things conceptually wrong with GI:

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GI is an indirect proxy for insulin. While rapid glucose spikes after refined starch lead to glycation and oxidative stress, it’s the insulin fluctuation that induces the other six subcellular pathologies (see Chapter 7), drives excess energy intake, and promotes obesity.

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GI assumes everyone responds to the same food in the same way. GI is computed based on responses of healthy people to certain foods, even though 88 percent of people have some form of metabolic dysfunction. Now that people are using continuous glucose monitors (CGMs; see Chapter 14), it’s very clear that people respond differently to the same food.

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The important parameter is glycemic load (GL). GL is different from GI—how much food do you have to eat to get the 50 grams of carbohydrate? GL takes into account the beneficial effect of fiber. A good example is carrots, which are high-GI (lots of carbohydrate) but low-GL (even more fiber). More fiber means a larger portion, because there’s less digestible carbohydrate. You can turn any high-GI food into a low-GL food by eating it with its original fiber. Real Food is by definition low-GL.

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Fructose! Fructose is the most egregious cause of liver insulin resistance and metabolic syndrome because of how the liver uniquely metabolizes it. Fructose isn’t glucose—when eaten, it doesn’t raise the blood glucose level (it’s not measured in the glucose assay). In fact, by definition, it’s low-GI, because it has no glucose. Still, this hasn’t stopped the food industry from trying to capitalize on the low-GI craze by adding fructose to foods. In fact, the Glycemic Index Foundation of Australia has the nerve to label sugar as low-GI, as if somehow that was a good thing. Keep insulin low by eating lots of fiber and by avoiding added sugar. Real Food is by definition a low-GL diet.

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A Fat Is Not a Fat

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The epic battle between British physiologist John Yudkin and Minnesota epidemiologist Ancel Keys for control of the American Diet, detailed in my book Fat Chance (2012) and Nina Teicholz’s The Big Fat Surprise (2017), is now sixty years old. Yudkin wrote Pure, White and Deadly (1972) targeting dietary sugar; Keys wrote The Seven Countries Study (1980) targeting dietary saturated fat. Both scientists had correlation but not causation; both had static data (single points in time) rather than longitudinal data (patterns over time). Both used ecologic (population) data, which is much flimsier than individual data. In other words, both had weak cases.

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However, Keys had a few more things going for him than Yudkin: hubris, bombast, cherry picking, and willful denial. Keys was also the beneficiary of three scientific discoveries of the 1970s that sealed Yudkin’s fate: people with familial hypercholesterolemia (FH; see Chapter 2) have high LDL and heart disease; dietary fat raises LDL levels; and LDL levels correlate with heart disease in populations. Never mind that smoking and trans-fats are bigger contributors, or that those countries eating the most fat had the lowest levels of heart disease. The die was cast, and the 1977 Dietary Guidelines assured that the world would go low-fat.

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There are one restriction study and two substitution studies that assessed the effects of the removal of saturated fat from diet—and the latter two had to be reanalyzed to get to the truth. The restriction study was done by the Women’s Health Initiative (WHI), which studied 161,000 women between 1993 and 1998 who reduced their consumption of saturated fat from 30 percent to 10 percent of calories. The verdict: no effect on either weight loss or heart disease. In the Sydney Diet Heart Study, which ran between 1966 and 1973, 458 men who had experienced a heart attack had the saturated fat removed from their diet and replaced with linoleic acid (from soybean oil), which is pro-inflammatory. All subjects experienced a decline in their LDL levels, yet their risk for heart attack increased by 62 percent, as well as their risk of dying by 70 percent. Perhaps the most egregious study was the Minnesota Coronary Study, which followed nine thousand patients over five years (1968 to 1973) at state mental hospitals and nursing homes, where meals were controlled by removing saturated fat and substituting linoleic acid (from corn oil). The study experienced the same results as Sydney—LDL went down, but heart attacks and deaths went up. The authors never published their findings, because they couldn’t explain them. Instead, the data lay in wait in the basement of the lead author, only to be discovered forty years later by his Mayo Clinic cardiologist son. In 2016, he published the findings. He was astonished, but he shouldn’t have been. Low-fat doesn’t work, and substituting with other fats doesn’t work either. It’s not about the LDL; it never was (see Chapter 2).

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Furthermore, the saturated fat story doesn’t take into account that all saturated fats are not the same. For example, the saturated fats in red meat are even-chain fatty acids (16 or 18 carbons), meaning they’re cardiovascularly neutral. The saturated fats found in dairy are odd-chain fatty acids (15 or 17 carbons), which are metabolized differently in the liver, and are associated with protection from chronic diseases like diabetes and heart disease. Therefore, the fat in dairy is likely protective—except we skim off that fat from cow’s milk and turn it into processed cheese. Good for the dairy producers, as they get two products out of one, but not so good for you, as an ingredient that could be protective against chronic disease has been removed “for your own good.” Even worse, sometimes we flavor the milk with chocolate or strawberry syrup for good measure (see Chapter 14).

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The Difference between Saturated Fat and Saturated Free Fatty Acids

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Despite all these data, and the fact that the FDA removed saturated fat from the Nutrition Facts label, people still think it’s the bogeyman. Let’s get the facts straight: there’s a difference between innocuous saturated fat and pernicious saturated free fatty acids. Saturated fat itself isn’t inflammatory, because it’s packaged into triglycerides (see Fig. 7–3d). Rather, the unpackaged moiety called free fatty acids or non-esterified saturated fatty acids (see Fig. 7–3a and c), in particular free palmitate (see Fig. 7–3a), is the inflammatory component, both in the body and in the brain. In particular, free palmitate seems to be the driver of liver and hypothalamic inflammation. However, you don’t eat free fatty acids. They’re produced and exist in only two places in the body. When stored triglyceride is released from the adipocyte (fat cell), the glycerol backbone must be cleaved off, liberating its three free fatty acids. It also happens when the liver turns excess sugar into triglyceride through the process of de novo lipogenesis (DNL), as it first must produce a free fatty acid. Both of these processes are related to each other through fructose, as fructose causes both insulin resistance and DNL. So is the saturated fat from food the problem? Or are the free fatty acids the metabolic by-product of dietary sugar?

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A Protein Is Not a Protein

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Companies are touting protein as a cure-all and for weight loss/muscle gain. They’re selling protein shakes, protein cookies, protein snack bars, even protein coffee. It’s true that protein is neither carbohydrate nor sugar nor fat, and you need it to maintain normal growth. However, your kidneys have a limited capacity to excrete the metabolic by-products of protein metabolism, and overexcretion can cause kidney damage. Therefore, protein quality is as important as protein quantity. For example, eggs and beans both contain protein, but are very different in quality. Dietary protein is made up of twenty separate amino acids strung together in different combinations and amounts. One of those amino acids, tryptophan, is rarer and therefore more important than others, because it’s the precursor of serotonin, an important brain neurotransmitter (see Chapter 19). Eggs, poultry, and fish are the best sources of this amino acid, while beans have very little. On the other hand, additional protein is needed if you’re building muscle, especially branched-chain amino acids (BCAAs; leucine, isoleucine, valine), which are 20 percent of muscle (see Chapter 18). BCAAs are in high concentration in corn products, and are what’s in those tubs of protein powder at the health food store. If you’re a bodybuilder, you need them; if you’re not a gym rat and consume excess BCAAs, your liver will take the amino groups off and turn them into organic acids, which will either be diverted into liver fat (through DNL) or into excess glucose, either of which can generate hyperinsulinemia and drive chronic disease. The goal is to get more tryptophan and less BCAAs in the protein you consume.

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What about Meat?

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Meat is relatively high in tryptophan, vitamins, and minerals, but it brings along several other less desirable items as well. With beef, health problems include: iron (oxygen radicals); BCAAs in corn-fed beef (DNL, liver fat, and insulin resistance); and choline, a by-product of which sticks to arteries, causes vascular disease, and leads to insulin resistance. However, red meat has a hazard risk (HR) ratio for diabetes of 1.24; in other words, high meat-eaters have a 24 percent increased risk over that of the general population. So if the general prevalence of diabetes is 9.4 percent, meat-eaters have a prevalence of 11.6 percent. While a 2.2 percent increase is not negligible, public health officials don’t worry about HR ratios unless they’re above 1.3. Further, when the iron and heme levels were adjusted, the HR ratio was reduced down to 1.13 (resulting in a diabetes prevalence of 10.6 percent, suggesting that other stuff in the meat isn’t a big driver of diabetes). In another study, unprocessed meat had a HR ratio for diabetes of 1.12 per 100 grams, while processed meat (bacon, sausage, salami) had a HR ratio of 1.51 per 50 grams. Thus, the difference in prevalence goes from 10.5 percent to 28.4 percent. Now, that’s notable. It’s the processing that renders the meat dangerous.

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Also, nitrates in processed meat are a known risk factor for colon cancer. Thus, it appears that processed meat is more problematic, presumably due to the additives and the iron, rather than due to the saturated fat. Some, although not all, of these concerns can be assuaged by purchasing grass-fed and nitrate-free meat instead.

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Mythology Begets Propaganda; Science Begets Public Health

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The New Battle Royale: Keto vs. Vegan

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Keto

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dietary composition of 10 percent carbohydrate, 70 percent fat, and 20 percent protein.

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The keto diet has been shown to result in significant and durable weight loss, improvement in insulin sensitivity in a majority of obese people, and diabetes reversal with medication discontinuation in a majority of patients.

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Most people, when faced with a life of no bread, no pasta, no sugar, say no way. This diet may be extreme, but it has sound principles. Explorer Vilhjalmur Stefansson was shipwrecked in the Arctic for fifteen months and forced to eat nothing but caribou and whale blubber. When he returned to the US, he felt healthier than before. Many years later, to prove the point, he and his colleague checked themselves into New York’s Bellevue Hospital and ate only meat for one year—they were healthier than the investigators, at least with the diagnostic tests available at the time.

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The science has now been researched extensively, and the keto diet works through two mechanisms. The first is that in the relative absence of carbohydrate and insulin, the adipocyte will release fatty acids into the bloodstream, which go to the liver and are turned into ketones (e.g., beta-hydroxybutyrate) to be used for energy in the rest of the body, especially the brain. The liver kicks in to utilize any stored liver fat, and reduces fatty liver, insulin resistance, and insulin levels. The reduction in insulin improves leptin resistance, which reduces appetite. Insulin reduction will also occur with the less stringent LCHF diet. The second mechanism is beta-hydroxybutyrate itself, which is a signaling molecule that is measured in the urine or breath to determine if you’re in ketosis. It tells the liver mitochondria to increase the production of sirtuin-1, which activates AMP-kinase and reduces mTOR, increasing metabolic rate, and induces autophagy (see Chapters 7 and 8). Further, beta-hydroxybutyrate alters the gut microbiome by reducing inflammatory cells and responses in the intestine. Last, beta-hydroxybutyrate also increases the synthesis of brain-derived neurotrophic factor (BDNF), which makes neurons grow and protects against dementia. This is why the keto diet has found favor among various Alzheimer’s researchers.

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Sounds pretty darn good, especially if you’re metabolically ill—what’s the downside? It’s really hard to stay in ketosis. After two months, most ketogenic diets aren’t ketogenic anymore because people aren’t that diligent. In addition, keto adherents tend to be low in selenium, magnesium, phosphorus, and vitamins B and C (however, they don’t have to be if they consume enough fiber in the form of leafy greens, as the micronutrients travel with the fiber). Newfangled ketone ester drinks are now on the market to try to biohack your body’s system by adding ketones to your bloodstream, but they don’t change your insulin, and as of yet there are no data that they can mitigate chronic disease states.

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Vegan and Other Plant-Based Diets

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Note that a vegan diet is not a low-fat diet, as olive oil, nuts, and avocados have plenty of saturated and unsaturated fats. That being said, several vegan diets have been promulgated to improve metabolic health. The Adventist Health Study (see Chapter 4) showed that vegans, lacto-ovo vegetarians, and pescatarians all had improved risk profiles compared with nonvegetarians (that is, those on the Standard American Diet), but adherents of each of these were not different from each other. Another diet with clear and robust data promoted by Dean Ornish (full disclosure, Dean is a friend) is an extremely low-fat and low-animal-product diet, but is all Real Food providing very large amounts of fiber. To be clear, Ornish advocates for both diet and stress reduction, which plays a unique role in reducing cortisol, thereby improving insulin sensitivity. So is it the diet or the stress reduction that is the primary therapy? We still don’t know.

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a standard vegan diet is low in iron, omega-3s, vitamin B12, and tryptophan (although you can supplement);

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Instead of restricting calories, you can just restrict meals. Intermittent fasting (IF) is a less painful way of jacking up the same subcellular processes. By depriving your liver of calories for fourteen to sixteen hours per day, IF gives it a chance to activate AMP-kinase, suppress mTOR, increase autophagy, chew up some of the liver fat that’s been stored, improve insulin resistance, and lower your insulin—the same outcomes that low-carb and ketogenic diets achieve. IF has also been shown to promote weight loss, blood glucose control, reduced inflammation, improvements in memory and stress resistance, slowed aging, and longer life span. Each of these benefits is a manifestation of improvement in insulin sensitivity. In this way, your leptin won’t drop so fast that you feel awful; and since insulin blocks leptin signaling, the lower your insulin levels go, the better your brain can see the leptin. This means your sympathetic nervous ratchets up, and you burn faster. All in all, most people find IF easier to adhere to long-term, and it’s better for you.

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Supplemental Earnings?

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Probiotic or Prebiotic?

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The latest research shows that the bacteria in your gut have a mind of their own; they want to be fed, and if they’re not, they’ll release neuroactive factors that change your behavior.

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Also, by not feeding the good bacteria, the bad bacteria proliferate and release inflammatory mediators that cause disease.

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But why is your microbiome broken in the first place? Maybe the caesarean section that delivered you at birth deprived your gut of beneficial vaginal flora. Maybe it was the antibiotics your doctor gave you for your ear infection when you were a toddler, or the antacid you took when you were twenty. Maybe it’s the antibiotics in your meat (see Chapter 20) or maybe it’s the diet sweeteners in the soda you drink to wash it down.

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So let’s repopulate your unhappy gut with a probiotic. Probiotics are living bacteria; logic says that if you eat them, they should multiply and grow. But they don’t. If they did, you wouldn’t have to keep taking them. Processed food has made the intestinal environment inhospitable, and the good bacteria can’t live in that environment. It would be like sending humans to Mars with no atmosphere. It doesn’t matter how many you keep sending, they’re not going to survive (unless they’re Matt Damon). You have to feed your gut, and processed food starves it. More processing means more functional intestinal problems, more autoimmune disease, and more metabolic syndrome. Probiotics can’t fix this because they can’t survive in the subsequent environment.

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There’s a more effective way to make sure those good bacteria set up shop: a prebiotic, which will alter the gut environment, and permit those probiotics to take. The simplest and most effective isn’t found in a supplement—but in dietary fiber. The microbiome will change for the better within two days of adopting a high-fiber diet. Add a probiotic with a prebiotic, and now maybe those bacteria will take because you’re changing your intestinal habitat. However, you have to continue to support the new environment by eating Real Food.

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The Gluten-free Craze

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In 2018, I finally learned why. Dr. Stefano Guandalini of the University of Chicago, one of the world’s foremost celiac disease researchers, explained this disorder to me. Wheat is a complex organism—it’s hexaploid (six nuclei) instead of diploid (two nuclei). It’s been selectively bred to cultivate certain traits—among them higher gluten content, which means better bread because gluten is “sticky” and therefore rises better, making a fluffier loaf. Wheat also has seven hundred different proteins you could have an intolerance to—only two of them are the ones in gluten. The other 698 are just as capable of generating an immune reaction. This is why there’s no biomarker in the blood for it; there are too many suspects. For example, if you take white blood cells from a celiac patient, put them in a petri dish, and throw either wheat, barley, rye, or purified gluten in as well, they’ll go bonkers. But if you take white blood cells from a patient with wheat intolerance and test them, they’ll react to the wheat but do nothing in response to the barley, rye, or purified gluten. Dr. Guandalini wants to rename this condition non-celiac wheat intolerance (NCWI), because these people can have a beer (made with barley)—and I do, without any problem.

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Chapter 16

What and How Fetuses, Infants, and Toddlers Eat

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Babies also have different metabolic needs than adults. For one, they have a rapidly growing brain.

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Since the brain is composed of 60 percent fat, there’s a lot that has to be laid down in a very short period of time, which means there has to be a lot of fat in the diet. But not just any fat.

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We’re talking omega-3s (see Chapter 19), which are essential fatty acids—fetuses must get them from their mothers, and babies must eat a lot of them very quickly.

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They come in two flavors: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Because of their three double-bonds, omega-3s are more flexible, meaning they bend in different directions. For this reason, they’re incorporated into cell membranes, especially neuronal membranes, where they increase fluidity (meaning they allow for easy cell deformation without rupture). This prevents cell aging and early cell death. Omega-3s also reduce inflammation at the nerve terminal, allowing for better neural transmission. Furthermore, omega-3s can be turned into endocannabinoids (ECs)—the brain’s version of marijuana, which helps heighten mood by alleviating anxiety. And that heightened stress is predetermined even before they are born. Lack of omega-3s during pregnancy in rats messes with insulin signaling and brain growth factor levels in the offspring, leading to increased anxiety. Conversely, omega-3s help repair the damage to neuronal membranes caused by toxins such as fructose. Omega-3s are so important to neonatal development that formula companies started supplementing with them back in 2003.

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So where do all those omega-3s come from? Breast milk is chock-full of them. But if mom is omega-3 deficient, there are immediate implications for all of us. First of all, what do we tell pregnant women not to eat? Seafood, out of concern for mercury poisoning. However, in the UK it’s been proven that maternal seafood consumption predicts improved neurodevelopmental outcomes in children. So are we making more trouble than we’re solving by advising against it?

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In the absence of Real Food, obstetricians can skirt the issue by giving the pregnant mom omega-3 supplements, fixing the deficiency. This provides a double bonus—the moms’ risk for depression is reduced, and the kids’ neurodevelopmental outcomes are improved.

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Sugar Babies 1

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Omega-3s aren’t all that babies’ brains need. Mother’s, cow’s, and other mammalian milks contain a special sugar called lactose, which is composed of two molecules—glucose and galactose bound together. You hear a lot about lactose because many people lack the enzyme that breaks the bond between the two molecules, a condition called lactose intolerance; affected individuals experience diarrhea, pain, and gas in response to milk or dairy consumption.

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However, you don’t hear much about galactose. When an adult consumes galactose, it goes straight to the liver and is converted immediately to glucose. Many adults don’t drink milk, and adults have no need for galactose. So why does it exist? Why is it important? Why is it exclusively in mammalian milk?

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Milk is food for babies; and babies, even more than children or adults, need to grow two parts of the body—the brain and the immune system. Galactose is an essential component of certain fats in the brain called cerebrosides and ceramides. Furthermore, the mammary gland is the only part of the human body that can make galactose, in order to properly feed the infant. But then is lactose-free formula a good idea? Parents often blame cow’s-milk formula or the lactose it contains for their babies’ feeding problems, fussiness, and other subjective symptoms. Currently, soy-based lactose-free formula is now 25 percent of all US formula sales. Is that good for all babies? A recent study showed breast-fed infants scored slightly higher on the mental development index than formula-fed infants at six and twelve months of age. They also showed higher psychomotor development index scores than soy-based lactose-free formula-fed infants.

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Galactose is also important in the development of both the innate and adaptive immune systems. A rare, genetic inability of the liver to turn galactose into glucose, called galactosemia, is also associated with immune problems. Many of these babies die of neonatal meningitis. If they survive the newborn period, they exhibit moderate cognitive deficits—although it’s not clear if it’s a function of withholding of galactose or of the disease itself. The point is that galactose is necessary for babies but not adults. A trial of lactose-free formula is often the first maneuver a doctor attempts for a fussy baby; it shouldn’t be. Talk with your doctor before you make the switch.

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Sugar Babies 2

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Then there’s that other sugar—fructose. Remember, there’s no biochemical reaction in any animal cell on the planet that requires fructose. So what happens when fructose enters a fetus? For a long time, it’s been assumed that the placenta protects the fetus from mom’s many missteps, but we now know this is false—otherwise we wouldn’t have crack- or opiate-addicted newborns.

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It turns out that fructose has effects on fetuses as well. If a pregnant mom drinks a Coke, the fructose crosses the placenta and the fetus gets a huge bolus (large amount), which has been shown to stimulate the liver to make even more free palmitate. In addition, the taste receptors on the tongue develop at thirty weeks’ gestation—way before the first taste of juice—meaning the fetus is sensing the fructose in the amniotic fluid. So yes, you can be addicted to soda at birth.

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Project Viva examined the associations between pregnancy, cognition, and childhood sugar consumption in the form of sugar sweetened beverages, other beverages (diet soda, juice), and fruit. Among 1,234 mother-child pairs enrolled, a mean maternal sucrose consumption of 50 grams/day—consistent with the upper limit of current USDA guidelines—negatively impacted mid-childhood cognitive testing. Also of note, prenatal diet soda consumption was shown to negatively impact mid-childhood verbal scores as well.

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Furthermore, cutting the umbilical cord only compounds the problem. Doctors used to think that fructose didn’t cross from the mother into the breast milk, but we now know that the only thing standing between mom’s 20-ounce Coke and the baby is mom’s intestine and liver. The amount of fructose that makes it into the breast milk correlates directly with the degree of weight and fat mass increase in six-month-old infants.

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Eighty-three percent of American infants start out breastfeeding, but that percentage is cut to 60 percent by three months, a function of race, education, poverty, and culture. A whole lot of infants are consuming some type of formula, either solely or as a supplement to breast milk. In fact, the formula industry is a behemoth and expected to gross $103 billion by 2026. The industry would like us to think that formula is as good for babies as is breast milk—but does the truth live up to the hype?

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A review of lactose-free infant formulas documents a dietary composition of half corn syrup solids and half sucrose, for a total of 10.3 percent of calories coming from sugar. While we don’t yet know if this is enough to lead to metabolic disturbances in infants, it certainly is in older children. In fact, based on EU guidelines, several US FDA-approved lactose-free formulas are illegal in Europe.

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Of course, infants eventually graduate from breast milk or formula up to baby food. Why? Because the marketers want them to. Was there always baby food? The first commercial baby food was marketed in the Netherlands in 1901 and in the US in the early 1920s. Gerber was founded in 1927, and Beech-Nut and Pablum (dried baby food) in 1931. Annually, the Gerber baby contest garners millions of submissions and views on social media—a brilliant marketing ploy. But what did babies eat before 1901?

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Back then, adult food was macerated and churned into chunky pastes, which is still what babies consume in many other countries. In order to get babies to eat the commercial stuff, manufacturers had to make it “appealing”—so they added sugar. Lots of it. The problem is that obese infants taste sugar less well than normal-weight infants, so the industry needed to add a greater amount for those infants to register their approval—just as they do for adults. But no matter—even thirty days of exposure can turn a sugar-ambivalent baby into a sugar-liker. It’s in the industry’s best interest to keep adding sugar so that the infant will only want to eat sweet foods—that they make. In fact, you have to introduce a savory food to an infant a median of thirteen times before they’ll accept it. That’s a lot of “here comes the choo-choo.” On the other hand, how many times do you have to introduce a sweet food to an infant before they’ll accept it? Just once.

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In 2015, the U.S. Centers for Disease Control and Prevention examined the nutritional information of 1,074 infant and toddler food products. It found 32 percent of toddler dinners, the majority of child-oriented snacks, and infant-aimed juices contained at least one source of added sugar. And 35 percent of all the calories in those foods or drinks came from sugar. Worse yet, a laboratory analysis of baby foods documents that their added sugar content is even higher than what’s reported on the Nutrition Facts label. Maybe the reason is that there are 262 different names for added sugar, so the industry can sneak it in without you even noticing?

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And then they’re hooked. By the time they hit six months of age, 60 percent of US infants consume some daily added sugars. After six months, that number jumps to 98 percent. The American Heart Association, UK Royal College of Paediatrics and Child Health, and the WHO all say that babies and toddlers shouldn’t be consuming any added sugar, and have all argued for mandatory guidelines on the sugar content of toddler foods to encourage reformulation. As a result, the newest 2020 Dietary Guidelines Advisory Committee (see Chapter 24) has written a section on infants and toddlers. We’ll see if their guidance makes it into the final document. However, to their credit, some food companies have publicly acknowledged the added sugar problem and are now reporting their practices on the Nutrition Facts label. All in all, commercial baby food is a minefield. If you can’t make your own, just remember this one piece of advice: avoid any food that comes in a pouch.

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Baby Teeth

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Baby Overjet

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weak chin. Dentists know it as retrognathia; you might know it as overjet. Similarly, malocclusion (not enough room for all the teeth in the mouth) has increased in the population over the last forty years; this was determined by looking at rates of orthodontia, even after controlling for financial concerns, which exhibit an increase in patient load between 1987 and 2004 (the years when children born in the late 1970s and 1980s would be fitted for braces). Why? Because sucking on mother’s nipple is far better than sucking on a plastic one. The infant has to suck harder to make a seal, and this action strengthens and grows the sixteen muscles of the tongue. The well-developed tongue then applies continuous pressure against the hard palate of infants so that it’s broad and flat (mimicking the shape of the tongue), thereby creating a larger space in the mouth and a wider airway. A low, lazy tongue means that the palate narrows and develops a high arch.

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Thumbs and pacifiers can vault the palate, keeping it narrow, and lead to future dental and airway issues. The position of the tongue and the vaulting of the palate is the difference between nose-breathers and mouth-breathers. The tongue has to be elevated in the palate for us to be nose breathers, and sucking on mother’s nipple instead of a plastic one reduces the risk for mouth breathing and overjet in later life.

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The problem mounts further in toddlerhood because of pureed baby food. What and how did babies eat after weaning off the breast before there was commercial baby food? As we explored earlier, they ate what their parents ate, and they gummed it to death. As a result, they got very strong mastication muscles (masseter, temporalis, and pterygoids), necessary to grow the jaw and increase the airway size. However, we’ve now abdicated this practice for defibertized and pureed baby food, because it’s yummier (added sugar), easier, and faster, and there’s a lower risk of choking.

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Furthermore, this isn’t just a cosmetic issue, it’s a metabolic one, too. Retrognathia, overjet, malocclusion, and a small airway set children and adults up for the development of obstructive sleep apnea (OSA), hypoxia (lack of oxygen), enzyme dyssynchrony (see Chapter 8), the eight subcellular pathologies (see Chapter 7), and obesity and metabolic syndrome in early childhood.

Note: add ADHD risk from the sleep issues

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As a kid gains weight, fat is deposited in the tongue, soft palate, and lateral pharyngeal walls, which results in enlargement of these tissues, narrowing the airway even further and contributing to the development of OSA. The OSA feeds the obesity and the obesity feeds the OSA. It’s this vicious cycle that can lead to metabolic syndrome. Today, 85 percent of sleep disordered breathing in children goes undiagnosed, and 24 percent of ADHD is really sleep disordered breathing that has been misdiagnosed. Is your kid snoring? It may be cute, but it’s not normal. Tell your dentist.

Note: oh nvm there it is lol

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Malocclusion is also the reason more wisdom teeth are being extracted. The jaw doesn’t grow enough, so there isn’t enough room for the third molars. Wisdom teeth are a biomarker, or sign and symptom of the problem started by a plastic nipple or pacifier. But when dentists take them out, the jaw and oral airway collapse even further. In fact, you could develop OSA after wisdom teeth extraction.

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Chapter 17

Food Classifications

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Nevin Scrimshaw, Hamish Munro, and Vernon Young—luminaries in the vitamin and protein fields who successfully researched and treated nutrient deficiencies. They were convinced it’s what’s in the food versus what’s missing, and if we can just add nutrients, so much the better. They were right—just not for everyone.

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But the food industry was happy to oblige my professors, as it gave them yet another selling point and front-of-package claim (see Chapter 24). It has been this kind of thinking, as well as the calorie hypothesis, that’s led to much of our ignorance and incompetency around food. It’s why consumers have no idea why America and the world continues its inexorable downward

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Processed food is defined by seven engineering criteria:

mass produced

consistent batch to batch

consistent country to country

uses specialized ingredients from specialized companies

consists of pre-frozen macronutrients

must stay emulsified so that the fat and water do not layer out

must have a long shelf life or freezer life

It’s exactly these engineering issues that make processed food toxic to human physiology by promoting the eight subcellular pathologies of Chapter 7.

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Pamphlets, Pyramids, and Plates

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The USDA is the primary sanctioned outlet for nutrition education. Its classification system started in 1902 with a brochure written by none other than Wilbur Atwater (see Chapter 4), entitled Principles of Nutrition and Nutritive Value of Food, in which he introduced the concept of calories to the American public. By 1917, the USDA issued Food for Young Children, a brochure providing guidance to parents trying to navigate the new foodscape that evolved from the Industrial Revolution, which then morphed into a revised brochure for adults titled How to Select Foods. The national bouts of malnutrition and starvation during the Depression and the Dust Bowl of the 1930s caused the USDA to invest in the “science” of nutrition. John Steinbeck got it when he wrote about a woman whose baby died, and instead breastfed a starving old man in The Grapes of Wrath (1939). By 1940, the USDA developed its guidance into the seven food groups (that is, carbohydrates, fats, dietary fiber, minerals, proteins, vitamins, and water). Notice that dietary fiber was its own food group prior to World War II. Why was that? Through the experience with malnutrition, the USDA knew about the importance of green vegetables for general health, and so fiber was considered an integral part of a balanced diet.

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However, over the course of the war and with food rationing, the American dairy and meat industries saw consumption dwindle. Then, after the war ended, they wanted to drum up business, so they made a push to gain relevance. This resulted in further refinement of the USDA food classification in 1956, which yielded the four basic food groups (dairy, meat, fruits and vegetables, breads and cereals; the one I learned in elementary school), in which dairy and meat both occupied prominent positions. Gone was any mention of fiber as a necessary nutrient. Furthermore, it was at this time that fruit juice was classified as a fruit by the USDA, further gutting any fiber requirement.

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The USDA Food Wheel of 1984 was the first classification system after the first Dietary Guidelines for Americans in 1980, which were strictly based on calories. This morphed into the 1992 Food Pyramid, with bread and grains at the base, because they were the least calorically dense of the macronutrients. Oils and sweets were placed at the top, because they were the most calorically dense (to be clear, sugar has the same caloric density as starch and protein at 4.1 kcal/gm, but sweets are usually a mixture of sugar and fat). The USDA followed up in 2005 with MyPyramid, which started favoring certain foods over others. But how did it become a pyramid in the first place?

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It turns out that the USDA didn’t invent the food pyramid, Sweden did. Sweden’s was scrapped, but the USDA adopted it anyway, because its 1980s policies of agricultural monoculture had generated a glut of cheap refined carbohydrate, which served as the base of the pyramid. USDA nutritionists had initially settled on 5 to 9 servings of fresh fruits and vegetables and 3 to 4 servings of whole grains per day, putting refined carbohydrate (like crackers) at the top. However, when the actual pyramid was revealed, the numbers were quite different: 2 to 3 servings of fruits and vegetables and 6 to 11 of all types of carbohydrate, including crackers. The nutritionists said “eat less,” but the pyramid said “avoid too much,” which is basically saying, “don’t eat more.”

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Who orchestrated this sleight of hand? The Reagan administration—which also advocated that ketchup was a vegetable. One of the originators of the Food Pyramid, Luise Light, is quoted as saying: “Ultimately, the food industry dictates the government’s food advice, shaping the nutrition agenda delivered to the public. In fact, to the food industry, the purpose of food guides is to persuade consumers that all foods (especially those that they’re selling) fit into a healthful diet.”

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The Food Pyramid came under immediate fire, even from those within government. In response to the growing obesity crisis, the USDA was forced to back away from it, and in 2011 introduced MyPlate, which endorsed the low-fat myth. To its credit, at least MyPlate didn’t tout refined carbohydrates; however, its low-fat imperative continues to miss the point and it somehow still categorizes fruit juice and fruit and veggie straws as a vegetable. The evidence base for any and all of these classification systems is spotty at best and nonexistent at worst. The USDA has promoted the corporate takeover of the American Diet by ultra-processed food—which was, in fact, their intent.

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The Distinction between Calories and Food

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Ultra-processed food now accounts for 70 percent of the items in the supermarket, the majority of the food consumed in the US. It also accounts for 85 percent of the fare produced by the top twenty-five food manufacturers, providing 60 percent of all of our energy intake. It provides 90 percent of the added sugar in the diet.

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Nutrition Facts or Fictions?

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The FDA is in charge of the Nutrition Facts label. The question is, does it alert people to any dangers inside the package? Does it tell you what’s been done to the food? Or whether that food is healthy or not? Has that label made any difference to anyone’s health?

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An educated consumer can spot certain code words on things that were added (see Chapter 20). For instance, the one thing on a food label that’s actually been shown to predict the development of disease were the words “partially hydrogenated.” Of course, this is code for trans-fats. Despite good data demonstrating the toxicity of trans-fats as early as 1957, it wasn’t until 2006 that the FDA altered the Nutrition Facts label to list trans-fats separately. The problem is that the current food label can’t tell you what’s been adulterated (see Chapter 18) or subtracted (see Chapter 19).

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Unfortunately for us, despite continued talk about revamping the US Nutrition Facts label to highlight individual components of food, there’s no movement to address the degree of food processing. However, other countries have gotten on the bandwagon. Two classification systems are worth mentioning. Hopefully, publicizing their success can move the needle on this side of the pond.

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Chapter 18

Food Adulterations

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Toxins and Heavy Metals

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Environmental toxins build up in animals and plants, unleashing their metabolic havoc inside us. Although ostensibly they’re not added by the industry, some are the by-products of industrial chemical and food processing. For instance, mercury contamination of seafood is a well-documented problem. The FDA says, “Nearly all fish and shellfish contain traces of methyl mercury. However, larger fish that have lived longer have the highest levels of methyl mercury because they’ve had more time to accumulate it. These large fish (swordfish, shark, king mackerel, and tilefish) pose the greatest risk.” Where did the mercury come from in the first place? Thermometers? Maybe. But mercury is also a by-product of various technological “advances,” including the processing of corn into high-fructose corn syrup.

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Of course, there are many other toxins in the water that concentrate in the fat of animals, such as PCBs and dioxins. You might be lured into complacency thinking that eating plants instead of fish or animals would fix this problem, but you would be wrong. Heavy metals concentrate in underground and aboveground plant parts, inhibiting the process of photosynthesis. To avoid toxicity, plants have developed specific mechanisms by which toxic elements are excluded, retained at root level, or transformed into physiologically tolerant forms—for them, not for us. For instance, arsenic, cadmium, chromium, mercury, antimony, and lead have been found in American rice and in forty-five prepackaged juices, according to Consumer Reports. Particularly high levels have also been found in processed baby food. All in all, food processing results in heavy metal runoff, which finds its way into our food supply.

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Fig 18–1: Cuts of Italian, Argentinean, and US beef. Picture taken through a restaurant window in Rome, Italy, 2016. The Italian and Argentinean beef is homogeneous, while the US beef is marbled, a sign of fat deposition in the muscle, insulin resistance, and metabolic syndrome.

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Branched-Chain Amino Acids (BCAAs)

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Take a look at Fig. 18–1. If you’re a carnivore, each of these cuts of meat should make you salivate. They’re all delicious, but they’re not the same. Take a good hard look. What do you see?

The Italian and Argentinean cows were raised on grass from birth to slaughter in eighteen months. The meat is pink and homogeneous. These steaks taste phenomenal, but they’re a little on the tough side. The US cow, on the other hand, was raised on corn from birth to slaughter in six months. Corn fattens them up faster, so they can go to market sooner—good for cash flow. American cattle ranchers prize their beef for being so tender you can cut it with a butter knife. You can see the fat, the marbling; this is intramyocellular lipid, meaning fat inside the muscle. That’s insulin resistance.

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How does corn perform this magic? It’s replete in valine, leucine, and isoleucine, known collectively as branched-chain amino acids, or BCAAs. These are essential amino acids; you must eat them. They collectively account for 20 percent of the amino acids found in human muscle. BCAAs are also what’s in protein powder, consumed by bodybuilders in order to augment muscle mass. If you’re a bodybuilder, you need lots of them. But what if you’re not? What if you’re a mere mortal, and you consume more BCAAs than your muscles need? The excess travels to the liver to be metabolized for energy. There, the amino group is removed by an enzyme called branched-chain amino-acyl transferase (BCAAT), where they’re turned into organic acids like oxaloacetate. They then enter the mitochondria either for burning or to be turned into liver fat. Like fructose, this can predispose people to insulin resistance.

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Christopher Newgard at Duke University School of Medicine has demonstrated that patients with metabolic syndrome exhibit higher levels of these amino acids in the bloodstream. Newgard also showed that animals who clear BCAAs faster are protected from metabolic disease. In other words, industrial feeding of animals is making both the animals and the humans sick at the same time. Furthermore, countries whose cattle are pastured have a lower prevalence of nonalcoholic fatty liver disease, while those that import American beef have a higher rate.

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Omega-6 Fatty Acids

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The advent of the cholesterol hypothesis of heart disease in the 1970s (see Chapters 2 and 12) brought about wide changes in our dietary predilections. Butter was out, but not frying. Eggs were out, but not chocolate cake. What could we fry foods in and substitute as a binder for baking, all at low cost? This was the advent of industrial monoculture; Iowa and Nebraska are now awash with corn and soybeans as far as the eye can see.

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A rapid switch to seed oils occurred in the 1980s—and our diet became replete in omega-6 fatty acids through industrial processing of corn and soybean oils. This was only made worse by industrial corn feeding of cows, chicken, and fish, increasing the omega-6 content of their diet, and therefore of ours. Overall, our consumption of omega-6s tripled in the twentieth century. As a result, the concentration of linoleic acid (the main dietary omega-6 fatty acid) in our adipose tissue increased from 9 percent in 1959 to 21 percent in 2008.

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The problem is that omega-6 fatty acids are pro-inflammatory (see Chapter 7). They’re the precursors to arachidonic acid, the molecule that gives rise to a bunch of inflammatory mediators, such as prostaglandins, leukotrienes, and thromboxanes. These chemicals are desirable when you’re fighting off a foreign invader like an infection, but not when you’re fighting a blood vessel blockage. Nutritionists talk about our omega-6 to omega-3 ratio as an index of inflammation balance; it’s supposed to be 1:1. On a processed food diet, this rises to 20:1. The good news is that grass-fed animals have lower levels of omega-6s and higher levels of omega-3s, so consuming less processed options can bring your ratio closer to 3:1 (see Chapter 19).

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Cooking Your Goose

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Perhaps the most neglected but insidious adulterations are what we do ourselves in the process of cooking. To be sure, this isn’t strictly a processed food problem, but some components in processed food provide more opportunity for these dangerous chemicals to be formed during cooking. Here are four that you make right in your own kitchen.

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Trans-fats

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Yes, you heard that right. Trans-fats are very low in Real Food, but you can make them right on your stove from any unsaturated fat. In fact, you can turn one of the healthiest fats in your kitchen (olive oil) into the deadliest (trans-fat) with just extra heat. The reason? Unsaturated fats have cis-double bonds (see Fig. 7–3c). If you heat an unsaturated fat past its smoking point, that cis-double bond can isomerize (flip) into a trans-double bond, and voilà—a trans-fat (see Fig. 7–3b). As an example, a recent study fried some falafel in canola oil at high temperature, and then mixed the spent oil into rat feed; those rats that ate spent canola oil had a higher incidence of colon tumors and gut inflammation than those who ate canola oil cooked at lower temperatures. The lower the oil’s smoking point, the easier it is to turn it into a trans-fat. Extra virgin olive oil has the lowest smoking point of all the fats, at 160°C (320°F).

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The exception to this smoking point rule: saturated fat—because there are no double bonds and therefore nothing to isomerize. Even though lard got a bad name as a saturated fat, it’s way safer to fry in than any other oil.

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Polycyclic Aromatic Hydrocarbons (PAHs)

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There’s no doubt that PAHs, which are found in coal and gasoline, lead to cancer. This has been known since the 1930s, when scientists painted coal tar on rats (see Chapter 6) to elicit tumors. Essentially, PAHs bind to DNA bases, generating oxygen radicals, which can cause cellular mutations. Of course, PAHs from vehicle exhaust and tire erosion promote lung disease and various cancers, but barbecuing or even smoking your meat leads to PAH formation as well. A set of studies showed that charcoal briquettes generate PAHs released into the air even without meat on the grill (propane doesn’t), and then it worsens with chargrilling meat, which has definitely been shown to lead to DNA mutations and cancer. Chargrilling vegetables also causes PAH formation, albeit at a lower level. Though grilling is definitely one of America’s favorite pastimes—I’m a grill-master extraordinaire—the PAH problem can become an issue. More grilling means more risk, so as with almost everything in this book, moderation is key.

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Dietary Advanced Glycation End Products (Dietary AGEs) and Acrylamide

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Glycation (see Chapter 7) occurs naturally in the body and in food—especially in response to heat. Have you ever made slow cooker caramel? You take white sweetened condensed milk in a can, heat it very hot, and you get brown caramel. This is because the heat drives the Maillard reaction to cause the glucose and fructose to bind to the milk proteins, which makes AGEs. This happens in many processed foods, because heating is a method for killing bacterial contaminants.

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Until recently, dietary AGEs found in processed food were thought to be benign. However, recent studies show that they are absorbed through the intestine, enter the bloodstream, and then bind to receptors for AGEs (called RAGEs—yes, really) on liver cells, which drives a molecular signal for mitochondria to stop burning and promote fat accumulation instead. My colleagues at Touro University looked at the blood level of RAGEs in teenagers, and found that they were higher in those who were obese. Furthermore, the level of RAGEs in those adolescents correlated with the degree of blood vessel damage, suggesting that they are not exactly benign. Another recent study looked at the diets of seventy-eight thousand women versus the risk of breast cancer over an eleven-year period; those who consumed the most dietary AGEs had a 30 percent increased risk of developing breast cancer. Neither of these correlative studies prove causation, nor do they prove that the RAGEs came specifically from processed food, but given the fact that many processed foods undergo flash heating to reduce risk for bacterial contamination, it seems probable that the food processing is contributing both to dietary AGEs and to our burden of chronic disease.

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One particular dietary AGE, called acrylamide, has garnered the most attention. It is formed when carbohydrate and fat meet at high temperature. It’s one of the things we love about French fries—that great crunch. Acrylamide is also a by-product of the coffee roasting process. Dietary acrylamide is absorbed, carried to the liver, and turned into a compound called glycidamide, which is a potent carcinogen. One study showed that one-third of cancers tested showed alterations in the cancer genome associated with this compound, which can only be made from food. Furthermore, a recent meta-analysis associated acrylamide exposure with premenopausal breast and uterine cancer. None of these studies reach the threshold of causation to prove that those AGEs are actually causing damage. But when you look at the data, there is enough prospective correlation for concern.

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3-Monochloropropanediol (3-MCPD) Fatty Acid Esters

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These bad boys occur in processed food when a free fatty acid (in fat) meets a chloride ion (in salt) during the procedure of flash heating at 204ºC (400ºF) or greater. They are particularly toxic to the kidney and testis, but may also have effects on the liver and other organs. The European Food Safety Authority (EFSA) has put an upper limit on the amounts in foods, but the FDA has only issued a guidance, not a limit.

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Raw Data

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To cook or not to cook? Raw restaurants have been popping up in trendy urban areas, primarily with a vegan menu. Ostensibly, eating raw food is better for nutrition, since heating can destroy as much as 50 percent of vitamins B and C. But of course, this has to be balanced against the inactivation of any viruses or bacteria during cooking. Perhaps fermentation (e.g., kimchi, sauerkraut, miso, tempeh, kombucha) is the best of both worlds. Some like the slightly sour taste, and the bacteria tend to be benign and can help improve microbiome diversity. Furthermore, the production of lactic acid during the fermentation process provides natural food preservation, and apparently vitamin and mineral availability can be greater after fermentation, possibly due to the degradation of phytic acid, which can inhibit intestinal vitamin absorption. Ah, but two caveats … processed food won’t ferment. And frozen yogurt doesn’t count—if the label doesn’t say “live cultures,” it’s just dessert.

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Chapter 19

Food Subtractions

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Once upon a time, people stone-ground wheat kernels and made a rustic bread out of the pulverized semi-smooth flour (today that would be an artisanal loaf that costs about $15, if you can find it). But once the wheat was ground, it couldn’t be stored. Why not? Well, each wheat kernel is made of three parts: on the outside is the bran, composed of soluble and insoluble fiber that coats the kernel; inside there’s the endosperm, which is pure starch or what makes white flour; and, last, there’s the germ, which is where the nucleic acids, polyphenols, flavonoids, vitamins, antioxidants, and other micronutrients reside (this is the goodie bag). I remember as a kid every day my mother reaching into the fridge to grab the Kretschmer Wheat Germ and forcing a tablespoon down my gullet, to my great displeasure. I found it pretty nasty, but it was kept in the fridge so it wouldn’t get even nastier. The micronutrients in wheat germ are amines, purines, and phenolic acids, all of which can be easily oxidized to quinones, which render them both nonnutritive and disgusting. But if during the milling, you separate the fiber and the germ from the starch, you can keep the starch in five-pound bags forever without spoilage. Good for depreciation; good for business; bad for nutrition.

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Fiber One or Fiber Zero

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Stephen Jones is a geneticist and director of the Bread Lab at Washington State University, a think tank and baking laboratory where scientists, bakers, chefs, farmers, maltsters, brewers, distillers, and millers congregate to experiment with flavor, nutrition, and functionality of wheats, barley, and other grains (which sounds better than Disneyland!). What do all grains share? Bran, endosperm, and germ. Jones demonstrated that, during the process of milling, between 20 and 30 percent of the weight of the grain is the husk, the fiber. That’s a lot of waste—if you waste it.

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As discussed in Chapter 12, fiber is perhaps the single most important nutrient for health, because it both protects the liver and feeds the gut. Yet it’s the nutrient you don’t absorb, because the fiber isn’t for you, it’s for your gut bacteria. You have to consume it to make them happy. You’re not eating for two—but for a hundred trillion.

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Remember (see Chapter 12), there are two kinds of fiber: soluble (e.g., pectins that hold jelly together) and insoluble (e.g., cellulose, the stringy stuff in celery). You need both, and the geometry of each, in order to both protect the liver and feed the gut. Of course, you can mill the kernel, but now the protective husk has been breached; the starch is out and readily available for digestion and absorption, thus raising the glucose and insulin response. The processed food industry can claim that their product is whole grain because it started with whole grain, but it’s not what’s in the food, rather it’s what’s been done to the food that really counts.

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Got Your Juices Flowing?

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When intact, the fiber in Real Food does double duty in both protecting the liver and feeding the gut. The best fiber is the combination of both soluble and insoluble fiber, and that’s pretty much everything that comes out of the ground—until it’s processed.

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What can be done? Insoluble fiber doesn’t freeze well. I’ll prove it to you. Take an orange, put it in the freezer overnight. Take it out the next morning, and let it thaw. Then try to eat it. It’s not an orange anymore. It’s turned to mush. The ice crystals have macerated the cell walls of the orange, so that upon thawing, the water rushes in, destroying the texture of the orange. Of course, Big Food knows this. So what do they do? They squeeze it and freeze it. Now it lasts forever and there’s no depreciation. They’ve turned an orange into a commodity, that is, storable food.

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The question is, was anything lost nutritionally in the process of juicing? The answer is an emphatic yes—all of the insoluble fiber is now gone. The soluble fiber alone still has some benefit; orange juice moves the food through the intestine faster (to generate the satiety signal sooner), and the soluble fiber can be converted to short-chain fatty acids. But those benefits pale in comparison to the suppression of the insulin response associated with the combination of the two. Remember, it doesn’t matter where the fructose comes from—fruit, sugar cane, beets—without the fiber, it all has the same metabolic effect on your body.

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Furthermore, juice is as egregious a delivery vehicle for sugar as is soda. Studies of juice consumption show increased risk of diabetes and heart disease even after controlling for calories, while whole fruit demonstrates protection. It’s the processing that causes the problems. Our ancestors didn’t have the health complications associated with fructose because they ate the whole fruit.

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Don’t believe it? This will make it clear—metabolically, is applesauce more like apples or apple juice? It turns out from a glycemic excursion standpoint, applesauce is like apple juice. It might feed the gut, but it’s not protecting the liver.

What about smoothies? The blades of the Vitamix, Breville, or Magic Bullet shear the insoluble fiber to smithereens, same as juice. As a result, the fiber can’t assemble the latticework for the gel in the duodenum—so it’s not protecting the liver from the onslaught of the sugar in the fruit smoothie. In fact, the European Society for Paediatric Gastroenterology, Hepatology and Nutrition has suggested refraining from giving smoothies to children. On the other hand, if it’s a green vegetable smoothie, then there’s nothing to protect the liver from, so have at it.

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Why can’t you just supplement with fiber? After all, there are enough Fiber One bars, oatmeal cookies, and Metamucil for everyone. Except it doesn’t work like that. Metamucil is a soluble fiber (psyllium), but has no insoluble fiber. Furthermore, thus far Metamucil hasn’t succeeded as a stand-alone therapy for type 2 diabetes. It has been shown to improve cholesterol and insulin, but only after a healthy diet was instituted. It did nothing to reverse the effects of a bad diet, and the FDA refused to approve even a qualified health claim.

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Raiding the Goodie Bag

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The bran surrounding the wheat kernel provides one kind of health benefit, while the germ confers a second. It’s a little goodie bag filled with cofactors needed to keep the eight subcellular pathologies (see Chapter 7) at bay. When you make bread or any grain product, our current methods of processing strip away all the good stuff.

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Antioxidants such as vitamins C and E, carotenoids, and alpha-lipoic acid within the germ are also removed during processing, which are then thrown away along with the fiber fraction or are diverted to nutritional supplement companies who isolate and sell them under their own brand. Not enough antioxidants in the diet means oxygen radicals run amuck, putting the cell at risk for dysfunction and death, which can later manifest as chronic disease.

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Unquenched oxygen radicals disrupt necessary protein folding within the cell, which leads to metabolic havoc. In the pancreas, if you can’t fold your insulin molecules, you get insulin deficiency; in the liver, you get insulin resistance. Without antioxidants, the liver is at risk from oxygen radicals, and inflammation ensues. The lack of Real Food means the lack of fiber, vitamins, polyphenols, polyamines, flavonoids, and other antioxidants that normally keep those eight subcellular pathways running smoothly.

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Selective Outbreeding

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Over the last fifty years, we’ve used selective breeding of crops so that they’re sweeter, but some nutritionists are concerned that we’ve outbred the micronutrients. Examining this claim can be somewhat difficult, as much of the research has been done by the food industry, which as we’ve discussed has a vested interest in the outcome.

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Let’s look at tomatoes as an example. The pigment in them is the antioxidant lycopene, a precursor to vitamin A, which has been credited with improving heart health and eyesight, as well as reducing cancer risk. However, the more sugar and sweeter the tomato, the less lycopene there is. Processing kicks it down another notch, because heating the lycopene molecule causes oxidation and isomerization from the all-trans (active) form to the all-cis (inactive) form. Same is true for grapes—the higher the sugar, the lower the vitamin C.

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Grass and Omega-3s

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Omega-3s are fish oil, not snake oil. Omega-3s might just be the healthiest thing you can put in your mouth. There are two kinds—docosahexaenoic (DHA) and eicosapentaenoic acids (EPA)—both of which reduce the inflammatory response in the fat cell and prevent the release of free fatty acids (see Chapter 12). This keeps them from hitting the liver, where they would be packaged into triglyceride. It’s also why omega-3s can prevent heart disease, but only in those people with high triglycerides at baseline, because they’re omega-3 deficient to start with.

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Even more important is the effect of omega-3s on the brain, which is why EPA and DHA have both been added to baby formula (see Chapter 16). Breast milk is chock-full of them, provided mom has been eating them herself. Omega-3s also indirectly affect serotonin release from nerve terminals throughout the brain. When the area surrounding the nerve terminal releasing serotonin is inflamed, it inhibits serotonin release, which may explain why people whose bodies and brains are undergoing inflammation tend to be so irritable, even if they’re taking an SSRI or other antidepressant. In fact, one study found that a Mediterranean diet improved symptoms of depression, and in another fish alone reversed depression. Omega-3 supplementation can also reduce risk for depression in children and adults, and can serve as an adjunct to antidepressants. Last, administration of omega-3s, with Real Food or a supplement, to patients with recurrent self-harm (e.g., cutting, picking, scratching, burning; the ultimate expression of anxiety) showed a reduction in suicidality, depression, and daily stress. A recent trial gave omega-3s along with minerals to eleven-year-old kids with oppositional defiant disorder (the kids who routinely find themselves in the principal’s office), and within three months their aggression was reduced. Omega-3s are not a magic bullet to cure all of our ills, but a lack of them seems to cause general havoc on our brains and bodies. Real Food is the best way to ingest them, but supplements can also work to fix the deficiency.

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So, where are omega-3s in the diet? Normally they’re found in fish, but not just any fish—wild fish. When omega-3s are made by algae, wild fish eat the algae, and in turn we eat the fish. However, farmed fish eat corn—filled with omega-6s and branched-chain amino acids (see Chapter 18). You can also get omega-3s from eggs, but only from pasture-raised chickens, because they’re eating grass as opposed to corn feed.

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This extends to meat as well. Pasture-raised is omega-3 rich. And if you’re vegan, flax is your best bet.

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Egg-static

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While all amino acids are important, tryptophan is the most important, because it’s the hardest to come by. It’s an essential amino acid, which means the only source is your diet. It’s highest in eggs, poultry, and fish. Furthermore, it’s the only amino acid that can be converted by the brain into serotonin, which as we discussed above is the happiness/anti-anxiety/anti-depression/pro-sleep neurotransmitter.

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Eggs aren’t often included in processed foods because they curdle with time, go rancid when not refrigerated, and enough people are allergic to them. Fish isn’t usually a big seller as an ingredient in processed food, in part because certain fish don’t freeze well and most people want to see the catch to determine how fresh it is. Nuts also have tryptophan, and spinach and soy have a little as well. But what about a tryptophan pill? It will definitely increase your blood level, but not without a bunch of side effects.

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four out of five Americans are deficient in the nutrients that contribute to a functioning immune system (vitamins A, C, D, E, and zinc).

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Chapter 20

Food Additions

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Germ Theory

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Bet you never thought of a rural farm as a clean place, but they are, because the manure feeds the plants by fixing nitrogen and bacteria into the soil where they belong. Conversely, concentrated animal feeding operations (CAFOs; see Chapter 25) aren’t clean, as there’s no soil for the manure to fix the nitrogen, and no grass for the animal to eat to maintain a healthy intestinal microbiome. Feedlot animals eating corn are not only carbohydrate- and BCAA-overloaded, but they’re also micronutrient malnourished, which leaves them open to infection. Furthermore, pathogenic bacteria can take hold in the unsanitary conditions of confined feedlots, so animals are routinely given low doses of antibiotics to prevent sickness, promote rapid growth, and therefore maintain cash flow. Of the antibiotics sold in 2014, 80 percent were for use on livestock and poultry; only 20 percent were for human use. Those antibiotics given to animals survive slaughter and processing, and are then delivered to our intestines. This results in two human health hazards that are now playing out: metabolic syndrome, and antibiotic resistance in bacteria that can cause illness. The last two decades have seen an emergence of drug-resistant organisms that are now affecting people and altering the bacterial flora of the human gut. As discussed earlier, intestinal dysbiosis occurs when the “bad bacteria” like Firmicutes outgrow the “good bacteria” like Bacteroides. These bad bacteria can attack the intestinal epithelial cells to cause leaky gut, which drives systemic inflammation and contributes to metabolic syndrome (see Chapter 7). The FDA has urged stricter limits for antibiotics in livestock and use has dropped 38 percent between 2015 and 2018. However, lots of serious challenges remain.

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To top it all off, a new sugar-loving bacterium inhabits our intestine, and apparently we invented it. Clostridioides difficile is a nasty denizen usually held at bay by the “good” bacteria. However, hospitalized people receive big-time antibiotics, which kill off the good guys in the intestine and allow the C. difficile to run rampant. This has resulted in a completely new strain (more than 5 percent DNA difference) that’s become specifically adapted to the high sugar content of processed food—so maybe this will become an equal opportunity offender, and not just inside hospitals.

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It’s a Jungle Out There …

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When you’re trying to keep food cheap, maintaining crop yield is paramount. But nature has other ideas. Insects, weeds, rodents, and fungi also call the American farm “home.” Even today, a species of locust threatens the entire African food supply. Toxicologists of the twentieth century did a bang-up job on finding chemicals to control these pests. But what they didn’t do very well was assess their toxicities to humans.

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Dichloro-diphenyl-trichloroethane (DDT)

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Pesticides have been around since World War II, with the advent of DDT, an estrogenic compound that inhibits the insect life cycle and protects crops. The trouble is that it inhibits our life cycle as well, and promotes cancer in estrogen-responsive tissues. This was the basis of Rachel Carson’s Silent Spring (1962), and the tipping point of the environmental revolution. Even though DDT was officially banned by the EPA in 1972, it’s never really disappeared and remains one of the persistent organic pollutants, or POPs. It’s still in the environment, and its breakdown product DDE is still found in babies today. It’s been linked to reducing mitochondrial metabolism and promoting insulin resistance.

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Glyphosate

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Understandably, the food industry needed a new pesticide right away, so it introduced glyphosate (Roundup) in 1974. It was such a big seller that by 2014, 826 million kilograms were sprayed worldwide annually. From a strictly agricultural standpoint, glyphosate has been a panacea, as it controls all manners of weed growth. To improve glyphosate’s actions, Monsanto genetically engineered corn and soy (the primary components in commodity foods) to be Roundup Ready, specifically so that their growth wouldn’t be inhibited and yields would be further increased. Here’s the problem: chemically, the active ingredient in glyphosate (N-phosphonomethyl-glycine) is a derivative of glycine, the smallest amino acid found in proteins. The glyphosate is taken up by the plant, incorporated into the structure of newly formed plant proteins in lieu of glycine (not human proteins), and inhibits the enzymatic pathways that can turn simple carbohydrates into complex aromatic amino acids (phenylalanine, tyrosine, tryptophan). Remember, phenylalanine and tryptophan are essential amino acids, which means you have to eat them, and tyrosine comes from phenylalanine—meaning glyphosate-treated crops are going to be low in these amino acids necessary to make the neurotransmitters serotonin, dopamine, and norepinephrine.

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Glyphosate has also been shown to contaminate all different kinds of crops. From a nutritional standpoint this can be problematic, especially for vegans who don’t have an alternative source for these amino acids, but ultimately it’s a problem for all of us. Remember, the bacteria in our gut are plants. Therefore, glyphosate affects the microbiome, which could contribute to leaky gut and subsequent inflammation. Although glyphosate has been implicated by some in the rise of celiac disease and cancer, this remains correlation, not causation. In animal studies, glyphosate also appears to alter methylation (see Chapter 7), which leads to epigenetic changes and obesity in subsequent offspring.

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Similar to the subterfuge of Big Tobacco, Monsanto knew as early as 1985 that glyphosate had carcinogenic potential in animals, but did nothing about it. Finally, the data became overwhelming, and in 2015 the WHO reclassified glyphosate as a probable carcinogen in humans. Since then, US courts have fielded forty-two thousand class action lawsuits against the industrial giant Bayer, which bought Monsanto in 2018. These concerns have been minimized by some scientists, and the upper limit for clinical toxicity has been increased from 6 to 100 by others—the only issue is that these scientists take money from Monsanto.

There’s been a call among academics to reassess the entire glyphosate toxicity profile, but the industry continues to resist. In 2020, Bayer settled all its glyphosate class actions suits for a mere $10 billion, and they’re still selling it worldwide.

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Atrazine

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This herbicide has been in use since 1958, in particular for corn. Atrazine (Buctril) inhibits photosynthesis, the primary energy pathway in plants. We humans don’t do photosynthesis, so it should be safe for us, right? Atrazine is a known teratogen (causes birth defects) in amphibians, so it’s affecting more than just plants. It’s also been shown to induce mitochondrial dysfunction and insulin resistance, diabetes, and methylation, influencing epigenetics. While Syngenta has always publicly maintained that atrazine is safe as used, it nonetheless paid $105 million in 2012 to settle a class action lawsuit alleging that it had contaminated Midwestern towns’ water supplies, having admitted no wrongdoing. Apparently the Trump administration agreed with Syngenta, as the EPA discarded the provisions of the Food Quality Protection Act (1996) to give atrazine a clean bill of health in September 2020. Many other pesticides have been shown to have detrimental effects on human mitochondria and insulin resistance. Perhaps even more concerning is that some of these pesticides may be acting like selective antibiotics, killing off both the animal’s microbiome and our own, letting the bad methane-producing bacteria take its place (see Chapter 25). This can result in leaky gut, inflammation, insulin resistance—and climate change.

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Flavor Enhancers

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Today, everyone expects bold flavors from their food. Scratch cooks can add spices. But processed food companies have to appeal to a wide array of palates, and many of those spices lose potency on the shelf. The industry has instead developed flavor enhancers to pique the palate of processed food consumers. Unfortunately, they have effects past the tongue that can promote chronic disease.

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Diacetyl

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Diacetyl is used as a butter flavoring in microwave popcorn and butterscotch. It easily decomposes to acetaldehyde, which is a known lung and liver toxin. Diacetyl is also associated with a severe and irreversible respiratory condition called bronchiolitis obliterans, which leads to inflammation and permanent scarring of the airways. In 2000, a microwave popcorn plant tested its employees, and 25 percent had compromised lung function. There was little or no response to medical treatment, and several of the workers, some only in their thirties, ended up on waiting lists for lung transplants. Breathing microwave popcorn is bad for you, although no one has yet shown that eating microwave popcorn is bad for you, unless you also have diverticulitis (inflammation of the colon), in which case you’ll have a flare and never do it again.

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Potassium Bromate

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Potassium bromate is used to strengthen bread and cracker dough, helping it rise during baking. It’s listed as a known carcinogen by the state of California, and a possible carcinogen by the International Agency for Research on Cancer. The process of baking converts most of the potassium bromate to benign potassium bromide, but not necessarily all of it. The UK, Canada, and the EU have all banned potassium bromate; the FDA issued an advisory in 1991, but the US still allows its use.

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Natural Flavors

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Did you ever wonder what a “natural” or “artificial” flavor was? Aside from salt, sugar, and water, natural or artificial flavor is the most commonly listed item, appearing on one out of seven food ingredient lists on the Nutrition Facts label. But what are they exactly? They’re chemicals, and the company doesn’t have to tell you what’s in it, and the FDA doesn’t require them to. Since most flavors are nonpolar, it usually means there’s an emulsifier (e.g., polysorbate 80), a solvent (e.g., propylene glycol), and a preservative (e.g., butylated hydroxyanisole; BHA), although it could be several of one hundred different items. The companies that make flavors also make fragrances. In general, the dose is small, so disease is unlikely—unless you have an allergy. But we don’t know for sure.

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Emulsifiers

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Lecithin (chocolate), polysorbate 80 (shortening), carboxymethylcellulose (salad dressing), and carrageenan (ice cream) are added to foods to maintain food consistency upon storage. After all, who wants clumpy ice cream? These molecules have one polar end and another nonpolar end, so they’re able to bind fat and water together to keep them from separating. However, emulsifiers are also detergents, and can strip away the mucin layer that sits on top of and protects intestinal epithelial cells from the bacteria, thus predisposing individuals to intestinal disease, food allergy, or leaky gut. Thus far, however, the FDA states they haven’t found cause for human concern.

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Don’t Talk to Me, I’m Hormonal

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Hormones are super important (spoken as an endocrinologist)—without them, the human species would die out. But what happens when extra hormones hit the food supply? In the case of the estrogenic pesticide DDT, it led to cancers. Unfortunately, we have not learned our lesson. Numerous hormones are used throughout the food supply to boost yield or prevent spoilage, but with numerous untoward side effects.

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Bovine Growth Hormone

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Recombinant bovine somatotropin (rBST; aka bovine growth hormone) is given to cows used for both dairy and beef production. It could influence human health in two ways.

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Dairy and cancer risk. rBST induces a hormone called IGF-1, which boosts a cow’s milk production by 15 percent—a boon to dairy farmers. IGF-1 is also a growth factor associated with human breast and prostate cancer. The concern is whether bovine IGF-1 present in milk is absorbed across the human intestine, predisposing milk drinkers to increased risk for cancer. The data demonstrates that milk drinkers do have a slightly increased blood IGF-1 level, but it’s not clear that this came from the milk itself, as almond milk consumers also have higher blood IGF-1 levels. Thus far, there hasn’t been any convincing epidemiologic evidence of an increase in human cancers from drinking milk. Today, the US is the third largest dairy exporter, annually shipping 2.2 million tons of milk powders, cheese, butterfat, whey, and lactose across the world. Considering the countries to which we sell our milk also have increased risk for metabolic syndrome and autoimmune disease, could this be a contributor? The good news is that rBST use has declined; in 2002, 22.3 percent of dairy cows were injected, but that number today is close to 10 percent.

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Beef and inflammation. The one thing we’re sure of is that rBST increases udder tissue inflammation and infection in the cow, which requires increased use of antibiotics for the animals. In 1999, the European Union’s Scientific Committee on Veterinary Measures Relating to Public Health said in a press release that six commonly used growth hormones had the potential to cause “endocrine, developmental, immunological, neurobiological, immunotoxic, genotoxic, and carcinogenic effects.” The EU subsequently banned imports of US beef because of scientific concerns about hormones. The US government successfully challenged the ban in the World Trade Organization.

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Estrogen

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In 1979, the island of Puerto Rico experienced an epidemic of early breast development in children, both in girls and boys. As it turns out, enterprising farmers were spiking the chickens with estrogen to increase their breast size, so they could sell the meat at a profit. If this were an isolated incident, you could just chalk it up to foolish avarice. But virtually the same thing happened again in 2002 at a Netherlands animal feed company. They used the contraceptive agents medroxyprogesterone acetate and estradiol in the feed marketed to thousands of farmers. Suddenly, young Dutch girls and boys were sprouting breasts. This caused a lot of damage in pig farming and the feed sector; lots of farmers went bankrupt. The Dutch government knew of the risks for cancer, diabetes, depression, obesity, cardiovascular disease, and immune and birth defects, yet instead of initiating a legal remedy, they concealed the threat and covered up the incident for years.

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There are many other estrogenic compounds floating around our environment, because it doesn’t take much for any molecule to be an estrogen—and the estrogen receptor is the most promiscuous of them all, binding to many classes of compounds, which is why everything seems to cause breast cancer. One common chemical is bisphenol A (BPA), added to baby bottles, cash register printer receipts, and food. It’s not added directly to the food, rather it’s indirectly added to the interior of the can, in order to protect the food from taking up metals and to retard spoilage. BPA seeps in anyway, and high levels in the blood correlate with obesity and insulin resistance (similar to that seen with DDT/DDE). Another class of compound called parabens is used as a preservative in cosmetics and lipstick, and in certain foods such as tortillas and muffins. They can alter the expression of genes, including those in breast cancer cells, and contribute to impaired fertility in women. My UC Berkeley colleagues and I even showed that parabens can advance the timing of puberty in girls.

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You’re So Well Preserved—for Your Age

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How long should food last on the shelf? It could rot, or it could mold, or it could go stale. But it doesn’t—witness the miraculously preserved twenty-year-old Hostess Twinkie and the ten-year-old McDonald’s cheeseburger, both stars on YouTube. Chalk it up to the chemicals the industry uses to preserve food. But, like formaldehyde, that doesn’t mean you want to ingest it; it might preserve your insides, too.

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Butylated Hydroxyanisole (BHA) and Butylated Hydroxytoluene (BHT)

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These are standard preservatives for chips and meats. However, the International Agency for Research on Cancer categorizes BHA as a possible human carcinogen, and it’s listed as a known carcinogen under California’s Proposition 65. These designations are based on consistent evidence that BHA and BHT causes tumors in animals—but data in humans are hard to come by.

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Propyl Gallate

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Propyl gallate is a preservative in products that contain fats, such as sausage, vegetable oil, soup bases, and even chewing gum. There’s some evidence that suggests it may also have estrogenic activity. It’s been implicated in a rat model of Parkinson’s disease, but not with any human disease at this point.

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Nitrates and Nitrites

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Nitrates and nitrites are the preservatives in cured meats, such as bacon, salami, sausages, and hot dogs. Although they can prolong a food’s shelf life and give it an attractive hue, they’re directly implicated in human disease. Nitrates turn into nitrites, which react with amino acids to form nitrosamines, which then react with nitrogen to form nitrosoureas. These are among the most potent carcinogens around and are associated with virtually every cancer of the alimentary tract: stomach, intestine, and colon. In 2010, the WHO declared nitrates as probable human carcinogens, and there are now regulations as to how many can be added to your cured meats, though we still don’t know what a safe amount actually is.

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Trans-fats

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Trans-fats were probably the single most important reason for the advent and success of processed food. Invented in 1911, the first trans-fat, called Crisco, hit the market, and by 1920 virtually every bakery product sold in America was laced with it, since it acts as a preservative and a hardening agent. Trans-fats can’t go rancid, because the trans-double bond can’t be oxidized by bacteria, as they don’t possess the enzyme to cleave it. The problem is that our mitochondria are refurbished and repurposed bacteria—they even have their own DNA—meaning they don’t produce the enzyme either, so trans-fats line our arteries and generate oxygen radicals, leading to metabolic syndrome.

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Gandhi said, “First they ignore you, then they laugh at you, then they fight you, then you win.” The first glimpse of the danger of trans-fats came in 1957, when an immigrant German biochemist at the University of Illinois named Fred Kummerow demonstrated their presence in arterial plaques of rats. This finding was ignored for thirty years, until corroboration in 1988. It was then that Kummerow launched a scientific campaign against trans-fats, and he was laughed at until 2006, when the FDA agreed that the science was strong enough to warrant a warning label on foods. Kummerow filed a petition with the FDA to ban trans-fats, while Big Food was kicking and screaming. He was ninety-nine years old when he sued the FDA in 2013, and finally trans-fats were taken off the generally recognized as safe (GRAS) list (see Chapter 24).

Nitrates and trans-fats are the only items that have ever been removed from the FDA GRAS list, so you know they must be bad (see Chapter 24).

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Sugar—It’s a Flavor Enhancer and a Preservative and an Endocrine Disruptor, and Oh So Much More

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Sugar makes food brown. Indeed, we love the brown color and caramel taste. Chapter 7 introduced the Maillard, glycation, browning, or aging reaction. Every time this reaction occurs, it throws off an oxygen radical that can damage the cell.

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Sugar raises the boiling point. This allows for caramelization to occur, which like we said is very tasty, but again this is just the Maillard reaction, which, over time, can cause your cells to age. There’s also data to suggest that fructose could “caramelize” your hippocampus, which might contribute to memory decline.

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Oh, and by the way, sugar is addictive. They don’t want you to know, they’ll deny, deny, deny; the same way the tobacco industry executives testified in Congress, “I believe that nicotine is not addictive.” Read on to examine the evidence.

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Chapter 21

Food Addictions

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There’s no doubt that we eat more than we used to. But why? We have a negative feedback system in our brains called leptin, which, until fifty years ago, told us that we had enough energy to burn, and therefore prevented us from overeating. However, as I explained in Chapter 2, insulin blocks leptin signaling (leptin resistance) at the hypothalamus, mimicking brain starvation, which causes us to overeat in an attempt to drive the leptin level

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higher. That being said, if insulin and leptin were the only problems, then we would overeat all types of foods—but we don’t usually overconsume fruits, vegetables, or beans/legumes/lentils. No, the foods we overeat are all found as components of fast food.

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Scientists have validated the Yale Food Addiction Scale (YFAS), which demonstrates that specific foods possess addictive properties. Furthermore, a pediatric YFAS argues that food addiction is common, especially among obese children.

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Yet, not everyone subscribes to the idea that specific foods or ingredients can function in this way. For instance, a group of academics in Europe called NeuroFAST doesn’t accept the concept of food addiction; they prefer to label it as “eating addiction.” In contrast to the YFAS, this group has proffered its own eating addiction scale in which all foods are treated similarly. NeuroFAST claims that it’s not the food, but rather the behavior that distinguishes the phenomenon.

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This isn’t just a semantic argument—if it’s about the food, then the food industry bears some culpability; but if it’s about eating, then it’s your fault and the industry gets off scot-free. NeuroFAST also states that even though specific foods can generate a reward signal in the brain, they still can’t be considered addictive because food is essential to survival. How could something essential be addictive? After all, nicotine, alcohol, heroin, and cocaine are not essential

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From their website, in their own words:

In humans, there is no evidence that a specific food, food ingredient or food additive causes a substance based type of addiction (the only currently known exception is caffeine) … Within this context we specifically point out that we do not consider alcoholic beverages as food …

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So NeuroFAST acknowledges caffeine’s addictive properties, but they separate it from food. NeuroFAST also recognizes alcohol as addictive, but they also separate it from food. Why? Natural yeasts constantly ferment fruit while still on the vine or tree, causing it to ripen, yet NeuroFAST says that purified alcohol isn’t a food. Rather, alcohol is a drug—we used to give it to women to stop premature labor. Once it’s processed and purified, its properties change.

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New Definition, New Rules

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Our UCSF research group has explored the question of addiction to specific components of food by using the opiate antagonist naltrexone, which blocks the reward system and is often prescribed for other addictions including alcoholism. From these studies, we’ve defined a phenomenon called reward eating drive (RED), which induces people to consume “tasty” foods unrelated to hunger or caloric needs. In a series of clinical research experiments, we showed that some people experience a loss of control with certain foods, and those that do tend to binge on high-sugar/high-fat foods (think chocolate cake). This aberrant behavior is driven by dysfunction of the reward system.

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Fast Food Nation

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Americans are fast food junkies—up to 37 percent of adults eat some form of it every day.

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Salt

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In humans, salt intake has traditionally been conceived as a learned preference rather than as an addiction. Four-to-six-month-old infants establish a salt preference based on the sodium content of breast milk, water used to mix formula, and diet. Fast foods are relatively high in salt, energy density, and caloric intake. On the other hand, studies show that people can reset their preference for less salty items. This has been demonstrated in adolescents deprived of salty pizza and hypertensive adults who were retrained to consume a lower sodium diet over eight to twelve weeks.

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Furthermore, salt intake is tightly regulated. For example, patients with a pediatric disease called salt-losing congenital adrenal hyperplasia (which I specialized in treating) lack the hormone that retains salt by acting on the kidneys. These kids urinate salt constantly, taking water with it, leading to low blood pressure and eventually shock. They drink the pickle juice right out of the jar. But when we give them back the missing hormone, called fludrocortisone, this craving stops.

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Last, the UK government engaged in a secret mass campaign with food manufacturers to reduce public salt consumption, and saw a 40 percent reduction in hypertension and stroke without signs of addiction. Why aren’t we doing that in the US?

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Fat

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The high fat content of fast food is vital to its rewarding properties. There may be a high-fat phenotype among some people, characterized by a preference for specific high-fat foods and weak satiety in response to them, which acts as a risk factor for obesity. However, it’s unlikely for most people, who get full from drinking whole milk as opposed to low-fat. So-called high-fat foods preferred by people are almost always also high in carbohydrate (e.g., potato chips, pizza, donuts)—then add sugar, and preference for high-fat foods goes up even more. Conversely, if you take the carbs out and just eat the fat (as in low-carb and ketogenic diets), people eat less.

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Caffeine

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Caffeine is a model drug of dependence, meaning it meets all the criteria for addiction in children, adolescents, and adults. People not only become tolerant of caffeine, but also experience physiological withdrawal when they try to kick it. However, in today’s fast-paced world, we’ve leaned even more into caffeine and as a result are sleep-deprived. To add insult to injury, most people ingesting caffeine do so with sugar—look at Red Bull, Coca-Cola, and low-fat vanilla lattes with two extra pumps of syrup. Starbucks and its signature Mocha Frappuccino have gone global. These drinks provide impetus for caffeine-dependent customers to frequent fast food franchises to get even more of their fix.

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Sugar

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Other than caffeine, the foodstuff with the highest score on the YFAS is sugar. In fact, adding a soda to a fast food meal increases the sugar content tenfold; multivariate analysis demonstrates that only soft drink intake, not animal products, is correlated with changes in BMI. Sugar has also been used for its analgesic effect in neonatal circumcision, suggesting a link between sugar and opioid tone in the brain’s reward center. Some, but not all, self-identified food addicts describe sugar withdrawal as feeling “irritable,” “shaky,” “anxious,” and “depressed,” symptoms also seen in opiate withdrawal. Other studies demonstrate the transference of addiction from one toxic addictive substance to caffeine, nicotine, and/or sugar—meaning sometimes when you stop smoking, you start drinking. Sometimes when you stop drinking, you start eating. All of these behaviors activate the same dopamine reward system.

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Human imaging studies also support the contention that sugar, and specifically the fructose molecule, is addictive. Fat activates sensory areas where you experience mouthfeel, while sugar activates the limbic system, the emotional part of the brain, where you experience reward. Taking the sugar molecule apart, glucose and fructose activate different parts of the brain, with fructose specifically lighting up the reward center. Sucrose establishes hardwired pathways for craving in these areas that can be identified by fMRI. Furthermore, the effects of fructose on dopamine are attenuated in obese adolescents, suggesting that they have fewer receptors due to tolerance.

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Animal studies also show that sugar, and specifically the fructose molecule, is addictive. Sugar administration induces behavioral alterations consistent with dependence (i.e., bingeing, withdrawal, craving, and cross-sensitization to other drugs of abuse, consistent with addiction). Indeed, sweetness surpasses cocaine as a reward in rats. In fact, addicting rats to opioids makes them binge on fructose instead, because of alterations in the reward center, and especially in adolescent rats. All in all, while sugar doesn’t exhibit the DSM-IV standards of tolerance and withdrawal, it sure as hell meets the DSM-5 standards of tolerance and dependence. So, whatever criteria you decide to use, it’s now obvious—sugar is addictive and many of us are junkies.

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Is Sugar a Gateway Drug?

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The prevalence of substance use disorders, such as opioids, has risen steadily. Could these people be primed for reward early on? And could sugar be their experience of this feeling? We know that sugar activates opioid pathways in the brain, even in newborns. We also know that certain genetic traits increase risk for both sugar seeking and drug addiction. While these are correlation, not causation, it’s not too far a stretch to imagine that some people are more susceptible to the addictive effects of sugar than others. This is similar to what is seen in alcohol—40 percent of Americans are teetotalers, 40 percent are social drinkers, 10 percent have a binge drinking problem, and 10 percent are bona fide alcoholics. We don’t know the percentage of people who are addicted to sugar, but how many people say, “I have a horrible sweet tooth”?

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So let’s say you’re one of these sugar-addicted people. Maybe you employ lots of restraint to stay away from the obvious triggers—soda, cakes, ice cream. But you still have to eat. What if food has sugar mixed or baked right into it, and you don’t even know it? Sugar is added to food as sucrose, high-fructose corn syrup (HFCS), honey, maple syrup, or agave. Can you break an addiction if the addictive substance is so pervasive that it’s in everything? In general, each sugar molecule is assumed to consist of half fructose, half glucose, although this percentage has recently come into question when an analysis of store-bought sodas in Los Angeles revealed a fructose content as high as 65 percent. The ultra-processed food category (see Chapter 17) is where 65 percent of the sugar in our diet lives—and it’s all been added. In fact, there’s only one place added sugar is not—Real Food.

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The hedonic nature of sugar is also revealed by examining its economics. For instance, coffee is price-inelastic (i.e., increasing price doesn’t reduce consumption). For example, when prices jumped in 2014 due to decreased supply, Starbucks sales didn’t budge an inch. As consumables go, soft drinks are the second most price inelastic, just below fast food. Raise the price 10 percent (e.g., with taxes), and consumption drops only 7.6 percent, mostly among the poor, as we saw in Mexico.

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Food or Food Additive?

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So how do we reconcile these two conflicting ideas of food addiction vs. eating addiction? It would appear that of the consumables prevalent in the Western diet, only sugar and caffeine have hedonic properties, that is, increasing food consumption independent of energy need. But if sugar is a food, meeting an energy need and necessary for survival, how could it qualify as being addictive?

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First, as discussed in Chapter 12, sugar isn’t necessary for survival. Second, does sugar legally qualify as food? Without appearing too lawyerly, it depends on how you define the word “food.” The Food, Drug, and Cosmetic Act (FDCA, 1938) 321.201(f) defines the term “food” as: (1) articles used for food or drink for man or other animals, (2) chewing gum, and (3) articles used for components of any such article. The first rule of vocabulary is that you are not allowed to use the word in the definition. The Merriam-Webster Dictionary defines “food” as: “a material consisting essentially of protein, carbohydrate, and fat used in the body of an organism to sustain growth, repair, and vital processes and to furnish energy.” Fructose supplies energy, so that makes it a food, right? But can you name an energy source that isn’t nutrition by any dietitian’s estimation, for which there is no biochemical reaction in the human body that requires it, and that causes disease when consumed chronically and at high dose implying addiction? Answer—alcohol. It has calories (7 kcal/gm), but it’s clearly not nutrition. When consumed chronically and in high dose, alcohol is toxic, unrelated to its calories or effects on weight. Not everyone who is exposed gets addicted, but enough do to warrant public health interventions. Clearly, alcohol is not a food. Similarly, sugar isn’t a food, as it’s also not essential for animal life, causes damage in chronically high dosage, and a sizable percentage of the population is addicted.

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It’s All in the Processing

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It’s true that certain foods are necessary for survival—while others aren’t. We need essential nutrients that our body can’t make out of other nutrients, but there are only five classes: 1) essential amino acids (nine out of the possible twenty found in proteins); 2) essential fatty acids (such as omega-3s and linoleic acid); 3) vitamins; 4) minerals; and 5) fiber. Furthermore, none of these essential nutrients are remotely addictive. Of the hedonic substances found in food, only alcohol, caffeine, and sugar are addictive—and these are food additives, not foods in themselves.

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When you process and purify something, you change its properties. Coca leaves are medicinal in Bolivia, but cocaine is a drug. Opium poppies were medicinal, but heroin is a drug. Caffeine is found in coffee (medicinal for many), but concentrated caffeine (e.g., in weight loss remedies) is a drug. In ancient times, sugar was a spice. Through the Industrial Revolution, it was a condiment. Now that it’s processed and purified, it’s a drug. How is this any different from refined sugar? Refined sucrose is the same compound found in fruit, but the fiber has been removed, and it’s been crystallized for purity. This process of purification turns sugar from food into drug, just like alcohol and caffeine. And just like these addictive consumables, sugar is a food additive. The minute the dose exceeds the liver’s capacity to clear and metabolize it, it’s in the brain, driving reward in all people, and addiction in some. And it’s being added by Big Food to 74 percent of the food supply, because when they add it, we buy more.

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Chapter 22

Food Fraud

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When asked to comment on food fraud, an executive of a well-known food manufacturer said, “We don’t want our company name and the words ‘food fraud’ in the same sentence.” Right. Don’t ask, don’t tell. This is the food industry’s dirty little secret, and they’ll do anything to keep it that way, because all food companies trade on trust. This also means there aren’t good data on food fraud—we really only hear about it when someone gets caught.

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We could literally be consuming anything and everything known to man—I’m sure some things not even known to man!—and remain completely oblivious to it. It’s estimated that 20 percent of the seafood sold is mislabeled, and the records show that 1.7 lawsuits per week are filed in the Northern District of California for some form of food fraud.

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Guilty of Passing Bad Food …

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Food fraud is literally defined as “misrepresentation as to the state of the food.” There are six different forms of it and some engender health risks while others don’t, but they all share three things in common—alteration of the food itself, lying to the consumer, and a profit motive. A seventh version, called misbranding or misrepresentation as to the state of the food label, will be discussed in reference to the FDA in Chapter 24. Below are six examples of food fraud that reached your restaurant’s or grocery store’s shelves without your knowledge:

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Dilution/adulteration. Something is added to the food to disguise or extend it. Milk is a common vehicle. In 2019 in India, milk was determined to have lower fat levels than advertised because the cows are inadequately fed. Another dilution is olive oil; it’s estimated that up to 80 percent of Italian virgin olive oil is neither Italian nor virgin.

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Substitution. It’s common for restaurants or food stands to substitute something of lesser value in an attempt to reap a higher profit. Vendors in New York City got caught selling beef gyros or goat gyros advertised as lamb; this occurs more frequently when the meat is shredded and mixed together. Another common substitution occurs in fish sales, where one study demonstrated that 21 percent of the fish underwent substitution, and that one out of every three establishments visited sold substituted seafood. Fish substitution is more likely to occur in restaurants (26 percent) than at grocery stores (12 percent). A common substitution occurs when tilapia (containing red dye), which costs $3.51 p er p o u n d, i ss w a pp e d o u t f ors na pp er, w hi c h cos t s ab o u t$ 15 per pound. Of the species tested, sea bass and snapper had the highest rates of mislabeling (55 percent and 42 percent, respectively). Much of the substituted seafood is labeled as a local favorite, while the truth is it may have been flown from halfway around the world.

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Intentional contamination/concealment. A famous international case occurred in 2008, where melamine was found in infant formula and other dairy products. In China, the milk was being diluted by dairy producers so more of it could be sold. The dilution decreased the amount of protein in milk, so the dairy producer replaced the natural milk protein with melamine, a nitrogen-rich compound used to make kitchen countertops. When ingested, melamine causes kidney stones and kidney failure. The melamine in milk killed six infants and sickened over 300,000 people in China, but dairy products laced with melamine were exported around the world and made it to our shores. Luckily no one in the US died. Another example is Parmesan cheese. In 2012, cellulose, a by-product of wood digestion, was added to several brands; in fact, one brand didn’t even have any cheese in the product at all.

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Country of origin. Many food items are prized because they come from unique places. But what if that place isn’t so unique? For instance, beer-battered pollock might come fresh from the waters of Alaska, or it might come frozen from a basin in China. More likely, the reason for this kind of fraud is to avoid paying duty on imported goods, such as alcohol.

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Organic. You might think that buying organic would save you from fraud. You would be wrong. The markup on organic is enormous, anywhere from 25 percent for avocados to 65 percent for milk. Furthermore, there’s a clear economic impetus to mark individual items as organic, as the only way to be caught is through laboratory analysis. One fraudster netted $142 million for faking organic on the label, and then spent his ill-gotten gains on Las Vegas casinos and sexual escapades. He eventually committed suicide rather than go to jail.

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Counterfeiting. Perhaps the most brazen of all food fraud occurs in the luxury space. Finding out that some high rollers were duped by the counterfeiting of rare wines and scotches may give you a moment of schadenfreude satisfaction, but this is a very alarming issue. If they can do that with something under that much scrutiny, imagine what they can do to you.

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Big Food’s Albatross

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You might think food fraud would be the purview of just a few bad apples, but it’s even more prevalent with processed food, where the source and identity of individual food components can be a “trade secret.” Consumers demand an abundant and constant food supply, so Big Food sources ingredients from the cheapest suppliers from abroad. Garlic, soy, chiles, rice—all imported. It doesn’t matter if the product is made in the US if the raw ingredients come from somewhere else. It is not unusual for processed foods to have five or more ingredients in them—for each additional ingredient, the chances of adulteration of that processed food increases to the 1.7 power. This is particularly true for the organic label on imported foods. Food producers in developing countries are entrusted with growing and purifying the raw materials with virtually no oversight. But why should Big Food care as long as it turns a profit, and no one gets acutely sick?

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Don’t Make a Federal Case Out of It

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When it affects public health (think melamine), we expect our USDA and FDA to spring into action. But do they? Can they? The FDA has largely steered clear of the issues of processed food fraud because they don’t have boots on the ground in every food-producing country in the world, and their charter is to ensure food is safe, not authentic.

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When discovered, food fraud can sour trade relations. For instance, in 2013, horsemeat and pork were found in 33 percent of European products that were represented to contain only beef, sometimes a complete substitution. In response, most countries in Europe chartered their own food fraud units, or at the very minimum, nominated a person or group to take on the responsibility for investigating domestic cases. Nonetheless, corruption and graft abound. In the UK, the food industry plays nice with the regulators—that way, if they get caught, they can ante up a settlement and keep it out of the newspapers.

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What distinguished the horsemeat fraud case of 2013 from the melamine fraud case of 2008 was geography, timing, and illness. Melamine was a China problem, but horsemeat was a Western problem. Serendipitously, the Global Food Safety Initiative (GFSI) conference was being held in Barcelona, Spain, in 2013, at the same time, and the food industry jumped on it. Their business is based on trust, which could be rapidly undermined if consumers really knew just how pervasive food fraud is.

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Big Food, trade associations, and some academics remain in an unholy alliance to cover up and paper this over. How are they entitled to self-regulate when they’re complicit in deceiving the public? But here’s the real problem: why is Big Food more worried about consumers’ trust regarding food fraud (which rarely kills), but less concerned about consumers’ trust about processed food and NCDs (which kill millions)? Because it’s easier for the public to understand and be horrified by horsemeat, rather than the science behind what will actually poison, addict, and kill them.

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Food “Truthiness”

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Big Food’s approach to dealing with fraud has always been flawed—though isn’t food fraud the responsibility of their food safety teams? The good news in the melamine case was that it was a problem both in food fraud and safety. It was the food safety leaders from Danone, Walmart, and Ahold who created the Food Fraud Think Tank, which reported directly to the board of directors of the GFSI. The Food Fraud Think Tank also consisted of INSCATECH, a US food fraud detection and prevention company; Eurofins, a food testing laboratory; and Professor John Spink of Michigan State University. The Food Fraud Think Tank was tasked with making recommendations to the GFSI Board of Directors as to how to handle food fraud going forward.

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The Board of Directors represent the largest food producers, restaurant chains, and retailers in the world. In other words, is Big Food the fox in charge of the henhouse? Unfortunately, only about half of the companies on the board of GFSI felt it was their responsibility to even address fraud. The Food Fraud Think Tank made two recommendations: companies must conduct vulnerability assessments (which they did); and they also must develop food fraud control plans (which they didn’t).

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Who’s in Charge? And Who’s Responsible?

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Right now, Big Food’s methods for detecting and remediating food fraud rest with the corporate executives in charge of safety, who aren’t fraud professionals. Rather, the food fraud professionals are those in charge of risk management, supply chain security, procurement, brand protection, and international law. They’re trained to combat fraud, but corporate execs are under orders to buy food at the lowest possible price, with the magical expectation that the food they are buying is authentic and high quality. Every day they go to work inherently conflicted.

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Big Food’s procurement system is like the Wild West; they’re at the mercy of other countries who supply us. But why does Big Food outsource in the first place? Sometimes it’s because certain foods only grow in certain regions, such as spices, vanilla, olive oil, cocoa, and coffee. However, the climate in the US is diverse enough to grow almost everything here. California, Florida, and Hawaii can sustain cocoa, coffee, and vanilla plants in addition to most citrus fruits. In other regions of the US, foods like honey, corn, wheat, cherries, grapes, pears, apples, peaches, plums, tomatoes, carrots, lettuce, grains, and a host of other produce can be grown in abundance. It would just cost more than our current outsourcing.

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Statistics vary slightly, but why does two-thirds of the apple juice in America come from China, and why does over 50 percent of orange juice and concentrate come from Brazil (especially since Brazil is dousing their oranges in glyphosate)? Why do we get milk powder from India, or seafood from Vietnam? Big Food has done the cost calculations down to the hundredth of a penny. Legitimate producers who grow or procure authentic food can’t compete with cheap imports. Yet the added cost—meaning the health difference—may or may not be known, and may or may not be quantifiable. Just wait for the mistake that costs lives. It happened with Katrina, Sandy, and coronavirus. It will happen with food fraud. Consumers will demand explanations, and Big Food will finger-point at the USDA, who will finger-point at the FDA, who will finger-point right back. At the end of the day, consumers must realize how vulnerable they really are.

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Food Sleuths

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what can you, the consumer, do to protect your health and your wallet from food fraud? It’s tough to say. But there are three precepts to remember:

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The more ingredients, the more risk (e.g., salted peanuts have three ingredients, Oreos have eleven ingredients). Avoid highly processed food.

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Buying organic may decrease your risk for cancer, but it increases the risk of fraud because fraudsters focus on organic due to the higher profit margin.

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Buy from the supplier directly (e.g., the farmer or the farmer’s market). Fewer middlemen mean fewer entities jacking up the price and people to hide behind, as well as more direct and face-to-face responsibility to the consumer.

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We are years, perhaps decades, away from truly fraud-free food. However, trust in food authenticity is essential to remaking the food system. We need and must demand more transparency; this is going to take a cultural movement. Growers have to believe that they will get a fair price and not be undercut. Consumers have to believe they’re getting what they want, and what they paid for. And manufacturers have to believe that they’ll get in trouble if they ignore us.

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Chapter 24

The USDA and the FDA Don’t Kill People; Rather They Let Them Die

🔮 The Cosmos

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