There is a politically expedient but problematic fiction that ‘consensus’ matters in science. Since a million matching opinions do not constitute a fact, a consensus — either real or apparent — is not a statement about evidence but an exercise in groupthink in which the status quo is made explicit.
Thus, scientific progress requires conservative and heretical thinkers — conservatives protect the authority and continuity of science, whereas heretics put forth creative dissent in an attempt to push the limits of what we know. Nevertheless, few people are willing and able to challenge the status quo — and those who have were often reviled, incarcerated, or executed (e.g., Galileo, Semmelweis, and Vavilov).
Consequently, when facts conflict with theory, academic researchers often ignore the facts rather than confront the consensus. As a result, the ‘marketplace of ideas’ — and research funding — are predestined to conformity, sycophancy, and stasis. In other words, the more pervasive the consensus, the more servile the research, the less probable the progress.
Although this unfortunate reality is evident across many fields, it has been extremely detrimental to nutrition science. For more than 50 years, ‘Diet-centrism’ — the theory that foods and beverages cause ill-health, obesity, and cardiometabolic diseases — has been accepted by physicians, researchers, and the public almost without question. Yet despite the unity and ubiquity of the consensus, there are centuries of evidence refuting diet-centric beliefs. Thus, because a million matching but ill-informed opinions do not constitute a fact, the consensus linking calories, ‘carbs’, meat, milk, sugar, salt, fat, cholesterol, and ‘ultra-processing’ to death and disease is not a statement about scientific evidence but the obsequious — and sterile — status-quo made explicit.
Accordingly, herein I present the heretical idea that the naïve determinism of ‘Diet-centrism’ — ‘you are what you eat’ and ‘what you eat is killing you’ — is not only simplistic and unscientific but specious because it ignores the fact that individual differences in metabolism (how the body ‘handles’ foods and beverages) is what matters most in diet-related health and disease.
Historical Evidence: It’s not the Food
Before the 20th century, obesity and cardiometabolic diseases such as type-2 diabetes mellitus (T2DM) were uncommon. Yet over the past 50 years, the prevalence of these maladies in horses, humans, dogs, cats, lab, and zoo animals increased to epidemic proportions. Given that these herbivores, omnivores, and carnivores have always consumed different diets, the claim that foods and beverages have suddenly caused parallel epidemics in different species is an extraordinary claim that requires extraordinary evidence. Yet there is no valid evidence supporting this belief.
To begin, humans have consumed highly palatable, ‘ultra-processed’ foods and beverages for thousands of years. Refined sugar, salt, butter, and cheeses date from 4000-8000 BC, and pasta, pizza, and pretzels were consumed in the 1st century AD. Although the consumption of ‘french-fries’ (‘chips’ in the UK) only began in the 17th century, potatoes fried in salt and animal fat quickly became the main source of nutrition in Ireland. By the 19th century, the Irish consumed ~4-5 lbs. of potatoes per person per day, with men consuming ~8-12 lbs./day. This is the equivalent of ~40 supersized servings of ‘french-fries’ every day for a lifetime. Yet despite consuming massive amounts of ‘carbs’, saturated fats, and salt, the Irish had little obesity or cardiometabolic diseases.
Similarly, the Amish — an ethno-religious group in the US — consume a high-calorie, highly-palatable diet that includes meat, potatoes, gravy, eggs, breads, pies, and cakes, and “is quite high in fat and refined sugar”. Yet the Amish have a greater life expectancy and substantially lower obesity, T2DM, heart disease, and cancer than other Americans.
Importantly, all humans start life consuming ~40% of their daily calories as dietary sugars and 25% as saturated fat — either in breast milk or infant formula (an ‘ultra-processed’, sugar-sweetened beverage with ‘added’ sugars, salts, and fats). Thus, recommendations to restrict ‘added’ sugars and ‘processed’ foods would prevent the feeding of most infants in industrialized nations. And contrary to current rhetoric, nations with the highest rates of sugar-sweetened beverage (formula) consumption by infants have the lowest rates of obesity and cardiometabolic diseases (Japan and Norway). Moreover, sugars added to foods and beverages enter the same metabolic pathways as intrinsic sugars. Thus, the glucose molecules in breast milk and the fructose molecules in fruit are exactly the same glucose and fructose molecules as in soda, sports drinks, and your favorite candy. This basic fact of biochemistry shows that the term ‘added sugar’ has no place in scientific discourse.
Furthermore, the medicinal use of sucrose (table sugar) for malnutrition and diarrheal diseases saves the lives of over 600,000 children each year. Thus, so-called ‘added’ sugars save more lives than any pharmaceutical agent. So if ‘food is medicine’, then table sugar is the greatest medicine of all. [Note: the phrase “let thy food be thy medicine” was fabricated by a journalist and attributed to Hippocrates to sell a diet book in the 1920s.]
Additionally, the most comprehensive report on dietary sugars — published before the current anti-sugar hysteria — concluded that “feeding normal human volunteers at levels of fructose approximating the 90th percentile intake levels of the U.S. population failed to demonstrate adverse effects on insulin sensitivity or glucose tolerance [cardiometabolic health].” And contrary to current rhetoric, over the last two decades the use of sugars & sweeteners in the US declined ~16% as obesity and T2DM increased almost 40% and severe obesity increased 96%. Thus, less sugar is linked to more obesity and diabetes — and this so-called ‘sugar paradox’ is ubiquitous (see Australia and the UK).
In sum, by ignoring contrary evidence, academic researchers and their ‘diet-centric’ consensus created a “fictional discourse on diet-disease relations”.
The Logic of Causality
The search for universal criteria by which to infer causality has eluded philosophers of science for centuries. Yet, at its simplest, the search for causes is the search for ‘differences that make a difference’ — mere associations are meaningless. For example, water (and other liquids) are associated with 100% of drowning deaths. Therefore, in the absence of water no one drowns. Yet despite the perfect correlation and counterfactual evidence, no educated person argues that water causes drowning because not everyone who drinks, bathes, or swims, drowns. In other words, water is not causal because it is not the ‘difference that makes a difference’.
To be precise, water is a sine qua non for drowning (an indispensable part or essential element) — not a cause. Thus, given the same environment (the presence of water), individual differences such as the inability to swim, intoxication, or insentience cause a person to drown.
The Illogicity of Blaming Food
Foods and beverages are a sine qua non for life — everyone must eat and drink. Yet just as water does not cause drowning because not everyone who drinks, bathes, or swims, drowns — diet does not cause poor metabolic health because not everyone who eats and drinks becomes obese or diabetic. Yet in contrast to the perfect correlation between water and drowning, there is no clear correlation between diet and obesity.
For example, muscular, male athletes consume more calories, ‘carbs’, sugars, salt, fat, cholesterol, and ‘ultra-processed’ foods than obese, sedentary women, yet have lower levels of adiposity and T2DM. Thus, more foods, beverages, and physical activity are linked with better health and less disease. Clearly, athletes’ bodies ‘handle’ their diets differently than those of sedentary people. Therefore, metabolism — not diet — is the ‘difference that makes a difference’ in health.
Similarly, in a 2013 study, my colleagues and I found that the people performing the least amount of physical activity gained the most fat mass — despite consuming less calories, less fat, and less sugar than those who ate more, performed more activity, and maintained their weight. Conversely, reducing physical activity causes an immediate decline in insulin sensitivity and metabolic health. Therefore, physical activity-induced differences in metabolism — not diet — cause differences in caloric intake, fat mass, and health.
Moreover, metabolism is the ‘difference that makes a difference’ in the ‘Oral Glucose Tolerance Test’ (OGTT) — a widely used test for diabetes and insulin resistance. In the OGTT, blood sugar is measured after patients consume a standard dose of dietary sugar. Over time, patients with weaker metabolisms have higher blood sugar than those with stronger metabolisms. Thus, given identical amounts of dietary sugar, differences in metabolism cause differences in blood sugar. It is nonsensical to argue that the dietary sugar caused the differences in blood sugar when each patient consumed the same amount.
What confuses most people — and [too] many researchers — is that different foods and beverages cause different metabolic responses. For example, consuming sugar or starch causes greater increases in blood sugar than consuming fat or protein. However, as the OGTT shows, it is not the increase in blood sugar after a meal that matters to cardiometabolic health but the decrease over time.
Stated simply, consuming dietary sugar increases everyone’s blood sugar — but not everyone’s blood sugar returns to ‘normal’ after a meal (e.g., diabetics). Thus, the diet-induced increase in blood sugar is irrelevant to cardiometabolic health because it is not the ‘difference that makes a difference’. What matters are the metabolic differences that cause blood sugar to decrease — or not — after a meal.
Yet most importantly, as a recent “intensive food-as-medicine program” showed, altering your diet has little effect on cardiometabolic health over time, whereas adequate physical activity “obliterates the deleterious effects of a high-caloric intake”. This explains why muscular athletes can consume massive amounts of calories, ‘carbs’, and ‘ultra-processed’ foods yet remain lean and healthy.
In sum, differences in metabolism — not diet — cause differences in cardiometabolic health.
‘Differences that Make a Difference’ in Obesity and Metabolic Strength
If people perform hard physical labor, they will consume more food, water, and oxygen than if they sat quietly in an office. Therefore, increased physical activity causes increases in metabolism that — in turn — cause increases in consumption (eating, drinking, and breathing). Therefore, if you ‘burn’ more calories through physical activity, you increase your metabolic strength, consume more calories, and maintain your weight. This fact explains why exercise rarely leads to weight-loss but is essential in health and preventing weight gain.
Conversely, when people reduce their physical activity ‘too much’ (below their ‘metabolic tipping point’), they weaken their metabolism. This causes them to consume more calories than they burn. In time, this leads to ‘acquired’ obesity and cardiometabolic diseases — independent of diet. In other words, a minimum amount of physical activity is needed for health, and individuals with extremely low levels will, over time, become obese, diabetic, or both — regardless of the foods and beverages they consume.
Importantly, if a woman’s physical activity is too low, her metabolism will be too weak to ‘handle’ pregnancy and she will consume too many calories. As a result, her children will be born fatter and with weaker metabolisms. In other words, they ‘inherit’ a life-long predisposition to obesity and cardiometabolic diseases. [Note: the non-genetic process of inheritance by which a mother’s prenatal metabolism irreversibly alters her descendants’ metabolism is known as a ‘maternal-effect’].
Consequently, the fact that women ’move less’ than they did five decades ago explains the recent rise in ‘inherited’ (childhood) obesity and adolescent T2DM. For example, from 1965 to 2010, the time women spent doing housework decreased by ~2 hours per day while sedentary time increased by 1 hour/day. This reduced the number of calories burned by ~250/day and doubled the amount of time spent sitting. By 2020, women spent more time sitting in front of the TV and using social media than cooking, cleaning, childcare, exercise, and laundry combined. As a result, their metabolisms became weaker — and because metabolic strength is essential for a healthy pregnancy, the decline produced successive generations of obese children with weak metabolisms.
Moreover, because all mammals share the metabolic pathways of pregnancy, my work suggests that ‘maternal-effects’ caused the parallel epidemics of obesity and cardiometabolic diseases in horses, humans, dogs, cats, lab, and zoo animals.
Conclusion
Consensus in academic research is rarely a statement about evidence. More often, it is an exercise in groupthink in which the status quo — right or wrong — is made explicit. Thus, progress needs heretics who are willing and able to challenge the consensus. Accordingly, I presented the heretical idea that humans have always consumed highly palatable, processed foods and beverages without increases in obesity or cardiometabolic diseases. Moreover, ‘acquired’ and ‘inherited’ differences in metabolism — not diet — cause obesity and poor metabolic health. Thus, the ‘diet-centric’ consensus linking calories, ‘carbs’, meat, milk, sugar, salt, fat, cholesterol, and ‘ultra-processing’ to death and disease is not only simplistic, but sterile and unscientific.
Nevertheless, given that science progresses ‘funeral by funeral’ and that food-based fears generate profitable marketing campaigns (e.g., low-fat and no ‘added’ sugars) and billions of dollars to fund academic research, ‘Diet-centrism’ will be the dominant paradigm in nutrition ‘science’ for the foreseeable future. Bon appétit.
