(Gary C. Smith, Colorado State University)
A lurking fear of “dietary fat as fattening” goes back to the 1920s in America, as staying slender was an important part of new middle-class fashions and lifestyles.1 Cutting back on calories was one of several competing theories at that time about how people should lose weight, and since fat packed more calories, many doctors advised their patients to cut back on this part of the diet.1
In 1930, Louis Newburgh (University of Michigan) declared that “those who have become fat did so because they over-ate or under-exercised – not because there was some endocrine or constitutional disorder.”2
Are the Causes of Obesity “Settled Science”?
The Los Angeles Times reported on Newburgh’s work in 1932 with the headline, “Just Gluttony Causes Obesity; Michigan Professor Strips Defense Of Portly.”2 Not much public attention was paid to causes of obesity between 1932 and 2001 because nutrition scientists and the federal government were obsessed with heart disease, dietary goals, and dietary guidelines. It seemed like “settled science” – people get fat because they take in more calories than they expend, or stay lean when they don’t.3
President’s Heart Attack Spurs Low-Fat Diet
In 1955, U.S. President Dwight D. Eisenhower had a heart attack; his personal physician (Paul D. White) immediately held a press conference calling for the American public to cut down on eating saturated fat and cholesterol.1 White based his dietary recommendation on research by Ancel Keys (University of Minnesota).4 Keys published another paper supportive of his “Diet-Heart Hypothesis.”5
Then, in 1961, Keys and White convinced the American Heart Association to officially recommend a low-fat, low-cholesterol diet (reduce total fat to 30% of calories, cap saturated fat at 10% of calories, increase carbohydrates to 55-60% of calories).6 Restricting total fat and saturated fat consumption while increasing carbohydrate consumption was codified in the Dietary Goals set by Senator George McGovern’s committee7, Dietary Guidelines For Americans: 19808, and DGFAs thereafter.
Little did we know, but these choices by AHA and the federal government – in their quest to conquer heart disease – were accompanied by lethal collateral damage to public health in America.
All We Know About Fat is Wrong, Study Finds
After an all-consuming nine-year investigation, Nina Teicholz concluded that all of our nation’s dietary recommendations about fat – the food ingredient about which our health authorities have obsessed for the past 60 years – are not just slightly off-track but completely wrong.1
When the low-fat, low-cholesterol diet was first officially recommended to the public by the American Heart Association (AHA) in 1961, 1 of 7 adult Americans was obese and 1 of 100 had diabetes; 40 years later, 1 of 3 adult Americans was obese and 1 of 9 had diabetes.9,10,11
Between 1961 and 2001, three scientific reports concluded that high-carbohydrate diets were more plausible explanations for heart disease than were total fat, saturated fat, or cholesterol – and warned that low-fat diets exacerbated the problem (because if you reduced the fat content of a diet, you automatically increased the content of carbohydrates).12,13,14
Researcher Blames Carbohydrates for Obesity Pandemic
The Women’s Health Initiative (WHI), started in 1993, was the first and only controlled randomized trial ever conducted of the low-fat diet; after 10 years of tracking the diet and health of >49,000 women, it was learned that the women not only failed to lose weight, but they also did not see any reduction in either heart disease or cancer.15
Researchers who opposed the low-fat diet dogma were ignored by most mainstream medical and nutrition communities until, in 2001, Gary Taubes wrote a critical history of the “Diet-Heart Hypothesis” for Science.1 He concluded that obesity was indeed a hormonal defect and not the result of gluttony and sloth; he described how the hormone causing obesity is most likely Insulin, which spikes when one eats carbohydrates.16,17
Among his primary conclusions were:
- Carbohydrates, not fat, are the drivers of obesity and many other chronic diseases;
- Dietary fat, itself, is the nutrient least likely to make you fat, because it’s the one macronutrient that doesn’t stimulate the production of Insulin;
- The refined carbohydrates and sugars in our diet are what cause obesity, diabetes, and related diseases, and not the dietary fat or the “excess calories” that are thought to come from eating more than we should.1,16,17
Eating Carbohydrates Throughout the Day Causes Your Body to Store Fat
Taube’s work shattered dogma to such an extent that most nutrition “experts” have been unable to respond except by simply dismissing him.1 But, a 2010 headline in the Los Angeles Times declared, “Fat Was Once The Devil. Now More Nutritionists Are Pointing Accusingly At Sugar And Refined Grains.”18
By 1953, we knew that:
- Hormones are responsible for the stockpiling of fat; Insulin – a hormone produced in the pancreas – trumps all others in the deposition of fat; and, the body secretes Insulin whenever carbohydrates are eaten.
- If carbohydrates are eaten only occasionally, the body has time to recover between the surges of Insulin; the fat cells have time to release their stored fat; and the muscles can burn the fat as fuel.
- If carbohydrates are eaten throughout the day, however, in meals, snacks, and beverages, then Insulin stays elevated in the bloodstream and the fat remains in a state of constant lockdown; fat accumulates to excess; and it is stored – not burned.1,19,20
If a person consumes a diet restricted in carbohydrates:
(1) The absence of carbohydrates would allow fat to flow out of the fat tissue, no longer held hostage there by the circulating Insulin, and this fat could then be used as energy.
(2) The person would lose weight – not because they ate less, but because the absence of Insulin was allowing the fat cells to release the fat and the muscle cells to burn it.21,22
Recent Research Identifies Hormones that Control the Urge to Eat
More recent research has revealed that there are two hormones that control our “urge to eat”: (a) Ghrelin – increases appetite, leads to weight gain, and (b) Leptin – suppresses appetite, contributes to weight loss.23
Research at the University of Alabama-Birmingham showed that sticking to an “Early Time-Restricted Feeding” (eTRF) regimen (“Eating breakfast like a king, lunch like a prince, and dinner like a pauper”) – a meal-timing strategy that involves intermittent daily fasting – was linked with reduced levels of the “appetite hormone” (i.e., Ghrelin) and increased levels of the “satiety hormone” (i.e., Leptin). Study participants reported more “even-keeled hunger,” increased feelings of “fullness,” and less inclination to eat.24
Beware of “One-Size-Fits-All” Dietary Guidelines
In retrospect, it was a huge mistake for the federal government to decide that it was prudent to issue “one-size-fits-all” dietary goals and dietary guidelines instead of having a range of advisory options that could – together – be a “Dietary Guidelines For ‘All’ Americans.”25 There is great danger to public health in “getting something wrong” – in which case the problem would be exacerbated rather than eliminated.
Sometimes there are solutions “in search of a problem that doesn’t exist.” The DGFA is the single most powerful influence on American food choices; Americans have followed the advice of DGFA since 1970, but has it worked?26 In 1980, 15% of Americans were obese; in 2017, 37.7% were obese.26
Is There a Genetic Component to Obesity?
There has to be a genetic component in the sequelae of obesity, diabetes, and cardiac mortality. Early on, scientists found communities (e.g., Eskimos and Inuits in the Artic; Samburus and Masai in Africa; Sikhs and Hunzas in India) of people who ate almost exclusively animal products (fish, game, meat, poultry, dairy, milk, blood, animal organs, eggs), yet almost never became obese or suffered heart attacks.1
In the general U.S. population, heritability of obesity ranges from 30% to 70%, and dozens of genetic variants have been associated with obesity.27 Investigators have discovered that variations within 13 genes, acting in the brain, can affect people’s food intake, hunger, satiety, etc.28
One gene instructs the fat tissues to burn more fat from food,29 another gene causes the body not to inform the brain to stop eating,28 and a third gene predicts weight loss.27 Three scientists agree that disclosing genetic information for “personalized nutrition” results in greater changes in intake of some dietary components, compared to general-population-based dietary advice.28,30,31
Obesity is a Hormonal Disorder
For nearly a century, “experts” have said, “obesity is caused by an imbalance between calories consumed and calories expended” (i.e., people get fat because they take in more calories than they use-up).3 That would be believable if the prevalence of obesity had not risen relentlessly in the past half-century.3
The failure to make meaningful progress by either treating or preventing obesity cannot be ignored; those in the field have been laboring under a fatally, tragically flawed paradigm.3 Obesity is not an energy-balance disorder – it is a hormonal disorder – a dysregulation of fat storage and metabolism and a disorder of fuel-partitioning.32
People don’t get fat because they eat too much, but because of the quantity and quality of carbohydrates in their diets, which establish a hormonal mileu that fosters the accumulation of excess body fat.32
“Carbohydrate-Insulin Model” Breaks onto the Scene
Because these hormonal responses are dominated by the Insulin signaling system, which in turn responds primarily to the form and amount of carbohydrates in their diet, this is called the “Carbohydrate-Insulin Model”.32
The “Carbohydrate-Insulin Model” is most certainly not settled science; both the Carbohydrate-Insulin Model and the Diet-Health Hypothesis are based on epidemiological (observational) data, which cannot be used to prove cause-and-effect relationships (only Randomized Controlled Clinical Trials can do that).33
Further Study Still Needed
Human-nutrition scientists have honed-in on the culprit (i.e., carbohydrates) and we know that “personalized health/nutrition” can be used to identify those individuals who are genetically susceptible to obesity, but there are still things that need further study. For example:
- When we feel “full” after eating a meal, some say the satiety-messaging is effected by Leptin,24 with signaling that originates from a full stomach,34 or a stretched intestine35, or sensory neurons in fat deposits near the spine,36 or bacteria from the gut microbiome.37,38
- There are research findings that connect addiction (similar to that of cocaine and nicotine39) to the consumption of large quantities of processed foods, fatty foods, and sugary foods/beverages,40 or sweet/fatty foods 39, or sugars, unhealthy fats, and refined flour, 41 or processed foods that “re-wire” the brain – causing it to elicit behavior that programs people to “crave” them.41
Ultra-Processed Foods May be a Driver of Obesity
Americans get 70% of their calories from plant-based foods and 30% from animal-based foods; 81% of their calories come from ultra-processed foods (i.e., those containing added sugars, fat, hydrogenated vegetable oils, and refined grains).42
So, 57% of all calories consumed by U.S. consumers come from ultra-processed foods. The high increasing consumption of ultra-processed foods in the 21st century may be a key driver of the obesity epidemic.43 Tons of evidence has come in within the last five years that ultra-processed foods should not be consumed regularly or in large amounts.44
The best of the evidence is that of a Randomized Controlled Clinical Trial conducted at the National Institutes of Health and published in Cell Metabolism.45
Those researchers concluded that:
- People were able to “gulp down” the ultra-processed food faster, which doesn’t allow sufficient time for the stomach-to-brain saying “the tank is full” – so they kept eating;
- On average, individuals on the ultra-processed diet ate 508 calories more per day (by taking extra helpings) and gained an average of 1 pound per week; those on the minimally processed diet lost an average of 1 pound per week;
- Limiting consumption of ultra-processed food by buying only those products with the least numbers of ingredients may be an effective strategy for obesity prevention and treatment.34,45,46,47
Cutting Sugar Could Prevent Millions of Cardiovascular Disease Events
Another NIH-funded study showed that cutting 20% of the sugar in packaged foods and 40% from beverages could prevent 2.48 million cardiovascular disease events such as strokes, heart attacks, and cardiac events, 490,000 cardiovascular deaths, and 750,000 diabetes cases in the U.S. over the lifetime of the current adult population.48
Very recently, FDA approved Tzield® as the first-ever immunotherapy to delay the onset of type 1 diabetes – hailing it as a “historic moment,” the “start of a seismic shift” in how that disease is treated, and as “the most important breakthrough for the condition since Insulin was discovered 100 years ago.”
For the first time, the immune system attack that is the root cause of type 1 diabetes can be addressed because Tzield® binds to, and deactivates, immune cells that attack Insulin-producing cells and increases the proportion of cells that help moderate immune response.49
USDA and USDHHS have released “Proposed Scientific Questions For Public Comment Regarding The 2025-2030 Dietary Guidelines For Americans.” New questions that the Dietary Guidelines Advisory Committee plans to address include ultra-processed foods.50 Hopefully, the DGFA Advisory Committee will allow the address of low-carb diets, sugars, refined grains, and genetic components to the sequelae of diabetes, obesity, cancer, and cardiac mortality.
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