Gary Taubes – The Old Mutual health Convention Presentation Summary

GARY TAUBES – Old Mutual Health Convention, Thursday February 19, 2015

Why We Get Fat – Adiposity 101 and the alternative hypothesis of obesity

Obesity and diabetes are global epidemics caused not from people eating too much and moving too little – the bibilical equivalent of greed and sloth. That view is the “original sin” of obesity research.

Research is available to show that the key driver of obesity is not “human weaknesses such as ignorance or indulgence”. Instead, it is hormonal imbalance, in particular dietary carbohydrate that is driving insulin that in turn is driving fat.

Obesity and diabetes rates have increased dramatically in the US since the 1960s. The conventional wisdom about obesity epidemics is the energy imbalance hypothesis.

According to the World Health Organisation: “The fundamental cause of obesity and overweight is an energy imbalance between calories consumed and calories expended.”

The Centres for Disease Control and Prevention says: “Weight management is all about balance— balancing the number of calories you consume with the number of calories your body uses or `burns off.’”

Obesity is said to be a result of “increased prosperity”
 and a toxic “obesogenic” environment.

As Kelly Brownell, director of the Rudd Center for Food Policy and Obesity at Yale, has noted:

“Cheese-burgers and French fries, drive-in windows and supersizes, soft drinks and candy, potato chips and cheese curls, once unusual, are as much our background as trees, grass, and clouds… Few children walk or bike to school; there is little physical education; computers, video games, and televisions keep children inside and inactive; and parents are reluctant to let children roam free to play.”

We think we understand obesity and diabetes. We have been giving roughly the same advice on them since 1960s; despite our belief that we think we understand them. We obviously don’t.

With obesity comes cluster of chronic diseases that include stroke, atherosclerosis, gall bladder disease, insulin resistance, diabetes, neurodegeneration, sleep apnea, asthma, fatty liver disease and cancer.

Conventional wisdom suggests that obesity is an energy imbalance disorder, the imbalance between calories consumed and expended. In biblical terms it would be called gluttony and sloth. Another observation has been that obesity is the result of increased prosperity and the presence of a toxic

“obesogenic” food environment.

The idea that too much food and too little physical activity are causing the obesity epidemic appears written in stone, and passed down from the mountain tops. It is more likely the original sin of obesity research.

There are counter examples in “black swans” – research on populations that have high levels of obesity but don’t have toxic “obesogenic” environments. For example:

  • Sioux of Sioux, South Dakota Crow Creek Reservation in 1928, showed that 40 % women, 10 % men, 25 % children “distinctly fat.” 20 % women, 25% men and children were “extremely thin”.
  • In African-Americans, Charleston, South Carolina in 1959, 18 % of men, 30 % of women are obese. Total family incomes were between $9 to $53/week .
  • In Trinidad, A third of women over 25 are obese and the per capita daily diet is less than 2000 calories (21 % fat): “Fewer calories than recommended by FAO.

Obviously there is something toxic about these levels of obesity, but it is not because these people have iPads and TVs. And these kids are running around free, yet they are growing up to be obese adults. Households are showing the double burdens of obesity and malnutrition.

Why were these populations fat? Occam’s razor can explain it: you don’t have to complicate hypotheses beyond necessity, and the simplest explanation is often the right one:

You expect rich countries to have high levels of obesity; in poor societies malnutrition and sub nutrition are common.

In the early 1970s, obesity was already considered a type of malnutrition, something that was wrong with the food supply. Since that time, it turned into nutrition caused by overeating, putting a belief system on top of observation.

Around 2005, researchers began to notice that overweight mothers had thin stunted children, and were showing signs of chronic undernutrition.

If you believe that these mothers took in too many superfluous calories, why didn’t they give those to their starving children. How many mothers would overeat while their children were starving? We have to throw out one of those paradigms.

As Rolf Richards from the University of the West Indies noted in 1973: “It is difficult to explain the high frequency of obesity seen in a relatively impecunious society such as exists in the West Indies, when compared to the standard of living enjoyed in the more developed countries… Malnutrition and subnutrition are common disorders in the first two years of life… Subnutrition continues in early childhood to the early teens. Obesity begins to manifest itself in the female population from the 25th year of life and reaches enormous proportions from 30 onwards.”

In 2005, Benjamin Caballero, of Johns Hopkins University, said: “A few years ago, I was visiting a primary care clinic in the slums of Sao Paulo [Brazil].The waiting room was full of mothers with thin, stunted young children, exhibiting the typical signs of chronic undernutrition. Their appearance, sadly, would surprise few who visit poor urban areas in the developing world. What might come as a surprise is that many of the mothers holding those under-nourished infants were themselves overweight… The coexistence of underweight and overweight poses a challenge to public health programs, since the aims of programs to reduce undernutrition are obviously in conflict with those for obesity prevention.”

Clearly, eating less doesn’t work,

The Cochrane Collaboration research in 2002 showed that “weight loss achieved in trials of calorie restricted diets is “so small as to be clinically insignificant”.

If we are obese, eat less, and end up fat anyway, it’s a pretty good sign that eating less doesn’t work. Clinical trials prove it.

Exercising more also doesn’t work.

The American Heart Association and the American College of Sports Medicine, in their physical activity guidelines in 2007 said: “It is reasonable to assume that persons with relatively high daily energy expenditures would be less likely to gain weigh time, compared with those who have low energy expenditures. So far, data to support this hypothesis are not particularly compelling.”

These hypotheses are about 100 to 150 years old. If centuries of testing thinking, and random controlled trials have shown them not to work, then you should seriously consider that the hypothesis is wrong.

The idea of energy in minus energy out, perverted appetite, eating too much with insufficient expenditure is supposedly based on the first law of thermodynamics. It doesn’t tell you anything about why people get fat.

It is nonsensical.

The alternate hypothesis I have found through research is that obesity is a hormonal regulatory disorder. Like type 2 diabetes, obesity is fundamentally a disorder of insulin signaling, hence it the term “diabesity”.

The carbohydrate content of the diet triggers it.

The key driver of insulin is carbohydrates and sugar in the diet, not fat and not saturated fat.

Obesity is shown to be disorder of excess fat accumulation (not energy balance, not over-eating, not sedentary behaviour)

Research also shows that people don’t need an excess of food to become obese. Mice make fat out of their food under the most unlikely circumstances, even when half starved. .

Every animal experiment I’ve ever found has showed that the animals didn’t get fat by overeating.

The degree of insulin resistance or sensitivity is a key factor in the equation of fat accumulation, and it explains why diabetes type 2 and obesity go together. This thinking is not new.

It is based on the theory of “lipophilia”, and goes back to 1933, when Erich Grafe said in Metabolic Diseases and Their Treatment: “A condition of abnormally facilitated fat production and impeded fat destruction . . . a sort of lipomatosis universalis, in the sense that the lipophilia in certain tissues is primary and the sparing in the energy expended is secondary.”

In 1938, Russell Wilder, of the Mayo Clinic, said: “The effect after meals of withdrawing from the circulation even a little more fat than usual might well account both for the delayed sense of satiety and for the frequently abnormal taste for carbohydrate encountered in obese persons… A slight tendency in this direction would have a profound effect in the course of time.”

Since then, researchers, including Dr Robert Atkins, began looking at low-carb, high-fat diets. Dozens of clinical trials and meta analyses have shown that everything gets better when you remove fattening carbs when you replace them with fat , including saturated fat. Yet there is still the tendency to think you are going to kill people with these diets, and dietary guidelines have emphasized carbohydrates in the diet, including for obesity and diabetes.

Understanding why restricting carbs and increasing fat is not a killer requires a lesson in Adiposity 101: Triglycerides vs fatty acids:

  • Fat is stored as triglycerides
  • Fatty acids are burned for fuel
  • Fat enters and exits fat cells as fatty acids
  • Inside the fat cell, fatty acids continually cycle into triglycerides and back out again.
  • Insulin is “the principal regulator of fat metabolism”.
  • When insulin is secreted or chronically elevated, fat accumulates in the fat tissue.
  • When insulin levels drop, fat escapes from the fat tissue and the fat depots shrink.
  • We secrete insulin primarily in response to the carbohydrates in our diet.

More and more research is proving that “carbohydrate is driving insulin is driving fat”, as 
George Cahill, said in 2005.

Yet the American Medical Association has trivialized this science as a debate about fad diets, saying in the JAMA in 1973: hat “fat is mobilized when insulin secretion diminishes” and yet low carbohydrate diets are “bizarre concepts of nutrition that should not be promoted to the public as if they were established scientific principles.”

In conclusion, there is solid science to show that:

  • Obesity is a disorder of fat accumulation, not energy balance (not overeating and sedentary behavior).
  • Fat accumulation is regulated fundamentally by insulin and dietary carbohydrates — “carbohydrate is driving insulin is driving fat.”
  • The solution to obesity and the obesity epidemics is not getting people to move more and eat less, but restricting the causative agent – ie, the refined grains and sugars.

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