Tim Noakes: Nutrition - The Butterfly Effect

By reducing "artery clogging saturated fats" overstuffed with calories, the USDGA's decision in 1977 was meant to prevent both heart disease and obesity. But as so often happens when theories are accepted on the basis of incomplete evidence, there is the probability that unintended consequences will result. The epidemic of obesity and diabetes that began after 1980 is a classic example. But how do we explain it? To understand it, we need to meet the principle player. The Appestat (the most important part of your body you've never heard of)

- The appestat is the part of the brain situated in the hypothalamus, thought to control the regulation of human body weight. Just as a thermostat controls temperature, the appestat controls your appetite

- For almost all of our existence, humans have been lean. It's only recently that we've become podgy, overweight and obese. The natural state of humans is to be lean

- We respond to biological cues that accurately regulate our energy (food) intake so that it matches precisely - to the final calorie - the amount of energy we need to sustain our daily physical activity and the integrity of our bodies

- Process known as homeostatic control of body weight through the precise matching of energy intake and energy expenditure. Some liken this control to the action of an appestat in the brain that regulates our appetite so that we are always just hungry enough to eat the exact number of calories that we need each day

- As humans have grown increasingly fat since 1980, then the cause must be damage to the appestat. If we understand what has damaged the appestat, we understand what is causing the modern obesity epidemic

- Increase is obesity occurred immediately after humans began to eat more carbohydrates and processed foods. That we may also have become less active is irrelevant since a properly functioning appestat simply reduces hunger and the desire to eat an exact proportion to the reduction in energy expenditure. (A properly functioning appestat would have no difficulty reducing our daily food intake)

- The obesity epidemic is the singular proof that something in our environment has damaged the proper functioning of the appestat

- Since it is much easier to overeat calories in food than to under-expend calories in physical activity, the most probable explanation is that the appestat was damaged by either (I) the increased intake of dietary carbohydrates following the direction of the USDGA to remove fat from the diet after 1977 or (II) the increased intake of processed foods since 1980. Or a combination of both

Argument 1: The Energy Balance Model of Obesity

- Regain control of our errant appestats

- According to this model the cause for the global obesity epidemic is really quite simple - it is the result of a massive global failure of human willpower that began with that generation of humans born after 1980. So if this is the cause, then the solution is also simple. We must regain our resolve: we must correct our suddenly wrong energy balances. By counting our calories, by controlling our portion sizes and by removing fat from our diets. We will again become lean. According to this logic a reduced calorie, high carbohydrate, low fat (HCLF) diet of the kind favoured by the Ancient Egyptians will be the most effective weight loss option

- What we fail to note is the nature of the foods that the obese eat

- We conclude that obesity is the result of a human character flaw and is incurable. Only the lean are strong willed; all the rest are unworthy of our efforts. (Or Tim Noakes understanding)

- The fundamental problem with the energy balance model is that it is brainless - it ignores any potential role for the human brain in regulating both energy intake and energy

expenditure. It ignores the role of the appestat that for all but the last three decades of human history has been absolutely precise in directing exactly how much we need to eat each day to keep our bodies at a stable weight. To reverse the obesity epidemic we have to fix the appestat. Dietary interventions based on brainless energy balance model will never do that since they do not even recognise its existence

Argument 2: The Hormonal (insulin) Lipophilic (fat loving) Model of Obesity

- Fundamentally different from the energy balance model since it predicts that fat does not accumulate in the body exclusively as a result of an energy imbalance.

- Rather the model foretells that hormones and especially the fat-building hormone, insulin, are crucial drivers of weight gain. The model also predicts that whilst all calories may be the same when measured outside the body, when ingested, calories from carbohydrate, fat and protein act quite differently. And calories from carbohydrate are uniquely obesogenic (obesity causing) for two different but complementary reasons

- First, carbohydrates stimulate the appetite and encourage the over consumption of calories; that is calories from carbohydrate act differently on the appestat than do calories from fat and protein. Second, calories from carbohydrate cause increased secretion of the fat-building hormone, insulin, that specifically stores as fat any excess calories ingested as carbohydrate. Third, calories from fat require an input of (wasted) energy before they can be stored or metabolised within the body whereas carbohydrates do not. As a result, calories from carbohydrate are not the same as calories from fat

- Persons with Type 1 Diabetes start to lose weight the instant their pancreas fails to produce enough insulin. Thus it was realised that "a functioning pancreas is essential for the fattening process." They also noted that fat accumulated in specific "lipophilic" areas of the body, more readily in the obese than in the lean. A sort of anarchy exists; the adipose tissue lives for itself and does not fit into the precisely regulated management of the whole organism

- "Insulin not only promotes fat storage but it also restrains fat mobilisation" and "Lipogenesis (fat storage) is high in the fed state and following carbohydrate administration, whereas it is suppressed by fasting, high-fat diets or insulin deficiency, such as uncontrolled diabetes

- Growing academic interest in the insulin theory of obesity and the rise of Banting as the potential solution for obesity. The key benefit of Banting is that being low in carbohydrate it stimulates neither appetite nor excessive insulin secretion

- Effects of Banting include weight loss, reversal risk factors for heart disease and improving athletic performance

- Dr Jeff Volek (PhD) and Stephen Phinney (MD), The Art and Science of Low Carb Living and The Art and Science of Low-carbohydrate Performance

- In summary, the evidence is absolute. The singular and direct cause of the epidemic of obesity and diabetes that began in the first generation born after 1977 was the adoption of the scientifically-unproven 1977 USDGA that encouraged all the world's people to adopt a low-fat, high carbohydrate diet. This also predicts that each succeeding generation since 1977 will be successively heavier

- Weight gain cannot occur without the ingestion of more calories than are needed by the body, but the point is that the over-ingestion of calories cannot occur if the brain appestat is functioning properly, as it did until 1980

- The appestat of the obese must fail because it is especially susceptible to the appetite-stimulating effects of high

carbohydrate foods, especially those found in modern processed foods that are designed with the single goal that they are highly addictive. It is those addictive foods that have invaded the human food chain in the past 30 years

- Weight gain will occur much more easily in those who have an impaired capacity to metabolise carbohydrate because their tissues are Insulin Resistant (IR). Thus in those with IR, carbohydrates are especially obesogenic because every time carbohydrates are eaten, they cause an exaggerated secretion of insulin, which directs the excess ingested calories to be stored as fat. In addition, the carbohydrates specifically cause the overconsumption of calories, not only because the fail to satisfy appetite but because they actively drive hunger