The cause of obesity has not been discovered yet because if it had, obesity would be no more a problem (nobody want to become nor to stay overweight).
More: if it had the last twenty-five years pandemic would have stopped its world-wide expansion from developed countries to emerging countries. And that is absolutely not the case.
Which of the following factors could be the ultimate candidate as obesity causal factor? Increased intakes?; Lack of physical exercise?; Sugar excess? And the winner is…
Sugar! At least it is according Dr Robert Lustig a paediatric who speaks in the video here enclosed. And an intermediate cause would be in one hand the increase of ghrelin, a hormone which provokes the craving for food intake and in the other hand the decrease of or the resistance to leptin which induces the opposite reaction (i.e. says to the brain you had enough).
Indeed in this post I will try to resume for you a one hour and twenty minutes long talk pronounced by Dr. Robert Lustig, Professor of Clinical Pediatrics in the Division of Endocrinology and Director of the Weight Assessment for Teen and Child Health (WATCH) Program at UCSF, on the topic of the pandemic of obesity.
All the slides stem from his course held before the Santa Cruz County Office of Education on March 24, 2011.
Due to the refinery process which is necessary to produce it, sugar (like wheat or alcohol) is not an aliment that is naturally available in a wild environment. Thus its abundance in our modern world is far to be natural and is solely the result of the food industry engineering. However the cost of sugar is very cheap. In the map here below we can see that the three factors cited here above appears to be geographically linked in the USA. But association doesn’t mean causation. Indeed a fourth confounding factor could play: perhaps a biochemical factor.
Thermodynamic would not be sufficient to solve the obesity issue. The true question should be where the calorie comes from? Eat less exercise more (it is all in the balance) is a dogma Dr Lustig struggle against in his stalk. Because since thirty years this dogma solved nothing with regard to obesity he says. Behavioural intervention all along the life time don’t work (no evidence has been brought that it work). Child obesity has doubled in every country that adopted western diet. The poor are disproportionately affected because they don’t have access to healthy choice. They don’t have a choice. Leptin is a hormone which tells your brain you have enough. This hormone could solve obesity. The concept of behaviour works best than the concept of thermodynamic to explain the epidemic of obesity. Behaviour understood as “a stereotyped motor response to a physiological stimulus”. Eating is a behaviour and physical exercise too. There is a biochemistry basis behind each behaviour. What is the biochemical underpinning of gluttony and sloth is the real question. Here comes the leptin hormonal theory. No one can exert a cognitive inhibition on a biochemistry process that’s why obesity relapses each time.
The cause of obesity could be the lack of leptin action. Because the leptin deficit lead to a starved brain which in turn provoke gluttony and sloth. Something in our diet could block the effects of leptin. During the last three decades calories intakes from fat reduced while calories from carbon hydrates increased due to the anti fat campaign undertaken for a cardiovascular risk concern. Nature-made fructose is hard to get, man-made fructose is easy to get. High Fructose Corn Syrup (HFCS) is cheap and thus is found everywhere in western alimentation and trend to replace sugar. All the more fructose brings a good taste to the food and it results in an increase of sales for food industry.
Carbo-hydrates encompass glucose, ethanol (alcohol) sucrose and fructose. Glucose is good (contained in potatoes for example and transformed in useful glycogen), alcohol is bad (well-known) but what is the statute for sucrose and fructose in the field of health? Like alcohol Fructose doesn’t metabolise in glycogen and does overload mitochondria leading to adverse events in chronic exposure. More: fructose triggers a leptin resistance.
In natural non refined aliments fructose is proportional with fibre.
Sugar is making us sick. Glucose is good but fructose is bad and sucrose contains half and half. Thus, AHA recommends a tremendous reduction in added sugar consumption in order to prevent cardiovascular disease. But fructose is good for the food industry because it makes food cheaper. And politicians know that across the world high price for food causes unrests and revolutions. That is the reason why they always support the food industry even when it’s against the public health interest. It’s useless to eat less of everything; instead it’s useful to reduce our fructose intake.
To reduce sugar consumption needs a policy because there is no medicine for that and it is beyond personal responsibility due to the biochemistry basement developed here above.
Obesity is thus a public health problem that is not on the way to be solved by a personal responsibility rationale such as “eat less, exercise more”.
Soda taxation could work to balance the sugar addiction now at work in western countries.
But conservative parties would say: “no for an additional governmental tax”!
A few slides excerpted from the talk:
1) Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite.Annals of internal medicine, Vol. 141, No. 11. (7 Dec 2004)Spiegel, Karine; Tasali, Esra; Penev, Plamen; Van Cauter, Eve
2) Teff KL, Elliott SS, Tschöp M, Kieffer TJ, Rader D, Heiman M, et al. Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women. Journal of Clinical Endocrinology & Metabolism. 2004 Jun;89(6):2963-2972. Available from: http://dx.doi.org/10.1210/jc.2003-031855.
3) Elliott SS, Keim NL, Stern JS, Teff K, Havel PJ. Fructose, weight gain, and the insulin resistance syndrome. The American Journal of Clinical Nutrition. 2002 Nov;76(5):911-922. Available from:http://www.ajcn.org/content/76/5/911.abstract.
4) Shapiro A, Mu W, Roncal C, Cheng KY, Johnson RJ, Scarpace PJ. Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding. American Journal of Physiology – Regulatory, Integrative and Comparative Physiology. 2008 Nov;295(5):R1370-R1375. Available from:http://dx.doi.org/10.1152/ajpregu.00195.2008.