In the last post we defined a hormonally horrible condition known as internal starvation. Let’s look at a simplified example of how this works. Consider Terri. She is internally starving and needs 500 calories of energy. Terri is also a yo-yo dieter and has already slowed down her metabolism and burned as much muscle as she can. Needing some calories, Terri eats 500 calories. Instead of those 500 calories getting into the cells needing it, only 250 make it in while the other 250 are ignored—thanks to insulin resistance—and stored as new body fat. Terri still needs 250 calories. She cannot slow down anymore. She cannot burn any more muscle. And thanks to all the excess insulin floating around, she does not have the ability to burn body fat. What is her only option? Overeat. Specifically, eat 250 extra calories.
So Terri snacks on 250 extra calories to keep her cells from starving. But now only a fraction of the 250 make it to the cells needing it while the rest is stored as body fat. Again, she must overeat even more. This process of overeating to keep a hormonally clogged metabolism running repeats itself until Terri eats 1,000 calories to meet her need for 500 calories. Terri’s metabolism is leaking calories into her fat cells and has to compensate by taking in extra calories.
Continue this “overeat to compensate for the clog” cycle day after day and Terri gains body fat. And on the surface it looks like she is gaining body fat because she is eating too many calories. But eating too many calories is not the cause of her new body fat. It is a symptom of a deeper problem: her hormonal clog. Terri’s high consumption of calories is not the cause of her weight gain. It is a symptom of the hormonal clog caused by inSANE low-quality calories.
“What passes for knowledge is often no more than well-organized ignorance.” – J.R.A. Mitchell, Queen’s Medical Centre
“The common aim of all science [is] the gradual removal of prejudices.” – Niels Bohr, physicist
Even the American Heart Association, which champions eating less and exercising more, acknowledged that calorie quantity does not cause obesity when they remarked: “One can argue that people become obese because they consume more calories than they expend, but this doesn’t tell us why the imbalance exists or the best way to correct it.” Put differently: “People become obese because they overeat, but that doesn’t tell us the cause of their overeating or how to fix it.”
Obesity is not caused by eating too many calories, and it is not cured by eating fewer calories. Hilde Burch at Baylor University concludes:
“Though [overeating] is observed with great regularity, it is not the cause of obesity; it is a symptom of an underlying disturbance…. The changes in weight regulation and fat storage are the essential disturbances.”
Telling an adult struggling to lose fat to eat less and exercise more is like telling a child struggling to see the chalk board to sit closer and squint more. Both confuse dealing with symptoms and fixing causes.
Problems are not solved by treating symptoms. That is why the calorie-quantity-based approach to fat loss, eating less and exercising more, fails 95% of the time long-term. It is only treating symptoms. It is based on the myth that gaining body fat is caused by calorie quantity, and that is wrong.
What do you think? Share. Get support. Learn simple science. Join us in the free Smarter Science of Slim Support Group today!
PS I like to think of the difference between “Eat Less. Exercise More. Harder.” and “Eat More. Exercise Less. Smarter.” like the difference between taking an expensive medication for the rest of our lives and curing a disease. Eating less and exercising more is one of the most expensive, time consuming, and painful “medications” around. And if we take it even more of it, forever, the symptoms of our clogged metabolism will be suppressed. But why not cure the underlying issue? Especially when eating SANE foods and doing smarter exercise takes less time and money, dramatically benefits our health, and never requires us to be hungry.
- Caro JF. Clinical review 26: Insulin resistance in obese and nonobese man. J Clin Endocrinol Metab. 1991 Oct;73(4):691-5. Review. PubMed PMID: 1890146.
- DeFronzo RA, Ferrannini E. Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. Diabetes Care. 1991 Mar;14(3):173-94. Review. PubMed PMID: 2044434.
- Kissebah AH, Peiris AN. Biology of regional body fat distribution: relationship to non-insulin-dependent diabetes mellitus. Diabetes Metab Rev. 1989 Mar;5(2):83-109. Review. PubMed PMID: 2647436.
- Apoundu J. Pi-Sunyer F. Obesity and Diabetes In: Bray GA, Couchard d, James WP, eds. Handbook of Obesity. New York: Marcel Dekker, 1997: 697-707.
- Lamarche B, Tchernof A, Mauriege P, et al. Fasting insulin and apolipoprotein B levels and low-density lipoprotein particle size as risk factors for ischemic heart disease. JAMA. 1998;279:1955-1961.
- Cordain L, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA, O’Keefe JH, Brand-Miller J. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005 Feb;81(2):341-54. Review. PubMed PMID: 15699220.
- Knowler WC, Pettitt DJ, Savage PJ, Bennett PH. Diabetes incidence in Pima indians: contributions of obesity and parental diabetes. Am J Epidemiol. 1981
- Haskell WL, Lee IM, Pate RR, Powell KE, Blair SN, Franklin BA, Macera CA, Heath GW, Thompson PD, Bauman A; American College of Sports Medicine; American Heart Association. Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association. Circulation. 2007 Aug 28;116(9):1081-93. Epub 2007 Aug 1. PubMed PMID: 17671237.
- Bruch, Hilde. The Importance of Overweight. New York: Norton, 1957. Print.
- J.R.A., Mitchell. “Diet and arterial disease? the Myths and the Realities.” Proceedings of the Nutrition Society 44.3 (1985): 363-370. http://journals.cambridge.org. Web. 27 Dec. 2010.