Hi! I'm your SANE concierge. What can I help you find today?

Your Set-Point Weight


“The set-point theory of body weight regulation is based on a large body of empiric evidence.”– D.S. Weigle, University of Washington

Our fat metabolism system automatically regulates our weight around a “set-point.” That set-point is why no matter how little we eat or how much we exercise, we generally end up weighing the same. It is why you can get sick, lose weight, but then gain it all back. It is also why heavy people do not keep getting heavier and heavier until they explode.

Set-Point Weight: The weight that our fat metabolism system automatically works to keep us at regardless of the quantity of calories we take in or exercise off.

I know that last part sounds silly, but let’s look at this point seriously. Why don’t obese people gain weight forever? If the quantity of calories they ate and exercised off raised them to 450 pounds, why doesn’t it raise them to 4,500 pounds? These individuals somehow automatically stop gaining weight. How does that work under the Calories In – Calories Out theory?

It doesn’t.

Here is how weight gain works in the real world: A person’s set-point rises and then their fat metabolism system fights to keep them weighing more regardless of how little they eat or how much they exercise. D.S. Weigle at the University of Washington notes: “Obesity is not a disorder of body weight regulation. Most obese patients regulate their weight appropriately about an elevated set-point weight.” A heavy person’s higher set-point keeps them at that higher weight like a thin person’s lower set-point keeps them at a lower weight. We all have a set-point. The issue is how high it is. Long-term fat loss comes from lowering it, not from starving it.

The set-point takes whatever quantity of calories we eat plus whatever quantity of calories we burn and balances us out automatically. That is why manually balancing calories fails 95% of the time over the long term. It is trying to override our set-point, and we generally do not win battles against our basic biological functions. As researcher Keith Frayn of Oxford University noted: “We should not be surprised that dieting is difficult because it is a fight against mechanisms which have evolved over many millions of years precisely to minimize its effects.”

J.M. Friedman of the Rockefeller University sums up the set-point: “[The simplistic notion] that weight can be controlled by ‘deciding’ to eat less and exercise more…is at odds with substantial scientific evidence illuminating a precise and powerful biologic system that maintains body weight within a relatively narrow range.” This point is also emphasized by P.J. Havel at the University of California: “Body weight…[is] tightly regulated over relatively long periods of time. Even after large alterations of body fat resulting from restriction of energy intake…body weight and fat stores tend to return to pre-intervention levels.”

Our body does not want us to starve. To lose weight, we need to lower the “relatively narrow range” where our “powerful biologic system” operates. In order to do that, we need to find out what causes the set-point to rise in the first place. We’ll do that in the next post.

  1. Friedman JM. A war on obesity, not the obese. Science. 2003 Feb 7;299(5608):856-8. PubMed PMID: 12574619.
  2. Friedman JM. Modern science versus the stigma of obesity. Nat Med. 2004 Jun;10(6):563-9. Review. PubMed PMID: 15170194.
  3. Garner, David, and Paul Garfinkel. Handbook of Treatment for Eating Disorders: 2nd Edition. 2 Sub ed. New York: The Guilford Press, 1997. Print.
  4. Havel PJ. Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Nutr Rev. 2005 May;63(5):133-57.Review. PubMed PMID: 15971409.
  5. Havel PJ. Update on adipocyte hormones: regulation of energy balance and carbohydrate/lipid metabolism. Diabetes. 2004 Feb;53 Suppl 1:S143-51. Review. PubMed PMID: 14749280.
  6. Hirsch J, Hudgins LC, Leibel RL, Rosenbaum M. Diet composition and energy balance in humans. Am J Clin Nutr. 1998 Mar;67(3 Suppl):551S-555S. Review. PubMed PMID: 9497169.
  7. Hirsch J. The regulation of food intake. Discussion. Adv Psychosom Med. 1972;7:229-42. PubMed PMID: 4485878.
  8. James W. Reeds P. Nutrient Partitioning In: Bray GA, Couchard d, James WP, eds. Handbook of Obesity. New York: Marcel Dekker, 1997: 555-571.
  9. Keesey RE, Hirvonen MD. Body weight set-points: determination and adjustment. J Nutr. 1997 Sep;127(9):1875S-1883S. Review. PubMed PMID: 9278574.
  10. Keesey RE. The body-weight set point. What can you tell your patients? Postgrad Med. 1988 May 1;83(6):114-8, 121-2, 127. Review. PubMed PMID: 3283713.
  11. Koopmans, Henry S. Experimental studies on the control of food intake.. In: Bray GA, Couchard d, James WP, eds. Handbook of Obesity. New York: Marcel Dekker, 1997: 273-311.
  12. Lönnqvist F, Arner P, Nordfors L, Schalling M. Overexpression of the obese (ob) gene in adipose tissue of human obese subjects. Nat Med. 1995 Sep;1(9):950-3. PubMed PMID: 7585223.Frayn, K. N. Metabolic Regulation: a Human Perspective. London: Portland, 1996. Print.
  13. Rosenbaum M, Vandenborne K, Goldsmith R, Simoneau JA, Heymsfield S, Joanisse DR, Hirsch J, Murphy E, Matthews D, Segal KR, Leibel RL. Effects of experimental weight perturbation on skeletal muscle work efficiency in human subjects. Am J Physiol Regul Integr Comp Physiol. 2003 Jul;285(1):R183-92. Epub 2003 Feb 27. PubMed PMID: 12609816.
  14. Trans Assoc Am Physicians. 1968;81:153-70. Experimental obesity in man. Sims EA, Goldman RF, Gluck CM, Horton ES, Kelleher PC, Rowe DW.
  15. Weigle DS. Human obesity. Exploding the myths. West J Med. 1990 Oct;153(4):421-8. Review. PubMed PMID: 2244378; PubMed Central PMCID: PMC1002573.