How to Lower Your Body’s Weight Set-Point

December 11, 2018

A body weight set-point is a number—your weight—that your body maintains within a narrow range through a feed-back and control system just like the thermostat in your home.

The body the set point involves your brain, gastrointestinal tract, circulating hormones, and fat cell mass.

What is known is that in adults, body weight is maintained at a relatively stable level for long periods (1). This observation is the basis for the set-point theory.

Information from the body is sent to a central controller located in an area in the brain’s forefront called the hypothalamus. The controller uses this information to change or maintain food intake (hunger), energy expenditure (metabolic rate) to correct any changes in body weight from this set-point. This involves hormone signals from the hypothalamus, fat cell mass, and gastrointestinal tract.

The set point management of body weight is more effective in response to weight loss than to weight gain (1).

During weight loss, the body’s metabolic rate—energy expenditure—decreases (2).

After weight loss, changes in the circulating levels of several peripheral hormones, including the hunger hormone Grehlin, increase (4). These hormone changes may remain in place for over one year (3).

These data help to explain the results of the Minnesota starvation study (5) during which subjects decreased calorie intake by 68.9% and lost 66% of their initial fat mass after 24 weeks of dieting. After a period of re-feeding with no restrictions, the subjects regained 145% of their original fat mass.

This is also the reason that diets alone will fail because the hypothalamus continues to counter the lower calorie intake by decreasing the metabolic rate and increasing the hunger hormone Grehlin.

In the Minnesota study, it took more than a year for some subjects to decrease their fat mass to within 5% of the initial value. These results suggest that in the USA, on a western diet, the body regulation of calorie deprivation is powerful, long lasting, and loosely controlled.

It is common for obese people on a diet to fail because they do not adhere to the diet. Most diets with no other intervention eventually fail [6].

Leptin

Leptin is another regulator of body weight or fat mass (7). Leptin is made in fat cells and is proportional to the amount of fat present in the body. The hypothalamus uses this information to regulate the hunger hormone, Grehlin, and the metabolic rate to maintain the set point (1). This is a very simple explanation.

There is a theory that pregnant women program the developing baby’s appetite regulatory centers in the brain. [8]

This idea is supported by a study that compared the weight in the babies of obese mothers who had pre-pregnancy by-pass surgery and lost weight to obese mothers who did not. The mothers who lost weight had 52% fewer overweight babies [9].

Increasing energy expenditure can increase calorie intake, whereas increasing calorie intake does not increase energy expenditure [activity] [10].

The metabolic response to underfeeding and overfeeding is complex and involves: specific metabolic rates in individual organs (heart, liver, kidneys, skeletal muscle, and brain); sympathetic nervous system activity; plasma concentrations of thyroid hormones and leptin; and insulin sensitivity [11].

In the long term, carbohydrate balance is tightly regulated [12].

By contrast, fat imbalances are not tightly regulated. Fat intake does not stimulate fat use as a source of energy [13].

These data show that variation in body weight is due to the fat content of the diet.

Leptin derived proportionally from fat cells is an important signal in body weight feedback and control. [14].

The blood level of leptin signals the hypothalamus to regulate energy intake and energy expenditure and maintains a “set point” of body weight. Current evidence suggests that leptin protects more for fat loss than for fat gain. [15].

This control system explains why it is easier to gain weight than to lose.

The body apparently does not compensate well to western high fat and high sugar diets as seen in the recent epidemic of obesity.

[16].

By contrast, a traditional Cameroonian diet containing high fiber carbohydrates and low fat led to a rapid return to initial body weight after massive over-feeding [17]. The set pint regulation of body weight appears more effective in non-western diets.

Can you change your weight set point?

There is no prospective controlled scientific studies that directly addresses this point. It is very difficult to completely control all the variables in humans.

Most articles on set point change recommend a long slow process of gradual weight loss. Medical weight loss programs with diet and prescription medication can counter act your brain’s set point as long as you take the drug.

A good example of this is the drug Phendimetrazine, which increases your metabolic rate because it is a stimulant and decreases your hunger. This effectively counter acts your brain. This method, like diet alone, will fail when the pill is no longer taken.

MY ANSWER

My answer is that exercise and low fat, low glycemic diets are the missing ingredients. With exercise and diet the set point will change because exercise will increase your metabolic rate and decrease your hunger and a low fat, low glycemic diet will enable your leptin-grehlin feedback system to work efficiently. This is another way of stating that your life style must change.

REFERENCES

1. Müller MJ, Bosy-Westphal A, Heymsfield SB. Is there evidence for a set point that regulates human body weight? F1000 Medicine Reports. 2010;2:59. doi:10.3410/M2-59.

2. Am J Clin Nutr. 1998 Sep;68(3):599-606. Adaptive reduction in basal metabolic rate in response to food deprivation in humans: a role for feedback signals from fat stores. Dulloo AG(1), Jacquet J.

3. N Engl J Med. 2011 Oct 27;365(17):1597-604. doi: 10.1056/NEJMoa1105816. Long-term persistence of hormonal adaptations to weight loss. Sumithran P(1), Prendergast LA, Delbridge E, Purcell K, Shulkes A, Kriketos A, Proietto J.

4.Reversible biological adaptations in obesity; Södersten, Per et al.The Lancet Diabetes & Endocrinology , Volume 3 , Issue 5 , 314

5. Keys, A., Brožek, J., Henschel, A., Mickelsen, O., & Taylor, H. L., The Biology of Human Starvation (2 volumes), University of Minnesota Press, 1950.

6. Svetkey LP, Stevens VJ, Brantley PJ, Appel LJ, Hollis JF, Loria CM, Vollmer WM, Gullion CM, Funk K, Smith P, Samuel-Hodge C, Myers V, Lien LF, Laferriere D, Kennedy B, Jerome GJ, Heinith F, Harsha DW, Evans P, Erlinger TP, Dalcin AT, Coughlin J, Charleston J, Champagne CM, Bauck A, Ard JD, Aicher K, Weight Loss Maintenance Collaborative Research Group Comparison of strategies for sustaining weight loss: the weight loss maintenance randomized controlled trial. JAMA. 2008;299:1139–48].

7 Blüher S, Mantzoros CS. Leptin in humans: lessons from translational research. Am J Clin Nutr. 2009;89(Suppl):991S–997S. doi: 10.3945/ajcn.2008.26788E.

8. Walley AJ, Asher JE, Froguel P. The genetic contribution to non-syndromic human obesity. Nat Rev Genet. 2009;10:431–42].

9. Kral JG, Biron S, Simard S, Hould F-S, Lebel S, Marceau S, Marceau P. Large maternal weight loss from obesity surgery prevents transmission of obesity to children who were followed for 2 to 18 years. Pediatrics. 2006;118: e1644–9]. These data point to the role of environmental factors in the regulation of body weight.

10. Westerterp KR. Physical activity, food intake, and body weight regulation: insights from doubly labelled water studies. Nutr Rev. 2010;68:148–54]. Very strenuous exercise and high energy expenditure can cause loss of body fat. [Westerterp K. Alterations in energy balance with exercise. Am J Clin Nutr. 1998;68:970S–974S.

11. Hall KD. Predicting metabolic adaptation, body weight change, and energy intake in humans. Am J Physiol Endocrinol Metab. 2010;298:E449–66. ; Bosy-Westphal A, Goele K, Later W, Hitze B, Kossel E, Settler U, Heller M, Glüer C-C, Heymsfield SB, Müller MJ. Contribution of individual organ mass loss to weight loss-associated decline in resting energy expenditure. Am J Clin Nutr. 2009;90:993–1001.]

12. Jebb SA, Prentice AM, Goldberg GR, Murgatroyd PR, Black AE, Coward WA. Changes in macronutrient balance during over- and underfeeding assessed by 12-d continuous whole body calorimetry. Am J Clin Nutr. 1996;64:259–66. ; Flatt JP. Carbohydrate balance and body-weight regulation. Proc Nutr Soc. 1996;55:449–65]

13. Flatt JP, Ravussin E, Acheson KJ, Jequier E. Effects of dietary fat on postprandial substrate oxidation and carbohydrate and fat balances. J Clin Invest. 1985;76:1019–24.]

14. Friedman JM. Leptin at 14y of age: an ongoing story. Am J Clin Nutr. 2009;89(Suppl):973S–979S; Blüher S, Mantzoros CS. Leptin in humans: lessons from translational research. Am J Clin Nutr. 2009;89(Suppl):991S–997S.)

15. Prentice AM, Moore SE, Collinson AC, O’Connell MA. Leptin and undernutrition. Nutr Rev. 2002;60:S56–S67.; Tam J, Fukumura D, Jain RK. A mathematical model of murine metabolic regulation by leptin: energy balance and defense of a stable body weight. Cell Metab. 2009;9: 52–63].

16. Prentice AM, Poppitt SD. Importance of energy density and macronutrients in the regulation of energy intake. Int J Obes. 1996;20(Suppl 2):S18–S23.

17. Pasquet P, Apfelbaum M. Recovery of initial body weight and composition after long-term massive overfeeding in men. Am J Clin Nutr. 1994;60:861–3.].

18.Is there evidence for a set point that regulates human body weight?