Perceive metabolic harm and adaptation


The term metabolic damage has gained widespread popularity over the years. The researchers1 first observed a decreased metabolic rate in subjects who had lost a significant amount of weight. This reduction is far from shocking, as reducing a person’s body weight also lowers their energy needs.

What was unique in this case, however, was that the metabolic rates of some individuals were well below the values ​​predicted by the researchers.

These results became popular in various fitness circles and quickly became labeled for metabolic damage. However, there is currently no convincing evidence for the existence of metabolic damage in this context. What the researchers observed is more precisely defined as metabolic adjustment and adaptive thermogenesis. 1

During a period of calorie restriction that accompanies a reduction in body weight, your body undergoes several physiological changes in order to adapt to the changing environment – both internally and externally.

Changes in hormones are associated with fat loss

Leptin is a hormone whose main function is to regulate energy levels and maintain body weight.

  • Often referred to as the satiety hormone, it helps regulate a person’s urge to consume food. Since leptin is synthesized in adipocytes, leptin is sensitive to body fat stores
  • When we lose body fat during a period of calorie restriction, serum leptin levels decrease. This decrease in leptin concentration is accompanied by a cascade of neurochemical changes that can significantly increase hunger and reward-seeking behavior
  • Various other hormones, including the thyroid, are also affected. Thyroid hormone has been shown to be a key variable in determining energy expenditure and basal metabolic rate (BMR) .4

Observations show that fat loss during a persistent calorie deficit can lower thyroid levels and thereby lower the basal BMR.5

Fat loss affects physiological energy processes

In addition, the adenosine triphosphate (ATP) synthesis becomes more efficient. Typically, ATP synthesis is around 40% efficient, which means that around 60% of energy is lost through thermogenesis.6 However, with low energy availability and reduced body fat, mitochondrial efficiency increases.

Proton leakage, a process regulated by the decoupling of proteins, results in energy being lost as heat. However, increased mitochondrial efficiency decreases proton leakage and increases ATP synthesis as an adaptive response

We also see other aspects of our physiology, such as: B. the efficiency of muscle work, the gain when calories are limited, and the weight loss

As these adaptations occur, we also see a decrease in non-exercise activity thermogenesis (NEAT). This decrease is associated with spontaneous physical activity unrelated to exercise and is the largest energy expenditure

Researchers have observed that calorie restriction and body weight loss can significantly reduce an individual’s NEAT. Unfortunately, this is mostly unconscious, so there isn’t much you can do about it.

Daily step counting is a common practice for recording and regulating energy consumption.

However, since this is specifically designed to use up calories, it is technically not NEAT. It is thermogenesis exercise activity. But I digress.

Researchers have found that our bodies like consistency. Enter the settling point theory. As one article put it,

“The set point model is based on physiology, genetics and molecular biology and suggests that there is an active feedback mechanism that links adipose tissue (stored energy) to intake and output via a set point that is believed to be encoded in the brain.” 10

While this does not account for all the relevant variables, it does, to some extent, explain the body’s desire to maintain homeostasis in terms of body weight and energy availability.

In essence, when the availability of energy from the outside, such as food, and from the inside, such as in body fat stores, decreases, our body tries to resist this change through various physiological and neurochemical changes.

As mentioned earlier, changes in thyroid gland, leptin levels, and even an increased hedonic dive for food are just a few of the numerous adaptive responses.

If you reduce your body weight, the energy requirements for locomotion decrease accordingly.11 NEAT can vary by 2,000 kcal per day between people of the same size.12

In a previous article I wrote for Kabuki Strength,

I mentioned: “An article by Rosenbaum and colleagues mentioned a 10-15% reduction in total energy costs (TEE) that was not explained by changes in body composition. Of this 10 to 15% reduction, around 85% could be explained by the reduction in non-dormant energy consumption, to which NEAT is the largest contributor. “13.14

Once we account for these changes, the vast majority of the discrepancies between the estimated BMR and the actual BMR are taken into account.

So is metabolic adaptation a problem? Absolutely. But does it indicate some form of harm? Well, at the moment there doesn’t seem to be any strong evidence for that. What can you do to manage some of these adaptive responses and successfully maintain your new body weight composition?? One possible approach is to use a high energy flow approach. 15

Increase physical activity

Researchers have consistently found that regular physical activity is strongly linked to successful weight management.

  • By increasing energy intake in proportion to energy expenditure, we can offset some of the adaptive responses of dieting and increase energy intake while staying within a given body weight range.
  • Increasing calories can reduce hunger, improve the thermal effects of foods, and help relieve mental fatigue accumulated during your diet.
  • A gradual approach to weight loss like 1% of your body weight loss per week can delay some of these adaptive responses because the acute change in energy availability is not dramatic.
  • In addition, it is important to set clear schedules and end dates for your diet periods.
  • Dieting for more than three months is usually not recommended as you will often see a drop in returns beyond this point.
  • If you use maintenance phases to slowly increase your energy intake while keeping your weight stable, you will have a higher calorie starting point by the beginning of the next phase of diet.

Metabolic damage doesn’t seem to have strong evidence right now. What we usually observe instead is a metabolic adjustment.

In the vast majority of cases, these adjustments are completely reversible.

When used correctly, diet can be an important aspect of healthy eating and optimizing body composition.


1. Michael Rosenbaum and Rudolph L. Leibel, “Adaptive Thermogenesis in Humans”. International Journal of Obesity, London. 2010 Oct; 34 (01): S47-S55.

2. RV Considin 1, MK Sinha, ML Heiman, A. Kriauciunas, TW Stephens, MR Nyce, JP Ohannesian, CC Marco, LJ McKee, TL Bauer et al. “New England Journal of Medicine. 1996, February 1; 334 (5): 292-5.

3. Miguel Alonso-Alonso, Stephen C. Woods, Marcia Pelchat, Patricia Sue Grigson, Eric Stice, Sadaf Farooqi, Chor San Khoo, Richard D. Mattes, and Gary K. Beauchamp. “Food Reward System: Current Perspectives and Future Research Needs.” Nutrition Report, May 2015; 73 (5): 296-307. Published online 9 April 2015.

4. Brian Kim, “Thyroid hormone as a determinant of energy expenditure and basal metabolic rate.” Thyroid, 2008 Feb; 18 (2): 141-13. 4th

5. Edward P. Weiss, Dennis T. Villareal, Susan B. Racette, Karen Steger-May, Bhartur N. Premachandra, Samuel Klein, and Luigi Fontana. “Calorie Reduction, but No Exercise-Induced Fat Mass Reduction, Reduces Triiodothyronine Plasma Concentrations: A Randomized Controlled Trial.” Rejuvenation Res. 2008 Jun; 11 (3): 605-609.

6. Sunil Nath, “The Thermodynamic Efficiency of ATP Synthesis in Oxidative Phosphorylation.” Biophysical Chemistry. 2016 Dec; 219: 69- 74th Epub 2016, October 15.

7. Martin Jastroch, Ajit S. Divakaruni, Shona Mookerjee, Jason R. Treberg, and Martin D. Brand, “Mitochondrial Proton and Electron Leaks”. Essays Biochem, 2010; 47: 53-67.

8. Michael Rosenbaum 1, Krista Vandenborne, Rochelle Goldschmied, Jean-Aime Simoneau, Steven Heymsfield, Denis R. Joanisse, Jules Hirsch, Ellen Murphy, Dwight Matthews, Karen R. Segal, Rudolph L. Leibel, “Effects of experimental weight disorders on the Skeletal muscles work efficiency in humans. “Am J Physiol Regul Integr Comp Physiol. 2003 Jul; 285 (1): R183-92. Epub 2003, February 27th.

9. Christian von Loeffelholz and Andreas Birkenfeld. “The role of thermogenesis of non-physical activity in obesity in humans.” Endotext, {Internet}. Last updated April 9, 2018.

10. John R. Speakman, David A. Levitsky, David B. Allison, Molly S. Bray, John M. de Castro, Deborah J. Clegg, John C. Clapham, Abdul G. Dulloo et al, settlement points and some alternative models : theoretical options to understand how genes and environments combine to regulate obesity in the body. “Disease Model Mech, 2011 Nov; 4 (6): 733-745.

11. Michael Rosenbaum 1, Krista Vandenborne, Rochelle Goldschmied, Jean-Aime Simoneau, Steven Heymsfield, Denis R. Joanisse, Jules Hirsch, Ellen Murphy. Dwight Matthews, Karen R. Segal, Rudolph L. Leibel, “Effects of Experimental Weight Disorders on Skeletal Muscle Efficiency in Humans.” Am J Physiol Regul Integr Comp Physiol. 2003 Jul; 285 (1): R183-92. Epub 2003 February 27th.