Metabolic Adaptation vs. Metabolic Damage: An In - Depth Analysis

I. Introduction

The term “metabolic damage” has witnessed a significant surge in popularity over recent years. Initial research by [Researchers1] identified a decline in the metabolic rate among subjects who had experienced substantial weight loss. This decrease is not entirely unexpected, as a reduction in an individual's body weight inherently leads to a corresponding decrease in their energy requirements. However, what was remarkable in this context was that the metabolic rates of some individuals were considerably lower than the projected values by the researchers.

These findings quickly gained traction within the fitness community and were promptly labeled as “metabolic damage.” Nevertheless, currently, there is a lack of compelling evidence to support the existence of metabolic damage in this particular context. What researchers were actually observing is more accurately defined as metabolic adaptation and adaptive thermogenesis, as per [1].

II. Physiological Changes during Caloric Restriction and Weight Loss

A. Hormonal Changes Associated with Fat Loss

Leptin, a hormone primarily responsible for regulating energy balance and maintaining body weight, is often referred to as the satiety hormone. It plays a crucial role in modulating an individual's appetite. Leptin is synthesized in adipocytes, making it highly sensitive to changes in body fat stores [2].

• During caloric restriction, as body fat is lost, serum leptin concentrations decline. This decrease in leptin triggers a cascade of neurochemical changes, which can significantly enhance hunger and reward - seeking behaviors [3].

• In addition to leptin, other hormones such as the thyroid hormone are also affected. The thyroid hormone is a key determinant of energy expenditure and the Basal Metabolic Rate (BMR) [4]. Observations indicate that sustained caloric deficit - induced fat loss can lead to a reduction in thyroid values, thereby lowering the basal BMR [5].

B. Impact of Fat Loss on Physiological Energy Processes

1. ATP Synthesis Efficiency

2. Adenosine Triphosphate (ATP) synthesis typically operates at approximately 40% efficiency, meaning that around 60% of energy is dissipated through thermogenesis [6]. However, in conditions of low energy availability and reduced body fat, mitochondrial efficiency increases. Proton leak, a process regulated by uncoupling proteins, causes energy to be lost as heat. An increase in mitochondrial efficiency reduces proton leak and boosts ATP synthesis as an adaptive response [7].

3. Other Physiological Adaptations

4. As calories are restricted and body weight decreases, other aspects of physiology, such as muscular work efficiency, also improve [8]. Simultaneously, Non - Exercise Activity Thermogenesis (NEAT) decreases. NEAT is associated with spontaneous, non - exercise - related physical activity and accounts for a significant portion of energy expenditure [9]. Researchers have noted that caloric restriction and weight loss can substantially reduce an individual's NEAT, often unconsciously. Although adopting a daily step - count routine is a common practice to monitor and regulate energy expenditure, this is technically exercise activity thermogenesis rather than NEAT.

III. The Settling Point Theory

Our bodies exhibit a preference for consistency, as described by the settling point theory. As stated in [10], “The set point model is grounded in physiology, genetics, and molecular biology, suggesting the presence of an active feedback mechanism that links adipose tissue (stored energy) to intake and expenditure via a set point, presumably encoded in the brain.” While this theory does not account for all relevant variables, it does offer some insight into the body's attempt to maintain homeostasis in terms of body weight and energy availability. As energy availability from external (e.g., food) and internal (e.g., body fat stores) sources diminishes, the body resists this change through various physiological and neurochemical adaptations, including changes in thyroid and leptin levels, as well as an increased hedonic drive for food.

Moreover, as body weight is reduced, the energy requirement for locomotion decreases proportionally. NEAT can vary by up to 2,000 kcal per day between individuals of the same size [12]. As previously mentioned in an article for Kabuki Strength [13], “A paper by Rosenbaum and colleagues cited a reduction in Total Energy Expenditure (TEE) of 10 - 15% which was not accounted for by body composition changes. Of this 10 - 15% reduction, approximately 85% could be attributed to reductions in non - resting energy expenditure, with NEAT being the largest contributor” [14]. Once these changes are taken into consideration, most of the discrepancies between estimated BMR and actual BMR can be resolved.

IV. Managing Metabolic Adaptation

A. The Significance of Metabolic Adaptation

Metabolic adaptation is indeed a crucial factor to consider. However, there is currently no strong evidence to suggest that it implies metabolic damage.

B. Strategies for Managing Adaptive Responses

1. Increase Physical Activity

2. Researchers have consistently demonstrated a strong association between regular physical activity and successful weight management. By increasing energy intake in proportion to energy expenditure, we can counteract some of the adaptive responses of dieting. This approach allows for an increase in energy intake while maintaining a predetermined bodyweight range.

3. Increasing calorie intake can alleviate hunger, enhance the thermic effect of food, and mitigate the psychological fatigue accumulated during the diet.

4. Adopting a more gradual weight - loss approach, such as losing 1% of body weight per week, may delay some of these adaptive responses, as the acute change in energy availability is less pronounced.

5. It is also essential to establish clear timelines and end dates for diet periods. Dieting for more than three months is generally not advisable, as diminishing returns often occur beyond this point. Utilizing maintenance phases to gradually increase energy intake while keeping weight stable can set a higher caloric starting point for the next diet phase.

In conclusion, at present, metabolic damage lacks strong supporting evidence. What is typically observed is metabolic adaptation, which is reversible in most cases. When implemented correctly, dieting can be an integral part of healthy eating and optimizing body composition.

References

1. Michael Rosenbaum and Rudolph L. Leibel, “Adaptive thermogenesis in humans.” International Journal of Obesity, London. 2010 Oct; 34(0 1): S47–S55.

2. R V Considine 1, M K Sinha, M L Heiman, A Kriauciunas, T W Stephens, M R Nyce, J P Ohannesian, C C Marco, L J McKee, T L Bauer, et al., “Serum immunoreactive - leptin concentrations in normal - weight and obese humans.” New England Journal of Medicine. 1996 Feb 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 Review, 2015 May; 73(5): 296–307. Published online Apr 9, 2015.

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

5. Edward P. Weiss, Dennis T. Villareal, Susan B. Racette, Karen Steger - May, Bhartur N. Premachandra, Samuel Klein, and Luigi Fontana. “Caloric Restriction But Not Exercise - Induced Reductions in Fat Mass Decrease Plasma Triiodothyronine 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.” Biophys Chemistry. 2016 Dec; 219: 69 - 74. Epub 2016, Oct 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 Goldsmith, Jean - Aime Simoneau, Steven Heymsfield, Denis R Joanisse, Jules Hirsch, Ellen Murphy, Dwight Matthews, Karen R Segal, Rudolph L Leibel, “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.

9. Christian von Loeffelholz, M.D. and Andreas Birkenfeld. “The Role of Non - exercise Activity Thermogenesis in Human Obesity.” Endotext, {Internet}. Last updated Apr 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., “Set points, settling points, and some alternative models: theoretical options to understand how genes and environments combine to regulate body adiposity.” Disease Model Mech, 2011 Nov; 4(6): 733–745.

11. Michael Rosenbaum 1, Krista Vandenborne, Rochelle Goldsmith, Jean - Aime Simoneau, Steven Heymsfield, Denis R Joanisse, Jules Hirsch, Ellen Murphy. Dwight Matthews, Karen R Segal, Rudolph L Leibel, “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.

12. Christian von Loeffelholz, M.D. and Andreas Birkenfeld. “The Role of Non - exercise Activity Thermogenesis in Human Obesity.” NCBI, Endotext {Internet}. Last updated Apr 9, 2018.

13. Debrocke, Daniel, “Preventing Weight Regain After A Diet.” Kabuki Strength, Apr 24, 2020. Accessed Feb 25, 2021.

14. Michael Rosenbaum and Rudolph L. Leibel, “Adaptive thermogenesis in humans.” Int J Obes (Lond). 2010 Oct; 34(0 1): S47–S55.

15. Gregory A Hand and Steven N Blair, “Energy Flux and its Role in Obesity and Metabolic Disease.” Eur Endocrinol. 2014 Aug; 10(2): 131–135. Published online 2014, Aug 28.