Metabolic Damage — Tearing Through the Science

The body is an amazing machine. It is capable of incredible athletic feats such as dead-lifting crazy amounts of weight, running a sub 4-minute mile, jumping nearly 50” in a vertical jump test or even non-athletic feats such as surviving in extreme climates, the immune system fighting off disease and the like. No matter what is thrown at it, most healthy individuals have probably seen firsthand just what the human body can do when tested or circumstances arise. No matter what happens to the body, it will find a way of compensating and adapting, and this also not surprisingly applies to your metabolism.

With the emergence of physique competitions gaining more and more popularity or even the general population being more body aware of maintaining a healthy body weight, many are looking to reduce their body weight. Armed with well-meaning advice of their friends or the common idea that eating less and exercising more is simply all you need to consider, this has also lead to many doing more harm than good. Fat loss stalls, people are looking soft and watery despite depleting in carbs, training sessions suck, the scale isn’t moving, and, in some cases, people even start gaining weight despite not changing anything.

This situation sound familiar? Of course it does. The body has adapted the metabolism to compensate for the decrease in calories being ingested and the stress placed on it from increased exercise and has adjusted accordingly as it likes homeostasis, and in this case, is an example of the body being protected by a mechanism that has evolved over thousands of years that protected your ancestors from starting to death when food wasn’t in abundance. Obviously, we aren’t in the stone age, so now that food is an abundance, this metabolic compensation is a hindrance for those looking to reduce body fat and is where the concept of metabolic damage now comes into play. Do remember that the whole point of body fat is to protect your internal organs, store energy for long periods and release when in an emergency scenario…it has no way of knowing when a deficit is ‘on purpose’ or if it is due to true starvation, so it only makes sense that adaptation takes place.

Metabolic Damage — What is it?

Defined as the non-clinical term as a step beyond adaptive thermogenesis, it all starts with the concept that the body has two responses to a caloric deficit (1). Further defined as that it is the fat-free mass (FFM)-independent reduction of resting energy expenditure (REE) to caloric restriction (CR). It should also be noted that adaptive thermogenesis attenuates weight loss and favors weight regain (2).

The first (and usually desired response) is that the body reduces stored body fat as is it releasing it to be burned as fuel to replace the calories that it was otherwise getting from caloric intake. The second is the less desirable, being the down-regulation of the metabolism to adapt to the stress caused by a caloric deficit. When an individual has the inability to lose body fat, even at a very low caloric intake and high levels of exercise, this is where metabolic damage comes into play as they are regarded to have a ‘damaged’ metabolism.

Now, the biggest misconception that is not supported by science is the permanence of this condition. There is no solid scientific evidence suggesting that this is a permanent state, and some will even go as far as saying that it isn’t a real condition, but simply a misnaming of adaptive thermogenesis. There is no scientific data supporting that the state of metabolic damage has a ‘definite’ indicator, but rather a combination of symptoms and testing parameters that come together to form a subjective state, and with that being said, many will circle and counter back to stating its simply AT.

Furthermore, one thing that needs to be stated is that since there is no scientific support for the state of actual metabolic damage, it should be noted that nearly all literature supports that when an individual starts to increase caloric intake, the metabolism ‘repairs’ itself gradually and elevates basal metabolic rate again. This will be discussed later in the article more as not surprisingly, there is some debate as to how one should ‘reverse’ or ‘fix’ said condition.

In summary, there really isn’t scientific support for their being a true state of ‘metabolic damage’, which implies that there is permanent damage to the metabolism long term, but rather what is often mistaken is metabolic damage is simply adaptive thermogenesis which can be reversed through introduction of more calories to bring the body out of this state over time. Let the emails flow in…I just said that metabolic damage is largely a myth and you simply are experiencing adaptive thermogenesis temporarily.

The Role of the Endocrine System

Now, just because we somewhat dispelled the notion of this ‘metabolic damage’ that many are worried about as simply saying that it is adaptive thermogenesis, let’s not throw in the towel, it simply means that there isn’t any permanent ‘damage’ occurring. With that being said, one of the biggest factors in this scenario is the role of the endocrine system as it plays an important regulation of body composition, energy intake, and energy expenditure.

Specifically, the hormones of the thyroid gland (particularly triiodothyronine (T3)) play a direct role in regulating metabolic rate (3). There is an inverse relationship with increases in circulating thyroid hormones are associated with an increase in the metabolic rate, whereas lowered thyroid levels result in decreased thermogenesis and overall metabolic rate (4). Leptin which is synthesized in adipocytes and functions as an indicator of both short and long-term energy availability; short-term energy restriction and lower body fat levels are associated with decreases in circulating leptin. Additionally, higher concentrations of leptin are associated with increased satiety and energy expenditure (5). The other hormone commonly associated with hunger/satiety, ghrelin, functions to stimulate appetite and food intake, and has been shown to increase with fasting, and decrease after feeding (6).

Testosterone is another key hormone affected by such states. Studies have indicated that testosterone plays a role in increasing muscle protein synthesis and muscle mass and may also play a role in regulating adiposity (7). Research has indicated that changes in fat mass have been inversely correlated with testosterone levels, and it has been suggested that testosterone may repress adipogenesis (fat storage), though the exact mechanism remains unclear and needs further research (8).

So how does this tie into adaptive thermogenesis? Results from a variety of research studies indicate that a general endocrine response to hypocaloric diets is that that they promote increased hunger, reduces metabolic rate, and threatens the maintenance of lean mass. Studies involving energy restriction, or very low adiposity, report decreases in leptin, testosterone and thyroid hormones…all negative things if you’re looking to achieve a physique with more lean muscle and less adipose tissue. (9).

Applications in The Real World

When we put the body in a hypocaloric state (less calories consumed than burned), the body has a variety of mechanisms that come into effect to prevent weight loss and start conserving energy as the natural preservation mechanism dictates. It is theorized that the degree to which a metabolic adaptation occurs is directly proportional to the size of the deficit that is occurring, and thus that is where the general wisdom where ‘slow and steady wins the race’ comes into effect. Not only does weight loss at a slower pace make a more sustainable practice for long term success as it entails a higher degree of lifestyle modification, but it prevents the body from having as large of a reaction to metabolic adaptation as an emergency from too large of a calorie deficit, too fast.

Whether you are a competitive bodybuilder, weekend warrior or someone that just wants to improve their body composition for better health an appearance, the guidelines of gradual deficits apply for the best result. Body weight reduction should be approached with a step-by-step process in which an individual adjusts the energy deficit that they are utilizing when the body reaches a plateau. This can be done by either adjusting intake (calories in) or expenditure (exercise via cardio for example). Not only will large deficits from a combination of calorie restriction and increased activity result in a faster plateau, but research has also shown that these higher caloric deficits are also more likely to result in greater loss of lean body mass (10) and compromise performance and recovery rates (11).

To help stack the deck in your favor and prevent muscle loss while keeping the fat loss rolling, you can also supplement accordingly with the advances in the thermogenic space. An ingredient that comes to mind here is NNB Nutrition’s MitoBurn® which is being built into a few of my upcoming products. This novel ingredient is perfect for this type of situation as it has been shown to help decrease fat mass and increase lean muscle while also helping to improve carbohydrate resistance and insulin sensitivity…all crucial things to avoid the dreaded ‘plateaus’ and keep you on your quest of improving body composition without stall (12) (13). Another crucial part of what makes this especially beneficial is that muscle is a metabolic tissue, and the more quality lean muscle, the higher calorie expenditure will be by default.

Now back to focusing on the nutrition aspect, another major reason that doing a ‘crash’ diet of restricting calories too fast in combination with excessive calorie burn from exercise is that research has indicated that following periods of restrictive dieting, the body will often revert to pre-diet values and the body essentially becomes hyper efficient as storing fat (12). This is known as ‘post-starvation obesity’ and a dramatic increase in calorie intake results in a rapid accumulation of fat mass with many overshooting their baseline levels of bodyfat and have a compromised metabolic rate, making the situation worse (13). Interestingly, it also appears that not only is there rapid fat regain if calorie intake is ramped up too quickly following restrictive dieting, but data also suggest that it may become more challenging to achieve that ideal body composition of decreased fat tissue in subsequent competitive seasons (14).

The best approach to avoid the phenomenon of rapid, post-dieting fat gain? Don’t get carried away with a huge deficit from calorie restriction or over-reaching with exercise to begin with! Obviously, it’s easy to play “Monday Morning Quarterback” and talk about ‘could have, should have’, so a real-world solution if you find yourself in this situation is to utilize ‘reverse dieting’. This is where following the cessation of a restrictive diet, you gradually increase calories in a step-wise fashion similar to in the cutting process, where when a plateau is reached, a small amount of calories is introduced to stimulate metabolism a little bit at a time rather than a large surplus. In theory, this allows the body to better restore circulating hormone levels and energy expenditure to pre-restrictive diet numbers while avoiding excess fat accrual. It is important to note that while many employ this approach, evidence is anecdotal at this point and more research is needed to prove this theory.

Adapting to Conclusions

Now that we’ve covered (and for the most part broken the heart of those thinking permanent metabolic damage exists), hopefully we now have a more accurate picture of what happens in the human physiology from restrictive dieting. While permanent damage has no research supported evidence, adaptive thermogenesis is indeed a very real thing. Going too hard, too fast with dieting can have negative outcomes associated with it both hormone and physical appearance wise, so it is best to take a measured, patient and calculated approach for optimal results in the short and long term. While this may disappoint some individuals out there that either claim they are long term metabolic damaged, or shoot holes in the ‘diet gurus’ that think it’s a thing, at the end of the day, science prevails.

For more information on MitoBurn, you can check it out here: https://nnbnutrition.com/products/mitoburn/

References

1. Adaptive thermogenesis in humans. Rosenbaum, M. 01, London : s.n., October 2010, Int J Obes, Vol. 34, pp. S47–55.

2. Metabolic adaptation to caloric restriction and subsequent refeeding: the Minnesota Starvation Experiment revisited. Muller, M. 4, October 2015, Am J Clin Nutr, Vol. 102, pp. 807–19.

3. Thyroid Hormone Regulation of Metabolism. Muller, R. 2, April 2014, Physiol Rev, Vol. 94, pp. 355–382.

4. Resting metabolic rate, body composition and thyroid hormones. Short term effects of very low calorie diet. Cavallo, E. 12, December 1990, Horm Metab Res, Vol. 22, pp. 632–5.

5. Leptin: a review of its peripheral actions and interactions. Margetic, S. NOvember 2002, Int J of Obesity, Vol. 26, pp. 1407–33.

6. Stomach is a major source of circulating ghrelin, and feeding state determines plasma ghrelin-like immunoreactivity levels in humans. Ariyashu, H. 10, October 2001, J Clin Endocrinol Metab, Vol. 86, pp. 4753–8.

7. Impact of testosterone on body fat composition. De Maddalena, C. 12, December 2012, J Cell Physiol, Vol. 227, pp. 3744–8.

8. Androgens inhibit adipogenesis during human adipose stem cell commitment to predipocyte formation. Chanzenbalk, G. 9, September 2013, Steroids, Vol. 78, pp. 920–26.

9. Body composition and endocrine profile of male Olympic athletes striving for leanness. Hagmar, M. 3, May 2013, Clin J Sports Med, Vol. 23, pp. 197–201.

10. Changes in fat-free mass during significant weight loss: a systematic review. Chaston, T. 5, London : s.n., May 2007, Int J Obes, Vol. 31, pp. 743–50.

11. Effect of two different weight-loss rates on body composition and strength and power-related performance in elite athletes. Garthe, J. 2, April 2011, Int J Sports Nutr Exerc Metab, Vol. 21, pp. 97–104.

12. Beta-Aminoisobutyric Acid as a Novel Regulator of Carbohydrate and Lipid Metabolism. Tanianskii, Dmitri. 3, March 2019, Nutrients, Vol. 11, p. 524.

13. β-aminoisobutyric Acid, L-BAIBA, Is a Muscle-Derived Osteocyte Survival Factor. Kitase, Yukiko. s.l. : March, March 2018, Cell Reports.

14. Weight regain after sustained weight reduction is accompanied by suppressed oxidation of dietary fat and adipocyte hyperplasia. Jackman, M. 4, April 2008, Am J Physiol Regul Integr Physiol, Vol. 294, pp. R1117–29.

15. Poststarvation hyperphagia and body fat overshooting in humans: a role for feedback signals from lean and fat tissues. Dulloo, A. 3, March 1997, Am J Clin Nutr, Vol. 65, pp. 717–23.

16. Weight cycling of athletes and subsequent weight gain in middleage. Saarni, S. March 2006, Int J Of Obes, Vol. 30, pp. 1639–44.