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How large is the impact of not being active on childhood, adolescent and adult obesity. Plus: Are there critical time periods in gestation, infancy childhood and adolescence?

You may have heard the claim that "fat cells form during childhood and puberty and stay forever" before, right? Well, if that's the case it would be logical to assume that our childhood may be a critical developmental windows in which we have the time-limited opportunity to shape or help shape our own or our kids body composition for the rest of our or their lives.

Scientists from Mater Health Services South Brisbane, the University College of London, and the Griffith University have now reviewed the relatively scarce experimental and abundant observational pertinent research in order to examine "the role of physical activity during periods of risk to reduce the probability of obesity onset and maintenance in adulthood" (Street. 2015).
Unfortunately, but not surprisingly, most of the experimental evidence comes from rodent studies. If we tried to summarize the results of these studies in a half-sentence it would say that they demonstrate general positive effects of early exercise on the outcomes for all animals irrespective of maternal obesity status or post-weaning diet.

"Although high-fat post-weaning diets resulted in generally fatter animals, the body composition, endocrine and immune system profiles of these animals were healthier than non-exercising high-fat diet animals and comparable to standard chow non-exercising animals" (Street. 2015).

Interestingly, these effects do not disappear when the animals stop exercising. Rather than that studies indicate that exercise at an early age can protect animals against obesity onset for 5 weeks following exercise cessation (Caruso. 2013) - that's quite impressive if we take into account that rodents have a much shorter lifespan and a rapid early development period compared to humans (five rodent weeks in the early life are similar to several human years).

In spite of the fact that we don't know for sure for how long these protective effects will last in humans, there's little doubt that the same up-regulation of markers associated with increases in the skeletal muscle mitochondrial function, of which scientists believe that they protect the young rodents from obesity, will occur in humans as well (Shindo. 2014). Luckily, this is not the only thing we already know about rodents and assume for humans. Here's more:

• Figure 1: If rodents are exercise in "childhood" (3WK), already, they will be significantly leaner - irrespective of whether they are fed an obesogenic HFD or the regular SMD diet (Wagener. 2012).

  the earlier, the better - the earlier young rodents are exercised (e.g. in the rodent equivalent of childhood), the more pronounced the protective effect against adult obesity (Wagener. 2012) - as you can see in Figure 1 earlier exercise will also yield significantly reduced body fat levels on standard rodent chow (SMD - 3WK);
• muscle & brain are involved - next to changes in the mitochondria, the "stay lean" effect is also mediated by changes in structure and/or function of brain regions involved in appetite regulation in mouse & man (Street. 2015); 
• males benefit more than females - the benefits of early exercise appear to be more pronounced for male vs. female animals (Schroeder. 2010); whether that's due to the higher muscle mass remains to be elucidated

"Each period is characterized by substantial yet qualitatively different changes in growth and maturation. The culmination of each period represents a milestone in development and a subsequent reduction in the developmental plasticity of the maturing system. Given the inherently greater plasticity of earlier periods, obesity risk later in the life course is greater if the pre-conditions for obesity are established and maintained early. Disrupting the trajectory of obesity during development is likely to pay dividends in adulthood with a healthier body composition and metabolic profile. The disrupting effect of physical activity is less well understood in relation to obesity risk during and following critical periods" (Street. 2015).

Let's briefly recap what we know about these periods and how exercise during gestation (obviously in this case the mother would exercise), early infancy and adolescence influence our obesity risk as adults:

• Figure 2: Body fat levels according to quartiles of physical activity in late pregnancy (Harrod. 2014).

  Gestation - Physical activity during pregnancy has been associated with reduced odds of a large-for-gestational age (LGA) infant, as well as reduced risk of small-for-gestational age, which are both linked to increased obesity risks later in life. In addition, there is evidence of reduced body fat levels, but identical lean mass and a significantly reduced risk of macrosomia (=excessive body weight) in babies born to mothers with higher levels of physical activity during pregnancy.
  
  Overall, however, the existing evidence - specifically for strength training - is conflicting and we are far from fully understanding the complex interactions between physical exercise, nutrition during gestation and the weight and body composition of the newborn baby (a usual more does not necessarily help mor). What appears to be certain though is that if beneficial effects occur, those will last for at least 12-24 months (Mattran. 2011; Chu. 2013). In one study scientists even found significantly reduced obesity risks up to age 5 even if the physical activity of the mother was the only significant difference between the kids (Clapp. 1996)

• Figure 3: Observational data shows that there is an inverse linear association between infant activity scores and body fat percentages as early as in year 1 (Li. 1995).

  Infancy - Although it is correct that our body composition in infancy is still largely influenced by our mother's physical activity during gestation, there's good evidence that an earlier achievement of gross motor milestones (sitting, crawling, etc.) gives us the activity headstart we need to stay lean. Based on the correlation between earlier motor milestones and lower subscapular and triceps skin-folds measurements of 12 month-old kids Street et al. conclude that  "more active infants depose less fat over the first year [...] because active energy expenditure has resulted in increased metabolic capacity".
  
  In contrast to rodents, the "early activity bonus" does not last long in humans. With 5 years "early active" children are no longer significantly leaner than their peers, unless they were continuously more active and/or were fed different diets.
  
  In spite of the fact that early life activity does not provide life-long protection against obesity, though, the experimental and observational evidence of an inverse relationship between physical activity and body fat levels in infancy (Li. 1995) highlights the importance of leading an "active life" - in the most general sense - as early as possible. This is also relevant, because activity builds, while inactivity "kills" muscle, which is in turn associated with a further reduction in physical activity: Overweight infants, for example, have been shown to reach motor milestones later than leaner counterparts (Slining. 2010). Now you've just learned about the link between these milestones and staying lean in a previous paragraph. Accordingly, you will know that this means that the "sweet", chubby babies and toddlers may be caught in a vicious cycle of "obesity > low activity > lower muscle > lower activity > more obesity > lower activity ... "even before the know what the word "activity" means.

  Figure 4: Normal body fat development during infancy (Street. 2015).

  This does not mean that babies have to be "ripped", but I guess we all have seen kids with body fat levels way beyond the normal ~30% at 6 months (see Figure 4). The real problem, however, occurs thereafter, when the slow and steady decline in body fat should be driven by increases in a kid's activity energy expenditure (AEE). The latter takes the role of the energetic needs of growing which have previously been every toddler's #1 energy consumer. If the growth process slows and "activity", which does by the way include "vocalization primarily in the form of crying [which] is the next greatest pre-ambulatory energy cost after the energy cost of growth" (Street. 2015), does not take it's place, obesity ensues.
  
  Obviously, you could counter that by calorically restricting your toddler, but this is (a) unhealthy and (b) the exact opposite of what the mums and dads do. In fact, way too many of them are priming their kids to become obese sugar addicts by giving their kids a sugar-sweetened beverage (a "healthy baby tea" *rofl*), whenever the kids utter a sound just to make them shut up do. It is thus no wonder that studies have linked infant temperaments that are characterized by negative affectivity/emotionality and a more frequent use of vocal signals such as crying and thus more frequent maternal feeding responses to increased fat gain (Baughcum. 1998; Darlington. 2006). That's alarming, even if it has not yet been conclusively shown that the two are causally and not just corollary related.

• Does the Optimal Meal Frequency Depend on Age? Study Suggests: Kids Better Eat Often, Adolescents Rather Step Away From Their Sugary Sins - Quality Counts! Read more!

  Childhood - An important feature of childhood development, particularly in terms of its association with increased obesity risk, is a fall in body mass index (BMI) until about 5–7 years of age, which is followed by the so-called "adiposity rebound" (AR).
  
  The earlier this rebound occurs, i.e. the earlier kids start to become fat again, the higher their risk of obesity as late as adulthood (Whitaker. 1998; Taylor. 2004). More specifically, studies like Whitaker et al. (1998) show that "early gainers" have a 20% higher obesity risk later in life and an extra 20% risk if they were already overweight - or I should say "over-fat" - at the age of 5-7 years.
  
  It is thus only logical that studies show that obese pre-schoolers often become obese adults (Nader. 2012). Next to the Western junk-food diet, research findings in the recent decades support a relationship between increased obesity risk, low physical activity and high sedentary pursuits during childhood (Reilly. 2010).
  

  Figure 5: Risk increase / decrease of becoming an obese teenager for weight status at AR, maternal and paternal BMI during; I think it's quite telling that even the "medium" weight (=average kids) already have increased obesity risks, these days (data from Whitaker. 1998).

  A recent study by Schuster et al., for example, shows that "overweight fifth-graders were more likely to become obese if they had an obese parent (P < .001) or watched more television (P = .02)" (Schuster. 2014); and that's only the last in a series of studies suggesting that children who engage in more vigorous physical activity are at reduced risk of obesity, while children who are more sedentary are at a significantly greater risk of becoming obese in adolescence, which happens to be the next and last developmental step we're going to discuss in today's waredownloadsoft obesity feature.
• Adolescence - Adolescence is a critical phase in the development of our fat stores. While the years before puberty are characterized by both fat cell hypertrophy (the fat cell size increases), hyperplasia (more fat cells are formed) and apoptosis (fat cells die), most experts agree that the number of apoptotic processes in our adipose tissue declines rapidly as we approach puberty.
  
  

  Figure 6: Difference of total fat mass of girls at age 10, 11, 12, 13; all values relative to girls who had a low and maintained a low activity levels (LL) - HH: high activity at baseline, low later, LH: low activity at baseline, high later, HL: high activity at baseline, low later (Völgyi. 2011).

  This decline in the adipose tissue turnover is really bad news and one of the reasons why scientists believe that the "critical window" from the headline of today's waredownloadsoft article closes during puberty:

  "It is generally thought that alteration in the size of fat cells in adulthood is achievable but maintenance of reduced fat cell size is likely to be difficult because of the mechanisms that may include, e.g. decreased leptin production. Furthermore, while an increase in adipo-cyte number is possible during adulthood, reversal of fat cell number does not occur. Consequently, adolescence represents an additional critical window when physical activity may affect obesity risk (reducing fat cell accretion) in ways it can-not during adulthood (reducing established fat cell number). " (Street. 2015)

  Since adolescence is also associated with an increase in lean mass, including skeletal muscle and bone, it is thus high time to start being, or - better - being even more active. After all, both muscle and bone mass are positively correlated with physical activity levels (Bailey. 1999; Völgyi. 2011).

• If you take a look at the data in Figure 6 it's yet not too late to start being active in puberty. The previously sedentary girls in Völgyi's study (Figure 6 | LH) who started to exercise regularly during puberty, for example,  were similarly lean as their "always active" peers (HH). Probably because they expended more energy, but also because their exercise left them less hungry than their sedentary peers ... that sounds like bogus? Well, take a look at the reduced 24h energy intake Thivel et al. measured in youths who were locked in a metabolic chamber in response to high intensity exercise vs. sitting around (Thivel. 2012 | Figure 7)  - exercise does not make you hungry.
  

  Figure 7: Much in contrast to what you may expect, obese kids actually eat less, when they are forced to work out. In that, doing high intensity exercise (HIE) is more "satiating" than low intensity (Thivel. 2012).

  Now, if exercise curbs your appetite, while being sedentary increases it and its obesogenic consequences, which in turn reduce your willingness and ability to exercise, it is obvious what Street et al refer to when they are talking about "a two way street" (Street. 2015). It's the previously hinted at vicious cycle in which lower physical activity predisposes to obesity, while obesity in turn predisposes to even greater reductions in physical activity.
  
  In view of the previously referenced physiological peculiarities, adolescence appears to be the last stage in our development, where increased activity, alone, can go a long and consequential way. It is thus all the more important to break the cycle of being sedentary <> getting fatter before the transition into adulthood takes place. After all, the currently available research leaves little doubt that physical activity during adolescence will promote an adult body composition and metabolic profile that is associated with a reduced obesity risk, and reduced morbidity: Adult women who were more active adolescents, for example, are 50% less likely to be abdominally obese - even if all covariates are controlled for (da Silva. 2015). Physical activity interventions in adults, on the other hand, yield very ambiguous results. In most cases, however, being more active alone will not make a significant enough difference to trigger fat loss and instigate health improvements. 

References:

• Bailey, D. A., et al. "A six‐year longitudinal study of the relationship of physical activity to bone mineral accrual in growing children: the University of Saskatchewan Bone Mineral Accrual Study." Journal of Bone and Mineral Research 14.10 (1999): 1672-1679.
• Baughcum, Amy E., et al. "Maternal feeding practices and childhood obesity: a focus group study of low-income mothers." Archives of Pediatrics & Adolescent Medicine 152.10 (1998): 1010-1014.
• Caruso, V., H. Bahari, and M. J. Morris. "The Beneficial Effects of Early Short‐Term Exercise in the Offspring of Obese Mothers are Accompanied by Alterations in the Hypothalamic Gene Expression of Appetite Regulators and FTO (Fat Mass and Obesity Associated) Gene." Journal of neuroendocrinology 25.8 (2013): 742-752.
• Chu, Lisa, et al. "Impact of maternal physical activity and infant feeding practices on infant weight gain and adiposity." International journal of endocrinology 2012 (2012).
• Clapp, James F. "Morphometric and neurodevelopmental outcome at age five years of the offspring of women who continued to exercise regularly throughout pregnancy." The Journal of pediatrics 129.6 (1996): 856-863.
• da Silva Garcez, Anderson, et al. "Physical Activity in Adolescence and Abdominal Obesity in Adulthood: A Case-Control Study Among Women Shift Workers." Women & health ahead-of-print (2015): 1-13.
• Darlington, Anne-Sophie E., and Charlotte M. Wright. "The influence of temperament on weight gain in early infancy." Journal of Developmental & Behavioral Pediatrics 27.4 (2006): 329-335.
• Harrod, Curtis S., et al. "Physical activity in pregnancy and neonatal body composition: the healthy start study." Obstetrics & Gynecology 124.2, PART 1 (2014): 257-264.
• Li, Ruowei, et al. "Relation of activity levels to body fat in infants 6 to 12 months of age." The Journal of pediatrics 126.3 (1995): 353-357.
• Mattran, Kelly, et al. "Leisure-time physical activity during pregnancy and offspring size at 18 to 24 months." Journal of Physical Activity and Health 8.5 (2011): 655.
• Nader, Philip R., et al. "Next steps in obesity prevention: altering early life systems to support healthy parents, infants, and toddlers." Childhood Obesity (Formerly Obesity and Weight Management) 8.3 (2012): 195-204.
• Reilly, John J. "Low levels of objectively measured physical activity in preschoolers in child care." Medicine and science in sports and exercise 42.3 (2010): 502-507.
• Rosenbaum, Michael, et al. "Effects of Weight Change on Plasma Leptin Concentrations and Energy Expenditure 1." The Journal of Clinical Endocrinology & Metabolism 82.11 (1997): 3647-3654.
• Rosenbaum, Michael, et al. "Low-dose leptin reverses skeletal muscle, autonomic, and neuroendocrine adaptations to maintenance of reduced weight." Journal of Clinical Investigation 115.12 (2005): 3579.
• Rosenbaum, Michael, et al. "Leptin reverses weight loss–induced changes in regional neural activity responses to visual food stimuli." The Journal of clinical investigation 118.7 (2008): 2583.
• Schroeder, Mariana, et al. "Post-weaning voluntary exercise exerts long-term moderation of adiposity in males but not in females in an animal model of early-onset obesity." Hormones and behavior 57.4 (2010): 496-505.
• Schuster, Mark A., et al. "Changes in obesity between fifth and tenth grades: A longitudinal study in three metropolitan areas." Pediatrics 134.6 (2014): 1051-1058.
• Shi, Haifei, et al. "Diet‐induced Obese Mice Are Leptin Insufficient After Weight Reduction." Obesity 17.9 (2009): 1702-1709.
• Shindo, Daisuke, Tomokazu Matsuura, and Masato Suzuki. "Effects of prepubertal-onset exercise on body weight changes up to middle age in rats." Journal of Applied Physiology 116.6 (2014): 674-682.
• Slining, Meghan, et al. "Infant overweight is associated with delayed motor development." The Journal of pediatrics 157.1 (2010): 20-25.
• Street, S. J., J. C. K. Wells, and A. P. Hills. "Windows of opportunity for physical activity in the prevention of obesity." Obesity Reviews (2015).
• Taylor, Rachael W., et al. "Rate of fat gain is faster in girls undergoing early adiposity rebound." Obesity research 12.8 (2004): 1228-1230.
• Thivel, David, et al. "The 24-h energy intake of obese adolescents is spontaneously reduced after intensive exercise: a randomized controlled trial in calorimetric chambers." PloS one 7.1 (2012): e29840.
• Wagener, A., A. O. Schmitt, and G. A. Brockmann. "Early and late onset of voluntary exercise have differential effects on the metabolic syndrome in an obese mouse model." Experimental and Clinical Endocrinology and Diabetes 120.10 (2012): 591.
• Whitaker, Robert C., et al. "Early adiposity rebound and the risk of adult obesity." Pediatrics 101.3 (1998): e5-e5.

People don't eat too much sugar. They simply make the wrong food choices.

With the publication of the latest issue of the Nutrition Bulletin from the British Nutrition Foundation, I am facing a whole host of potentially news-worthy recent papers. Of actual significant interest are yet only two of them. One that focuses on the involvement of different sugars in the obesity epidemic and a second paper that's actually a summary of an expert meeting discussing "what's new in sports nutrition". I have to admit, though, "new" is a relative term - specifically if you are not just reading each and every waredownloadsoft article, but also all the waredownloadsoft Facebook News, these "news" shouldn't be that "new" for you.

• Sugars and obesity: Is it the sugars or the calories? - In this article Choo et al. (2015) discuss the emerging evidence pointing towards sugars containing fructose as potential motors of the obesity epidemic.
  
  As the reviewers point out, the hypothesis that fructose may be at the heart of the obesity epidemic "is largely supported by ecological observations, rodent models of overfeeding and select human trials" (Choo et al.). This does also imply that...

  "[h]igher level evidence from systematic reviews and meta-analyses of controlled dietary trials has yet to show convincingly that fructose-containing sugars behave differently from any other forms of energy (especially refined starch and fat)" (Choo. 2015).

  Prospective cohort studies, which provide the strongest observational evidence, have shown an association between risk of overweight and obesity and fructose-containing sugars consumed as sugar-sweetened beverages but not as total sugars or other important sources of added sugars such as cakes, pastries and sweets. I mean, it's no coincidence that potato chips and French fries, not 100% fruit juices have been identified as the driving motors of the belly development in the the Nurses’Health Study, the Nurses’ Health Study II and the Health Professionals Study from the US (see Figure 1 | Choo. 2015).
  
  

  Figure 1: Bodyweight changes (kg) over a 4-year period associated withan increase in the consumption of different food items in the Nurses’Health Study, the Nurses’ Health Study II and the Health Professionals Study from the US (Choo. 2015).

  Comparative analyses show that high intakes of other highly palatable foods such as refined grains, processed meats, red meats, French fries and potato products, as well as physical inactivity may play an equal or greater role in weight gain and the risk of overweight and obesity. The contributions of these factors are also difficult to disentangle from that of sugar-sweetened beverages owing to their collinearity with sugar-sweetened beverages as part of a Western dietary pattern and lifestyle.
  
  Therfore, the scientists demand that "[a]ttention needs to remain focused on decreasing overconsumption of all foods associated with overweight and obesity." In that, they admit that "[s]ugar-sweetened beverages and foods are certainly an important place to start," but also highlight that one "should not draw attention away from the issue of overconsumption in general" (Choo. 2015).
• What's new in sports nutrition? The  British Nutrition Foundation's half-day symposium ‘What's new in sports nutrition?’ brought together world-leading sports nutrition experts to discuss the latest and most significant findings in sports nutrition.
  
  Discussion centred on injury and illness prevention, training adaptation and competition performance, with particular focus on the role of nutrition in bone health, immunity, skeletal muscle changes and the interplay of sports nutrition with sleep. Dr Kevin Currell chaired proceedings. For the former, i.e. the prevention of inury and illness, the most interesting study was one in male gymnasts. A study that used a 2g/kg bodyweight protein + low GI carbohydrate + high fiber diet wit 400ml of milk and creatine supplementation to effectively reduce the body weight and thus the load on the joints and prevent injury in male gymnast who frequently experienced injury post competition.
  

  Figure 2: Muscle mass and body fat in response to 6 weeks high protein, high fiber, low GI carb diet in male gymnasts with who frequently experienced injury post competition (unpublished data according to Alerton. 2015).

  In fact, the gymnast lost 5 kg over the 6-week period (from 71 to 66 kg), percentage body fat fell by 8% (from 17% to 9%) and lean body mass stayed relatively similar (56.6–57.1%). Most intriguingly, the change in bodyweight led to reduced injury and increased training capacity.
  
  The researchers who had been invited to the conference also presented evidence in favor of the gut and immune protective prowess of colostrum, which has

  Figure 3: Colostrum supplementation has been shown to blunt the exercise induced reduction in endogenous anti-oxidants and potentiates its beneficial effects (Appukutty. 2012 | learn more)

  "[...] considerable evidence to suggest that [...] supplementation can maintain immunity and decrease the risk of URTIs [upper respiratory tract infections], particularly during periods of heavy training. Supplementation can also limit exercise-induced increases in gut permeability, which in turn may confer benefits on immune function and reduce GI complaints. 

  However, beneficial effects of colostrum are less pronounced following acute intake; longer term supplementation (>2 weeks) is required for maximal effects. Moreover, many previous studies have used high doses of bovine colostrum (10–60 g/day) and further work is needed to establish dose–response effects and optimal dosing" (Alderton. 2015).

  That's not exactly news, just like the importance of sleep for optimal athletic performance or the beneficial of glycogen depletion on mitochondrial adaptation to exercise I discussed back in back in 2012, already.

References:

• Alderton, S. and Chambers, L. (2015), What's new in sports nutrition?. Nutrition Bulletin, 40: 140–148. doi: 10.1111/nbu.12144
• Choo, V. L., Ha, V. and Sievenpiper, J. L. (2015), Sugars and obesity: Is it the sugars or the calories?. Nutrition Bulletin, 40: 88–96. doi: 10.1111/nbu.12137
• Green, H. (2015), Dietary carbohydrates: A food processing perspective. Nutrition Bulletin, 40: 77–82. doi: 10.1111/nbu.12135

You may argue that it is unfair, but there's no way to negate that people who have been sign. overweight once are at a high risk of ending up with a reduced metabolic rate when they've achieved the same weight and body comp. as people who have never been obese.

You will probably have heard of, maybe even experienced the nasty reduction in basal energy expenditure that occurs during and often persists after energy restricted diets. In today's waredownloadsoft article, I will briefly summarize the results of a couple of recent studies that may yield new insights into a phenomenon some people call "metabolic damage".

Now, "metabolic damage", or as I prefer to call it, the diet-induced (semi-)permanent down-regulation of our basal energy expenditure wouldn't be a problem if our appetite would decrease to the same degree. Unfortunately, there's a disconnect between appetite and energy expenditure of which a recent study from the University of Leeds suggests that it may be particularly pronounced in the obese.
As J.E. Blundell et al. point out, the prevailing model of homeostatic appetite control envisages two major inputs: (1) signals from adipose tissue and (2) signals from peptide hormones in the gastrointestinal tract. As a waredownloadsoft reader you are familiar with both inputs - the role of leptin and adiponectin and the satiety hormone induced appetite reduction.

Figure 1: An increase in energy expenditure increases the already existing correlation between total daily energy intake and the amount of fat-free mass in obese individuals (Blundell. 2015).

In contrast to the amount of lean mass which is a decently reliable predictor of energy intake in both lean and (especially active) obese individuals, neither the total amount of fat mass, nor the signals it's sending are reliable predictors of energy intake in the obese. The signalling system appears to be disturbed in both obese (too much leptin + leptin resistance) and reduced obese (too little leptin for the remaining body fat) individuals.
Only recently, Teresa Jiménez Jaime and colleagues from Universidad de Chile confirmed in a three-month study on twenty-two women aged 23-44 years with a body mass index (BMI) of 25-32 kg/m² who underwent a calorie restriction treatment (20 kcal / kg initial weight) and were encouraged to increase their physical activity.

Figure 2: Changes in resting and total energy expenditure during diet + exercise intervention (Jiminéz Jaime. 2015).

In the compliant group, the scientists observed a sign. reduction in resting energy expenditure (REE) in absolute terms and adjusted for fat free mass (-164 ± 168 kcal/day (10,6%) and -4,3 ± 4,6 kcal/kg FFM (10,5%)). Accordingly, the significant correlation between FFM and REE (r = 0, 56 p < 0,05), that existed at the beginning of the study was lost at the end of the intervention.
This was not the case in the subjects who didn't adhere strictly to the energy reduced diets. If we take into account that neither of the two groups lost sign. amounts of fat-free mass it is obvious that the mismatch between the theoretically required energy (i.e. calculated based on fat-free mass) and the real energy intake during a diet is mediated by a reduced energy expenditure that could be mediated, at least partly, by a borderline sign. reduction in thyroid function (the reduction in T3 and free T3 Jiminéz Jaime et al. observed didn't reach stat. significance). To become "metabolic damage" this reduction would have to persist even when the subjects returned to an energy sufficient diet.

Figure 3: Quotient of measured (RMRm) & predicted / calculated (RMPp) resting metabolic rate in subjects after 8w on a protein-enriched formula diet  that provided 2.1 MJ/day according to the relative weight change (Camps. 2013).

If we take a look at the data from a study by Camps et al. (2013), it appears as if it would depend on the amount of weight that is lost, whether this will or won't happen. Only the subjects who lost more than 10% of their body weight on a protein-enriched formula diet  that provided 2.1 MJ/day (51.9 grams of protein, 50.2 grams of carbohydrates and 6.9 grams of lipids) actually suffered from "metabolic damage", i.e. a disconnect between the measured (RMRm) and the predicted / calculated (RMPp) resting metabolic rate. And what's worst: The effect may diminish over time, but it won't disappear even after 44 weeks of eating "normal" again.
References:

• Blundell, J. E., et al. "The Biology of Appetite Control: do Resting Metabolic Rate and Fat-Free Mass drive Energy Intake?." Physiology & behavior (2015).
• Bray, GeorgeA. "Effect of caloric restriction on energy expenditure in obese patients." The Lancet 294.7617 (1969): 397-398.
• Camps, Stefan GJA, Sanne PM Verhoef, and Klaas R. Westerterp. "Weight loss, weight maintenance, and adaptive thermogenesis." The American journal of clinical nutrition 97.5 (2013): 990-994.
• Camps, Stefan GJA, Sanne PM Verhoef, and Klaas R. Westerterp. "Weight loss–induced reduction in physical activity recovers during weight maintenance." The American journal of clinical nutrition 98.4 (2013): 917-923.
• Camps, S. G., et al. "Genetic predisposition and energy restriction induced adaptations in resting energy expenditure and physical activity." How humans economize (2015): 93.
• Camps, S. G. J. A. How humans economize: energy restriction and end energy expenditure. Diss. Maastricht University, 2015.
• Jimenez Jaime, T., et al. "Efecto De La Restricción Calórica Sobre El Gasto Energético En Mujeres Adultas Con Sobrepeso U Obesidad." Nutrición Hospitalaria 31.6 (2015): 2428-2436.