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Will slimming down from a 120 cm to a 60 cm waist always ruin your metabolic rate and set you up for weight regain or can high GI protect you from yoyoing?

Broscience tells us: "Carb up to preserve your resting metabolic rate." And in fact, there is some scientific evidence that suggests a link between high(er) carbohydrate intakes and increased thyroid function. The same amount of T3 will trigger a sign. higher stimulation of lipolysis and fat oxidation, for example, on high vs. low carb diets (Mariash. 1980). Low carb diets, on the other hand, lead to significant reductions of the active thyroid hormone and increases in the 'thyroid receptor inhibitor' rT3 - even in healthy individuals and if the energy intake is standardizes (Serog. 1982; Ullrich. 1985). So, is broscience right? Well, overfeeding studies show a similar increase in T3 in response to protein, fat and carbohydrates (Danforth Jr. 1979). So refeeds should work, irrespective of their carbohydrate content...
As you can see, it is hardly possible to confirm or reject the "carb up to prevent metabolic damage" (=prevent the diet induced over-proportional reduction in resting energy expenditure) hypothesis based on the existing evidence. A recent study by J. Philip Karl and colleagues who tried to determine "the effects of diets varying in carbohydrate and glycemic index (GI) on changes in body composition, resting metabolic rate (RMR), and metabolic adaptation during and after weight
loss" (Karl. 2015), however, may yet take us one step further towards rejecting or confirming this commonly heard of idea.

Figure 1: Overview of the key parameters of the study design and dietary composition (Karl. 2015).

In said study, Karl et al. randomly assigned adults with obesity (n = 91) to one of four diet groups for 17 weeks. As you can see in Figure 1, the diets all subjects were provided with differed in percentage energy from carbohydrate (55% or 70% | Figure 1, top-right) and GI (low or high, Figure 1, bottom-right) but were matched for protein, fiber, and energy. The study design itself comprised 5 phases:

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"Phase 1 was a 5-week weight maintenance phase in which weight maintenance energy needs were determined by adjusting provided energy intake to maintain stable weight. Mean Phase 1 energy intake was 12.2 MJ/day with 48% energy provided as carbohydrate, 16% as protein, and 36% as fat. Following Phase 1, participants were randomized by the study statistician to their Phase 2 dietary assignment using computer-generated randomization. The four diets differed in carbohydrate content (55%, ModCarb or 70%, HighCarb of total energy) and dietary GI (less than 60, LowGI or 80, HighGI), and were provided for 12 weeks at 67% of the weight maintenance energy intake determined in Phase 1. 

Participants were allowed to increase their energy intake during Phase 2 by requesting additional, randomization-appropriate foods from the metabolic kitchen if too hungry to be adherent. Phase 3 was a 5-week weight maintenance phase during which food was provided according to randomization. Energy intake during Phase 3 was prescribed to support weight maintenance at the new, lower body weight, and was predicted from body weight and energy intake measured at the end of Phase 2, with adjustment for self-reported physical activity. Phase 4 was a 12- month follow-up period during which participants selected and pre pared their own meals after being provided with instructions on fol lowing the diet to which they were randomized" (Karl. 2015)

To assess the effects of this sequence of induction (weight maintenance), and weight stabilization phases, the body weight, body composition, RMR, and metabolic adaptation (measured RMR vs. predicted resting metabolic rate = RMR) of the middle aged study participants (49-64 years) were measured before and after all phases of the study.

Figure 2: (A) Weight loss and (B) percentage of total weight loss attributable to fat mass and fat free mass while consuming provided-food diets differing in glycemic index (GI) and percent energy from carbohydrate (55%, ModCarb and 70%, HighCarb) for 17 weeks (n = 79). Values are mean 6 SEM. Weight loss analyzed by repeated measures ANCOVA, body composition by two-factor ANOVA. a,bMain effect of time; asignificant decrease from baseline (P < 0.001), bsignificant difference from Phase 2 end (P < 0.001). No diet effects (main effects or interactions) for any comparisons. GI, glycemic index; HighCarb, 70% energy from carbohydrate; ModCarb, 55% energy from carbohydrate (Karl. 2015).

Interestingly, the analysis of this data revealed no significant inter-group differences in terms of any of the relevant study outcomes. Yes, you read me right: This means that neither the GI, nor the GL, nor the carbohydrate content of the diet had statistically significant effects on weight loss, body composition, RMR, or the metabolic adaptation aka "metabolic damage" due to weight loss.

Figure 3: Measured resting metabolic rate as a function of predicted metabolic rate (Karl. 2015). Note: If there was no "metabolic damage", the solid line which represents the ideal body-weight dependent decline of energy expenditure and the dashed line which represents the actual ratio of the measured to the predicted RMR should be congruent.

While there were no inter-group differences and neither the amount or the type of carbohydrates had an effect on the reduction of the metabolic rate, there is still one interesting result you can see in the right graph in Figure 3. Said graph depicts the ratio of the measured to the predicted metabolic rate during the 5-week weight maintenance phase. If you look closely, you will realize that it suggests that having a high predicted RMR, i.e. being heavier, being taller and being more muscular, is associated with a non-significant decline of the non-predicted reduction of the energy expenditure (=metabolic damage) and thus a narrowing of the gap between the solid and dashed line.

"Solid and dashed? I don't get it!"

You're asking how I can support this hypothesis? Well, the dashed line that represents the true ratio of the actual to the predicted RMR approaches the theoretical one (the solid line) for higher RMR values. If this was more than a trend, it would suggest that two things: (a) Losing less weight and thus maintaining a higher predicted metabolic rate protects against metabolic damage (that would be useless). And (b) being tall and muscular and thus having a naturally high(er) predicted RMR can protect you from suffering metabolic damage when you lose weight.

Unfortunately, it's not possible to tell which (if any) of the two options is correct. If I had to make an educated guess, though, I would say it's a combination of both: The weight change of an average 5.5 kg did not wary too much and was withing 95% confidence intervals of [-7.1 kg, -4.6 kg]. In conjunction with individual physiological qualities of people with higher baseline RMRs, it could still explain the narrowing of the gap between predicted and true RMR after dieting.
References:

• Danforth Jr, Elliot, et al. "Dietary-induced alterations in thyroid hormone metabolism during overnutrition." Journal of Clinical Investigation 64.5 (1979): 1336.
• Karl, J. Philip, et al. "Effects of carbohydrate quantity and glycemic index on resting metabolic rate and body composition during weight loss." Obesity 23.11 (2015): 2190-2198.
• Mariash, C. N., et al. "Synergism of thyroid hormone and high carbohydrate diet in the induction of lipogenic enzymes in the rat. Mechanisms and implications." Journal of Clinical Investigation 65.5 (1980): 1126.
• Serog, P., et al. "Effects of slimming and composition of diets on VO2 and thyroid hormones in healthy subjects." The American journal of clinical nutrition 35.1 (1982): 24-35.
• Ullrich, Irma H., Philip J. Peters, and M. J. Albrink. "Effect of low-carbohydrate diets high in either fat or protein on thyroid function, plasma insulin, glucose, and triglycerides in healthy young adults." Journal of the American College of Nutrition 4.4 (1985): 451-459.

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.