Twin power vs. heterogenity
As Bouchard, Tchernof and Tremblay rightly point out, "human heterogeneity in the response to the much described “obesogenic environment” created by affluent societies represents a critical aspect of the obesity epidemic" (Bouchard. 2013) And while this is certainly right it is, from a scientist's perspective, a huge problem. After all, we want to study the influence of a given parameter in isolation.
Twin studies can provide us with pairs of subjects where these inter-individual differences are minimized and while the focus of previous observational studies has been on the hitherto more or less fruitless and above all practically 100% irrelevant (what does it help you to know that you are "at risk" of getting obese) identification of genotype-overfeeding interaction, Bouchard et al. are
"[...]taking advantage of the extensive panel of pre-overfeeding traits to investigate the most parsimonious predictors of the gains in body mass, FM, FFM, and total body energy (BE), with a particular focus on the partitioning of the energy gains between adipose and lean tissues." (Bouchard. 2013)The goal is to identify biomarkers of body composition changes in response to chronic overfeeding may allow us to develop new hypotheses about the endogenous (genetic) and environmental causes of human heterogeneity in the response to chronic overfeeding.
|Figure 1: Factors that predispose to weight & fat gain on a caloric surplus (adapted from Bouchard. 2013)|
In a previously published paper, the researchers have already reported that their subjects, 24 young lean men (12 pairs of identical twins) exhibited individual differences in body weight and composition gains in response to a standardized 353 MJ (84 000 kcal) overfeeding protocol over 100 days
"The mean (+SD) gains in fat mass (FM) and fat-free mass (FFM) were 5.4+1.9 kg and 2.7+1.5 kg for a total body energy (BE) gain of 221+75 MJ representing 63% of the energy surplus consumed." (Buchard. 2013)In this follow up publication, Buchard et al. were now taking a closer look at the most important baseline correlates of these overfeeding-induced changes with the aim of identifying biomarkers of the response.
Unfortunately, the subjects daily energy expenditure was highly limited, as they were "kept sedentary" except for a supervised 30min walk, over the whole study period, in the course of which their body weight was measured daily, while their body density was assessed on three occasions from a series of underwater weighing tests.
"The subjects were studied eight at a time (four pairs of twins) over a period of 18 months. Subjects were housed in a closed section of a dormitory on the campus of Laval University 24-hour supervision.
"From 16 to 8% body fat" a cross-fitesque training-style may be right for those with high baseline fitness (learn more).
Each subject stayed in the unit for 120 days, which included a 14-day baseline observation period, a 3-day pre-overfeeding testing period, a 100-day experimental overfeeding treatment, and a 3-day post-overfeeding testing period." (Buchard. 2013)
An "intermittent overfeed" protocol
The actual overfeeding protocol comprised a 6-day binge with 1,000 extra kcal per day that was followed by a backlash to the calculated maintenance level on day 7. Thus, subjects overfed during 84 of the 100 day experimental phase.
- the total excess energy intake was 84 000 kcal
- the macronutrient ratio as 15/35/50% for protein, fat and carbs
- a higher protein intake (30g+ of a high EAA protein source w/ every full meal, 15-20g of protein with snacks),
- the usefulness of a sane carbohydrate intake (low GL instead of low carb),
- the avoidance of a skewed n6-PUFA to other dietary fat intake, and
- an intense, but not overexerting workout routine with a focus on heavy compound lifts, a minimal amount of HIIT and the occasional very low intensity (walking on a treadmill steady state cardio)
Now, talking about the study would be pointless, if the only thing to take away from the experiment were recommendations based on papers that were discussed in previous blogposts, right? So what are the new insights this study brings to the table, then?
- Total, not relative, increases in calorie intakes matter: First of all, it is kind of surprising that the changes in body composition did not depend on the pre-overfeeding levels of body weight, FM, BE, and daily caloric intake. In other words, for these lean healthy men, the changes the scientists observed were almost fully determined by the absolute increase in energy consumption - irrespective of how lean they were and even more surprisingly irrespective of whether those 1,000kcal extra were a surplus of 30% or 40% of their baseline energy intakes.
- Muscle has a "repartitioning effect": Contrary to the fat mass, which did not correlate with changes in any of the measured parameters, the scientists observed a statistically significant inverse correlation between the amount of muscle, the subjects were carrying on their frames and the changes in the lean-to-fat mass ratio (r=-0.41; p=0.05) - this means: the more muscle the guys had to begin with the more muscle and less fat they were gaining in response to the 1,000 extra kcal they were consuming.
- RMR and food induced thermic effects don't influence the total gains, but... While neither the resting metabolic rate, nor the thermic effect of food influenced the changes in body weight, FM, FFM, or BE, the thermic effects in the 4h after a meal had a significant and highly beneficial effect on the ratio of muscle to fat, the subjects gained (clear-cut evidence in favor of a high(er) protein diet yielding better results).
Learn about the fallacies of the training in the "fat burning" zone and why burning fat for fuel does not equate fat loss (read more)
"[t]here was no correlation between RQ during the RMR measurement and at various time points of the TEM test with the overfeeding-induced gains in body weight, FM, FFM, or BE." (Bouchard. 2013)is perfect evidence that this is also, or I guess I'd better say, "even more so" the case when you are bulking.
- Fitness is a negative predictor of fat gains: In view of the fact that a high VO2max correlates with higher mitochondrial capacities (and often higher muscle mass) it is not surprising that "VO2max per kilogram of body weight was negatively correlated with the gains in body weight,
FM, and BE, with coefficients ranging from -0.41 to -0.49, all p<0.05" (Bouchard. 2013); and that the overfeeding-induced increases in fat mass relate to those in lean mass were negatively related to baseline VO2max per kilogram of body weight and the maximum O2pulse (r=-0.43; p<0.05)
- A high(er) count of type I fiber count protects against fat gains: In line with the previously mentioned negative correlation between fitness (endurance type) and fat gains, there was a strong trend for the proportion of type I fibers in the vastus lateralis muscle to correlate negatively with (r = -0.40) with fat gains. Accordingly, the oxidative potential of the skeletal muscle, the scientists quantified by assessing the maximal activity of OGDH (Alpha-ketoglutarate dehydrogenase is an enzyme that's involved in the oxidative process by which the citric acid cycle converts fats to energy) in a muscle homogenate, was negatively correlated with the gains in FM, as well as in the FM–to-FFM ratio. According to Bouchard, et al. these correlations ranged from -0.42 to -0.48 (p<0.05).
Fiber composition of bodybuilders, recreational lifters, endurance rowers and sedentary control; determined via myosin heavy chain (MHC) isoform content of the triceps brachii muscle (data adapted from Jurimäe. 1997; figure originally published as part of the Intermittent Thoughts on Building Muscle)
- Thyroid hormones don't matter that much: While they can make all the difference when you are cutting, the basline TSH levels and the subjects response to a TRH challenge (this is test to evaluate, whether the pituitary response to the hormone that will trigger TSH release is normal) did not influence total weight gain, body fat or fat free mass gains. It should be said, though that all subjects were euthyroid and obviously not overtraining (learn why this matters)... well, there is one thing that did show a correlation though: Although it's not quite clear what the implications are, the early 30-45min TSH response during the TRH challenge was correlated positively with the fat mass to fat free mass gains. In other words, the more pronounced the spike in TSH, the more likely you'll gain fat, not muscle. Without seeing the corresponding thyroid response this could yet mean either that the thyroid is sluggish to react, so that the negative feedback takes longer to occur, or that the opposite is the case and a HPTA that produces larger spikes in thyroid metabolism is to blame for the increased propensity for fat gain.
- Plasma glucose and insulin don't matter: We are approaching the end of the list and I have to admit that this is one of the things that kind of surprised me. In the end, the non-significant influence of both basal, as well as glucose stimulated increases in blood glucose and insulin levels had no effect on the overfeeding-induced changes in body weight, fat mass and fat free mass does confirm that "the fattening hormone" and the purported reason "why we are fat" is not an issue for those of us who are lean and healthy and whose body easily manages his glucose levels just the way it is supposed to be.
- The restless ones don't get muscular: The fact that high baseline norepinephrine levels showing a significant negative association (r = -0.41) with increases in fat-free mass should remind you of something I want to scream at 50% of the people emailing me questions like "What happens if I eat another gram of carbs extra?" I can tell you if you are stressing out about these 100% irrelevant details all the time this and the corresponding constant psychological stress is going to do more harm to your progress than eating 200g of carbs extra, folks... but I guess those of you for whom this is an important message will continue to ignore this. So keep freaking out that you missed your macros by a blueberry, today - obviously you must be enjoying it more than the beautiful things in life.
- Leptin and the rest of the hormonal pack: With a positive associated with the changes in body weight and fat mass gains the "fat hormone" (actually it's an adipokine, but since a "hormone" is a signaling molecule produced by an organ and the adipose tissue is imho an organ, it would be valid to call it a hormone), leptin, appears to be a fattening. On the other hand, higher baseline leptin levels are usually the result of higher baseline body fat mass and since fat begets fat, the latter is probably the common determinant. Leptins "good" cousin adiponectin, but also ghrelin and even IGF and hGH were totally void of pro- or anti-obesogenic effects.