Friday, November 11, 2016

Why's Maintaining 'Ur Fat Loss so F* Hard? Calorie Counter Will Ramp Up Your Appetite, No Matter What - Lifelong Anti-Weight-Gain Efforts Required in Formerly Obese Subjects

If  obesity is a chronic disease it cannot be surprising that it cannot be cured and weight loss maintenance requires life-long effort(s) on part of the formerly obese (note: things are different for non-obese individuals trying to shed extra-pounds).
I've discussed the issue of "metabolic damage" in a series of previous SuppVersity articles and pointed out that the scientific evidence supporting the disproportionate down-regulation of your metabolic rate with (significant) weight loss cannot support the exorbitant weight rebound we see in many so-called "weight-reduced individuals", who return to their "normal" dietary habits.

Now, a recent study from the US (Polidori. 2016) shows that this weight gain is mostly driven by a hitherto largely overlooked increase in appetite - an increase that goes way beyond any effects of "metabolic damage".
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Before we get into a discussion of the implications of this research, though, I would like to briefly summarize what Polidori et al. did to arrive at their important conclusion that...
"feedback control of energy intake plays an even larger role [than energy expenditure adaptations when it comes to the post-diet jojo-effect] and helps explain why long-term maintenance of a reduced body weight is so difficult" (Polidori. 2016)
Using a validated mathematical method the authors calculated the energy intake changes of 153 patients who lost a significant amount of weight over the course of a 52-week placebo-controlled trial with canagliflozin, a sodium glucose co-transporter inhibitor, a commonly used diabesity drug that increases urinary glucose excretion.
Association between adaptive thermogenesis and weight loss in 151 overweight patients from three studies after dietary or bariatric surgery-induced weight loss.
"Metabolic damage" does not scale with weight loss: While it would be logical to assume that there was a linear increase in "metabolic damage", i.e. the reduction of your resting metabolic rate, in response to each pound of body weight you've lost. The existing evidence, which has recently been reviewed by Müller et al. (2016), however, suggests that this link does not exist (see Figure on the left). This is also in line with the results of the study at hand and previous studies which didn't find an effect of increasing weight loss on the subjects' appetite (this is discussed in detail below).
In spite of the fact that we are talking about experimental evidence, the scientists still had to rely on math / statistics to come up with data on the actual energy intake of their subjects.
Metabolic damage in Biggest Losers | more
"We calculated the free-living energy intake changes in 153 patients treated with 300 mg/day canagliflozin over a 52-week trial using the mea-sured body weight data and an assumed mean UGE [urinary glucose excretion] of 90 g/day as inputs to a mathematical model that has recently been validated against an expensive biomarker method" (Polidori. 2016 | note: it is still debatable how accu-rate this calculation is as it depends on a relatively simple formula that uses a bunch of input parame-ters based on theoretical assumptions).
Now, this use of a sodium glucose co-transporter inhibitor and the resulting urinary loss of approximately 90 g of glucose per day (that's 360 kcal/day) is an important qualifier here, as it is a way of creating an energy deficit of which the scientists argue based on previous scientific evidence that the way the scientists induced an energy deficit ...
  • does not alter the subjects' energy expenditure (regular dieting would acutely decrease their metabolic rate) or central pathways controlling energy intake (hunger & appetite) and 
  • allows for weight loss even though the patients are not directly aware of being in an energy deficit - or, put more simply, without any 'dieting efforts' or austerity
As Polidori et al. point out, any observed increased energy intake countering the weight loss induced by SGLT2 inhibition therefore likely reflects the activity of the feedback control system - your body's very own 'calorie counter' as I have called it in the headline.
Learning from those who did it: Wyatt et al. used data from the National Weight Control Registry (Wyatt. 2005) to follow a still barren path in obesity research: studying what those who manage to lose weight and keep it off did right. Until now, way too much effort is spend on identifying diet mistakes; mistakes that would be automatically avoided if you did the right things. Unfortunately, there's no magic bullet or, as the authors say: "If weight loss maintenance requires “swimming upstream” against the environment, then these are the best swimmers" (Wyatt. 2016).

The use of refeeds was not part of Wyatt's research interest, but there's experimental evidence that refeeding twice a week promotes fat loss | more.
What Wyatt et al. were able to show, however, is that people who have successfully maintained weight loss share similarities in how they keep weight off. And here's what they did: (1) They didn't rely on dieting, only, but have increased their total physical activity (to 3,293 kcal per week) as well (only 9% of those who kept the weight off did it with dieting, only); (2) they didn't stop dieting / return to their old habits after losing a certain amount of weight, but maintained a tightly energy controlled diet; (3) they constantly monitored their weight and intervened when they saw weight gain of more than 3-5 pounds; (4) cheri-shing improvements in quality of life and self-confidence.

Aspects I wouldn't include in the list, yet, are: consuming a low fat diet (that was probably due to the popularity of low fat back in the day), eating breakfast everyday (there simply is no convincing evidence that this will mechanistically promote weight loss and maintenance), and improve.
Beware: Chronic dieting at low deficit can make you fat | more!
It is also noteworthy that the study at hand provides additional evidence of the mechanisms which are driving the post-dieting weight regain (i.e. an increase in appetite and thus usually food intake) - a mechanism that is weight and not deficit dependent. This, in turn, may be considered further evidence of the existence of something many people call a "set point" (i.e. a given weight at which your body is "happy" and your appetite will match your energy requirements pretty well). Unfortunately, Polidori, et al. cannot explain why the weight-controlling appetite increase does not scale with the amount of weight the subjects lost. Why's that important? Well, if you lose 10kg or 20kg, your appetite will increase to the same extent. If we assume that this increase in appetite translates directly into increases in food intake, the rate of weight gain will be the same - regardless of whether you lose 10kg or 20kg of body weight - it's the total amount that counts.
Is it futile to even try to lose weight? An excellent comment by Priya Sumithran & Joseph Proietto says NO - (1) Modest (5–10 %) weight loss confers significant reductions in the risks of several weight-related conditions such as type 2 diabetes, obstructive sleep apnoea and non- alcoholic fatty liver disease [18], and is likely to be accompanied by milder metabolic adaptation | (2) Although the majority of people will eventually regain much of the lost weight, results are variable, and a proportion of people manage to maintain clinically beneficial weight loss even in the long-term: more than 4000 U.S. adults in the National Weight Control Registry database (97 % Caucasian, 80 % women), for example, have maintained a loss of at least 13.6 kg (30 lbs) for a mean of over 5 years |  (3) New pharmacological therapies that help weight loss and maintenance are becoming available (e.g. GLP-1 agonists) and other drugs that mimic the effects of RYGB surgery are in the development pipeline. And still, while there's hope, it's important to acknowledge that "[l]ike other chronic con-ditions, obesity is not cured after the phase of treatment (weight loss), and strategies for long-term management (maintenance of weight loss) are required " (Sumithran. 2016).
So does the study just confirm that people who have gotten fat once are doomed forever? That's difficult to tell, after all, some interventions such as RYGB weight loss surgery appear to have a decent rate of success. While the subjects may not turn into fitness models, many manage to maintain a decently healthy weight after crash-dieting down to a normal BMI-range.

Surgery may yet not be the only option. After all, there's reason to believe that there's a threshold level of weight loss after which the previously discussed compensation effects occur. It may thus well be possible that small weight changes are uncompensated by changes in energy intake. If we consider the previously referred to concept of a weight set-point to be dynamic in both directions, it is thus not impossible that losing your weight in baby-steps with adequate periods at an energy equilibrium (calories in = calories out) and no further weight loss in-between the short dieting periods may help you to lower your set-point and achieve (in the long-run) meaningful weight-loss without compensatory increases in appetite that will get you back to your original weight in no time | Comment on Facebook!
References:
  • Müller, Manfred J., Janna Enderle, and Anja Bosy-Westphal. "Changes in Energy Expenditure with Weight Gain and Weight Loss in Humans." Current Obesity Reports 5.4 (2016): 413-423.
  • Polidori, David, et al. "How strongly does appetite counter weight loss? Quantification of the feedback control of human energy intake." Obesity 24.11 (2016): 2289-2295.
  • Sumithran, Priya, and Joseph Proietto. "Maintaining weight loss: an ongoing challenge." Current Obesity Reports 5.4 (2016): 383-385.
  • Wyatt, Holly R., et al. "Lessons from patients who have successfully maintained weight loss." Obssity Management 1.2 (2005): 56-61.