While I’m here at the 10th Canadian Obesity Network Summer School (Boot Camp), in the Canadian Rockies, it is perhaps of interest to note that one of the founding faculty of this school, Denis Richard from Laval University, has just published a paper in Nature Reviews Endocrinology, which nicely reviews the complex neurobiology of energy balance.
The paper focuses largely on the “energy out” part of energy homeostasis, which is partly determined by the themogenesis of brown adipose tissue and mediated by the sympathetic nervous system.
Thus, several areas of the brain work together in complex neuronal networks involving a host of neuronal systems including the opioid, endocannabinoid and melanocortin systems, that not only control appetite and eating behaviour but also thermogenesis.
These neuronal systems, in turn receive inputs from a wide range of peripheral organs including the gut, liver and adipose tissue via hormonal and neuronal pathways that signal energy stores and nutritional status.
The paper also discusses how some of these findings may be relevant to the development of novel treatments for obesity.
For researchers and students: the paper includes a number of excellent graphics that nicely illustrate these systems.
With all the concern about the impact of obesity on metabolic and cardiovascular health, it is often forgotten that after smoking, obesity is the single most important risk factor for many common cancers, including of course breast cancer.
The importance of this relationship is again documented by Marian Neuhouser and colleagues in a paper published in JAMA Oncology.
The study examines the associations of overweight and obesity with risk of postmenopausal invasive breast cancer after extended follow-up (about 13 years) in the Women’s Health Initiative (WHI) clinical trials, involving over 67,000 postmenopausal women ages 50 to 79 years at 40 US clinical centers..
Overall, 3388 invasive breast cancers were observed over the follow-up period with women who were overweight or obese having increased risk that was related to their degree of excess weight.
Compared to normal weight women, individuals with Class II and III obesity had a 60% greater risk for invasive breast cancer with an almost 2-fold greater risk for estrogen receptor–positive and progesterone receptor–positive breast cancers.
Class II and III obesity was also associated with a 2-fold greater risk for larger tumor size, positive lymph nodes and deaths.
Furthermore, risk was increased in women with a baseline BMI of less than 25.0 who gained more than 5% of body weight over the follow-up period.
Given this importance of obesity for breast cancer, one can only wonder just how much of the Cancer research funding raised by the Pink Ribbon campaign and other Cancer charities, finds its way into research on obesity treatment and prevention – can’t say I know of any cancer funding that has knocked on the doors of my fellow obesity researchers.
Note: see comment #1
One of the most persistent notions about equating caloric deficit to weight loss is the 3500 Cal “rule”.
I have previously posted about why this is nonsense and not exactly helpful when it comes to thinking about clinical weight loss or weight (you’re dealing with physiology NOT physics!).
Now, Nicholas Gwerder, a student from the University of Sacramento, in his Master Thesis, has apparently reviewed the literature on this and concludes that if anything, one pound of weight loss comes closer to 4,500 calories.
Gwerder reaches this conclusion by analysing data from 28 studies in which he compares the theoretical weight loss to the actual weight (and fat) lost in these studies.
Although, I do not have access to Gwerder’s Master Thesis, here is what he says in the summary:
“The energy equivalent of body weight loss varied considerably, dependent upon the constituent portions of fat, water, protein, carbohydrate and mineral lost. Adipose tissue also varied with type and was dependent upon the composition of lipid, water, and protein. The most valid theoretical equivalent for a pound of fat was calculated at 4,423.90 kilocalories based on in vivo extraction of human intracellular lipid samples.”
Thus, as Gwerder points out, the 3,500 per pound notion tossed around (including by a number of guidelines and associations)
“…severely underestimates the caloric values needed to achieve desired fat mass loss. This use of the proper caloric value for fat mass loss has the potential to improve exercise and nutrient recommendations for achieving healthy body fat values.”
Thus, if this number holds true, a daily 500 Cal deficit maintained over 10 weeks will not give you a 10 pound weight loss, but rather only about 7.5 lbs.
All the same, in practice over time this never really works out, not just because of the individual variability (Gwerder notes about 20% variation in this relationship) but because as you reduce your caloric intake, your individual metabolic requirements will very quickly shift to living off fewer calories, which means that pretty soon into your diet, the initial 500 Cal deficit is no longer a deficit (thank your physiology). This is the feared weight-loss plateau – the frustration of every dieter.
So, whether 3,500 or 4,500 Cal per pound, the relationship between calorie restriction and weight loss is not linear and thus extrapolating the amount of expected weight loss based on this deficit seldom works out in practice.
Indeed, I know from my patients that this “rule” is a matter of endless frustration and seldom helpful.
Managing weight is not simply about energy in and energy out.
And finally, to conclude this week’s discussion of evidence to support the notion that weight cycling predicts weight (fat) gain especially in normal weight individuals, I turn back to the paper by Dulloo and colleagues published in Obesity Reviews, which quotes these interesting findings in US Rangers:
“…U.S. Army Ranger School where about 12% of weight loss was observed following 8–9 weeks of training in a multi-stressor environment that includes energy deficit. Nindl et al. reported that at week 5 in the post-training recovery phase, body weight had overshot by 5 kg, reflected primarily in large gains in fat mass, and that all the 10 subjects in that study had higher fat mass than before weight lost. Similarly, in another 8 weeks of U.S. Army Ranger training course that consisted of four repeated cycles of restricted energy intake and refeeding, Friedl et al. showed that more weight was regained than was lost after 5 weeks of recovery following training cessation, with substantial fat overshooting (∼4 kg on average) representing an absolute increase of 40% in body fat compared with pre-training levels. From the data obtained in a parallel group of subjects, they showed that hyperphagia peaked at ∼4 weeks post-training, thereby suggesting that hyperphagia was likely persisting over the last week of refeeding, during which body fat had already exceeded baseline levels.”
Obviously, association (even in a prospective cohort) does not prove causality or, for that matter, provide insights into the physiological mechanisms underlying this observation.
All we can conclude, is that these observations in US Rangers (and the other studies cited in Dulloo’s article) are consistent with the notion that weight loss in normal weight individuals can be followed by significant weight gain, often overshooting initial weight.
Incidentally, these findings are also consistent with observational studies in women recovering from anorexia nervosa, famine, cancer survivors and other situations resulting in significant weight loss in normal weight individuals.
Certainly enough evidence to consider a work of caution against “recreational” weight loss, especially in individuals of normal weight.
Dulloo AG, Jacquet J, Montani JP, & Schutz Y (2015). How dieting makes the lean fatter: from a perspective of body composition autoregulation through adipostats and proteinstats awaiting discovery. Obesity reviews : an official journal of the International Association for the Study of Obesity, 16 Suppl 1, 25-35 PMID: 25614201
My recent reading of the paper by Dulloo and colleagues on post-dieting weight gain in non-obese individuals, reminded me of my clinical observation that a surprisingly large proportion of patients I see in our bariatric clinic report a history of competitive sports.
When I have previously discussed this observation with colleagues, the answer I often get is that this weight gain is simply due to the fact that active athletes are used to eating a lot, which they continue to do after their activity levels decline, thus resulting in weight gain – a theory, I don’t quite buy largely because it appears far too simplistic (and I have yet to see any evidence to support it).
Rather, if the phenomenon of weight-cycling induced weight gain is real, one would assume that not all athletes are at risk, but rather that this phenomenon would be limited to athletes in disciplines where weight cycling (e.g. to meet certain weight criteria), often referred to as “weight cutting”, is part of the culture of that sport. Examples of such sports include wrestling, boxing, and weight lifting.
It turns out that this very issue has been studied by Saarni and colleagues, who, in a paper published in the International Journal of Obesity, report their findings on a large national cohort of 1838 male elite athletes who had represented Finland in major international sport competitions in 1920-1965.
This cohort included 370 men engaged in sports in which weight-related performance classes are associated with weight cycling (boxers, weight lifters and wrestlers) and 834 matched control men with no background in athletics.
Over the 20+ years of follow-up, the weight-cycling gained a whooping 5.2 BMI units from age 20 years to their maximum mean weight (at around age 60) conpared to only 3.3 BMI units in non-weight-cycling athletes or just 4.4. BMI units in the non-athletic controls.
Indeed, weight-cycling athletes were about three times as likely to develop obesity (defined as a BMI > 30), than their non-weight cycling colleagues or controls.
This enhanced risk of developing obesity in weight-cycling athletes remained significant even after correction for a number of potential confounders including health habits (smoking, alcohol use, use of high-fat milk or physical activity) or weight at age 20 years.
While this paper does not prove causality, or for that matter, provide any insights into possible biological mechanisms that would promote weight gain, it is certainly consistent with the hypothesis that repeated cycles of weight loss and regain in people who start out with a normal weight (in this case elite athletes) strongly predicts subsequent weight gain and the development of obesity.
Or, as the authors put it,
“The weight cycling behavior of the former athletes engaged in power sports at a young age resembles that of young dieters who lose weight temporarily and soon regain it. The present observations concerning the enhanced weight gain of these athletes raise the concern that the repeated cycles of weight loss and regain caused by dieting at a young age could similarly affect weight in the long term.”
Saarni SE, Rissanen A, Sarna S, Koskenvuo M, & Kaprio J (2006). Weight cycling of athletes and subsequent weight gain in middleage. International journal of obesity (2005), 30 (11), 1639-44 PMID: 16568134