Save Your Carbs For Dinner?

Diurnal changes in hormones and metabolism are well known and how these can be influenced by timing and sequencing of external stimuli (e.g. eating, exercise, sleep, etc.) has always been of considerable interest. A study by Sigal Sofer and colleagues from the Hebrew University of Jerusalem, Israel, published in OBESITY, suggests that eating most of your carbs at dinner may have beneficial effects on hormonal patterns, metabolism, and lead to more weight loss than eating a similarly calorie-restricted diet with carbs spread out throughout the day. The rationale for the study as stated by the researchers is that: “…consumption of carbohydrates mostly in the evening would modify the typical diurnal pattern of leptin secretion as observed in Muslim populations during Ramadan. The experimental diet induced a single daily insulin secretion in the evening, thus it was predicted that the diet would lead to higher relative concentrations of leptin starting 6–8 h later i.e., in the morning and throughout the day. This may lead to enhanced satiety during daylight hours and improve dietary adherence.” In addition, “Studies have shown that there is a negative correlation between insulin and adiponectin levels. Since the experimental diet used in this study reduces insulin secretion during the day, it was also hypothesized that adiponectin concentrations would increase throughout the day improving insulin resistance, diminishing symptoms of the metabolic syndrome and lowering inflammatory markers.” A total of 78 male subjects (policemen) with a BMI greater than 30 were randomized to 6 months of 1,300–1,500 kcal/day diets, with either the carbs served mostly at dinner (test) or throughout the day (control). Subjects eating their carbs in the evenings lost more weight (11.6 vs. 9.06 kg) and had lower hunger scores as well as greater improvements in fasting glucose, average daily insulin concentrations, and insulin-resistance. There were also greater improvements in lipid profiles, CRP, and other relevant markers in the intervention group. While leptin levels dropped in both groups (not surprising given the weight loss), the leptin decrease was less in the late-carb-eaters than in the control group, and adiponectin levels increased significantly only in the intervention group. The authors suggest that these hormonal changes may perhaps explain the improved metabolic control and lower hunger scores in this group. However, the authors are also careful to point out that: “Further research is required to confirm and clarify the mechanisms by which this relatively simple diet approach enhances satiety,… Read More »

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South Asians Have Larger Fat Cells and Higher Risk

I am currently in Cambridge, UK, as part of the faculty of SCOPE (Specialist Certification of Obesity Professional Education), the official inter-professional educational program of the International Association for the Study of Obesity (IASO). This year’s participants include a significant delegation from India, which is in the midst of its very own obesity epidemic. While it is rare to see severe obesity (BMI levels over 40) in people of South Asian origin, there is now ample evidence suggesting that this population is particularly prone to the cardiometabolic complications of obesity even at a rather moderate increase in BMI. In a study I co-authored with Sonia Anand and other colleagues from McMaster University, Hamilton, ON, published online today in PLoS one, we show that this increased risk may be attributable to adipocyte hypertrophy and increased ectopic fat deposition. For this study, we recruited 108 healthy South Asians (defined as parents and grandparents who originated from India, Pakistan, Sri Lanka, or Bangladesh) and white Caucasians (ancestors originated from Europe) into one of three BMI strata: ≤25 kg/m2, 26–29 kg/m2, ≥30 kg/m2, matched for sex and age. Measurements included body composition, adipocyte size, abdominal fat area (MRI studies), and hepatic adiposity (MRI-spectroscopy) were assessed and related to fasting glucose, insulin, lipids and adiponectin levels. After adjustment for age, sex, and BMI, South Asians had more body fat, lower lean muscle mass, increased waist to hip ratio, less superficial subcutaneous abdominal adipose tissu, more deep/visceral to superficial adipose tissue ratio, and more liver fat than their Caucasian counterparts. South Asians also had higher fasting insulin, lower HDL cholesterol, and lower adiponectin levels. Most interestingly, fat cell size, measured as adipocyte area, was increased in South Asians compared to white Caucasians, and this difference in adipocyte size accounted for almost all of the observed differences in metabolic parameters and fat distribution. Thus, this form of ‘ethnic’ lipodystrophy’ may well play an important role in the increased risk of South Asians even at lower BMI levels. Although, this is a small cross-sectional study, the consistency of our findings with other reports in the literature, lead us to consider the following clinical implications: 1) Young, apparently healthy South Asians have greater metabolic impairment compared to white Caucasians who tend to develop metabolic changes at higher levels of obesity and at a more advanced age, supporting earlier screening for abdominal adiposity and elevated glucose among South Asians. 2)… Read More »

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Why Hyperleptinaemia is Not Leptin Resistance

Yesterday, I posted about the presentation of Columbia University’s Rudy Leibel on how losing weight results in a hypometabolic and orexogenic response mediated largely by a fall in plasma leptin levels that, as a rule, accompany any attempt at reducing fat stores. This post elicited a number of responses that I will try to address in this follow-up post. Several readers wanted to know whether there is a way to readjust your ‘leptin sensitivity’ so that the brain no longer wants to restore body weight to pre-weight loss levels. The short answer is ‘no’. Although there are several proposed strategies (special diets, refeeding days, exercise strategies, etc.) floating around in the popular literature, there is very little scientific evidence that this can actually be done. The sad fact is that anyone, who has ever lost weight, has to continue with efforts to keep it off – this includes people who have had bariatric surgery, who if they ever decide to reverse their surgery – will rapidly gain their weight back (even after years of keeping it off). This, by the way, is why bariatric surgery has to be seen as a definitive and permanent solution and why temporary devices like gastric balloons, which have to be eventually removed, are not a permanent treatment for obesity. Another reader wanted to know, that if this was true, why some people are successful in maintaining long-term weight loss. The answer to this is that these individuals somehow manage to continue their efforts (whatever those may be) in the long-term. The best studied group of individuals who have succeeded in the long-term are perhaps those represented by the National Weight Control Registry, who, using various strategies manage to reduce their caloric intake to about 1400 KCal (the same amount that is effectively eaten by successful post-bariatric surgery patients) combined with considerable amounts of exercise (upto 400 KCal worth every day). Such ongoing efforts are clearly beyond what most people can do without completely changing their lives. So, what the NWC participants actually demonstrate, is not so much that sustaining weight loss is possible but rather that this requires an almost ‘superhuman’ effort (some would say ‘obsession’) – indeed the NWC registrants represent a rare minority of people attempting to lose weight by diet and exercise alone (the NWC registry has a few thousand registrants compared to the tens of millions who try losing weight… Read More »

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Why is it so Hard to Maintain a Reduced Body Weight?

Yesterday, I had the pleasure of attending a lecture by Rudy Leibel from Columbia University, who is perhaps best known for his considerable contributions to our current understanding of energy metabolism. The talk was hosted by William Colmers as part of the University of Alberta Merck Translational Lecture Series. In his presentation, Leibel addressed the issue of why it is so hard to keep weight off – in fact, even in people who undergo bariatric surgery, weight always comes back when surgery is reversed. One of the key underlying problems is that when people lose weight, their energy expenditure does not simply fall to that of the energy expenditure of a person ‘naturally’ at that lower weight – it drops to levels far greater than expected. Thus, a formerly-obese person burns 20% less calories than a never-obese person of that lower weight – or in other words a 200 lb person, who loses 40 lbs burns about 20% fewer calories than someone who is 160 lbs, but has never been obese. On top of this, the formerly-obese person experiences hunger, cold intolerance, and other behavioural and metabolic changes that make sustaining this lower body weight difficult. From an evolutionary sense, this makes a lot of sense, as maintaining or ‘defending’ fat stores in the past has always been vital for human survival and therefore complex biological systems have evolved to readily take up and store excess calories when available and reduce caloric expenditure when times are tough. In a large series of carefully conducted energy balance studies in humans, Leibel examined the impact of weight loss on energy expenditure, energy intake, neuroendocrine function, autonomic physiology, metabolism and brain imaging. Whereas a short-term increase in body weight by 10 % results in a transient increase in energy expenditure, this returns to baseline, when the weight is lost. This means that weight-loss per se does not reduce energy expenditure. On the other hand, a 10% drop in body weight immediately reduces energy expenditure by as much as 20%. Interestingly, this fall in energy expenditure is not simply due to a fall in metabolic rate, but largely due to a decline in activity expenditure. This means that the body ‘saves’ energy not simply by turning down the furnace, but by becoming substantially more ‘fuel efficient’ during activity. In other words, someone who loses weight, will burn substantially fewer calories for a given amount… Read More »

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How Obesity Affects Your Liver

Obesity is rapidly overtaking alcohol as one of the major causes of fatty liver disease. The term non-alcoholic fatty liver disease (NAFLD) is now widely used to describe hepatic steatosis resulting from excess weight in the absence of a history of significant alcohol use or other known liver diseases. Already NAFLD is one of the most common liver disease worldwide with approximately 30% of the population affected in industrialized, western countries. But how exactly does excess weight lead to a fatty liver and how damaging is this effect on liver function? This is the subject of a comprehensive review by Alexander Wree and colleagues from the University of Duisburg-Essen, Germany, published in the latest issue of DIGESTION. As the authors point out, visceral adipose tissue secretes free fatty acids (FFAs) and hormones (adipokines) that appear to play a major role in the development of NAFLD. Toxic FFAs can activate the intrinsic apoptosis pathway in hepatocytes (via c-Jun N-terminal kinase_mediated Bax activation) in a process known as ‘lipoapoptosis’. Not surprisingly, apoptotic cell death is a prominent feature in the progression of NAFLD to nonalcoholic steatohepatitis (NASH). In addition, reduced adiponectin levels commonly associated with obesity may establish a proinflammatory milieu, thus increasing vulnerability to lipotoxicity, which promotes progression from simple steatosis to NASH and even advanced hepatic fibrosis. Interestingly, obesity also appears to be a significant and independent risk factor for hepatocellular carcinoma, the most frequent type of liver cancer. There is also data to suggest that excess body weight can adversely affect the progression of chronic hepatitis C and B. Fortunately, NAFLD is a treatable condition, which responds (often dramatically) to weight loss interventions. Thus, some readers may be aware that many bariatric surgeons now routinely recommend two weeks of weight loss prior to laparoscopic surgery, as this has been shown to dramatically reduce liver size and improve visibility during the surgical procedure. As for so many other obesity related conditions, preventing and treating obesity will be a key measure in preventing and controlling this epidemic of fatty liver disease. AMS Edmonton, Alberta Wree A, Kahraman A, Gerken G, & Canbay A (2010). Obesity Affects the Liver – The Link between Adipocytes and Hepatocytes. Digestion, 83 (1-2), 124-133 PMID: 21042023

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