Now, a randomised controlled study by Mark Ng Tang Ful and colleagues, published in BMC Medicine, suggests that treatment with testosterone may help promote diet-induced loss of fat mass and limit loss of muscle mass.
The study included 100 middle-aged men with obesity, who had a total testosterone level of or below 12 nmol/L, the lower limit reported for healthy young men.
Subjects received 10 weeks of a very low energy diet (VLED) followed by 46 weeks of weight maintenance during which they were randomly assigned to 56 weeks of 10-weekly intramuscular testosterone undecanoate or placebo.
Of the 82 men, who completed the study, participants treated with testosterone had an about 3 Kg greater reduction in fat mass with a greater reduction in visceral fat.
While both groups lost the same amount of lean mass during the VLED, participants treated with testosterone, quickly regained the lean mass so that they had about 3.4 more lean mass than the controls at the end of the study, so that virtually all of the greater weigh loss by these participants over the course of the trial was attributable to fat loss.
These findings are consistent with what is known about testosterone function in men with obesity.
Thus, as the authors remind us,
“Experimental studies in humans suggest that fat-derived adipokines and pro-inflammatory mediators may play a role in central gonadal axis suppression. In addition, preclinical evidence has shown that testosterone deficiency promotes adipose tissue accumulation but reduces myogenesis via an androgen receptor mediated pathway.”
Thus, these findings suggest that dieting men may benefit from adjunct treatment with testosterone to promote fat loss and conserve muscle mass.
Every two years the Canadian Obesity Network holds its National Obesity Summit – the only national obesity meeting in Canada covering all aspects of obesity – from basic and population science to prevention and health promotion to clinical management and health policy.
Anyone who has been to one of the past four Summits has experienced the cross-disciplinary networking and breaking down of silos (the Network takes networking very seriously).
Of all the scientific meetings I go to around the world, none has quite the informal and personal feel of the Canadian Obesity Summit – despite all differences in interests and backgrounds, everyone who attends is part of the same community – working on different pieces of the puzzle that only makes sense when it all fits together in the end.
The 5th Canadian Obesity Summit will be held at the Banff Springs Hotel in Banff National Park, a UNESCO World Heritage Site, located in the heart of the Canadian Rockies (which in itself should make it worth attending the summit), April 25-29, 2017.
Yesterday, the call went out for abstracts and workshops – the latter an opportunity for a wide range of special interest groups to meet and discuss their findings (the last Summit featured over 20 separate workshops – perhaps a tad too many, which is why the program committee will be far more selective this time around).
So here is what the program committee is looking for:
- Basic science – cellular, molecular, physiological or neuronal related aspects of obesity
- Epidemiology – epidemiological techniques/methods to address obesity related questions in populations studies
- Prevention of obesity and health promotion interventions – research targeting different populations, settings, and intervention levels (e.g. community-based, school, workplace, health systems, and policy)
- Weight bias and weight-based discrimination – including prevalence studies as well as interventions to reduce weight bias and weight-based discrimination; both qualitative and quantitative studies
- Pregnancy and maternal health – studies across clinical, health services and population health themes
- Childhood and adolescent obesity – research conducted with children and or adolescents and reports on the correlates, causes and consequences of pediatric obesity as well as interventions for treatment and prevention.
- Obesity in adults and older adults – prevalence studies and interventions to address obesity in these populations
- Health services and policy research – reaserch addressing issues related to obesity management services which idenitfy the most effective ways to organize, manage, finance, and deliver high quality are, reduce medical errors or improve patient safety
- Bariatric surgery – issues that are relevant to metabolic or weight loss surgery
- Clinical management – clinical management of overweight and obesity across the life span (infants through to older adults) including interventions for prevention and treatment of obesity and weight-related comorbidities
- Rehabilitation – investigations that explore opportunities for engagement in meaningful and health-building occupations for people with obesity
- Diversity – studies that are relevant to diverse or underrepresented populations
- eHealth/mHealth – research that incorporates social media, internet and/or mobile devices in prevention and treatment
- Cancer – research relevant to obesity and cancer
…..and of course anything else related to obesity.
Deadline for submission is October 24, 2016
To submit an abstract or workshop – click here
For more information on the 5th Canadian Obesity Summit – click here
For sponsorship opportunities – click here
Looking forward to seeing you in Banff next year!
It is now well established that the almost non-existant rates of long-term weight loss are not because of lack of will power or lack of motivation. Rather, they are firmly embedded in human (and animal) physiology, that is designed to defend body weight at all costs through complex neuroendocrine homeostatic mechanisms that will eventually wear out even the staunchest dieter.
But just how strong is the physiological drive to defend and regain lost body weight? Or even more specifically, how much does an increase in appetite counteract weight loss?
This is the topic of a paper by David Polidori and colleagues, prepublished on bioRxiv*.
The researchers use data from a 52-week trial of canagliflozin, a sodium glucose co-transporter (SGLT2) inhibitor leads to a urinary glucose loss of approximately 90 g/day throughout the duration of treatment.
This amounts to a net daily energy loss of ~360 kcal/day that occurs without directly altering central pathways controlling energy intake and without the patients being directly aware of the energy deficit.
Based on the observed changes in body weight over time, the researchers used a validated mathematical method to calculate changes in daily energy intake using principles from engineering control theory.
The complex mathematical formula takes into account a wide range of parameters including changes in the energy expenditure rate and density of fat and fat-free mass, energy cost of fat and protein turnover, dietary and adaptive thermogenesis as well as changes in physical activity (no change in physical activity was assumed in this study).
Subjects in the treatment arm showed the typical initial weight loss (of about 5 Kg) followed by the maintenance of a weight-loss plateau throughout the remainder of the study, a pattern which, in light of a continuing daily energy loss of about 360 kcal is consistent with a proportional feedback control system that serves to limit the amount of weight loss and creates a drive towards weight regain (think of this as the tension that counteracts a steady pull on a rubber band).
Based on their calculations, the amount of daily increase in caloric intake required to maintain the weight loss plateau (rather than continuing to lose weight), was in the order of about 100 Kg/day per Kg weight loss. This is substantially more than the reduction in metabolic rate generally seen with weight loss (of about 10-20% of body weight) is only about 30 kcal/day per Kg weight loss).
When applying these finding to the typical weight-loss curve seen in the usual commercial weight loss programs (an initial weight loss followed by gradual weight regain), the researchers show that the difference between the homeostatic drive to eat and the actual energy intake, a quantitative index of the ongoing effort to sustain the intervention in the face of the continuing biological signals to overeat, requires that subjects have to demonstrate a persistent effort to avoid overeating above baseline during the intervention even when the average energy intake returns to near baseline levels.
“…homeostatic feedback control of energy intake is likely a primary reason why it is so difficult to achieve large sustained weight losses in patients with obesity. Rather, weight regain is typical in the absence of heroic and vigilant efforts to maintain behavior changes in the face of an omnipresent obesogenic environment. Unfortunately, there is no evidence that the energy intake feedback control system resets or relaxes with prolonged maintenance of lost weight – an effect similar to the long-term persistent suppression of energy expenditure in weight-reduced humans. Therefore, the effort associated with a weight loss intervention persists until either body weight is fully regained or energy intake increases above baseline to match the homeostatic drive to eat.”
I am currently in Rio de Janeiro, speaking at the 21st World Congress of the International Federation for the Surgery of Obesity & Metabolic Disorders – IFSO 2016.
As Lee Kaplan from Harvard University reminded the audience, obesity is a disease of energy homeostasis, where everything seems to be working just fine, except that the “setpoint” of the system is set too high.
Kaplan used the analogy of the temperature in a room, where the thermostat is set too high – say to 30 Centigrade.
Everything else in the room works just fine: nothing wrong with the heater, or the air-conditioning, or the ventilation system, or the isolation. In fact, even the thermostat is working just fine doing its job – except that it is set too high!
Dieting would be like tearing open a window to lower the temperature in the room. Yes, if you open the window, things may cool down, but the thermostat will only make the heating work extra hard trying to heat the room and, once you close the window, the thermostat will rapidly bring the temperature back to 30 Centigrade (or come off your diet).
So how do we reset the set point?
Well, that appears to be exactly what bariatric surgery does to the system – it somehow manages to lower the set point, allowing the body to regulate its weight at a lower level than before (something that does not happen when you lose weight simply with diet and exercise).
How exactly surgery does this, remains unclear, but there is no doubt that this happens and there are a lot of experiments showing that after sugery, the body actively regulates body weight at a lower “setpoint”.
Unfortunately, this “resetting” is not permanent.
If you reverse the surgery, the body goes right back to regulating its weight at the higher level, resulting in the rapid weight regain, which is why I consider obesity surgery a “treatment” rather than a “cure”.
Kaplan went on to talk about the role of the bacteriome and bile acid metabolism (both dramatically changes with bariatric surgery – but very little with diet and exercise).
Figuring out how bariatric surgery changes the setpoint (even temporarily) will hopefully lead to new medical treatments for obesity.
Till then, anyone losing weight (no matter what diet, exercise, or medication) needs to remember that they stand to regain the weight, the minute they stop the “treatment”.
Rio de Janiero
While many folks have no problem seeing how “excess” body fat can often lead to health problems, they may wonder what exactly is meant by “abnormal” body fat and are perhaps unsure as to why this would be included in the definition of obesity.
This is where we need to take a moment to remind ourselves that fat tissue is actually a vital organ, without which, we would experiences all kinds of health problems. Not only, is our ability to store excess calories vital to prepare for the next major illness or famine, it is also a vital organ for reproduction (women stop having periods when their fat stores get too low).
That said, the safest place to store all those excess calories is in your fat tissue, especially the fat tissue directly underneath your skin. This is where the excess calories cause the least trouble, not affecting the functioning of other organs or clogging up your blood stream, and where they can sit for decades, until they are perhaps one-day called upon in a time of need.
It is also “normal” to have a small amount of fat in other depots such as around the gastrointestinal tract, the heart, or the kidneys – here the fat serves both a mechanical and immunological function – again, the fat here generally does not cause any health problems (indeed, lack of fat in these locations may).
All of this is not very interesting from a medical or health perspective, as this kind of fat generally does not cause any real health problems, unless, it perhaps expands to a size that causes mechanical issues simply due to its sheer mass.
In contrast, the term “abnormal” refers to fat accumulation in parts of the body where you would not normally find fat in a “healthy” person. This, is commonly referred to as “ectopic” fat and refers to fat accumulation within organs like the liver, pancreas, heart, skeletal muscle or other organs, where you would rather not have any fat.
These “abnormal” fat accumulations can substantially disrupt organ function, leading to all kinds of metabolic problems.
Interestingly enough, there is not a very strong relationship between the total amount of body fat and the location of that body fat.
The extreme example of this is seen in patients with lipodystrophy, who, being unable to store excess calories in “normal” subcutaneous fat depots, deposit their fat in the liver and other organs, thus presenting with all of the problems generally associated with obesity.
Exactly why some people are more prone to “ectopic” fat deposition that others, who can apparently tuck away all their extra calories underneath their skin with little, if any, impact on their health, remains largely unknown, except that genetics appears to play a very substantial role.
But, whatever the reason, the bottom line remains that even very little extra body fat, if stored in the wrong location, can cause all of the metabolic problems generally associated with obesity.
In contrast, even large amounts of body fat, if safely sequestered away in subcutaneous depots may have little (if any) impact on health.
This is why the WHO included both the presence of “excess” as well “abnormal” body fat in their definition of obesity.
Again, none of this can be measured by stepping on a scale or looking at a BMI chart.
If your excess or abnormal body fat affects your health – you have obesity – if it doesn’t, you don’t.