That depends entirely on what you think obesity is.
If you think the defining feature of obesity as a medical condition is the presence of a certain amount of body fat (e.g. greater than 20% in boys and greater than 30% in girls), then, as outlined in a systematic review and meta-analysis by Simmonds and colleagues, published in Obesity Reviews, BMI is a reasonably good measure (when compared to actual body composition as measured by densitometry (hydrostatic weighting or air displacement plethysmography), deuterium dilution, or DXA).
However, if you believe that the defining feature of obesity (in contrast to simple adiposity or fatness) should be a measure of whether or not excess or abnormal body fat actually impairs health in a given individual, then this analysis is not really helpful.
This distinction is important if we embrace the notion that obesity is a disease – a disease impairs health. A risk factor, on the other hand, is just that – a risk factor for a disease.
They are not the same.
Risk for diabetes is not diabetes.
Risk for heart disease is not heart disease.
Risk for cancer is not cancer.
Thus, the onus on anyone describing anyone as having the disease “obesity”, is to demonstrate that that person actually is “diseased” or in other words, is experiencing an impairment in health directly related to the presence of abnormal or excess body fat.
Thus, as this paper shows, BMI may well be a reasonable diagnostic measure of adiposity (more so in girls than in boys) – whether or not it helps diagnose obesity is another question entirely.
Exposure to endocrine disrupters in humans included our diets, personal care products, antimicrobial soaps, household or agricultural pesticides, and cleaning products.
Now, the Endocrine Society has produced its second Scientific Statement on environmental endocrine-disrupting chemicals (EDC-2), published in Endocrine Reviews. (a summary appears in JAMA Internal Medicine)
The major EDC classes reviewed were industrial chemicals (polychlorinated biphenyls [PCBs], dioxins), pesticides, plastics and plasticizers (bisphenol A [BPA] and phthalates), perfluorinated compounds, and flame retardants.
As for the relationship between ECDs and obesity, the authors summarize:
“In animals, several EDCs now referred to as obesogens and diabetogens were associated with obesity and DM2, respectively, with results dependent on the chemical, dosage, and age of exposure. The evidence is strongest for tributyltin, persistent organic pollutants (POPs), pesticides, and BPA. Some EDCs exert actions on adipogenesis, or on pancreatic β- and α-cells. Developmental EDC exposures also led to insulin resistance and hyperinsulinemia and were associated with alterations in serum adiponectin and leptin. Although the mechanisms varied, they included effects mediated via the aryl hydrocarbon receptor, peroxisome proliferator-activated receptor γ (PPARγ), and estrogen receptors (ERs). Furthermore, limited evidence suggests that the hypothalamic control of energy balance may be perturbed. Cross-sectional epidemiological data showed associations between EDCs, obesity, and/or DM2, although causality cannot be inferred. Less is known about EDCs and cardiovascular disease, but emerging work suggests that this merits further research.”
I have little doubt that both exposure and susceptibly varies widely between individuals, however there are currently no tests that would allow us to discern the contribution of ECDs to obesity in a given individual.
Thus, while the magnitude of the contribution of ECDs to any given person’s weight problem may be hard to diagnose and even harder to manage, the findings do remind us that the environmental drivers of obesity may well go beyond just our foodscape and sedentariness.
Free access to the Executive Summary of the Statement is available here
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!
Continuing in my miniseries on the recent “Clinical Discussion” on obesity, published in the New England Journal of Medicine, I now turn to the second question that we need to answer before jumping into giving our patient any advice about managing her weight.
The first question, as discussed in yesterday’s post, is to understand the possible “root-causes” of her weight gain, as these may not only have to be targeted during treatment but can also pose important barriers to management (e.g. emotional eating, depression, lack of time, stress, etc.).
Unfortunately, as I noted yesterday, the case presentation did not provide much in terms of helping us understand, why this patient has a BMI of 32 in the first place.
Not only did we not get any information regarding her weight trajectory, we were also only told that she eats out often and is largely sedentary – not really much to go on, given that the same could be said about the vast majority of people living in the US (or in Canada), irrespective of their size or weight.
As for the second question that we now need to answer, before giving any advice, is whether or not she even has a health issue that needs to be addressed.
Thus, while we may be led to believe that her BMI of 32 in itself justifies the diagnosis of “obesity”, we must remember that BMI is a essentially a measure of body size, in fact, not much better than a dress size.
Although statistical risk for certain health problems (e.g. diabetes, hypertension, joint problems, sleep apnea, etc.) may rise with increasing BMI, this relationship is far weaker than most people think.
Indeed, as we have previously noted, as many as 25-30% of individuals in the BMI 30-35 range may have no clinically significant health impairments whatsoever. This is particularly true for younger individuals and for women – out patient just happens to be a 29 year-old female.
Thus, it is in fact not all that surprising, that the case report goes on to note that Ms Chatham has neither a history of coronary artery disease nor diabetes (which would indeed be rather unusual if did), and, apart from a marginally elevated blood-pressure, her health status is largely “unremarkable”. Although not mentioned in the case vignette, we can perhaps also assume that all her lab values are normal.
Thus, even if we assume that the blood pressure reading is reliable, this information would at best put her at an Edmonton Obesity Stage 1, a stage where her long-term mortality risk would be almost indistinguishable from “normal”.
And, if we apply the actual WHO definition of obesity (the presence of excess or abnormal body fat that impairs health), we may in fact have to bend over backwards to diagnose this woman as having obesity at all.
So if there is no relevant health impairment from her BMI of 32, why is she even concerned about her weight?
Because, as we learn from the case study, she has been told indirectly, by her friends and family, that she is “overweight.”
Which brings me back to our question at hand: does this woman even have a health problem that needs to be addressed?
My answer would be a rather enthusiastic, “not really”.
We could of course leave it at that, and simply reassure her that she is pretty healthy (although she may perhaps want to have her blood pressure rechecked in the near future).
If however, she does persist in her intention to lose weight, and continues to insist that we advise her on what she can do to improve her health (which are really two very different questions), we may need to have a much longer discussion with her.
This is something we will look at tomorrow, when we address the third question:
What would be the best management plan for this patient?