Nevertheless, epidemiologists (and folks in health promotion) appear to like the notion that there is such a weight (at least at the population level), and often define it as the weight (or rather BMI level) where people have the longest life-expectancy.
Readers of this literature may have noticed that the BMI level associated with the lowest mortality has been creeping up.
Case in point, a new study by Shoaib Afzal and colleagues from Denmark, published in JAMA, that looks at the relationship between BMI and mortality in three distinct populations based cohorts.
The cohorts are from the same general population enrolled at different times: the Copenhagen City Heart Study in 1976-1978 (n = 13 704) and 1991-1994 (n = 9482) and the Copenhagen General Population Study in 2003-2013 (n = 97 362). All participants were followed up to November 2014, emigration, or death, whichever came first.
The key finding of this study is that over the various studies, there was a 3.3 unit increase in BMI associated with the lowest mortality when comparing the 1976-1978 cohort with that recruited in 2003-2013.
Thus, The BMI value that was associated with the lowest all-cause mortality was 23.7 in the 1976-1978 cohort, 24.6 in the 1991-1994 cohort, and 27.0 in the 2003-2013 cohort.
Similarly, the corresponding BMI estimates for cardiovascular mortality were 23.2, 24.0, and 26.4, respectively, and for other mortality, 24.1, 26.8, and 27.8, respectively.
At a population level, these shifts are anything but spectacular!
After all, a 3.3 unit increase in BMI for someone who is 5’7″ (1.7 m) is just over 20 lbs (~10 Kg).
In plain language, this means that to have the same life expectancy today, of someone back in the late 70s, you’d actually have to be about 20 lbs heavier.
While I am sure that these data will be welcomed by those who would argue that the whole obesity epidemic thing is overrated, I think that the data are indeed interesting for another reason.
Namely, they should prompt speculation about why heavier people are living longer today than before.
There are two general possible explanations for this:
For one these changes may be the result of a general improvement in health status of Danes related to decreased smoking, increased physical activity or changes in social determinants of health (e.g. work hours).
On the other hand, as the authors argue, this secular trend may be that improved treatment for cardiovascular risk factors or complicating diseases, which has indeed reduced mortality in all weight classes, may have had even greater beneficial effects in people with a higher BMI. Thus, obese individuals may have had a higher selective decrease in mortality.
There is in fact no doubt that medical management of problems directly linked to obesity including diabetes, hypertension and dyslipidemia have dramatically improved over the past decades.
Thus, it appears that the notion of “healthy” weight is a shifting target and that changes in lifestyle and medical management may have more than compensated for an almost 20 lb weight increase in the population.
This is all the more reason that the current BMI cutoffs and weight-centric management of obesity both at a population and individual level may need to be revisited or at least tempered with measures of health that go beyond just numbers on the scale.
The GLP-1 analogue liraglutide (Saxenda), recently launched in North America for the treatment of obesity, has now also been shown to improve symptoms (apnea-hypopnea index – AHI) of obstructive sleep apnea (OSA).
This, according to a paper by Blackman and colleagues published in the International Journal of Obesity.
This 32-week randomized, double-blind trial was conducted in about 360 non-diabetic participants with obesity who had moderate (AHI 15-29.9 events/h) or severe (AHI ⩾30 events/h) OSA and were unwilling/unable to use continuous positive airway pressure therapy (CPAP).
After 32 weeks, the mean reduction in AHI was greater with liraglutide (3.0 mg) than with placebo (-12.2 vs -6.1 events/h).
This improvement in sleep apnea was largely explained by the greater mean percentage weight loss compared with placebo (-5.7 vs -1.6%).
Additional findings included a greater reductions in HbA1c and systolic blood pressure in the participants treated with liraglutide versus placebo.
Liraglutide was generally well tolerated with no unexpected adverse effects.
Thus, it appears that in addition to weight loss, treatment with liraglutide 3.0 mg results in clinically meaningful improvements in the severity of obstructive sleep apnea, an important issue that affects both the cardiometabolic risk and quality of life of so many individuals living with obesity.
Disclaimer: I have received honoraria as a consultant and speaker for Novo Nordisk, the maker of liraglutide
While this approach can be highly effective, it does require training, resources and ongoing (lifelong?) interventions (not unlike most other chronic diseases).
Now a rather comprehensive paper by Soleyman and colleagues from the University of Birmingham, Alabama, published in Obesity Reviews provides an overview of obesity management in primary care.
As readers are well aware, our body weight are tightly regulated by a complex neuroendocrine system and defends us agains weight loss through a multi-faceted physiological response to prevent further weight loss and restore body weight.
As the authors note,
“To maintain weightloss, individuals must adhere to behaviours that oppose these physiological adaptations and the other factorsfavouring weight regain. However, it is difﬁcult for peoplewith obesity to overcome physiology with behaviour over the long term. Common reasons for weight regain include decreased caloric expenditure, decreased self-weighing frequency, increased caloric intake, increased fat intake and eating disinhibition over time.”
The paper provides a succinct overview of the evidence supporting behavioural, medical and surgical obesity treatments.
It also reiterates the basic principles of obesity management as outlined in the various guidelines:
1. Obesity is a chronic disease that requires long-term management. It is important to approach patients with information regarding the health implications.
2. The goal of obesity treatment is to improve the health of the patient, and it is not intended for cosmetic purposes.
3. The cornerstone of therapy is comprehensive lifestyle intervention from informed PCPs or other healthcare professionals.
4. The initial goal of therapy is a weight loss of 5–10% in most patients, as this is sufﬁcient to ameliorate many weight-related complications. However, weight loss of ≥10% may be needed to improve certain weight-related complications, such as obstructive sleep apnoea.
5. Consideration should be given to the use of a weight-loss medication or possible bariatric surgery, as the addition of these treatment modalities to lifestyle therapy can promote greater weight loss and maintain the weight loss for a longer period of time.
6. It is important for clinicians to evaluate the patient for weight-related complications, that can be improved by weight loss, and to consider such patients for more aggressive treatment.
As for how to get more primary care clinics to actually implement these approaches, the authors note that,
“Primary care practitioners need to address the problem of obesity in their patients, just as they would with any other chronic condition such as hypertension or type 2 diabetes, and to ensure that their patients are aware of the health risks of obesity.”
Again something that the Canadian Obesity Network is working hard to promote in this country.
A blood pressure that is too high can kill you – so can a blood pressure that is too low.
A blood sugar that is too high can kill you – so can a blood sugar that is too low.
It turns out that BMI is no different – too high and too low both carry a risk – a risk, however, that is substantially confounded by actual body fat%, which is not reliably measured by BMI.
This is basically the message in a paper by my colleagues Raj Padwal and co from the University of Alberta in a paper published in the Annals of Internal Medicine.
The researchers looked at data from about 50,000 women and 5,000 men (mean age, 63.5 years; mean BMI, 27.0 kg/m2) referred for bone mineral density (BMD) testing with dual-energy x-ray absorptiometry (DXA), which they linked to administrative databases.
Given the size and demographics of the cohort, death occurred in almost 5000 women over a median of 6.7 years and 1000 men over a median of 4.5 years.
Women in the lowest BMI and body fat% quintiles had a 40% higher risk of dying (compared to quintile 3). Risk of dying were also about 20% greater in the highest body fat% quintile for women.
Similarly in men, both low BMI (HR, 1.45 for quintile 1) and high body fat percentage (HR, 1.59 for quintile 5) were associated with increased mortality.
The exciting bit about this study is that the researchers had both BMI and body fat% available to them and were able to show that both variables independently of each other contribute to mortality risk.
Thus, the worst possible combination in both men and women was low BMI and high body fat%.
Or, as the authors put it,
“Low BMI and high body fat percentage were both associated with increased all-cause mortality. Mortality increased as BMI decreased and body fat percentage increased…..Thus, our results suggest that BMI may be an inappropriate surrogate for adiposity, and this limitation may explain the presence of the obesity paradox in many studies.”
As the authors discuss, these finding should have clinical implications as they clearly demonstrate the limitations of BMI as a measure of health risk.
“..our findings underscore that the risk for all-cause mortality increases with both increasing adiposity and decreasing BMI in a general population of middle-aged and older adults. These findings also suggest the importance of using direct measures of adiposity when building prognostic or even exploratory models.”
Now a study by Crump and colleagues published in JAMA Intern Medicine suggests that some of this risk may be mitigated by increased physical fitness.
The cohort study involving over 1.5 million Swedish young men in Sweden, who underwent standardized aerobic capacity, muscular strength, and BMI measurements obtained at a military conscription examination and were followed for up to 40 years.
Almost 100,000 men went on to develop hypertension, whereby both high BMI and low aerobic capacity (but not muscular strength) were associated with increased risk of hypertension, independent of family history or socioeconomic factors.
A combination of high BMI (overweight or obese vs normal) and low aerobic capacity (lowest vs highest tertile) was associated with the highest risk of hypertension.
The association with aerobic fitness was apparent at every level of BMI.
Form this study the authors conclude that high BMI and low aerobic capacity in late adolescence are associated with higher risk of hypertension in adulthood.
Although one must also be cautious in assuming causality with regard to associations found in such studies, the observations are certainly compatible with the notion that increased cardiorespiratory fitness may well mitigate some of the impact of increased BMI on hypertension risk.