Regular readers will be quite familiar with the findings that cardiometabolic health appears to be far more related to “fitness” than to “fatness” – in other words, it is quite possible to mitigate the metabolic risks commonly associated with excess body fat by improving cardiorespiratory fitness.
Now, a study by Kathy Do and colleagues from York University, Toronto, published in BMC Obesity, shows that this relationship also holds for people with quite severe obesity.
The researcher studied 853 patients from the Wharton Medical Clinics in the Greater Toronto Area, who completed a clinical examination and maximal treadmill test. Patients were then categorized into fit and unfit based on age- and sex-categories and in terms of fatness based on BMI class.
Within the sample, 41% of participants with mild obesity (BMI<35) had high fitness whereas only 25% and 11% of the participants with moderate (BMI 35-40) and severe obesity (BMI>40), respectively, had high fitness.
Individuals with higher fitness tended to be younger and more likely to be female.
While overall fitness did not appear to be independently associated with most of the metabolic risk factors (except systolic blood pressure and triglycerides), the effect of fitness in patients with severe obesity was more pronounced. Thus, the prevalent relative risk for pre-clinical hypertension, hypertriglyceridemia and hypoalphalipoproteinemia and pre-diabetes was only elevated in the unfit moderate and severe obesity groups, and fitness groups were only significantly different in their relative risk for prevalent pre-clinical hypertension within the severe obesity group.
Similarly, high fitness was associated with smaller waist circumferences, with differences between high and low fitness being larger in those with severe obesity than with mild obesity.
Based on these findings, the researchers conclude that the favourable associations of having high fitness on health may be similar if not augmented in individuals with severe compared to mild obesity.
However, it is also apparent based on the rather low number of “fit” individuals in the severe obesity category (only about 1 in 10), that maintaining a high level of fitness proves to be more challenging the higher the BMI.
The 2018 JAMA special issue on obesity also includes a brief paper by Ann Blair Kennedy and colleagues reviewing the debate (which really isn’t much of a debate to anyone who knows the data) on whether it is more important to be fit than to worry about being fat (it is).
As the authors review, there is now ample data showing that cardio-respiratory fitness (CRF) is far more important for the prediction of cardiovascular mortality than the level of fatness (measured as BMI or otherwise).
In fact, once you account for differences in “fitness”, actual BMI levels almost cease to matter in terms of predicting longevity.
Unfortunately, as the authors point out, most studies linking obesity to cardiovascular outcomes (including studies on the so-called obesity “paradox”), fail to properly measure or account for cardiovascular fitness, thereby ignoring the most important confounder of this relationship.
For clinicians (and anyone concerned about their excess weight), it is helpful to remember that while achieving and maintaining a significant weight loss is a difficult (and often futile) undertaking, achieving and maintaining a reasonable degree of cardiorespiratory fitness is possible at virtually any shape or size.
Thus, as the authors point out,
“…in current US society, many people progressively gain weight and lose CRF as they age. Conceivably, maintaining CRF may be more important than preventing the development of obesity. However, for people who are overweight or have mild to moderate obesity, there are effective ways to improve CRF, including exercise and lifestyle interventions and there is general agreement that having low levels of PA is unhealthy. Increasing PA to help keep individuals from becoming unfit can be achieved if patients meet current PA guidelines of 150 minutes of moderate or 75 minutes of vigorous PA per week.”
Clearly, if your primary concern related to your patients’ excess body fat is about their cardiovascular health, you would probably be doing them a far greater service by getting them to improve their cardiorespiratory fitness rather than simply lose a few pounds (and no, exercise is not the best way to lose weight!).
On the other hand, if there are other health issues that are of primary concern (e.g. sleep apnea, osteoarthritis, fatty liver disease, etc.) or the degree of excess fat significantly affects mobility or other aspects of quality of life, then perhaps a frank discussion about available and effective “weight-loss” treatments appears warranted.
Let us not forget that it is never a good idea to simply treat numbers on the scale.
The assessment of weight history is no doubt a key feature of obesity assessment. Not only can weight history and trajectories provide important insights into obesity related risk but, perhaps more importantly, provide key information on precipitating factors and drivers of excessive weight gain.
Now, in a short article published in MedEdPublish, Robert Kushner discusses how the well-known OPQRST mnemonic for assessing a “chief complaint” can be applied to assess body weight.
In short, OPQRST is a mnemonic for Onset, Precipitating, Quality of Life, Remedy, Setting, and Temporal pattern. Applied to obesity, Kushner provides the following sample questions for each item:
Onset: “When did you first begin to gain weight?” “What did you weight in high school, college, early 20s, 30s, 40s?” “What was your heaviest weight?”
Precipitating: “What life events led to your weight gain, e.g., college, long commute, marriage, divorce, financial loss?” “How much weight did you gain with pregnancy?” “How much weight did you gain when you stopped smoking?” “How much weight did you gain when you started insulin?”
Quality of life: “At what weight did you feel your best?” “What is hard to do at your current weight?”
Remedy: “What have you done or tried in the past to control your weight?” “What is the most successful approach you tried to lose weight?” “What do you attribute the weight loss to?” “What caused you to gain your weight back?”
Setting: “What was going on in your life when you last felt in control of your weight?” “What was going on when you gained your weight?” “What role has stress played in your weight gain?” “How important is social support or having a buddy to help you?”
Temporal pattern: “What is the pattern of your weight gain?” “Did you gradually gain your weight over time, or is it more cyclic (yo-yo)?” “Are there large swings in your weight, and if so, what is the weight change?”
As Kushner notes,
“These features provide a contextual understanding of how and when patients gained weight, what efforts were employed to take control, and the impact of body weight on their health. Furthermore, by using a narrative or autobiographical approach to obtaining the weight history, patients are able to express, in their own words, a life course perspective of the underlying burden, frustration, struggle, stigma or shame associated with trying to manage body weight. Listening should be unconditional and nonjudgmental. By letting patients tell their story, the clinician is also able to assess the patients’ awareness, knowledge, motivation, decision-making, and resiliency regarding weight management. The narrative provides a basis for approaching the patients’ weight holistically, as well as beginning to formulate diagnostic and therapeutic options.”
There is no doubt much to be gained in understanding obesity by allowing patients to tell their own weight stories.
In my talks, I have often joked about how to best keep weight off – just carry around a backpack that contains the lost pounds to fool the body into thinking the weight is still there.
It turns out that what was intended as a joke, may in fact not be all too far from how the body actually regulates body weight.
As readers of these posts are well aware, body weight is tightly controlled by a complex neuroendocrine feedback system that effectively defends the body against weight loss (and somewhat, albeit less efficiently, protects against excessive weight gain).
Countless animal experiments (and human observations) show that following weight loss, more often than not, body weight is regained, generally precisely to the level of initial weight.
With the discovery of leptin in the early 90s, an important afferent part of this feedback system became clear. Loss of fat mass leads to a substantial decrease in leptin levels, which in turn results in increased appetite and decreased metabolic rate, both favouring weight regain and thus, restoration of body weight to initial levels.
Now, an international team of researchers led by John-Olov Jansson from the University of Gothenburg, Sweden, in a paper published in the Proceeding of the National Academy of Science (PNAS), provides compelling evidence for the existence of another afferent signal involved in body weight regulation – one derived from weight-bearing bones.
Prompted by observations that prolonged sedentariness can promote weight gain, independent of physical activity, the researchers hypothesised that,
“…there is a homeostat in the lower extremities regulating body weight with an impact on fat mass. Such a homeostat would (together with leptin) ensure sufficient whole body energy depots but still protect land-living animals from becoming too heavy. A prerequisite for such homeostatic regulation of body weight is that the integration center, which may be in the brain, receives afferent information from a body weight sensor. Thereafter, the integration center may adjust the body weight by acting on an effector.”
In a first series of experiments, the researchers observed that implanting a weight corresponding to about 15% of body weight into rodents (rats and mice), resulted in a rapid “spontaneous” adjustment in body weight so that the combined weight of the animal plus the weight implant corresponded more-or-less to that of control animals.
Within two weeks of implanting the weights, ∼80% of the increased loading was counteracted by reduced biological weight, largely due to reduced white adipose tissue (WAT), accompanied by a corresponding decrease in serum leptin levels. (Interestingly, this weight loss was also accompanied by a substantial improvement in insulin resistance and glucose homeostasis).
The decrease in “biological” body weight was mainly attributable to a reduction in caloric intake with no changes in fat oxidation, energy expenditure or physical activity.
Removal of the implanted weights resulted in rapid weight regain to initial levels, showing that the “weight sensor” was active in both directions.
Experiments showed that this “weight sensing” mechanism was largely independent of the leptin pathway and did not appear to involve grehlin, GLP-1, a-MSH, estrogen receptor-a, or the sympathetic nervous system.
Now for the interesting part: the observed effect of weight loading was not seen in mice depleted specifically of DMP1 osteocytes, demonstrating that the suppression of body weight by loading is dependent on osteocytes.
As the authors note, these findings are consistent with a growing body of data indicating that the skeleton is an endocrine organ that regulates energy and glucose metabolism. Indeed, it is well known that osteocytes can sense dynamic short term high-impact bone loading for local bone adaptation – now it appears, that osteocytes may also play a vital role in sensing overall body weight and signalling this to the brain centres that regulate energy balance and body weight.
Thus, in summary, not only have the authors provided compelling evidence for a “weight-sensing” role for bone osteocytes (presumably through their presence in the long weight-bearing bones of our lower extremities) but also provide a plausible biological explanation for the weight gain and change in fat mass seen with prolonged sedentariness (which literally takes the weight off the bone).
These findings may also finally explain why rats held at increased gravity for extended periods of time (simulated G2) become lean even when their energy intake matches their expenditure.
Perhaps, carrying around a heavy backpack may indeed help with long-term weight loss maintenance after all – who knew?
Hat tip to Jean-Philippe Chaput for alerting me to this article
This morning, I am presenting a plenary talk in Berlin to about 200 colleagues involved in childhood obesity prevention.
The 1-day symposium is hosted by Plattform Ernährung und Bewegung e.V. (Platform for Nutrition and Physical Activity), a German consortium of health professionals as well as public and private stakeholders in public health.
Although, as readers are well aware, I am by no means an expert on childhood obesity, I do believe that what we have learnt about the complex socio-psycho-biology of adult obesity in many ways has important relevance for the prevention and management of childhood obesity.
Not only do important biological factors (e.g. genetics and epigenetics) act on the infant, but, infants and young children are exposed to the very same societal, emotional, and biological factors that promote and sustain adult obesity.
Thus, children do not grow up in isolation from their parents (or the adult environment), nor do other biological rules apply to their physiology.
It should thus be obvious, that any approach focussing on children without impacting or changing the adult environment will have little impact on over all obesity.
This has now been well appreciated in the management of childhood obesity, where most programs now take a “whole-family” approach to addressing the determinants of excess weight gain. In fact, some programs go as far as to focus exclusively on helping parents manage their own weights in the expectation (and there is some data to support this) that this will be the most effective way to prevent obesity in their offspring.
As important as the focus on childhood obesity may be, I would be amiss in not reminding the audience that the overwhelming proportion of adults living with obesity, were normal weight (even skinny!) kids and did not begin gaining excess weight till much later in life. Thus, even if we were somehow (magically?) to completely prevent and abolish childhood obesity, it is not at all clear that this would have a significant impact on reducing the number of adults living with obesity, at least not in the foreseeable future.
Let us also remember that treating childhood obesity is by no means any easier than managing obesity in adults – indeed, one may argue that effectively treating obesity in kids may be even more difficult, given the the most effective tools to managing this chronic disease (e.g. medications, surgery) are not available to those of us involved in pediatric obesity management.
Thus, I certainly do not envy my pediatric colleagues in their struggles to provide meaningful obesity management to their young clients.
I am not sure how my somewhat sobering talk will be received by this public health audience, but then again, I don’t think I was expected to fully toe the line when it comes to exclusively focussing on nutrition and activity (as important as these factors may be) as an effective way to prevent or even manage childhood obesity.