New study claims that “healthy obesity” is a myth

Recently, researchers from Mount Sinai Hospital in Toronto attempted to determine whether healthy obesity really exists. This report recently splashed into the news after an editorial published in the Annals of Internal Medicine declared that “healthy obesity is a myth“.

Consistent with this statement, the original report by Kramer and colleagues found that metabolically “healthy” obese people have a 24% higher rate of all-cause mortality relative to metabolically healthy people of normal weight. In reality, this 24% boost is little more than rounding error. In the same study, people with poor metabolic health had a 165-214% increase in mortality, regardless of body mass, Yes, even the skinny ones.

Study overview

Kramer and colleagues conducted a meta-analysis of studies that looked at the relationship between BMI (normal weight, overweight, obese), mortality (all-cause or cardiovascular deaths) and metabolic health. Metabolic health was determined in these studies based upon key determinants of health like waist circumference, fasting triglyceride (e.g. fat) levels, fasting glucose levels, blood pressure, high-density lipoprotein (HDL or “good”) cholesterol levels and the use of anti-hypertensive or glucose-lowering medications. Some studies also looked at inflammatory markers and insulin resistance (which is associated with diabetes).

In their analysis, the researchers included 12 prospective studies with a total of 67,127 participants that studied the relationship between BMI, mortality and metabolic health. About half of these studies had a follow-up for 10 years or longer duration, which represents a key difference between this study and past reports that have generally considered durations of less than 10 years.

I have reproduced one key observation that didn’t make it into the headlines in Figure 1 (below). As is apparent, there is a strong relationship between body mass index and metabolic health, with the ratio of healthy to unhealthy individuals shifting from about 7:1 in the normal weight category, less than 2:1 in the overweight class and less than 1:1 among obese individuals.

Figure 1. Proportion of individuals in the overall sample by BMI category (normal weight, overweight, obese) as a function of metabolic health. The proportion of metabolically healthy individuals decreases from about 7:1 in the normal weight group to less than 1:1 in the obese group.

Figure 1. Proportion of individuals in the overall sample by BMI category (normal weight, overweight, obese) as a function of metabolic health. The proportion of metabolically healthy individuals decreases from about 7:1 in the normal weight group to less than 1:1 in the obese group. More than 40% of obese people are classified as “healthy”.

In other words, people with higher body mass tend to have poorer metabolic health. Still, a large proportion of these obese people (>40%) were still classified as healthy.

Additionally, the researchers divided participants into a series of groups: metabolically healthy people who were i) normal weight, ii) overweight or iii) obese and metabolically unhealthy people who were iv) normal weight, v) overweight or vi) obese.

When they compared these groups, a number of interesting findings emerged.

First, people who were metabolically healthy, regardless of body weight, had similar mortality rates, slightly favoring the normal weight group (by between 10% and 24%). However, this small difference was only significant when the researchers compared “healthy” obese with “healthy” normal weight individuals in studies that had a 10-year follow-up, with a relative risk of 1.24x higher in the obese group (24% difference). When studies with shorter follow-ups were included, the relative risk was similar but not significant.

In other words, there is a small, but significant effect of body mass on mortality in metabolically healthy individuals.

Second, when metabolically unhealthy individuals were compared to metabolically healthy people of normal weight, there was a massive effect of poor metabolic health, regardless of BMI. The relative risk of mortality was between 2.65-3.14 for all groups of metabolically unhealthy individuals (obese, overweight, normal weight). This represents a whopping 165-214% increase in the incidence of mortality among these groups, relative to the healthy normal weight individuals.

In short, having good metabolic health puts you in the clear. Being obese at the same time doesn’t have much of an effect.

The key factors that clearly predicted higher mortality in all groups of unhealthy individuals were elevated systolic blood pressure, decreased HDL levels, modestly elevated LDL levels and elevated fasting triglyceride and glucose levels. Healthy obese and healthy normal weight individuals differed more modestly on a number of factors, including waist circumference, insulin resistance, cholesterol levels and blood pressure.


What conclusions can we draw from this study?

1) It looks as though being obese leads to poor metabolic health, and poor metabolic health produces a major increase in mortality. Moreover, people with normal weight were 3-4 times more likely to be metabolically healthy than obese individuals. That’s number one, and should not be downplayed.

2) It is clear that for those people who are metabolically healthy, body mass has a small effect on mortality, which is tiny compared to the effect of poor metabolic health. Based upon this, I cannot agree with the conclusion that “healthy obese” individuals do not exist. Clearly they do, and in large numbers. In fact, the 1.24x increased risk in this healthy obese group was compared to healthy normal weight individuals. Relative to all normal weight individuals, it is unlikely that there is any significant difference in mortality.

While the authors of this paper propose that metabolically healthy obese individuals are slowly developing disease risk, this study does not directly test this hypothesis. It is true that people in the “healthy obese” category have higher levels of some metabolic markers of poor health than normal weight individuals, but clearly these markers have not caused large increases in mortality over the 10-year span studied here. In order to show that healthy obese individuals are transitioning to unhealthy obesity (rather than being a completely distinct group of people), a long-term follow-up comparing metabolic markers of health across the obesity cycle would be necessary.

Overall, I suspect that the safest bet is to avoid obesity in general. This should cut the risk of poor metabolic health dramatically and lead to a reduced chance of mortality, consistent with most health advice. However, there doesn’t seem to be much evidence to completely ignore people who are both healthy and obese. Based upon this study, there are likely lots of these “healthy obese” individuals, and further, they only appear to have slightly elevated levels of mortality. This doesn’t imply that everyone should assume that metabolic health is simply a stroke of luck: while there are probably a number of genetic factors involved, I suspect that lifestyle (diet, exercise) also plays a pretty big role in this metabolic advantage. I will have to look into this at some future date.

ResearchBlogging.orgKramer CK, Zinman B, & Retnakaran R (2013). Are Metabolically Healthy Overweight and Obesity Benign Conditions?: A Systematic Review and Meta-analysis. Annals of internal medicine, 159 (11), 758-69 PMID: 24297192


The Free Will Fallacy

I have used quite a bit of space on this blog in search for the enigma that is “free will”. This isn’t a chemistry experiment. My aim isn’t to isolate a fraction of “essence of free will” to be resold for profit. Instead, I would just like to narrow down its purpose and meaning.

Wikipedia provides a straightforward, if altogether too generic, definition, stating that:

“Free will is the ability of agents to make choices unconstrained by certain factors.”

It’s pretty apparent that the operative phrase here is certain factors. For example, if human choices are, in fact, tightly constrained and yet still remain free of the influence that arises from the reverse motion of Mercury, then I think it’s fair to say that free will becomes redundant. If astrology is the only outside influence that our choices are free from (“Phew!”), but otherwise our choices follow a whole host of physical laws, then it makes sense to resort to those laws in order to understand the causes behind human decisions.

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New gene associated with post-traumatic stress symptoms

A group of researchers operating out of Emory University, in Atlanta, and the Scripps Research Institute and University of Miami, in Florida, recently reported on a novel gene that regulates fear both in mice and humans with Post-traumatic Stress Disorder (PTSD). Their work was published in the upstart, cutting-edge journal Science Translational Medicine last month.

Following now-popular trend in the sciences, the researchers conducted a full-scale, animal-to-human translational research program to demonstrate the potential importance of this new gene to human “fear-related” disorders like PTSD. Given the recent push in the sciences to make basic research results “translate” to the clinic, this trend is at once both exciting and a little disconcerting. For example, while the breadth of this report is admirable, it does give me the sense that the researchers stitched together two distinct research papers into a single, over-extended compilation.

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What is post-traumatic stress disorder?

Soldiers in World War I, many of whom suffered from “shell shock”, a condition which commonly arose during “trench warfare”, when military personnel were frequently exposed to long periods of artillery barrage. Credit: Public domain, via Wikimedia Commons

Post-traumatic stress disorder or PTSD has a surprisingly long and tortuous history in the annals of psychiatric medicine (a brief history can be found in Chapter 18 of this book). The symptoms of this disorder were recognized early on in the form of “soldier’s heart” and “shell-shock”, but for decades official psychiatric manuals in both the United States and around the world assumed that such conditions were transient and would resolve without much intervention. It wasn’t until the 1980s, during the “post-Vietnam era” when both the DSM-III and ICD-9 first defined PTSD as a profound and chronic condition.

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Transcranial stimulation: How-to

There has been an extended buzz in the news media about the use of transcranial “stimulation” techniques to enhance or impair learning and other “mental” abilities. Popular methods typically involve the application of a magnetic field or an electrical current to the surface of the skull, which can selectively disrupt (inhibit) or excite cells near the cortical surface.

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Transcranial electrical stimulation does not enhance planning abilities

Electrical stimulation for cognitive enhancement is starting to look an awful lot like snake oil. Drink up. Credit: Benjamin Chung, on Flikr (CC BY-SA 2.0).

The saga of electrical stimulation for cognitive enhancement continues.

The next on my list is a 2009 study by Colleen Dockery and her colleagues from the Max Planck Institute in Tuebingen, Germany. This study is another popular citation used to promote the efficacy of transcranial electrical stimulation for performance enhancement and represents one of the first trials to assess the effectiveness of transcranial direct current stimulation (tDCS) for enhancing planning capabilities, in particular.

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Running out of control: do any interventions enhance performance?

Don’t pick the wrong placebo control. Credit: IronGargoyle, via Wikipedia Commons (Public Domain).

Researchers from Florida State University, Boot and colleagues recently reported on a pervasive problem in psychological intervention research that undermines, if not entirely invalidates, the entire field.

The concern? Psychological interventions are rarely double-blinded, because the experimental group always knows they are receiving a treatment. Most reasonably designed studies attempt to obviate this concern by including a second “control” group, which undergoes a similar, but distinct, intervention in order to isolate the specific “treatment” effect of the experimental intervention.

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Action video games–brain drain or brain trainer?

Some gamers have even advanced beyond vision. Martin Leung at Video Games Live (Toronto).   Credit: Ian Muttoo, via Flikr (CC BY-SA 2.0).

Some gamers have even advanced beyond vision. Martin Leung at Video Games Live (Toronto). Credit: Ian Muttoo, via Flikr (CC BY-SA 2.0).

Lately, I have begun discussing recent research in the field of “cognitive enhancement”. Studies in this field explicitly aim to develop techniques that improve mental functions such as attention, memory, higher-level reasoning, etc, either to assist individuals in recovery from injury and impairment or to enhance “normal” functions.

A major complication of performance enhancement training is that while performance gains are easy to demonstrate in specific domains, enhancement tends to be selective and does not generalize to overall performance across various tasks. For example, if I wanted to improve my overall level of intelligence, I could easily boost my scores by completing a large number of practice intelligence tests, but this would be unlikely to benefit my general intellectual capacities (eg). While I am certain that this is a hotly-debated topic, I aware of very little evidence to suggest that any specific intervention would allow me to boost my overall level of intelligence. (Sorry, Bradley Cooper.)

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Deep brain stimulation for anorexia nervosa

Radiograph showing deep brain stimulation of the thalamus

Radiograph showing bilateral electrode implants into the striatum of a patient with Parkinson’s Disease. Credit: Hellerhoff (own work), via Wikimedia Commons (CC BY-SA 3.0).

In a recent issue of Nature Medicine, a leading pre-clinical experimental medicine journal, an article penned by Eric Nestler places the spotlight on recent trials which use DBS to treat severe cases of Anorexia Nervosa, whereas Jennifer Warner-Schmidt discusses future directions for this therapy based upon recent impressive studies in the animal literature. An implicit assumption of the discussion is that if DBS proves effective, it should be integrated into the broader framework for how we understand and treat mental illness.

But is DBS truly effective? This is a question more easily asked than answered.

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