Tuesday, January 15, 2013

Is it really healthier to be a few pounds overweight? That’s not what the study says.

Source: Wikimedia Commons

by Jennifer Gunter, MD, FRCS(C), FACOG, DABPM
[This post first appeared at Dr. Gunter's blog, where she wields the lasso of truth.]

A new study published in the Journal of the American Medical Association (JAMA) indicates that a body mass index or BMI of 25-29.9 (overweight) is associated with the lowest risk of death and that class 1 obesity (BMI 30-34.9) is not associated with an increased risk of mortality. As this study hit the presses January 2nd (and I’m sure no editorial thought was given by JAMA to such a study coming out at the first of the year) when many people are thinking about weight loss resolutions, it was covered widely in the press and I read several op-eds claiming vindication for obesity. One op-ed on a major news site was indignant that CT scanners couldn’t accommodate a friend (some CT scanners have difficulty accommodating patients over 300 lbs). The author’s solution? Build bigger CT scanners because obesity isn’t bad at all. This new study proves it.

My answer? Back the truck up.

First of all the study doesn’t say that being overweight is good for you and that being an ideal weight is bad. What the study does tell us is that people who have a BMI of 35 or greater are more likely to die. This is not new information. A BMI of 35 is a lot of extra weight, depending on your height it could easily mean 70 extra pounds or more.15% of Americans have a BMI of 35 or greater.Only people with a BMI over 35, way over 35, need bigger CT scanners. I’m not saying that severely obese people shouldn’t have access to imaging studies, but the answer to the epidemic of severe obesity is not to claim vindication based on the inaccurate interpretation of one study and simply build bigger equipment.

What about the lower risk of death in the overweight and class 1 obesity groups compared with the normal BMI group? Well, this can be explained by a variety of factors:
  • The wrong control group. Many researchers question whether the control group should really be a BMI of 22-24.9, not the wider range of 18.5-24.9 used in this study. The reason, many people at the thinner end of the scale are thin because of illness and this obviously skews mortality statistics.
  • BMI is an imperfect tool with which to predict mortality when the result isn’t one extreme (< 18.5) or the other (>34.9). This is not a new finding. BMI just looks at weight, not the proportion of weight that is muscle mass vs. fatty tissue. Many people with a normal BMI have very little muscle mass and thus are carrying around excess fat and are less healthy than their BMI suggests. There are better metrics to look at mortality risk for people who have a BMI in the 18.5-34.9 range, such as waist circumference, resting heart rate, fasting glucose, leptin levels, and even DXA scans (just to name a few). The problem is that not all these measurement tools are practical on a large-scale.
  • A small amount of fat may provide an extra energy reserve for someone who becomes chronically ill, thus skewing the survival stats. For example, consider the dramatic weight loss associated with chemo…if you can’t eat due to extreme nausea and you have a little extra fat then you burn fat, but if you have no fat and can’t eat then you start breaking down muscle. This is a phenomenon has popped up in a few studies and definitely requires more research, because obesity is definitely associated with worse outcomes in many cancers.
  • Not all fat is created equal. Belly fat, the metabolically active muffin top, is what contributes to diabetes and other inflammatory conditions. Having a few extra pounds around the middle is far worse than having a few extra pounds on the hips. Again, not new information. BMI doesn’t distinguish between belly fat and thigh fat.
What is very important is that we don’t take erroneous messages from this study (hello, health reporters for major news outlets looking for attention-grabbing headlines). This study says nothing more than we need better tools than BMI to assess mortality risk for people who have a body mass index between 18.5 and 34.9 and that BMI doesn’t predict “ideal weight,” it only tells us that extremes are bad. This study also confirms that the 15% of Americans with a BMI of 35 are at increased risk of dying prematurely, a point sadly missed by many.

Body mass index simply doesn’t convey enough information to assess mortality risk for 85% of the population, but that fact (which isn’t new) shouldn’t stop each and every one of us from striving everyday to be the healthiest that we can be.

And with that, I’m off for my run.

Dr. Jennifer Gunter is an OB/GYN and a pain medicine physician who has authored the book,The Preemie Primer, a guide for parents of premature babies. In addition to her academic publications, her writing has appeared in USA Today, the A Cup of Comfort series, KevinMD.comEmpowHer.comExceptional ParentParents PressSacramento Parent, and the Marin Independent Journal.


  1. Fat isn't a storage unit it's an endocrine organ and being the healthiest you can be involves understanding that it is not a storage unit and its size is a highly heritable trait that shouldn't be messed with.

    Also, I'm not a fan of point form that dismisses a peer-reviewed paper with no clinical trial data to back up the points made.

    Many have attempted to dismiss Flegal and her colleagues' careful and systematic review, over the past 7 years, of the NHANES data on the (incorrect) assumption that somehow the cohorts were not sufficiently screened for pre-existing conditions, but it hasn't held up on scrutiny.

    And in fact the entire body of Flegal and her colleagues' work does indeed show that there are some 87,000 fewer deaths than expected for those BMI 25-30 and that's pretty irrefutable however you might like to pick apart the science.

    It's all well and good to suggest that BMI is an imperfect measuring tool, and it is, however that only tends to be used as the convenient "get-out clause" when the results are unsavoury to the author. There is indeed no such thing as an ideal or healthy BMI range, you have a healthy weight set point for you. The BMI bell curve simply displays the averages and 70% of all women will naturally fall between BMI 21-27.

    We know that obesity onset and the presence of obesity are not tied to food intake or activity levels [W. Kulesza, 1982; JA Baecke et al., 1983; RJ Myers et al., 1988; ML Johnson et al., 1956; L Lissner et al., 1989; AM Prentice et al., 1986; R Jeffrey et. al. 2006; P Togo et. al., 2001; J Holsten, 2009; J Couzin, 2005; MA Grediagin et. al., 1995; BS Metcalf et. al., 2011; JS Speakman et. al., 2006 and H Pontzer et. al., 2012 ].

    I certainly agree that the 15% of Americans beyond BMI 35 who are at increased risk of dying prematurely might deserve attention, but perhaps we might want to turn our attention to the worrisome overlap of SES/exposure to endocrine disruptors in hygiene and home products/genetic predispositions/sleep deprivation and stress rather than the thoroughly trounced concepts of exercise and diet as any way to treat inflammatory obesity (although exercise will improve health markers, it does not lower weight appreciably -- G. Gaesser's body of work a good starting point for data on that).

    And that brings me to the final point: there is a distinct difference between being naturally BMI 35+ and developing that weight through the onset of inflammatory obesity which involves concurrent metabolic chronic conditions (diabetes, etc. etc.). Between 5-11% of the population actually has inflammatory obesity that may predispose them to early death [KM Flegal et. al., 2005] and mortality for diabetes is still lower in the obese than 'normal' weighted individuals [A Jerant, P Franks, 2012].

  2. Hi Gwyneth:

    Thanks for your comment. I would like to make a few clarifications, but would like to come out first saying that I have trained as a metabolic biologist for over a decade, specializing in cellular fat synthesis and storage. While my research has focused primarily on basic science, I am also able to comment on some clinical aspects of fat metabolism.

    My first clarification is a response to your opening point about fat being an endocrine organ. This is actually not quite accurate - "fat" is a type of molecule. In the case of obesity, the major fat storage molecule is triacylglycerol (also known as triglycerides, and abbreviated TG), which is largely stored in specialized cells called adipocytes (there are also cells in the liver that can store TG, but their capacity is much more finite). The endocrine function to which you are referring actually pertains to the property of the adipocyte cell/tissue itself, though this can be influenced by the amount of TG found in the adipocyte cell.

    As for heritability - there are certainly some genetic predispositions to obesity, but we cannot at all dismiss the incredible effects of the environment.

    As for the post itself, I agree with Jen's interpretation of the JAMA study cited (also note, this is the study that is being scrutinized, not others). In the specific JAMA article being discussed, the range for "normal" is cited in their methods, and is 18.5-<25. Her arguments against using this range are definitely valid.

    I also agree that using BMI as predictor of mortality is a flawed strategy, and this argument is, by no means a "get out" clause. Because BMI does not take into account the ratio of adipose to non-adipose tissue, we have no real way of telling how much fat is related to the weight. Someone who is an athlete (high proportion of muscle) but weighs in at 225 pounds is certainly not at the same risk as someone a 225 pound person with a high proportion of fat. I don't think we need to cite clinical data to suport this discrepancy as it is common sense.

    Also, I can't disagree with you more regarding the notion that obesity is not tied to food intake/activity levels (it is as simple as going to NIH for this: http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0004552/). Diet and exercise play a HUGE factor in how much someone weighs, regardless of genetics. Though, I will say that the physiology of obesity and related maladies is extremely complicated, and we are still working to uncover how genetics, epigenetics, and environment dictate this condition.

    Also, because of the nature of adipose tissue and their ability to secrete inflammatory factors (TNF-alpha, interleukins, etc), it is certainly valid to make a point that obesity is a condition of chronic mild inflammation, but, again, this is only a small part of the pathophysiology of obesity.

    And, to your last point, as a person who spent their PhD research studying lipotoxicity (cell death from fat overload), there is way more to the story than inflammation regarding the development of diabetes, etc. etc.

    -Jeanne (biology editor)