Regular readers will have followed the track of studies demonstrating that BMI is but a poor measure of health. This is why we came up with the Edmonton Obesity Staging System, that defines obesity based on the actual presence of physical, mental, and/or functional problems and limitations. Readers will recall, that we have previously shown that Obesity Stage – in contrast to BMI – is a powerful predictor of CV and all-cause mortality.
Now, yet another study, which looks at the relationship between BMI and mortality, again shows that ‘metabolically healthy’ obese individuals do not have an increased risk for CV mortality and in fact have a lower risk than ‘metabolically unhealthy’ non-obese individuals.
This study by Mark Hamer and Emmanuel Stamatakis from University College London, UK, published in the Journal of Clinical Endocrinology and Metabolism, looks at data from an observational study with prospective linkage to mortality records in community-dwelling adults from the general population in Scotland and England.
The sample includes 22,203 men and women [aged 54.1 y, 45.2% men] without known history of CVD at baseline followed for an average of about 7 years.
Based on blood pressure, high-density lipoprotein-cholesterol, diabetes diagnosis, waist circumference, and low-grade inflammation (C-reactive protein ≥ 3 mg/liter), participants were classified as metabolically healthy (0 or 1 metabolic abnormality) or unhealthy (two or more metabolic abnormalities). Obesity was defined as a body mass index of 30 or greater.
Compared with the metabolically healthy nonobese participants (about 20% of the obese population), their obese counterparts were not at elevated risk of CVD or all cause mortality.
On the other hand, both non-obese and obese participants with two or more metabolic abnormalities were at elevated risk.
Not surprisingly, metabolically unhealthy obese participants were at elevated risk of all-cause mortality compared with their metabolically healthy obese counterparts.
These data fit nicely with our findings using the obesity staging system. Thus, in our studies of the NHANES and Cooper Longitudinal Fitness Study, we found that Stage 0 and 1 obese individual (i.e. those with no or pre-clinical risk factors) did not have an increase risk compared to Stage 2+ individuals (those with comorbidities and/or endorgan damage).
Consistent with the present study, we also found that about 50% of non-obese individuals (in the BMI 25-30 range), would in fact fall into the Stage 2+ categories based on metabolic or other abnormalities.
Thus, simply using BMI as an indication for treatment would ‘over treat’ a substantial number of ‘obese’ individuals while missing an even greater number of ‘non-obese’ individuals, who are at risk.
As pointed out in an accompanying editorial by JP Després,
“Thus, obesity assessed by the BMI cannot properly estimate CVD and all-cause mortality risk. Furthermore, the therapeutic objective of achieving a normal BMI to prevent/manage cardiometabolic diseases may also be questioned on the basis of the emerging evidence…..The study by Hamer and Stamatakis provides robust evidence that a paradigm shift is needed: obesity can no longer be assessed the old-fashioned way.”
This is why the 5As of Obesity Management recommend the assessment of Obesity Stage in addition to BMI prior to giving patients any advice on managing their weight.
AMS
Edmonton, Alberta
Hamer M, & Stamatakis E (2012). Metabolically healthy obesity and risk of all-cause and cardiovascular disease mortality. The Journal of clinical endocrinology and metabolism, 97 (7), 2482-8 PMID: 22508708
Després JP (2012). What is “metabolically healthy obesity”?: from epidemiology to pathophysiological insights. The Journal of clinical endocrinology and metabolism, 97 (7), 2283-5 PMID: 22774209.
In The News
July 20th, 2012 at 7:58 am
BMI is nonsense.
July 20th, 2012 at 8:46 am
From: Chaldakov et al.
Adipoparacrinology: an Emerging Field in Biomedical Research.
Balkan Med J 2012; 29: 2-9 • DOI: 10.5152/balkanmedj.2012.022
Until recently, physicians have looked upon obesity as an
accumulation of external adipose tissue (subcutaneous and
abdominal). This was routinely evaluated by anthropometric
measurements including BMI and waist, hip and, recently,
neck circumference. However, recent data using non-invasive
imaging, such as echography, computed tomography, MRI
and positron emission tomography, reveal a new picture of
adipotopography (fat mapping). We should therefore focus
our attention not only on anthropometric values of external
adipose tissue, but – more importantly – the “weight” of internal,
organ-associated adipose tissue, including PAAT/tunica
adiposa. Thin outside, fat inside (TOFI) and other phenotypes
of WAT distribution are illustrated in Table 5. A predictive
message of adipoparacrinology therefore might be that “being
thin does not automatically mean you are not fat”, quoting
Dr Jimmy Bell, Head of Molecular Imaging Group at Hammersmith
Hospital, London, UK, the Master of fat mapping (64).
Table 5. Adipotopography (fat mapping): variations+
___________________________________________________________________
TOFI** thin outside, fat inside
TOTI***** thin outside, thin inside
FOFI* fat outside, fat inside
FOTI** fat outside, thin inside
_____________________________________________________________________
+The number of asterisks indicates the quality of cardiometabolic health, as related
to adipose tissue distribution. Thus, TOTI represents a highest quality and FOFI–the lowest. From Rančič et al (81)