The tape measure: a powerful predictive ‘instrument’ for mortality

More research recently published in the Archives of Internal Medicine further validates the power of waist circumference measurements to predict death from all causes. This study provides evidence that its accuracy is far superior to body mass index (BMI).

Waist circumference (WC), a measure of abdominal obesity, is associated with higher mortality independent of body mass index (BMI). Less is known about the association between WC and mortality within categories of BMI or for the very high levels of WC that are now common.”

The authors examined the association between WC and mortality among 48 500 men and 56 343 women between 1997 and 2006, during which 9315 men and 5332 women died. Considering the adverse metabolic and hormonal activity of visceral (intra-abdominal versus subcutaneous) fat, their data is not surprising:

“After adjustment for BMI and other risk factors, very high levels of WC were associated with an approximately 2-fold higher risk of mortality in men and women…The WC was positively associated with mortality within all categories of BMI.”

Very high levels of WC means 47 inches for men and 43 inches for women. Waist circumference is a more reliable indicator than weight or BMI. If you’re losing weight without your WC getting smaller, you’re probably losing more muscle than fat. As the authors state in their conclusion:

“These results emphasize the importance of WC as a risk factor for mortality in older adults, regardless of BMI.”

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Even modest visceral fat gain causes blood vessel dysfunction

An interesting study just published in the Journal of the American College of Cardiology offers evidence that even a modest amount of fat around your waist prevents blood vessels from dilating properly. But there is good news too. The authors refer to endothelial function (the endothelium is the inner lining of the blood vessel; it regulates constriction and dilation):

“The aim of this study was to determine the impact of fat gain and its distribution on endothelial function in lean healthy humans…Endothelial dysfunction has been identified as an independent predictor of cardiovascular events.”

Study subjects were assigned to either gain weight or maintain the same weight while a number of functional indicators were tracked along with body composition. The metric for endothelial function was brachial artery flow-mediated dilation [FMD]. The weight gainers then lost the added weight for the final measurements. What did the data show? First the bad news, then the good:

FMD decreased in fat gainers but recovered to baseline when subjects shed the gained weight.

Subcutaneous fat gain did not degrade endothelial function. The authors sum up their findings by concluding:

“In normal-weight healthy young subjects, modest fat gain results in impaired endothelial function, even in the absence of changes in blood pressure. Endothelial function recovers after weight loss. Increased visceral rather than subcutaneous fat predicts endothelial dysfunction.”

So ‘it’s not over until the fat lady loses the weight around her waist.’

Fructose even worse than glucose for fat and insulin

Journal of Clinical InvestigationThis is why the ubiquitous high-fructose corn syrup is such a disaster for public health. The authors of this study published in The Journal of Clinical Investigation note that “Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance.” When they examined the effect in humans they found that all the following were increased markedly in the subjects on fructose but not glucose: visceral adiposity (fat around the organs), plasma triglycerides, fat in the liver, small dense LDL, oxidized LDL, fasting glucose and fasting insulin. At the same time insulin sensitivity decreased in the subjects consuming fructose but not glucose. The authors conclude: “These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.” [DNL = de novo lipogenesis which means making fat from scratch in the liver.] An accompanying commentary in the same journal states: “In the event that any readers harbor some remaining skepticism, an unprecedented thorough analysis in close to 900,000 participants from almost 60 prospective studies was very recently published, proving beyond any possible doubt that progressive excess mortality is caused by increased body adiposity…Stanhope and colleagues provide major scientific progress by demonstrating marked differences in the metabolic effects of these two major sugars with respect to their ability to promote intraabdominal lipid deposition and hepatic lipid production, while shifting cholesterol metabolism in an unfavorable manner and diminishing insulin sensitivity in humans.” Public health is groaning under a burden of overweight/obesity; how much disease could we prevent just by cutting out most of the sweet drinks (including most fruit juices) for children and adults?