With all the talk about obesity as a risk factor for diabetes and heart disease, we may often forget that excess weight affects all organ systems.

One set of organs that appears particularly sensitive to the ill-effects of excess weight are the kidneys.

This is nicely illustrated in a study just published in the American Journal of Kidney Disease by John Munkhaugen and colleagues from the Norwegian University of Science and Technology, Trondheim, Norway.

The researchers examined the combined effect of blood pressure (BP) and body weight on the risk for end-stage renal disease or chronic kidney disease (CKD)-related death.

Participants included data from 74,986 adults of the first Health Study in Nord-Trøndelag (88% participation rate), which were linked to the Norwegian Renal Registry and Cause of Death Registry.

During a median follow-up of 21 years (1,345,882 person-years), 507 men (1.4%) and 319 women (0.8%) initiated renal replacement therapy (n = 157) or died of CKD (n = 669).

The risk associated with body weight started to increase from a BMI of 25.0, but this increased risk was not seen in participants with BP less than 120/80 mm Hg.

In contrast, in participants with even moderately increased BP (pre-hypertension or hypertension), there was a progressive increase in the risk for kidney disease with increasing BMI suggesting an almost 6-fold increased risk in participants with a BMI greater than 35.

The study strongly suggests that individuals with a BMI greater than 30 are increasingly vulnerable to kidney disease even with a modest increase in blood pressure.

This finding has several important clinical implications:

1) Blood pressure should be carefully monitored in all individuals with BMI greater than 30.

2) Even moderately elevated blood pressure (pre-hypertension) should be addressed with lifestyle and, if necessary, pharmacological treatment in obese individuals.

3) Blood pressure treatment targets in obese patients may need to be similar to targets in patients with diabetes (i.e. below 130/80 mm Hg).

AMS
Edmonton, Alberta

Regular readers are certainly familiar with my many posts on the limitations of BMI and on the idea that not all fat is bad and that different fat depots may have quite different effects on cardiometabolic risk.

You can now find much more on this topic in a comprehensive review article by Konstantinos Manolopoulos and colleagues at Oxford University, UK, published in this month’s issue of the International Journal of Obesity.

The review not only concludes that there is now ample evidence to support the notion that not just the amount of body fat, but rather its distribution is an important determinant of the metabolic and cardiovascular risk associated with obesity. In fact there is now increasing evidence that being too skinny may well be bad for you and that carrying a few extra pounds of fat on your hips and thighs may actually be protective.

Thus, studies show that increased hip and thigh fat is independently associated with protective lipid and glucose profiles. This protective effect may be in part due to the fact that gluteofemoral fat can absorb and store excess fatty-acids, thereby removing them from the circulation. In addition, leptin and adiponectin levels tend to be positively associated with gluteofemoral fat while the level of inflammatory cytokines is negatively associated.

As the authors point out, the loss of gluteofemoral fat, as observed in Cushing’s syndrome and lipodystrophy is in fact associated with an increased metabolic and cardiovascular risk.

This may not be good news for people seeking medical help to reduce the size of their hips and thighs - I would probably have to advise them against it - definitely not a message many of my patients want to hear.

On the other hand, if the excess fat is largely located around your midsection, then, this excess “belly” fat is probably the biggest driver of your risk for type 2 diabetes and heart disease.

So really, not much new for regular readers of my blog, but certainly a noteworthy article that nicely summarizes what is currently known about this issue.

Wonder what it’ll take to make large butts and thighs more socially acceptable?

AMS
Edmonton, Alberta

Recently, I blogged about Jennifer Kuk’s study showing that even so called “metabolically healthy” obese folks may have an increased risk of premature death. This study certainly supported the notion that the term “healthy obese” may well be an oxymoron.

Now, a new study Johan Ärnlöv and colleagues from Uppsala University, Sweden, published online in Circulation, provides further support for the idea that obesity may still kill you even if you have no other apparent metabolic risk factors.

The researchers looked at deaths in 1758 fifty-year old male participants without diabetes in the community-based Uppsala Longitudinal Study of Adult Men (ULSAM).

After adjustment for age, smoking, and LDL cholesterol, as expected, an increased risk for cardiovascular disease was observed in normal-weight (hazard ratio 1.63), overweight (HR 1.74), and obese (HR 2.55) participants with metabolic syndrome (MetS).

However, even in participants without MetS, overweight (HR 1.52) and obesity (HR 1.92) were associated with a significantly greater risk for cardiovascular disease.

Thus, as in the previous study by Kuk and colleagues, it again appears that excess weight is a significant predictor of heart disease even in people who appear to be metabolically healthy.

Clearly, taken together, these studies challenge the notion of so-called “healthy” or “benign” obesity.

What does this mean for clinical practice and weight-loss recommendations?

As blogged before, unfortunately losing weight and keeping it off is by no means easy and most people will tend to regain any weight they lose. For this reason alone, prevention of further weight gain is a far more achievable and realistic goal than losing weight and keeping it off.

For practical reasons, I have therefore previously recommended that we focus our expensive and limited weight-loss treatments on people with apparent obesity related complications (EOSS Stage 2 and 3). 

But let us not kid ourselves into believing that excess weight can be a benign condition and that simply continuing to gain weight can be OK as long as medical check ups show no sign of obesity-related illness.

It is always the right time to stop the gain!

AMS
Edmonton, Alberta

A few weeks ago, while attending the American Heart Association meeting in Orlando, I met with my friend and colleague Steven Smith, who has just taken on the position of Executive Director of the Translational Research Institute for Metabolism and Diabetes, Florida Hospital and Burnham Institute.

This week, Steven penned a most interesting essay for the New England Journal of Medicine, in which he discusses potential downsides of a low-carb diet. Most of his argument is based on a recent study that showed progresson of artherosclerotic plaques with a low-carb diet in apolipoprotein E-deficient mice, a model commonly used to study arteriosclerosis.

It turns out that the same article was recently also discussed on OBESITY PANACEA, an obesity blog run by Peter Janiszewski and Travis Saunders, two PhD students, who work in obesity research and are very active members of the Canadian Obesity Network.

As they point out, the two key possibilities that Steven presents in his article are that increased level of free fatty acids in the blood (released from insulin resistant fat cells and implicated in the initiation of inflammatory processes) or a reduced level of circulating endothelial progenitor cells (produced in bone marrow and help maintain the health of the blood vessels), both possible effects of a low-carb diet, could explain these detrimental effects, but I will leave it to OBESITY PANACEA to explain…

AMS
Toronto, Canada

Over the past 15 years, smoking rates in the US have declined by 20%, whereas obesity rates have increased by 48%.

A new analysis published in the New England Journal of Medicine by Susan Stewart and colleagues from Harvard University, Boston, MA, forecasts the effect of trends in obesity and smoking on future U.S. life expectancy and quality-adjusted life expectancy.

The researchers used data from the past three decades to forecast future rates of obesity and smoking and estimate their effects on length and quality of life.

The net effect of the declines in smoking and the increases in BMI for an 18-year old is a reduction in life expectancy of 0.71 years and a reduction in quality-adjusted life expectancy of 0.91 years relative to the trend. This pattern of results is seen for every year between 2005 and 2020 and becomes more pronounced over time.

The calculations assume that if past trends continue, almost half the U.S. adult population will meet the WHO criteria for obesity by 2020 (currently the obesity rate already exceeds 35% in some states).

Obviously, these forecasts are at a population level and do not apply to a particular person who loses weight or stops smoking.

While these results do not imply that life expectancy will fall, they do suggest that as a result of increasing obesity rates life expectancy will rise less rapidly than it otherwise would.

While these are US data, there is little reason to assume that similar trends will not also be apparent in other countries including Canada.

Clearly, policy makers will likely now need to address obesity with the same vehemence as they did smoking - unfortunately, finding and implementing effective policies to reduce obesity makes smoking bans look like a walk in the park (no pun intended).

AMS
Edmonton, Alberta