Tag Archives: obesity

Which Cancers Are Linked to Obesity?

American Institute for Cancer Research has the list along with a helpful article.  You’d think that a person moving from obese down to overweight or normal weight would reduce future cancer risk, but I’m not sure that’s ever been proven.  We’ve learned in the last decade that obese and overweight patients with heart disease seem to live longer if they stay overweight – an example of the obesity paradox.

Why Do Obese People Have More Asthma?

It may be related to leptin, a hormone produced by fat cells (adipocytes).  ScienceDaily has all the details, most pertinent of which is that the study at hand was done in mice.  So not ready for prime time (humans).  Some of the sickest asthmatics I’ve cared for have been morbidly obese.

Is Fructose the Cause of Our Obesity Epidemic?

Mainly because of its low cost, HFCS [high fructose corn syrup] consumption replaced approximately one-third of the total sugar consumption in the USA between 1970 and 2000, paralleling to some extent the increasing prevalence of obesity during this period. Consequently, HFCS has been a particular focus of possible blame for the obesity epidemic. However, HFCS consumption has remained very low in other parts of the world where obesity has also increased, and the most commonly used form of HFCS contains about 55% fructose, 42% glucose, and 3% other sugars, and hence is associated with similar total fructose and glucose intakes as with sugar. Furthermore, sucrose is hydrolyzed in the gut and absorbed into the blood as free glucose and fructose, so one would expect HFCS and sucrose to have the same metabolic consequences. In short, there is currently no evidence to support the hypothesis that HFCS makes a significant contribution to metabolic disease independently of the rise in total fructose consumption.

Given the substantial consumption of fructose in our diet, mainly from sweetened beverages, sweet snacks, and cereal products with added sugar, and the fact that fructose is an entirely dispensable nutrient, it appears sound to limit consumption of sugar as part of any weight loss program and in individuals at high risk of developing metabolic diseases. There is no evidence, however, that fructose is the sole, or even the main factor in the development of these diseases…

— Luc Tappy in BMC Biology, May 21, 2012 (the article is a review of fructose metabolism and potential adverse effects of high consumption)

PS: Luc Tappy believes that excessive calorie consumption is an important cause of overweight and obesity.

Steve Parker, M.D.

For Weight Loss, What’s More Important: Exercise or Food?

This is NOT diet food

What you eat, and how much, are more important than your physical activity.  By far.

  • Your genetics largely determines your response to an exercise program
  • Physical activity isn’t a great way to lose weight
  • School-based or other programs to increase childhood physical activity probably won’t reverse childhood obesity statistics
  • Disregarding weight loss, exercise has other worthwhile metabolic advantages
  • Highly advanced societies shouldn’t blame our overweight problem on decreased levels of physical activity

Skyler Tanner slaughters some sacred cows in his blog post June 4, 2012. I pulled these bullet points from his post. Click on his embedded links for details.

Steve Parker, M.D.

Are We Fat Because We Eat Too Much, Or Lack Physical Activity?

Are we fat because we eat too much, or lack physical activity?

Most people would say, “It’s both.” Most people would be wrong, at least in terms of populations rather than individuals.

Obesity results from a protracted imbalance between energy intake (calories we eat) and energy expenditure (physical activity and resting metabolism).

Overweight and obesity have increased significantly over the last 25 years in most of the developed world. Is it because we started eating more, or that we have so many energy-saving devices that we now expend less energy on physical activity? If we are less active due to technologic advances, yet keep eating as much as in the past, we will gain weight as the excess calories are stored as fat.

Technologic advances over the last 150 years have allowed us to transform from a labor-intensive agrarian economy to one based on services and information. Computers, in particular, have made it much less labor-intensive to get our jobs done. For example, when I was a hospital intern 30 years ago, I made multiple daily trips from the patient care floors downstairs to Radiology to look at x-ray films. Now, the “films” are at my fingertips on computers close to the bedside.

Have trends in technology over the last 25 years continued to reduced the energy expenditure needed to get through our days? Alternatively, are we exercising less? Either explanation would lead to weight gain if caloric intake remained the same.

Researchers in 2008 studied populations in Europe and North America, examining trends in physical activity energy expenditure over time, since the 1980s. Energy expenditure was evaluated with a highly accurate method called “doubly labelled water.” They found that physical activity energy expenditure actually increased over time, although not by much. They conclude that the ballooning waistlines in the study populations are likely to reflect excessive intake of calories.

(All I have is the abstract of the article. I’ll try to get the full article and report back here if anything additional is interesting.)

So according to Westerterp and Speakman, the problem has not been lack of physical activity. We’re simply eating too much.

On the other hand, a 2011 study found that daily work-related energy expenditure decreased by over 100 calories in the U.S. over the last 50 years.  That could certainly contribute to our expanding waistlines.

Steve Parker, M.D.

Reference: Westerterp, K.R., and Speakman, J.R. Physical activity energy expenditure has not declined since the 1980s and matches energy expenditures of wild mammals. International Journal of Obesity, 32 (2008): 1256-1263. Published online May 27, 2008. doi: 10.1038/ijo2008.74

Prostate Cancer Deaths Linked to Overweight and High Insulin Levels

Lancet Oncology in 2008 published a report associating worse prostate cancer outcomes—death, that is—with overweight, obesity, and hyperinsulinemia.

Grapes are an iconic Mediterranean fruit

Researchers looked at data from the respected Physicians’ Health Study, finding 2,546 men who developed prostate cancer during many years of observation. Of these men, 38.8% were overweight (body mass index 25–30) and 3.4% were obese (BMI over 30).

(For definitions of overweight and obesity, and to calculate your body mass index, click here.)

Compared with normal-weight men (BMI under 25) who developed prostate cancer, overweight men with prostate cancer were one-and-a-half times more likely to die from the cancer. Obese men with prostate cancer were two-and-a-half times more likely to die.

A blood test called C-peptide is a marker of insulin resistance and hyperinsulinemia. Obesity is often accompanied by high insulin levels and insulin resistance. Overweight, not so much. Eight hundred twenty-seven of the men with prostate cancer had C-peptide levels drawn at baseline, before diagnosed with cancer. Men with the highest C-peptide levels were almost two-and-a-half times more likely to die of prostate cancer than men with the lowest C-peptide levels.

Study participants having both excess body weight and high C-peptide levels had the worst outcome.

Prostate cancer is the most common invasive cancer in U.S. men, with about 185,000 cases diagnosed every year. It is one of the cancers that can be prevented by following the traditional Mediterranean diet for years. The other prevented cancers are breast, uterus, and colorectal. Obesity predisposes men to cancer of the prostate, colon, rectum, kidney, and esophagus.

The study at hand suggests that if you are overweight or obese and then develop prostate cancer, you have a greater risk of dying from the cancer compared with healthy-weight men. Given that prostate cancer is so common, why not cut your risk of getting it and dying from it by controlling your weight with a Mediterranean-style diet?

Steve Parker, M.D.

Reference: Ma, Jing, et al. Prediagnostic body mass index, plasma C-peptide concentration, and prostate cancer-specific mortality in men with prostate cancer: a long-term survival analysis. Lancet Oncology, online publication October 6, 2008. DOI: 10.1016/S1470-2045(08)70235-3

Are We Fat Because We’re Less Active Now?

Less active

Much of the globe has seen a significant decline in populaton-wide physical activity over the last few decades, according to Nike-sponsored research reported in Obesity Reviews.

Countries involved with the study are the U.S., U.K., Brazil, China, and India.  How did they measure activity levels?

Using detailed historical data on time allocation, occupational distributions, energy expenditures data by activity, and time-varying measures of metabolic equivalents of task (MET) for activities when available, we measure historical and current MET by four major PA domains (occupation, home production, travel and active leisure) and sedentary time among adults (>18 years).

The authors note the work of Church, et al, who found decreased work-related activity in the U.S. over the last half of the 20th century.

Inexplicably, they don’t mention the work of Westerterp and colleagues who found no decrease in energy expenditure in North American and European populations since the 1980s.

More active

My gut feeling is that advanced populations around the globe probably are burning fewer calories by physical activity over the last 50 years, if not longer, thanks to technologic advances.  We in the U.S. are also eating more calories lately.  Since the 1970s, average daily consumption by women is up by 150 calories, and up 300 by men.  Considering both these trends together, how could we not be fat?

Steve Parker, M.D. 

Fat Cell Turnover: Implications for Weight Loss

The number of fat cells in our bodies is constant throughout adult life for both lean and overweight people. When adults gain fat weight, it’s because our individual fat cells store more fat, thereby enlarging. We don’t gain more fat cells. Conversely, when we lose weight, the fat cells shrink.

Our number of fat cells is set during childhood and adolescence. Lean individuals generally have fewer fat cells than overweight people.

In many living tissues, individual cells gradually die off and are replaced by new cells. For example, we shed dead skin cells all the time, but they are replaced just as quickly by new skin cells. A red blood cell lives three months then dies and is replaced. The percentage of cells that die and are replaced over a period of time is called “turnover.”

Researchers in Stockholm recently studied the turnover of fat cells in humans. They measured turnover by analysing the incorporation of carbon-14 derived from nuclear bomb tests in genomic DNA. They found that 10% of fat cells die off and are renewed yearly at all adult ages in both skinny and overweight people.

So what?

Well, if 10% of your fat cells die every year, what if you could prevent them from being replaced with new ones? You would lose weight, as long as your remaining fat cells didn’t swell with more stored fat. Next year, another 10% of your fat cells die, and so on.

How can we prevent dead fat cells from being replaced by new ones? Nobody knows . . . yet. You can bet that pharmaceutical companies are thinking about this.

But I wouldn’t hold my breath. Pharmaceutical intervention will not be available for at least eight to 10 years, if ever.

We already have available, in 2009, a tried and true method for reducing fat mass: Eat Less, Move More.

Steve Parker, M.D.

Reference: Spalding, K.L., et al. Dynamics of fat cell turnover in humans. Nature, 453 (2008): 783-787. Epub May 4, 2008. PMID: 18454136.

Yet Another Epidemic: Fatty Liver In Teens

MedPage Today on May 25, 2012 has an article documenting the rise of fatty liver disease in U.S. teenagers.  Prevalence is now up to one in 10 teens.

An expert quoted in the article says it’s tied in with the rise of childhood obesity.

Youth obesity in the U.S. tripled from the early 1980s to 2000, ending with a 17% obesity rate. Overweight and obesity together describe 32% of U.S. children. Some experts believe this generation of kids will be the first in U.S. history to suffer a decline in life expectancy, related to obesity.

I wrote about a small research study that found a very-low-carb diet more effective against fatty liver, compared to a low-calorie diet.  But that involved adults.

University of Colorado researchers indicate that for weight loss, a low-carb, high-protein diet is safe and effective in adolescents.

Diet researchers found in 2008 that a modified low-carbohydrate Mediterranean diet had significant potential to reduce fatty liver.  My Low-Carb Mediterranean Diet (minus the wine option) would probably help overweight teens with fatty liver disease, but it’s never been tested in such a clinical trial.

Steve Parker, M.D.

Is a Low-Carb Diet Safe for Obese Adolescents?

I answered this question last year at the Diabetic Mediterranean Diet Blog, based on research from the Department of Pediatrics, University of Colorado.

It’s an important question. Childhood obesity in the U.S. tripled from the early 1980s to 2000, ending with a 17% obesity rate. Overweight and obesity together describe 32% of U.S. children. Some experts believe this generation of kids will be the first in U.S. history to suffer a decline in life expectancy, related to obesity.

Steve Parker, M.D.