You Can't Blame the Obese and the Smokers For Everything

With all this talk of banning the corpulently gifted from eating in public; flying on airplanes; riding on amusements; boating in Disney, etc. and banning the smokers from existing at all, we should keep in mind that both groups keep cost down. We cannot blame our rounder or our oxygen challenged citizens for increasing health care expenditures nor can we blame them for the senior citizen population exploding beyond our capability to take care of them. Nope, we can blame our vain, fitness-obsessed, self-disciplined, population who want to live forever.

It is true, until the age of 56-years old, annual health expenditure is highest for obese people. At older ages, smokers incurred higher costs. However, because of lower life expectancy, lifetime health expenditure was highest among healthy-living people and lowest for smokers. The "More-to-Love" category held an intermediate position.

Although obesity prevention leads to a decrease in costs of obesity-related diseases, this decrease is offset by cost increases due to diseases unrelated to obesity in the people who are in constant search for the fountain of youth. Obesity prevention and eliminating those who like to inhale may be an important to improving the quality of live, but it is not a cure for increasing health expenditures.

Here's another interesting study about climate change, sex ratio and longevity.

The theory that natural selection has conserved mechanisms by which women subjected to environmental stressors abort frail male fetuses implies that climate change may affect sex ratio at birth and male longevity. Using time series methods, we find that cold ambient temperatures during gestation predict lower secondary sex ratios and longer life span of males in annual birth cohorts composed of Danes, Finns, Norwegians, and Swedes born between 1878 (earliest year with complete life tables) and 1914 (last birth cohort for which male life span can be estimated). We conclude that ambient temperature affects the characteristics of human populations by influencing who survives gestation, a heretofore unrecognized effect of climate on humanity.

Read more...

Rankings of World's Major Economies by Topic

The Economist provides rankings from Rankings from the Pocket World in Figures on over 200 topics and statistical profiles of more than 65 of the world’s major economies.

Including:

Biggest Coffee Producers

Biggest Economies

Change in Population

Cigarette Consumption

Computer Ownership

Current Account, Biggest Deficit

Current Account, Largest Surplus

Highest Car Ownership

Highest Forested Area

Highest Life Expectancy

Highest Obesity

Highest Office Rent

Higest Purchasing Power

Largest Population

Largest Stock Market Capitalization

Lowest Life Expectancy

Population per doctor

Read more...

Bone Cells Affect How Much You Weigh

The skeleton affects energy metabolism.

If your blood glucose is out of whack, the problem may be in your bones. Research in mice shows that bone cells exert a surprising influence on  how the body regulates sugar, energy, and fat. The discovery could lead to new ways to treat type-two diabetes, a disease involving poor regulation of blood glucose. It also means that skeletons act as endocrine organs, which affect other body tissues by releasing hormones into the bloodstream.

The team announcing the finding, led by Gerard Karsenty of Columbia University, had previously found that fat cells secrete a hormone that influences bone-forming cells called osteoblasts. Because hormone regulation between two cell types is often reciprocal, Karsenty and his  team reasoned that osteoblasts might also be emitting hormones that control fat tissue. Osteoblasts make bone throughout a healthy person's lifetime,  while cells called osteoclasts tear down bone processes that constantly remodel the skeleton. Osteocalcin, a somewhat enigmatic protein produced  only by osteoblasts, seemed like a good hormone candidate, Karsenty says.

"[It] has been the flagship molecule of the [bone-research] field for 30 years, but nobody knew what it was doing." -- Gerard Karsenty

Karsenty's team fed a normal diet to mice engineered to lack the gene for osteocalcin. The mice became  obese and had low blood concentrations of insulin, a key hormone for controlling blood glucose. The animals also had poor sensitivity to insulin, a hallmark of people with diabetes. Another group of mice, which had been engineered to have extra osteocalcin, stayed thin despite being fed a high-calorie diet. These animals also maintained higher insulin concentrations and better sensitivity to insulin than the mice lacking osteocalcin did, the team reports in the Aug. 10 Cell. Further tests on mice showed that osteocalcin causes the insulin-making cells in the pancreas to proliferate and ramp up insulin production. The bone protein also causes fat cells to store less fat and to secrete a hormone called adiponectin. In people as well as in mice, this substance improves cells' sensitivity to insulin. Previous research has shown that many people with type 2 diabetes have low blood concentrations of osteocalcin. "Osteocalcin, if everything goes well, could be a treatment for type 2 diabetes. That's where the excitement is," Karsenty says.

"This could also have important ramifications for cardiovascular disease because of the effect on metabolic syndrome," a condition related to diabetes, comments Dana T. Graves of Boston University. "The fact that bone cells regulate energy metabolism, and that they do it through osteocalcin, is a major finding," he saysIt is already known that fat cells secrete a hormone that affect bone cell growth and because the hormone secreting process is often a reciprocal process, Gerard Karsenty of Columbia University assumed that the bone cells may be secreting hormone(s) that affect fat cells or fat tissue and he was right.

Read more...

Obesity Cured by Antibiotics??

Dec. 20, 2006 -- A link between obesity and the microbial communities living in our guts is suggested by new research at Washington University School of Medicine in St. Louis. The findings indicate that our gut microbes are biomarkers, mediators and potential therapeutic targets in the war against the worldwide obesity epidemic.

In two studies published this week in the journal Nature, the scientists report that the relative abundance of two of the most common groups of gut bacteria is altered in both obese humans and mice. By sequencing the genes present in gut microbial communities of obese and lean mice, and by observing the effects of transplanting these communities into germ-free mice, the researchers showed that the obese microbial community has an increased capacity to harvest calories from the diet.

"The amount of calories you consume by eating, and the amount of calories you expend by exercising are key determinants of your tendency to be obese or lean," says lead investigator Jeffrey Gordon, M.D., director of the Center for Genome Sciences and the Dr. Robert J. Glaser Distinguished University Professor. "Our studies imply that differences in our gut microbial ecology may determine how many calories we are able to extract and absorb from our diet and deposit in our fat cells."

That is, not every bowl of cereal may yield the same number calories for each person. People could extract slightly more or slightly less energy from a serving depending upon their collection of gut microbes. "The differences don't have to be great, but over the course of a year the effects can add up," Gordon says.

Trillions of friendly microbes reside in the intestine, where they help to digest food that the body can't on its own, such as the complex sugars found in grains, fruits and vegetables. As part of the digestive process, the microbes break down nutrients to extract calories that can be stored as fat.

The researchers focused on two major groups of bacteria - the Bacteroidetes and the Firmicutes - that together make up more than 90 percent of microbes found in the intestines of mice and humans. In an earlier study, they compared genetically obese mice and their lean littermates. The obese mice had 50 percent fewer Bacteroidetes and proportionately more Firmicutes. Moreover, the differences were not due to a bloom of one species in the Firmicutes or a diminution of a single or a few species of Bacteroidetes: virtually all members of each group were altered.

In one of this week's Nature articles, Ruth Ley, Ph.D., a microbial ecologist in Gordon's group, reports on her investigation into whether these findings also held true among obese humans. She followed 12 obese patients at a Washington University weight loss clinic over a one-year period. Half the patients were on a low-calorie, low-fat diet and half were on a low-calorie, low carbohydrate diet.

At the outset of the study, the obese patients had the same type of depletion of Bacteroidetes and relative enhancement of Firmicutes as the obese mice. As the patients lost weight, the abundance of the Bacteroidetes increased and the abundance of Firmicutes decreased, irrespective of the diet they were on. Moreover, not one particular species of Bacteroidetes but the entire group increased as patients lost weight.

In a companion paper in the same journal, Peter Turnbaugh, a Ph.D. student in Gordon's lab, compared the genes present in the gut microbial communities of the obese and lean mice using the newest generation of massively parallel DNA sequencers.

The results of these so-called comparative metagenomic studies revealed that the obese animals' microbial community genome (microbiome) had a greater capacity to digest polysaccharides, or complex carbohydrates. By transferring the gut microbial communities of obese and lean mice to mice that had been raised in a sterile environment (germ-free animals), he confirmed that the obese microbial community prompted a significantly greater gain in fat in the recipients.

Gordon notes that these findings represent steps in a long journey designed to understand the contributions of our microbial self to our health. "Our microbial cells outnumber our human cells by as much as 10 fold and, and they may contain 100 times more genes than our own human genome," Gordon says.

These studies raise a number of questions, according to Gordon. "Are some adults predisposed to obesity because they 'start out' with fewer Bacteroidetes and more Firmicutes in their guts?" he asks. "Can features of a reduced Bacteroidetes-Firmicutes enriched microbial community become part of our definition of an obese state or a diagnostic marker for an increased risk for obesity? And can we intentionally manipulate our gut microbial communities in safe and beneficial ways to regulate energy balance?"

Read more...