BLACKS ARE FATTER AND MALE DROPOUTS ARE FATTER

The article below is a bit hard to follow and its political correctness does not help. IQ was of course not examined but I think that "Males with a disadvantaged background who experienced early transitions into the labor force" can be decoded in one word as "dropouts" -- and they were found to be fatter. And blacks were found to be fatter too, perhaps reflecting that many of them are dropouts. Why an early dropout from education is asssociated with being overweight one can only speculate but it would appear consistent with the usual finding that high IQ people have better biological functioning generally. So low IQ people may have worse functioning even in trivial ways

Obesity, Race/ethnicity and Life Course Socioeconomic Status across the Transition from Adolescence to Adulthood

By Melissa Scharoun-Lee et al.

Background: Differences in the association of socioeconomic status (SES) with obesity may underlie racial/ethnic disparities in obesity that increase dramatically across the transition to adulthood in the US.

Objective: To examine racial/ethnic differences in the influence of life course SES on longitudinal obesity patterns from adolescence to adulthood.

Methods: Latent class analysis was used on a nationally representative, diverse sample of 12,940 adolescents followed into young adulthood (mean age=21.7 years) to identify life course SES group profiles based on SES data in adolescence and young adulthood. Gender-stratified multinomial logistic regression models estimated the association of SES groups with obesity incidence and persistence versus staying non-obese.

Results: No significant interactions with race/ethnicity were observed, though racial/ethnic minorities had the highest obesity risk across SES groups. Racial/ethnic-pooled associations between disadvantaged SES exposure and higher obesity risk were strong but differed by gender. Males with a disadvantaged background who experienced early transitions into the labor force, marriage and residential independence had the highest risk of obesity incidence (RRR=1.64; 95%CI: 1.12, 2.40), while females exposed to persistent adversity were at highest risk (RRR=3.01, 95%CI: 1.95, 4.66). In general, SES group membership had a stronger relationship with obesity persistence than incidence.

Conclusions: The relationship between SES and obesity patterns is similar across race/ethnicity and differs by gender during the transition to adulthood. However, stronger associations with obesity persistence and enduring racial/ethnic disparities in obesity risk across SES groups suggest that these social factors play a larger role in disparities earlier in the life course.

J Epidemiol Community Health. Published Online First: 31 October 2008




The Catch-22 of Aging

It seems there's just no way to beat Father Time. As we age, our chromosomes fracture, and specialized proteins rush in to reverse the damage. But new research shows that in doing so, these proteins inadvertently switch on genes that can contribute to aging, allowing senescence to march ever onward.

The idea that a protein might patch up a rickety, aging chromosome is not new. About a decade ago, researchers identified a protein called Sir2 that zooms to the spot of broken DNA in yeast cells and repairs the breaks. But to do that, Sir2 has to abandon its job of inactivating a sterility gene elsewhere in the yeast genome. The result is yeast cells that have intact DNA but are sterile, a symptom of aging in the fungi. Since then, researchers have drawn more connections between Sir2 and its protein family, the sirtuins, to aging in yeast, insects, and mice (Science, 18 June 2004, p. 1731). But they didn't know if the mammalian equivalent of Sir2, a protein called SIRT1, caused the same genetic catch-22.

To find out, molecular biologist David Sinclair of Harvard Medical School in Boston and colleagues studied SIRT1 in mice. In mouse embryonic stem cells, the researchers saw that SIRT1 hangs out near strands of DNA that don't seem to produce proteins, suggesting that it plays a gene-silencing role like Sir2 plays in yeast.

Next, the researchers mimicked aging in mouse cells by exposing them to hydrogen peroxide. The chemical simulates oxidative stress, a buildup of reactive oxygen that often occurs in older cells; many researchers believe that oxidative stress damages cell structures, such as chromosomes, and causes the problems we associate with aging. After 1 hour in the peroxide solution, more than 90% of the SIRT1 proteins left their original locations on the chromosome and moved to the breaks, the researchers report today in the journal Cell.

What was the effect of SIRT1 leaving its post? Further work in the brains of aging rodents suggested that many of the genes associated with SIRT1 turn on in older mice, possibly because SIRT1 has left the scene to repair a broken chromosome. The result could be a liver gene turning on in the brain, disrupting the brain's function, says Sinclair. Such faulty gene activity contributes to a multitude of age-related problems, such as diabetes and dementia.

Overall, the findings indicate that a mammalian cell's effort to stave off old age can actually promote the symptoms of aging. "This may be a very fundamental Achilles' heel of life," says Sinclair. Still, understanding how SIRT1 contributes to the process can help researchers develop better treatments for aging-related problems, Sinclair says. For example, in further experiments, his team showed that mice fed SIRT1 lived more than 25 days longer than did control mice after exposure to genome-altering radiation.

Leonard Guarente, a molecular biologist at the Massachusetts Institute of Technology in Cambridge who conducted some of the original sirtuin studies in yeast, says the work provides greater insight into aging in mammals, including humans. It also, he notes, shows that simple organisms like yeast still have something to teach us.

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