Clearly, we’ve got a lot of work to do:

The Cat in the Hat

Via Jim at Frederick County Biotech Community.

(For previous installments of Sunday Funnies, see here.)


I have two words for you: rat lipsuction.

One of the common features of aging throughout the Class Mammalia is the accumulation of body fat in specific deposits — specifically, the growth of visceral (or abdominal fat). We do it, monkeys do it, dogs do it, and rodents do it. Visceral fat (VF) has been implicated in a variety of age-related disorders, including metabolic syndrome and chronic inflammation, both of which have in turn been linked to frailty.

If VF produces a factor or factors that limits lifespan (either by promoting the aforementioned conditions or by another mechanism), then removing it should make those factors go away and concomitantly lengthen lifespan. (I suppose the alternative would be a parabiosis experiment in which a rat with lots of VF shared a blood supply with a rat with little VF, though (a) the results would be difficult to interpret due to myriad confounding factors; (b) I’m not sure what one would do if the fat rat died while the thin rat was still alive; and (c) the entire exercise would be a horrifying abomination.) Muzumdar et al. have collected just that sort of data: They removed the VF from rats consuming an ad libitum chow diet, and showed that the rats aged almost as successfully as calorie-restricted (CR) rats (which, by the way, never accumulate VF):

Visceral adipose tissue modulates mammalian longevity

Caloric restriction (CR) can delay many age-related diseases and extend lifespan, while an increase in adiposity is associated with enhanced disease risk and accelerated aging. Among the various fat depots, the accrual of visceral fat (VF) is a common feature of aging, and has been shown to be the most detrimental on metabolic syndrome of aging in humans. We have previously demonstrated that surgical removal of VF in rats improves insulin action; thus, we set out to determine if VF removal affects longevity. We prospectively studied lifespan in three groups of rats: ad libitum-fed (AL-fed), CR (Fed 60% of AL) and a group of AL-fed rats with selective removal of VF at 5 months of age (VF-removed rats). We demonstrate that compared to AL-fed rats, VF-removed rats had a significant increase in mean (p < 0.001) and maximum lifespan (p < 0.04) and significant reduction in the incidence of severe renal disease (p < 0.01). CR rats demonstrated the greatest mean and maximum lifespan (p < 0.001) and the lowest rate of death as compared to AL-fed rats (0.13). Taken together, these observations provide the most direct evidence to date that a reduction in fat mass, specifically VF, may be one of the possible underlying mechanisms of the anti-aging effect of CR.

The authors argue (a bit too strongly, in my opinion) that their experiment demonstrates that prevention of VF accumulation is a major mechanism of the lifespan extension due to CR. A skeptic could easily argue that it works the other way: VF represents a really large storehouse of energy, and its removal could force the rat to deplete other fat reserves and enter a state that mimics CR. The parabiosis experiment that I parenthetically described above (or some less repellent and [not entirely incidentally] more scientifically valuable version thereof, e.g., one in which candidate factors secreted by VF were introduced back into lipectomized rats) would go a long way toward bolstering the authors’ interpretation.

Regardless, it’s a good reminder not to skip yoga and jogging this weekend.

Sarcopenia (muscle wasting) is one of the most devastating aspects of the frailty syndrome that accompanies old age. Ryall et al. have a review of the molecular and cellular mechanisms underlying age-related degeneration of skeletal muscle.

Two of the great scourges of old age are insulin resistance (often leading to late-onset diabetes) and frailty (a suite of symptoms that may have their roots in runaway inflammatory signaling). A review by Paolisso and Abbatecola investigates the possible connections between the two:

Is There A Relationship Between Insulin Resistance and Frailty Syndrome?

Due to the fact that the percentage of aged subjects in the populations of industrialized countries is dramatically increasing, the scientific community has been obligated to focus their attention on age related disease states and peculiar consequences of aging such as, frailty. Frailty is defined as a syndrome of decreased reserve and resistance to stressors and is clinically expressed as muscle weakness, poor exercise tolerance, factors related to body composition, sarcopenia, and lower extremity mobility. Some biochemical markers of frailty in older persons, including pro-inflammatory markers, hormones and free radicals have been suggested. However, there is growing evidence that a rise in insulin resistance [IR] occurs as individuals age and IR is not only considered a simple metabolic finding, but has been identified as a major risk factor for many age-related diseases due to altered lipid metabolism, increased inflammatory state, impaired endothelial functioning, pro-thrombotic status and atherosclerosis. Considering that IR is related to many of the clinical features of frailty such as, skeletal muscle weakness, lower extremity mobility disability, cognitive decline and body composition changes, we will analyze the relationships among IR and such individual components while highlighting potential pathophysiologic mechanisms of IR on the activation of the downward spiral of the frailty syndrome in older persons. In particular, we will address the issue that IR may also be considered a pivotal biological component of some clinical aspects of the frailty syndrome in aging individuals.

When they look back from fifty years hence, will we seem as primitive and misguided?

Senile agitation? Have some Thorazine!

(Via My[Confined]Space)

A meeting devoted to clinical research in aging. This is mainstream geriatrics, with a twist: the organizers have a higher-than-usual interest in work related to translating basic biogerontological findings into the clinic.

The UCSD Clinical Investigation Institute (CII) and Nature Medicine invite you to attend the third annual Frontiers of Clinical Investigation Symposium, Aging 2007: Bench to Bedside to be held October 18-20, 2007 in La Jolla, California. The theme for this year’s symposium explores innovative approaches to bridge laboratory investigation to clinical research in aging. The topic stands at the crossroads of many disciplines, including endocrinology and cardiology as well as neurodegenerative and musculoskeletal diseases. Multi-disciplinary sessions will include basic, translational, and clinical presentations on cutting edge research to provide an integrated approach to understanding the science of healthy aging. This symposium will provide unique insights and tools for optimizing and streamlining clinical investigation from discovery to drug development.

Abstract submission deadline is August 27th; registration gets costlier after September 16th.

More at the conference website.

(Hat tip to reader and biogerontologist John Cumbers for bringing this conference to our attention.)

A group of preschoolers were asked what happens to people when they get old. Some of the answers are hilarious; others poignant.

“You don’t die, but your body dies”

Some of the responses hint at an awareness of frailty, tissue decline (especially of the skin), and loss of mobility, but overall it sounds like they’re mostly unaware of the true ravages of advanced age. In a way it’s a mercy that none of the young ones mentioned (i.e., were aware of) incontinence, neurodegeneration, cancer, sexual dysfunction, diabetes, hearing and vision loss …

Via BoingBoing

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