Weight Battle

From the Star-Telegram: "At 140 pounds and 6 feet tall, Fagg is bone thin. But his body mass index of 20 puts him within the optimal range for health. He might appear frail, but he is strong enough to do yoga and cardio workouts. If anyone doubts his fitness level, the 60-year-old Fagg is quick to challenge them to a hike from his home in Hurst to downtown Fort Worth. In 2007, he hiked down the north rim of the Grand Canyon and up the south rim, for a total of 65 miles, 13 of them straight up. 'My goal is to hike it again at 75,' Fagg said. He sees no reason why he won't be able to make it. Like many followers of the calorie restriction, or CR, lifestyle, Fagg hopes to live to be 100. But life extension is not the reason he eats so little. For Fagg and others, it's the health benefits that matter. ... Since the 1930s, researchers have documented the health benefits of calorie-restriction in animals, including a reduction in certain cancers. Although not a lot of research has been done on humans, two studies found that the probability of someone who practices CR coming down with diabetes was virtually nil."

View the Article Under Discussion: http://www.star-telegram.com/living/story/1338341.html
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Via ScienceDaily: "moderate amounts of exercise alone can reduce the inflammation in visceral fat ... benefits of exercise were apparent, even without a change in diet. We saw improvements in insulin sensitivity, less fat in the liver, and less inflammation in belly fat ... Scientists now know that obesity is associated with a low-grade systemic inflammation. Obese people have higher levels of circulating inflammatory markers, such as C-reactive protein (CRP), which are produced and secreted by fat tissue. This inflammation then triggers the systemic diseases linked with metabolic syndrome, such as Type 2 diabetes and heart disease ... mice were assigned to either a sedentary group, an exercise group, a low-fat diet group, or a group that combined a low-fat diet with exercise ... The surprise was that the combination of diet and exercise didn't yield dramatically different and better results than diet or exercise alone." This suggests that the level of visceral fat is more important than other factors and whatever strategy you choose to get rid of it is going to provide some benefit. Which is not an excuse not to exercise or to overeat - a partial benefit is only a partial benefit.

View the Article Under Discussion: http://www.sciencedaily.com/releases/2009/04/090423154237.htm
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Here is an interesting open access paper at PLoS ONE: "We generated microarray gene expression data from livers of male mice fed high calorie or [calorie restriction] CR diets, and we find that CR significantly changes the expression of over 3,000 genes, many between 10- and 50-fold. We compare our data to the GenAge database of known aging-related genes and to prior microarray expression data of genes expressed differently between male and female mice. CR generally feminizes gene expression and many of the most significantly changed individual genes are involved in aging, hormone signaling, and p53-associated regulation of the cell cycle and apoptosis. Among the genes showing the largest and most statistically significant CR-induced expression differences are Ddit4, a key regulator of the TOR pathway, and Nnmt, a regulator of lifespan linked to the sirtuin pathway. ... Our data show that CR induces widespread gene expression changes and acts through highly evolutionarily conserved pathways, from microorganisms to mammals, and that its life-extension effects might arise partly from a shift toward a gene expression profile more typical of females." So yet another theory to add to the many on the cause of longevity differences by gender.

View the Article Under Discussion: http://dx.doi.org/10.1371/journal.pone.0005242
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A good example of the sort of cellular hacking going on in the laboratory and early trials these days via EurekAlert!: researchers "have developed a nanoparticle - about one thousandth smaller than a printed period - that can travel through the blood stream. 'Decorated' with a tumor-targeting antibody, the nanoparticle is able to locate primary and hidden metastatic tumor cells and deliver its payload: a fully functioning copy of the P53 tumor suppressor gene. ... Normal cells have two copies of the functioning P53 gene. The protein produced by the P53 gene is activated to either coordinate the repair process in cells or induce cell suicide. ... In earlier work using animal models, [researchers] delivered functional p53 genes to tumor cells and tumor metastases in 16 different types of cancer, including prostate, pancreatic, melanoma, breast cancer and head and neck cancer. The presence of the replacement genes dramatically improved the efficacy of conventional cancer therapy. ... When the job of reinstating a normal P53 suppressor gene is done, the nanoparticle - essentially a little fat droplet wrapped around the gene - simply melts away, unlike non-biodegradable delivery systems. ... Clinical trials are now underway ... The trial already has enrolled six patients with various cancers and anticipates a total of 14."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2009-04/foas-fdn040509.php
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

As I've mentioned in the past, autophagy - the process by which cells destroy and replace damaged or old components - seems to be very important in the natural longevity you are granted by the operation of your metabolism. It's required for the longevity boost given by calorie restriction, for example. Some groups would go so far as to say that most or all longevity-inducing tweaks to metabolism operate through increased autophagy: "Autophagy is involved in cellular protein and organelle degradation, which is mediated by the lysosomal pathway. [Autophagy] has a key role in cellular housekeeping by removing damaged organelles. During aging, the efficiency of autophagic degradation declines and intracellular waste products accumulate. In Caenorhabditis elegans, there is clear evidence that lifespan is linked to the capacity to regulate autophagy. Recent studies have revealed that the same signaling factors regulate both aging and autophagocytosis, thus highlighting the role of autophagy in the regulation of aging and age-related degenerative diseases. Here, we examine in detail the interactions of the signaling network involving longevity factors SIRT1, mTOR, FoxO3, NF-kappaB and p53 in the regulation of autophagy. We discuss the possibility that these well-known stress resistance and longevity factors regulate the aging process via autophagy."

View the Article Under Discussion: http://pmid.us/19380253
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