We examined the association of coffee drinking with subsequent total and cause-specific mortality among 229,119 men and 173,141 women in the National Institutes of Health–AARP Diet and Health Study who were 50 to 71 years of age at baseline. Participants with cancer, heart disease, and stroke were excluded. Coffee consumption was assessed once at baseline.

[...]

In this large prospective study, coffee consumption was inversely associated with total and cause-specific mortality. Whether this was a causal or associational finding cannot be determined from our data. (Funded by the Intramural Research Program of the National Institutes of Health, National Cancer Institute, Division of Cancer Epidemiology and Genetics.)

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And make no mistake about it, you are dumb. You’re a group of incredibly well-educated dumb people. I was there. We all were there. You’re barely functional. There are some screw-ups headed your way. I wish I could tell you that there was a trick to avoiding the screw-ups, but the screw-ups, they’re a-coming for ya. It’s a combination of life being unpredictable, and you being super dumb.

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A major goal in aging research is to improve health during aging. In the case of mice, genetic manipulations that shorten or lengthen telomeres result, respectively, in decreased or increased longevity. Based on this, we have tested the effects of a telomerase gene therapy in adult (1 year of age) and old (2 years of age) mice. Treatment of 1- and 2-year old mice with an adeno associated virus (AAV) of wide tropism expressing mouse TERT had remarkable beneficial effects on health and fitness, including insulin sensitivity, osteoporosis, neuromuscular coordination and several molecular biomarkers of aging. Importantly, telomerase-treated mice did not develop more cancer than their control littermates, suggesting that the known tumorigenic activity of telomerase is severely decreased when expressed in adult or old organisms using AAV vectors. Finally, telomerase-treated mice, both at 1-year and at 2-year of age, had an increase in median lifespan of 24 and 13%, respectively. These beneficial effects were not observed with a catalytically inactive TERT, demonstrating that they require telomerase activity. Together, these results constitute a proof-of-principle of a role of TERT in delaying physiological aging and extending longevity in normal mice through a telomerase-based treatment, and demonstrate the feasibility of anti-aging gene therapy.

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The TOR kinase, which is present in the functionally distinct complexes TORC1 and TORC2, is essential for growth but associated with disease and aging. Elucidation of how TOR influences life span will identify mechanisms of fundamental importance in aging and TOR functions. Here we show that when TORC1 is inhibited genetically in C. elegans, SKN-1/Nrf, and DAF-16/FoxO activate protective genes, and increase stress resistance and longevity. SKN-1 also upregulates TORC1 pathway gene expression in a feedback loop. Rapamycin triggers a similar protective response in C. elegans and mice, but increases worm life span dependent upon SKN-1 and not DAF-16, apparently by interfering with TORC2 along with TORC1. TORC1, TORC2, and insulin/IGF-1-like signaling regulate SKN-1 activity through different mechanisms. We conclude that modulation of SKN-1/Nrf and DAF-16/FoxO may be generally important in the effects of TOR signaling in vivo and that these transcription factors mediate an opposing relationship between growth signals and longevity.

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Last week, Harvard’s Faculty Advisory Council revealed that the school now spends $3.75 million annually on academic journal subscriptions. Why so much? According to a memo the council sent out, some journals cost the school up to $40,000 every year, with the two top publishers increasing the price of content 145% over the last six years.

This is troubling for a number of reasons. First, in an age where the public can browse nearly 4 million articles for free on Wikipedia, a curious person looking to read up on the latest scientific research can expect to spend nearly $30 to $40 for a single paper from publishers such as Elsevier and Springer.

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Several factors are at play here, scientists say. One may be that because journals are now online, bad papers are simply reaching a wider audience, making it more likely that errors will be spotted. “You can sit at your laptop and pull a lot of different papers together,” Dr. Fang said.

But other forces are more pernicious. To survive professionally, scientists feel the need to publish as many papers as possible, and to get them into high-profile journals. And sometimes they cut corners or even commit misconduct to get there.

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In recent years, there has been an explosion of interest in biologics. (The list of people who have also experimented with Regenokine reportedly includes Fred Couples, superagent Ari Emanuel, and the late Pope John Paul II.) Those willing to pay out of pocket can now treat their ailing joints with everything from platelet rich plasma (PRP) therapy, in which blood is spun until it contains a high concentration of healing platelets, to concentrated bone marrow injections, dense with stem cells. What all of these biologics have in common is the same appealing logic: Instead of cutting with a scalpel, or administering a synthetic drug — these treatments have long recovery times and nasty side effects — the healing mechanisms of the flesh should be put to work. The body heals best when it heals itself.

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New DNA sequencing methods will soon make it possible to identify all germline variants in any individual at a reasonable cost. However, the ability of whole-genome sequencing to predict predisposition to common diseases in the general population is unknown. To estimate this predictive capacity, we use the concept of a “genometype”. A specific genometype represents the genomes in the population conferring a specific level of genetic risk for a specified disease. Using this concept, we estimated the capacity of whole-genome sequencing to identify individuals at clinically significant risk for 24 different diseases. Our estimates were derived from the analysis of large numbers of monozygotic twin pairs; twins of a pair share the same genometype and therefore identical genetic risk factors. Our analyses indicate that: (i) for 23 of the 24 diseases, the majority of individuals will receive negative test results, (ii) these negative test results will, in general, not be very informative, as the risk of developing 19 of the 24 diseases in those who test negative will still be, at minimum, 50 – 80% of that in the general population, and (iii) on the positive side, in the best-case scenario more than 90% of tested individuals might be alerted to a clinically significant predisposition to at least one disease. These results have important implications for the valuation of genetic testing by industry, health insurance companies, public policy makers and consumers.

We stick our hand in a cow stomach, get a window into our core (thanks to a hunter who became a walking science experiment in the 1800s), and listen in on the surprising back-and-forth between our gut and our brain. And we talk to a man who kind of went out of his mind when a medical procedure left him (for a little while) gutless.

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