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"After controlling for potential confounders, higher monthly ejaculation frequency was associated with a statistically significant decreased risk of total prostate cancer compared to the reference group at every time period."
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Charlie Stross lays out the state of aging: "cognitive functioning burdened by decades of memories to integrate, canalized by prior experiences, dominated by the complexity of long-term planning at the expense of real-time responsiveness...truck by intricate, esoteric cross-references to that which has gone before."
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Bloomberg Visual Data reports on the ways people die, and how they have changed over time. The most interesting part of the report is about dementia and Alzheimer's:
The downside to living so long is that it dramatically increases the odds of getting dementia or Alzheimer's. That's why total deaths in the 75+ category has stayed constant despite impressive reductions in the propensity to die of heart disease.
The rise of Alzheimer's and other forms of dementia has had a big impact on healthcare costs because these diseases kill the victim slowly.
About 40% of the total increase in Medicare spending since 2011 can be attributed to greater spending on Alzheimer's treatment.
A few days ago, I saw this photo on a friend's Facebook feed, accompanied by a caption claiming that it showed a truck driver who had exposed half his face to the sun for 30 years.
There wasn't any link and naturally, being Facebook, I assumed this was probably not an accurate description of what was going on in the photo and kind of just brushed it aside.
And then Mo Costandi posted the same photo on Twitter along with a link to its original source—The New England Journal of Medicine. Oh, s&*%.
The patient reported that he had driven a delivery truck for 28 years. Ultraviolet A (UVA) rays transmit through window glass, penetrating the epidermis and upper layers of dermis. Chronic UVA exposure can result in thickening of the epidermis and stratum corneum, as well as destruction of elastic fibers. This photoaging effect of UVA is contrasted with photocarcinogenesis. Although exposure to ultraviolet B (UVB) rays is linked to a higher rate of photocarcinogenesis, UVA has also been shown to induce substantial DNA mutations and direct toxicity, leading to the formation of skin cancer. The use of sun protection and topical retinoids and periodic monitoring for skin cancer were recommended for the patient.
Basically, this gentleman does not yet seem to have skin cancer. Instead, the skin on that side of his face had thickened (a sign that his skin cells aren't growing and sloughing off in a normal way). The elastic tissue on that side of the face had also started to degenerate, leaving deep wrinkles, as well as wide pores that became multiple blackheads. Also, small cysts had formed around the follicles of fine hairs on his face.
Read more about how exposure to UVA rays from the sun can cause skin damage and premature aging.
Video Link. YouTuber Adam Forgie of Utah, the person behind the camera, shoots these lovely videos with some regularity. "I take care of my legally-blind, near-deaf grandmother," he explains. "She may be blind, but she can still dance! She likes the attention." You can follow her on Twitter here.
Update: Boing Boing readers in various spots around the world report that the video is blocked in certain countries outside the US. This is dumb. Sorry.
There was some interesting research out of the Mayo Clinic announced this week. The study focused on a new method to combat aging, though not, significantly, one that could extend life. Instead of living forever, Darren Baker and colleagues would just like to help people enjoy the time they do have—by reducing the physical downsides of aging, such as lost muscle and stiff joints.
Their method centers around something called senescent cells, normal cells that have basically shut down all growth, but continue to release chemicals into the body. Some scientists have suspected this process of cellular senescence contributes to the negative physical effects of aging and Baker's team was able to provide some big support for that theory. They killed senescent cells in the bodies of fast-aging mice. Those mice went on to age more gracefully, delaying the physical breakdown of their bodies. Ed Yong explains:
Baker exploited the fact that many senescent cells rely on a protein called p16-Ink4a. He created a genetic circuit that reacts to the presence of p16-Ink4a by manufacturing an executioner: a protein called caspase-8 that kills its host cell. Caspase-8 is like a pair of scissors – it comes in two halves that only work when they unite. Baker could link the two halves together using a specific drug. By sneaking the drug into a mouse’s food, he activated the executioners, which only killed off the cells that have lots of p16-Ink4a. Only the senescent ones get the chop.
Baker tested out this system in a special strain of genetically engineered mice that age very quickly. It worked. The senescent cells disappeared, and that substantially delayed the onset of muscle loss, cataracts, and fat loss. Typically, around half of these mice show signs of muscle loss by five months of age. Without their senescent cells, only a quarter of them showed the same signs at ten months. Their muscle fibres were larger, and they ran further on treadmills. Even old mice, whose bodies had started to decline, showed improvements.
It really should go without saying that there's a big jump between getting something to work in mice and getting it to work in people. So do not expect your doctor to be able to kill off your senescent cells anytime soon, if ever. There's also potential risks to this therapy and a lot we don't yet know about it. Will this work as well in mice that age at a normal rate? Will killing senescent cells allow us to delay or eliminate other signs of aging, or just muscle loss and cataracts? If you kill of senescent cells, will damaged cells continue to grow, producing cancer?
When you're thinking about a study like this, it's probably best to treat it as an interesting discovery about the way mammal biology might work, rather than something that has any immediate practical medical applications for humans. From that perspective, this is pretty cool science.
Bonus fun: Read Ed Yong's write-up of the study. Then read this version written by a reporter at the New York Times. Then think about how much you would have misunderstood about this study if you'd only read the New York Times story.
If a centenarian jumped off a bridge while eating a bag of jelly donuts and chain-smoking, would you do it, too?
That's basically the message in a new column by LiveScience's Christopher Wanjek, which looks at why the people who live the longest should not necessarily be health role models for the rest of us.
It seems that longevity goes hand-in-hand with some funny yesbuts. What you eat and how active you are doesn't seem to matter ... if you're one of the very, very lucky folks with a genetic predisposition toward surviving into extreme old age. For everybody else, there's pretty good evidence that healthy habits actually do extend your lifespan. Part of what fascinates me about the studies that show that is that they often compare Seventh Day Adventists to the general population. Why? Because Seventh Day Adventists generally don't eat meat (the first time I ever saw lentil loaf, it came from SDA cookbook), and are discouraged from booze, cigarettes, drugs, and caffeine. It also doesn't hurt that they run a massive, and well-respected, healthcare system, centered around Loma Linda University. Makes 'em easier to study like that.
For the general population, there is a preponderance of evidence that diet and exercise can postpone or ward off chronic disease and extend life. Many studies on Seventh Day Adventists — with their limited consumption of alcohol, tobacco and meat — attribute upward of 10 extra years of life as a result of lifestyle choices.