Researchers in Japan manipulated mouse eggs to grow mice that were bi-maternal, having genetic material from two female parents, but no male parent. They then studied these mice alongside mice with one male and one female parent. The bi-maternal mice and the control mice were kept in the same conditions and fed the same diet, but the bi-maternal mice were significantly smaller and lighter, seemed to have better immune systems, and had an average lifespan 186 days longer than the control mice.

Tomohiro Kono from the Tokyo University of Agriculture, one of the researchers, believes that the bi-maternal mice might have lived longer because of the absence of a gene mice inherit from their fathers, though further study is needed:

"We believe that the most likely reason for the differences in longevity relates to the repression of a gene called Rasgrf1 in the BM mice. This gene normally expresses from the paternally inherited chromosome and is an imprinted gene on chromosome 9 associated with post-natal growth. Thus far, it's not clear whether Rasgrf1 is definitively associated with mouse longevity, but it is one of the strong candidates for a responsible gene. Furthermore, we cannot eliminate the possibility that other, unknown genes that rely on their paternal inheritance to function normally may be responsible for the extended longevity of the BM mice."

If Rasgrf1 is responsible for mouse longevity, it could be responsible for human longevity as well, and could go a long way toward explaining why women tend to live longer than men.

Why Females Live Longer Than Males: Is It Due to the Father's Sperm? [Science Daily — Thanks to Robert Atlas]

A team of researchers in the UK explored the role of a protein known as S6K1, which turns out to play an extraordinary role in aging and age-related disease. When the researchers grew mice lacking the gene to produce S6K1, their mice lived significantly longer (see chart - the red lines are mice without S6K1). They also developed fewer age-related debilitating conditions.

Female mice without S6K1 lived slightly longer than their male counterparts, and over 160 days longer than the control group. That means the female mouse lifespan increased by twenty percent.

Mice without S6K1 also lost weight, even if they ate more than ordinary mice. In other words, a substance that could block the expression of S6K1 would trick the body into thinking that you'd gone on a very rigorous diet. And it would make you healthier into an older age. The best part?

In their paper, the researchers conclude:

It might be possible to develop drug treatments that manipulate S6K1 and AMPK to achieve improved overall health in later life. Indeed, short-term rapamycin treatment reduces adiposity in mice, and metformin treatment [often used against type 2 diabetes] extends lifespan in short-lived mice.

This is good news, because often when researchers make discoveries related to longevity there is no immediate pathway to manufacturing a life-extending drug. For all of us who want to stay healthy in old age while still eating sugar and fat once in a while, let's hope this research team starts testing a drug based on their S6K1 discovery - and soon.

via Science

The system of caloric restriction has been studied in yeast and mice, and now a long-range study in monkeys has confirmed what many suspected. Primates who reduce their calorie intake live much longer, healthier lives than their counterparts who eat whatever they wish. This gives hope to people hoping to apply this insight to humans, since humans are close genetic cousins of monkeys.

According to a release from Science:

Ricki Colman and colleagues began their study at the Wisconsin National Primate Research Center in 1989 by assigning adult rhesus monkeys, each between age seven and 14, to either a caloric restriction group or a control group. Once the monkeys were assigned to a group, the researchers determined their baseline food intake and began reducing the diets of those monkeys in the caloric restriction, or CR, group by ten percent for three months until they reached the desired 30 percent restriction. At the end of the study, 37 percent of the control group had died of age-related causes while only 13 percent of the CR group had. This finding means that the control monkeys experienced a death rate from age-related conditions such as diabetes, cancer, cardiovascular disease, and brain atrophy three times that of the CR group.

Adds researcher Sterling Johnson:

Both motor speed and mental speed slow down with aging. Those are the areas which we found to be better preserved. We can't yet make the claim that a difference in diet is associated with functional change because those studies are still ongoing. What we know so far is that there are regional differences in brain mass that appear to be related to diet.

If you'd like to try this experiment on yourself, keep in mind that eating fewer calories does not mean giving up healthy items. You'll want to eat more veggies and fruits, as well as complex carbohydrates, and cut out fats. The researchers suggest that the ideal amount of restriction is 30 percent fewer calories than you currently consume, which you should achieve gradually over time. So first restrict yourself by 10 percent, then 10 more, and so on. Losing a few desserts is worth it if it means your brain will be healthy when you're 90.

via Science

Researchers at the University of North Carolina have found a protein, called p16INK4a, that is tied to aging. In a forthcoming article in Aging Cell, the team describes this protein's presence in the human blood stream. Higher amounts of the protein are also tied to tobacco use and inactivity. Interestingly, the study found that inactivity contributed more to this aging marker than a high body mass index, which seems to show that activity slows down aging more than preventing obesity does.t

The research team says that this discovery could help with stabilizing organ transplants, recovery from surgery, or cancer treatment. As of now, it's a way to see just how far your body has aged molecularly, regardless of how you have aged chronologically. It also might lead to further development of age-prolonging procedures.

Aging is traditionally coupled with a process called "senescence," which is generally understood to be the wearing out and breaking down of cells over time. There are many theories of aging, but many biologists theorize that the effects of aging are a naturally evolved part of life. The corollary to this is that aging (or even death) isn't necessarily a requirement for life. It might be something we can prevent entirely.

The research into prolonging peoples' lives is expansive. A group called the Methuseleh Foundation is constantly working to cure aging, and a governmental agency, the National Institute on Aging, is working on the problem as well. This new research, which gives researchers a tool for documenting and measuring the aging process, could eventually contribute to longer lives for humanity.

Test detects molecular marker of aging in humans [UNC School of Medicine, via Science Daily]

Here are all the technologies they're interested in, and the age-related problems they're designed to cure.

via Xenophilia

The researchers found two fly genes, known as magu and hebe, that are responsible for causing older female flies to continue laying eggs. And they noticed that when those genes "over-express," or go into overdrive, that they also extend the natural lifespan of the flies by up to 30 percent. Humans have a gene, SMOC2, which is similar to the magu gene, so it's possible that these findings will be relevant to humans as well. Scientists already know of reliable ways to make genes over-express.

John Tower and Yishi Li, who conducted the research, are publishing the results this month in Molecular Genetics and Genomics. They suggest that hebe and magu genes have life-extending effects because they promote the formation of stem cells. Stem cells keep bodies young, and are also crucial to reproductive health. So when hebe and magu over-express, they stimulate the growth of new stem cells, and that has a cascade effect on the body's youthfulness.

Said Tower:

This would appear to be stimulating the stem cells to divide more in the old fly and therefore produce more offspring. It both makes females lay more eggs and live longer, so it really argues against any kind of obligatory tradeoff between reproduction and lifespan.

Add to your purses of the future a little bag of life-extension pills that will keep you fertile and lively well into your 100s.

Adult-Specific Over-Expression of the Drosophila Genes magu and hebe [via Molecular Genetics and Genomics]

Apparently the chinchilla and other small rodents of its type have cells that are better than humans' at sensing when cancer is developing. As soon as cancerous growths are detected, the rodent's body slows down cell division, halting the expansion of the tumor and preventing metastasis. Gorbunova and colleagues suspect that the human body could be induced to do the same thing, essentially curing its own cancer by becoming very efficient at self-monitoring.

One of the interesting outcomes of this study had to do with the rodents' levels of telomerase, an enzyme that regulates cell aging and also causes cancer. According to the University of Rochester:

Gorbunova and colleagues showed that it was not life expectancy, but body mass that regulated the expression of telomerase. Simply having more cells increases the likelihood that one will become cancerous. We humans, as large animals, would likely develop cancer much more often and much earlier if we didn't suppress our telomerase.

So the bigger you are, the more likely you'll start mutating.

Said Gorbunova:

We haven't come across this anticancer mechanism before because it doesn't exist in the two species most often used for cancer research: mice and humans. Mice are short-lived and humans are large-bodied. But this mechanism appears to exist only in small, long-lived animals.

I'm ready to become the first human-chinchilla chimera if it will make me cancer-proof.

Image via FurryAnimalsOhMy.

Novel Anti-Cancer Mechanism Found in Small Rodents [via University of Rochester]

As they explain in an article published this week in Nature Structure and Molecular Biology, researchers at the Salk Institute for Biological Studies, led by molecular and cell biology professor Vicki Lundblad, have discovered how Est3 keeps telomeres long each time yeast cells divide. Telomeres are made with an enzyme known as telomerase, and Est3 helps pack extra telomerase onto the ends of newly-divided chromosomes. Then the telomerase builds longer telomeres to keep those cells youthful.

But what's really intriguing about all this is that Est3, which you'll recall is in yeast cells, has an analog in mammals known as TPP1. This is where things get really exciting. If it turns out that TPP1 is involved in keeping our telomeres long, scientists can start researching it and determining whether it could provide a key to keeping humans young for much longer than ever before.

There is a danger, though. As the researchers point out in a release about their work:

Factors that regulate telomerase activity are a very hot topic in biomedicine: sluggish telomerase activity promotes premature cell death and may underlie diseases of aging via telomere shortening, while hyperactive telomerase could promote uncontrolled cell division and cellular immortality associated with cancer.

So we don't want too much telomerase, or our cells will go cancerous. But the discovery of Est3 bodes well for anyone who wouldn't mind a little protein intervention to keep their cells (and bodies) young.

Keeping Cells Useful [Eurekalert via Salk Institute]

Decades ago, nutritionists lobbied the US government to add iodine to salt, because most US residents weren't getting enough iodine in their diets. Today, most of us here in the US accept that salt comes with iodine (though you can buy it without). Chemists like UC Santa Barbara's Bruce Lipshutz, who studies CoQ10, hope that in the future we will also accept the idea that CoQ10 comes in drinking water, perhaps along with several other vital vitamins and enzymes. So even if you want to grow old and die in the old-fashioned way, you may not be able to — at least, if you plan to drink water.

Nanotechnology Adds Vital Enzyme to Drinking Water [via ZDNet]

It turns out that when you're under stress, your body releases more of the hormone cortisol, which stimulates that hyper-alert "fight or flight" reflex. While cortisol is good in small doses, over time it erodes the small caps at the end of your chromosomes known as telomeres (the little yellow dots at the end of those blue chromosomes in the picture). Many researchers have long suspected that telomeres would provide a key to longevity because they are quite large in young people and gradually shrink over time as cells divide.

Rita Effros, the researcher who led the UCLA study, believes that she can synthesize a pill that combats stress by putting more telomerase — the substance that builds telomeres — into the body. This would keep those telomeres large, even in the face of large amounts of cortisol. It might also make your body live a lot longer too.

Effros told Eurekalert:

When the body is under stress, it boosts production of cortisol to support a "fight or flight" response. If the hormone remains elevated in the bloodstream for long periods of time, though, it wears down the immune system. We are testing therapeutic ways of enhancing telomerase levels to help the immune system ward off cortisol's effect. If we're successful, one day a pill may exist to strengthen the immune system's ability to weather chronic emotional stress.

And, perhaps, to live much longer lives.

UCLA Study Identifies the Mechanism Behind the Mind-Body Connection [Eurkalert]

According to the authors of the study, diabetes and lung disease were the biggest life-shorteners. In an introductory note to their study, PLoS editors write:

The researchers looked at differences in death rates between all counties in US states plus the District of Columbia over four decades, from 1961 to 1999. They obtained the data on number of deaths from the National Center for Health Statistics, and they obtained data on the number of people living in each county from the US Census. The NCHS did not provide death data after 2001. They broke the death rates down by sex and by disease to assess trends over time for women and men, and for different causes of death.

Over these four decades, the researchers found that the overall US life expectancy increased from 67 to 74 years of age for men and from 74 to 80 years for women. Between 1961 and 1983 the death rate fell in both men and women, largely due to reductions in deaths from cardiovascular disease (heart disease and stroke). During this same period, 1961-1983, the differences in death rates among/across different counties fell. However, beginning in the early 1980s the differences in death rates among/across different counties began to increase. The worst-off counties no longer experienced a fall in death rates, and in a substantial number of counties, mortality actually increased, especially for women, a shift that the researchers call "the reversal of fortunes." This stagnation in the worst-off counties was primarily caused by a slowdown or halt in the reduction of deaths from cardiovascular disease coupled with a moderate rise in a number of other diseases, such as lung cancer, chronic lung disease, and diabetes, in both men and women, and a rise in HIV/AIDS and homicide in men. The researchers' key finding, therefore, was that the differences in life expectancy across different counties initially narrowed and then widened.

Not surprisingly, the factors are: diet, smoking, and exercise. The worst killer is smoking. People who, at the age of 70, eat lots of vegetables and get daily exercise, have a 54 percent probability of living to be 90 or older. If they don't get a lot of exercise, they still have a 44 percent chance of making it to the century mark. But if they smoke, they only have a 22 percent chance of living to 90.

The good news is that there are a lot of things people can do to extend their lives even without miracle drugs. The bad news is that a lot of people live in places where the air is so filled with smoke and pollution that they are effectively smokers even if they don't want to be. AP Photo/Misha Japaridze

Exceptional Longevity in Men [Archives of Internal Medicine]