In a 10-year U.S. study, people who drank coffee regularly were less likely to die of many causes, including heart disease and diabetes, than those who didn’t drink coffee at all.

The more coffee study participants consumed, the lower their risk of dying, and decaf drinkers showed a similar pattern.

“Coffee contains numerous biologically active compounds, including phenolic acids, potassium, and caffeine,” said lead author Dr. Erikka Loftfield of the National Cancer Institute in Rockville, Maryland.

Many studies have found that coffee consumption is associated with lower risk of overall and heart-related mortality, Loftfield told Reuters Health by email.

The researchers used data from a previous study on 90,317 adults without cancer or history of cardiovascular disease who were followed from 1998 through 2009. They had reported their coffee intake, along with other dietary and health details, at the start of the study.

By 2009, about 8,700 people had died. After accounting for other factors like smoking, the researchers found that coffee drinkers were less likely to have died during the study than nondrinkers.

The risk of death was lowest for those who drank four to five cups of coffee per day. A similar association was seen among drinkers of decaffeinated coffee as well, according to the results in American Journal of Epidemiology.

Coffee drinkers had a reduced risk of death from heart disease, chronic respiratory diseases, diabetes, pneumonia and influenza and suicide, but not cancer, the researchers found.

“Although coffee drinking has also been inversely associated with incidence of certain cancers, like liver, in epidemiological studies, we did not observe an association between coffee and overall cancer mortality,” Loftfield said. “This may be because coffee reduces mortality risk for some cancers but not others.”

People who consumed two to three cups of coffee per day had approximately an 18 percent lower risk death during follow-up compared to those who reported drinking no coffee, she said. Drinking up to five cups per day, or 400 milligrams of caffeine per day, is not associated with any long-term health risks, Loftfield added.

Moderate caffeine intake, up to 200 milligrams per day, is even safe for pregnant women, according to a statement by the American College of Obstetricians and Gynecologists.

“There is an accumulating number of studies of very high quality that show that people who drink more coffee tend to have better health outcomes,” said Dr. Marc J. Gunter of Imperial College London, who was not part of the new study.

“Coffee drinking is correlated with other health behaviors,” and those who drink it regularly may have other healthy habits, like exercising and keeping to a healthier diet, though the researchers tried to account for those other factors, Gunter told Reuters Health.

The study doesn’t prove that coffee extends life.

“You could argue that people who are already sick might not be drinking as much coffee,” Gunter said.

But coffee may also have a direct effect on inflammation or cardiovascular health, he said.

“It doesn’t seem to do you any harm, if you like drinking coffee then carry on,” Gunter said.

Coffee can be part of a healthy, balanced lifestyle, and it may even do some good, though we can’t yet recommend than non-drinkers adopt the habit for health reasons, he said.

Human supercentenarians share at least one thing in common–over 95 percent are women. Scientists have long observed differences between the sexes when it comes to aging, but there is no clear explanation for why females live longer. In a discussion of what we know about stem cell behavior and sex, Stanford University researchers Ben Dulken and Anne Brunet argue that it’s time to look at differences in regenerative decline between men and women. This line of research could open up new explanations for how the sex hormones estrogen and testosterone, or other factors, modify lifespan.

It’s known that estrogen has direct effects on stem cell populations in female mice, from increasing the number of blood stem cells (which is very helpful during pregnancy) to enhancing the regenerative capacity of brain stem cells at the height of estrus. Whether these changes have a direct impact on lifespan is what’s yet to be explored. Recent studies have already found that estrogen supplements increase the lifespan of male mice, and that human eunuchs live about 14 years longer than non-castrated males.

More work is also needed to understand how genetics impacts stem cell aging between the sexes. Scientists have seen that knocking out different genes in mice can add longevity benefits to one sex but not the other, and that males in twin studies have shorter telomeres–a sign of shorter cellular lifespan–compared to females.

“It is likely that sex plays a role in defining both lifespan and healthspan, and the effects of sex may not be identical for these two variables,” the authors write. “As the search continues for ways to ameliorate the aging process and maintain the regenerative capacity of stem cells, let us not forget one of the most effective aging modifiers: sex.”

The fatter we are, the more our body appears to produce a protein that inhibits our ability to burn fat, suggests new research published in the journal Nature Communication. The findings may have implications for the treatment of obesity and other metabolic diseases.

Most of the fat cells in the body act to store excess energy and release it when needed but some types of fat cells, known as brown adipocytes, function primarily for a process known as thermogenesis, which generates heat to keep us warm. However, an international team of researchers from the Wellcome Trust-Medical Research Council Institute of Metabolic Sciences at the University of Cambridge, UK, and Toho University, Japan, have shown that a protein found in the body, known as sLR11, acts to suppress this process.

Researchers investigated why mice that lacked the gene for the production of this protein were far more resistant to weight gain. All mice — and, in fact, humans — increase their metabolic rate slightly when switched from a lower calorie diet to a higher calorie diet, but mice lacking the gene responded with a much greater increase, meaning that they were able to burn calories faster.

Further examinations revealed that in these mice, genes normally associated with brown adipose tissue were more active in white adipose tissue (which normally stores fat for energy release). In line with this observation, the mice themselves were indeed more thermogenic and had increased energy expenditure, particularly following high fat diet feeding.

The researchers were able to show that sLR11 binds to specific receptors on fat cells — in the same way that a key fits into a lock — to inhibit their ability to activate thermogenesis. In effect, sLR11 acts as a signal to increase the efficiency of fat to store energy and prevents excessive energy loss through unrestricted thermogenesis.

When the researchers examined levels of sLR11 in humans, they found that levels of the protein circulating in the blood correlated with total fat mass — in other words, the greater the levels of the protein, the higher the total fat mass. In addition, when obese patients underwent bariatric surgery, their degree of postoperative weight loss was directly proportional to the reduction in their sLR11 levels, suggesting that sLR11 is produced by fat cells.

In their paper the authors suggest that sLR11 helps fat cells resist burning too much fat during ‘spikes’ in other metabolic signals following large meals or short term drops in temperature. This in turn makes adipose tissue more effective at storing energy over long periods of time.

There is growing interest in targeting thermogenesis with drugs in order to treat obesity, diabetes and other associated conditions such as heart disease. This is because it offers a mechanism for disposing of excess fat in a relatively safe manner. A number of molecules have already been identified that can increase thermogenesis and/or the number of fat cells capable of thermogenesis. However to date there have been very few molecules identified that can decrease thermogenesis.

These findings shed light on one of the mechanisms that the body employs to hold onto stored energy, where sLR11 levels increase in line with the amount of stored fat and act to prevent it being ‘wasted’ for thermogenesis.

Dr Andrew Whittle, joint first author, said: “Our discovery may help explain why overweight individuals find it incredibly hard to lose weight. Their stored fat is actively fighting against their efforts to burn it off at the molecular level.”

Professor Toni Vidal-Puig, who led the team, added: “We have found an important mechanism that could be targeted not just to help increase people’s ability to burn fat, but also help people with conditions where saving energy is important such as anorexia nervosa.”

Jeremy Pearson, Associate Medical Director at the British Heart Foundation (BHF), which helped fund the research, said: “This research could stimulate the development of new drugs that either help reduce obesity, by blocking the action of this protein, or control weight loss by mimicking its action. Based on this promising discovery, we look forward to the Cambridge team’s future findings.

“But an effective medicine to treat obesity, which safely manages weight loss is still some way off. In the meantime people can find advice on healthy ways to lose weight and boost their heart healthy on the BHF website — bhf.org.uk.”

Reference:

Andrew J. Whittle, Meizi Jiang, Vivian Peirce, Joana Relat, Sam Virtue, Hiroyuki Ebinuma, Isamu Fukamachi, Takashi Yamaguchi, Mao Takahashi, Takeyoshi Murano, Ichiro Tatsuno, Masahiro Takeuchi, Chiaki Nakaseko, Wenlong Jin, Zhehu Jin, Mark Campbell, Wolfgang J. Schneider, Antonio Vidal-Puig, Hideaki Bujo. Soluble LR11/SorLA represses thermogenesis in adipose tissue and correlates with BMI in humans. Nature Communications, 2015; 6: 8951 DOI: 10.1038/ncomms9951

As we age, we typically experience declines in the quality of our sleep. Mindfulness meditation is a self-administered approach that intentionally focuses one’s attention on the emotions, thoughts and sensations occurring in the present moment. David Black, from University of Southern California (California, USA), and colleagues enrolled 49 men and women, ages 55 years and older, whoe experienced moderately (or greater) disturbed sleep, who were divided into two groups. One group visited the study center for six weekly two-hour sessions of a course in Mindfulness Awareness Practices for daily living. Those included meditation, eating, walking, movement and friendly or loving-kindness practices. A certified teacher led the exercises and also instructed participants to meditate for five minutes daily, gradually increasing to 20 minutes daily. The other group attended six weeks of a sleep hygiene and education course, where they learned about sleep problems, and self-care methods for improving sleep, and weekly behavioral sleep hygiene strategies. Prior to the start of the six-week programs, the average sleep quality questionnaire score was 10. At the end of the study period, those in the meditation group demonstrated improvement in their sleep score by an average of 2.8 points, compared to 1.1 points in the sleep hygiene group. Among those in the meditation group, daytime impairments, including symptoms of insomnia, fatigue and depression, were improved as well. The study authors conclude that: “Formalized mindfulness-based interventions have clinical importance by possibly serving to remediate sleep problems among older adults in the short term, and this effect appears to carry over into reducing sleep-related daytime impairment that has implications for quality of life.”

Reference:

David S. Black, PhD, MPH1; Gillian A. O?Reilly, BS1; Richard Olmstead, PhD2; Elizabeth C. Breen, PhD2; Michael R. Irwin, MD2. Mindfulness Meditation and Improvement in Sleep Quality and Daytime Impairment Among Older Adults With Sleep Disturbances

Out of a ‘haystack’ of 40,000 genes from three different organisms, scientists at ETH Zurich and a research consortium in Jena have found genes that are involved in physical ageing. If you influence only one of these genes, the healthy lifespan of laboratory animals is extended and possibly that of humans, too.

With advancements in molecular genetic methods in recent decades, the search for the genes involved in the aging process has greatly accelerated. Until now, this was mostly limited to genes of individual model organisms such as the C. elegans nematode, which revealed that around one percent of its genes could influence life expectancy. However, researchers have long assumed that such genes arose in the course of evolution and in all living beings whose cells have a preserved a nucleus from yeast to humans.

Combing through 40,000 genes

Researchers at ETH Zurich and the JenAge consortium from Jena have now systematically gone through the genomes of three different organisms in search of the genes associated with the aging process that are present in all three species and thus derived from the genes of a common ancestor. Although they are found in different organisms, these so-called orthologous genes are closely related to each other, and they are all found in humans, too.

In order to detect these genes, the researchers examined around 40,000 genes in the nematode C. elegans, zebra fish and mice. By screening them, the scientists wanted to determine which genes are regulated in an identical manner in all three organisms in each comparable aging stage young, mature and old; i.e. either are they upregulated or downregulated during aging.

As a measure of gene activity, the researchers measured the amount of messenger RNA (mRNA) molecules found in the cells of these animals. mRNA is the transcript of a gene and the blueprint of a protein. When there are many copies of an mRNA of a specific gene, it is very active; the gene is upregulated. Fewer mRNA copies, to the contrary, are regarded as a sign of low activity, explains Professor Michael Ristow, coordinating author of the recently published study and Professor of Energy Metabolism at ETH Zurich.

Out of this volume of information, the researchers used statistical models to establish an intersection of genes that were regulated in the same manner in the worms, fish and mice. This showed that the three organisms have only 30 genes in common that significantly influence the aging process.

Reduce gene activity, live longer

By conducting experiments in which the mRNA of the corresponding genes were selectively blocked, the researchers pinpointed their effect on the aging process in nematodes. With a dozen of these genes, blocking them extended the lifespan by at least five percent.

One of these genes proved to be particularly influential: the bcat-1 gene. “When we blocked the effect of this gene, it significantly extended the mean lifespan of the nematode by up to 25 percent,” says Ristow.

The researchers were also able to explain how this gene works: the bcat-1 gene carries the code for the enzyme of the same name, which degrades so-called branched-chain amino acids. Naturally occurring in food protein building blocks, these include the amino acids L-leucine, L-isoleucine and L-valine.

When the researchers inhibited the gene activity of bcat-1, the branched-chain amino acids accumulated in the tissue, triggering a molecular signalling cascade that increased longevity in the nematodes. Moreover, the timespan during which the worms remained healthy was extended. As a measure of vitality, the researchers measured the accumulation of aging pigments, the speed at which the creatures moved, and how often the nematodes successfully reproduced. All of these parameters improved when the scientists inhibited the activity of the bcat-1 gene.

The scientists also achieved a life-extending effect when they mixed the three branched-chain amino acids into the nematodes’ food. However, the effect was generally less pronounced because the bcat-1 gene was still active, which meant that the amino acids continued to be degraded and their life-extending effects could not develop as effectively.

Conserved mechanism

Ristow has no doubt that the same mechanism occurs in humans. “We looked only for the genes that are conserved in evolution and therefore exist in all organisms, including humans,” he says.

In the present study, he and his Jena colleagues from the Leibniz Institute on Aging, the Leibniz Institute for Natural Product Research and Infection Biology, the Jena University Hospital and the Friedrich Schiller University purposefully opted not to study the impact on humans. But a follow-up study is already being planned. “However we cannot measure the life expectancy of humans for obvious reasons,” says the ETH professor. Instead, the researchers plan to incorporate various health parameters such as cholesterol or blood sugar levels in their study to obtain indicators on the health status of their subjects.

Health costs could be massively reduced

Ristow says that the multiple branched-chain amino acids are already being used to treat liver damage and are also added to sport nutrition products. “However, the point is not for people to grow even older, but rather to stay healthy for longer,” says the internist. The study will deliver important indicators on how the aging process could be influenced and how age-related diseases such as diabetes or high blood pressure could be prevented. In light of unfavourable demographics and steadily increasing life expectancy, it is important to extend the healthy life phase and not to reach an even higher age that is characterised by chronic diseases, argue the researchers. With such preventive measures, an elderly person could greatly improve their quality of life while at the same time cutting their healthcare costs by more than half.