Like spicy food? If so, you might live longer, say researchers at the Larner College of Medicine at the University of Vermont, who found that consumption of hot red chili peppers is associated with a 13 percent reduction in total mortality in a large prospective study.

For centuries, peppers and spices have been thought to improve health and longevity, but only one other scientific study conducted in China and published in 2015 has previously examined chili pepper consumption and its association with mortality. This new study corroborates the earlier study’s findings.

Using National Health and Nutritional Examination Survey (NHANES) III data collected from more than 16,000 Americans who were followed for up to 23 years, medical student Mustafa Chopan ’17 and Professor of Medicine Benjamin Littenberg, M.D., examined the baseline characteristics of the participants according to hot red chili pepper consumption. They found that consumers of hot red chili peppers tended to be “younger, male, white, Mexican-American, married, and to smoke cigarettes, drink alcohol, and consume more vegetables and meats,” in comparison to participants who did not consume red chili peppers. They examined data from a median follow-up of 18.9 years and observed the number of deaths and then analyzed specific causes of death.

“Although the mechanism by which peppers could delay mortality is far from certain, Transient Receptor Potential (TRP) channels, which are primary receptors for pungent agents such as capsaicin (the principal component in chili peppers), may in part be responsible for the observed relationship,” say the study authors.

There are some possible explanations for red chili peppers’ health benefits, state Chopan and Littenberg in the study. Among them are the fact that capsaicin is believed to play a role in cellular and molecular mechanisms that prevent obesity and modulate coronary blood flow, and also possesses antimicrobial properties that “may indirectly affect the host by altering the gut microbiota.”

“Because our study adds to the generalizability of previous findings, chili pepper or even spicy food consumption may become a dietary recommendation and/or fuel further research in the form of clinical trials,” says Chopan.

Reference: Mustafa Chopan, Benjamin Littenberg. The Association of Hot Red Chili Pepper Consumption and Mortality: A Large Population-Based Cohort Study. PLOS ONE, 2017; 12 (1): e0169876 DOI: 10.1371/journal.pone.0169876

Abstract: “The evidence base for the health effects of spice consumption is insufficient, with only one large population-based study and no reports from Europe or North America. Our objective was to analyze the association between consumption of hot red chili peppers and mortality, using a population-based prospective cohort from the National Health and Nutritional Examination Survey (NHANES) III, a representative sample of US noninstitutionalized adults, in which participants were surveyed from 1988 to 1994. The frequency of hot red chili pepper consumption was measured in 16,179 participants at least 18 years of age. Total and cause-specific mortality were the main outcome measures. During 273,877 person-years of follow-up (median 18.9 years), a total of 4,946 deaths were observed. Total mortality for participants who consumed hot red chili peppers was 21.6% compared to 33.6% for those who did not (absolute risk reduction of 12%; relative risk of 0.64). Adjusted for demographic, lifestyle, and clinical characteristics, the hazard ratio was 0.87 (P = 0.01; 95% Confidence Interval 0.77, 0.97). Consumption of hot red chili peppers was associated with a 13% reduction in the instantaneous hazard of death. Similar, but statistically nonsignificant trends were seen for deaths from vascular disease, but not from other causes. In this large population-based prospective study, the consumption of hot red chili pepper was associated with reduced mortality. Hot red chili peppers may be a beneficial component of the diet.”

Like everything else in the body, the white-matter fibers that allow communication between brain regions also decline with age. In a new study, researchers found a strong association between the structural integrity of these white-matter tracts and an older person’s level of daily activity not just the degree to which the person engaged in moderate or vigorous exercise, but also whether he or she was sedentary the rest of the time.

The study, reported in the journal PLOS ONE, tracked physical activity in 88 healthy but “low-fit” participants aged 60 to 78. The participants agreed to wear accelerometers during most of their waking hours over the course of a week, and also submitted to brain imaging.

“To our knowledge, this is the first study of its kind that uses an objective measure of physical activity along with multiple measures of brain structure,” said University of Illinois postdoctoral researcher Agnieszka Burzynska, who conducted the research with U. of I. Beckman Institute director Arthur Kramer and kinesiology and community health professor Edward McAuley.

Most studies ask subjects to describe how much physical activity they get, which is subjective and imprecise, Burzynska said. The accelerometer continuously tracks a person’s movement, “so it’s not what they say they do or what they think they do, but we have measured what they are actually doing,” she said.

The researchers assumed that participants’ activity levels over a week accurately reflected their overall engagement, or lack of engagement, in physical activity.

The study also relied on two types of brain imaging. The first, diffusion tensor imaging, offers insight into the structural integrity of a tissue by revealing how water is diffused in the tissue. The second method looks for age-related changes in white matter, called lesions. Roughly 95 percent of adults aged 65 and older have such lesions, Burzynska said. While they are a normal part of aging, their early onset or rapid accumulation may spell trouble, she said.

The team found that the brains of older adults who regularly engaged in moderate-to-vigorous exercise generally “showed less of the white-matter lesions,” Burzynska said.

The association between physical activity and white-matter structural integrity was region-specific, the researchers reported. Older adults who engaged more often in light physical activity had greater structural integrity in the white-matter tracts of the temporal lobes, which lie behind the ears and play a key role in memory, language, and the processing of visual and auditory information.

In contrast, those who spent more time sitting had lower structural integrity in the white-matter tracts connecting the hippocampus, “a structure crucial for learning and memory,” Burzynska said.

“This relationship between the integrity of tracts connecting the hippocampus and sedentariness is significant even when we control for age, gender and aerobic fitness,” she said. “It suggests that the physiological effect of sitting too much, even if you still exercise at the end of the day for half an hour, will have a detrimental effect on your brain.”

The findings suggest that engaging in physical activity and avoiding a sedentary lifestyle are both important for brain health in older age, Burzynska said.

“We hope that this will encourage people to take better care of their brains by being more active,” she said.

Reference: Agnieszka Zofia Burzynska ,Laura Chaddock-Heyman,Michelle W. Voss,Chelsea N. Wong,Neha P. Gothe,Erin A. Olson,Anya Knecht,Andrew Lewis,Jim M. Monti,Gillian E. Cooke,Thomas R. Wojcicki,Jason Fanning,Hyondo David Chung,Elisabeth Awick,Edward McAuley,Arthur F. Kramer. Physical Activity and Cardiorespiratory Fitness Are Beneficial for White Matter in Low-Fit Older Adults. PLoS ONE 9(9): e107413. doi:10.1371/journal.pone.0107413

The stem cells in our teeth can be energized to fill in chips, cracks, and cavities, researchers say, and the findings could one day possibly make dental cement obsolete.

The work has been conducted just in mice so far, but the research, published Monday in the journal Scientific Reports, highlights a way to motivate stem cells to repair tooth defects at a scale they normally can?t, with a drug that already has some safety testing behind it. It also demonstrates the potential of a type of stem cell therapy in which the cells are stimulated in place, rather than taken out, manipulated, and put back in.

?We?re mobilizing stem cells in the body and it works,? said Paul Sharpe, a researcher at King?s College London and an author of the new paper. ?If it works for teeth, chances are it could work for other organs.?

Experts not involved with the work noted that while it is in early stages, the simplicity of the approach should ease its path into the next phases of research that show whether it might produce the same results in people.

?These important steps close down the translational gap and bring this discovery a step closer to future clinical applications,? Dr. Vanessa Chrepa, a researcher at the University of Washington, wrote in an email. ?This work will hopefully set the stage for clinical studies in the near future.?

When teeth lose some of their dentin ? the bony tissue beneath the enamel that makes up the bulk of the tooth ? the stem cells tucked deep inside mount a recovery effort and manufacture new dentin (which is also spelled dentine). The problem, Sharpe said, is that the natural repair mechanism can only regrow small amounts of dentin and can?t make up all that is lost when a tooth suffers a serious injury, contracts a major infection, or takes on the sharp end of a dentist?s drill.

Because of the limits of the teeth?s ability to repair themselves, dentists have to fill or seal teeth to prevent further infection and degradation. But dental cement also prevents the tooth from ever returning to its natural, pearly white self.

Sharpe and his team have been trying to understand how the natural repair mechanism works in hopes of converting that understanding into a way to super-power it. As part of their research, they discovered that a group of molecules called glycogen synthase kinase inhibitors (or GSK-3 inhibitors) boosts the stem cells? ability to stimulate production of dentin beyond what normally occurs.

For the new study, the researchers drilled tiny holes into mice?s molars to expose the tooth?s pulp, where the stem cells live. They then inserted collagen sponges that had been soaked in one of three types of GSK-3 inhibitors and covered the tooth.

After six weeks, the researchers removed the teeth and found that the sponges had dissolved and the lost dentin had mostly been regenerated.

?They?ve harnessed the signaling pathway that promotes natural repair,? said Megan Pugach, a researcher at the Forsyth Institute in Cambridge, Mass., and at the Harvard School of Dental Medicine, who was not involved with the research.

Sharpe and his team are now conducting similar studies in rats to make sure the approach can generate enough dentin to fill in larger holes in larger teeth before trying to study the method in people. But two aspects of the approach could help ease its path into clinical trials.

A new study shows that older people who followed a Mediterranean diet retained more brain volume over a three-year period than those who did not follow the diet as closely. The study is published in the January 4, 2017, online issue of Neurology?, the medical journal of the American Academy of Neurology. But contrary to earlier studies, eating more fish and less meat was not related to changes in the brain.

The Mediterranean diet includes large amounts of fruits, vegetables, olive oil, beans, whole grains, moderate amounts of fish, dairy and wine, and limited red meat and poultry.

“As we age, the brain shrinks and we lose brain cells which can affect learning and memory,” said study author Michelle Luciano, PhD, of the University of Edinburgh in Scotland. “This study adds to the body of evidence that suggests the Mediterranean diet has a positive impact on brain health.”

Researchers gathered information on the eating habits of 967 Scottish people around age 70 who did not have dementia. Of those people, 562 had an MRI brain scan around age 73 to measure overall brain volume, gray matter volume and thickness of the cortex, which is the outer layer of the brain. From that group, 401 people then returned for a second MRI at age 76. These measurements were compared to how closely participants followed the Mediterranean diet.

The participants varied in how closely their dietary habits followed the Mediterranean diet principles. People who didn’t follow as closely to the Mediterranean diet were more likely to have a higher loss of total brain volume over the three years than people who followed the diet more closely. The difference in diet explained 0.5 percent of the variation in total brain volume, an effect that was half the size of that due to normal aging.

The results were the same when researchers adjusted for other factors that could affect brain volume, such as age, education and having diabetes or high blood pressure.

There was no relationship between grey matter volume or cortical thickness and the Mediterranean diet.

The researchers also found that fish and meat consumption were not related to brain changes, which is contrary to earlier studies.

“It’s possible that other components of the Mediterranean diet are responsible for this relationship, or that it’s due to all of the components in combination,” Luciano said.

Luciano noted that earlier studies looked at brain measurements at one point in time, whereas the current study followed people over time.

“In our study, eating habits were measured before brain volume was, which suggests that the diet may be able to provide long-term protection to the brain,” said Luciano. “Still, larger studies are needed to confirm these results.”

Reference: 1.Michelle Luciano, Janie Corley, Simon R. Cox, Maria C. Vald?s Hern?ndez, Leone C.A. Craig, David Alexander Dickie, Sherif Karama, Geraldine M. McNeill, Mark E. Bastin, Joanna M. Wardlaw, Ian J. Deary. Mediterranean-type diet and brain structural change from 73 to 76 years in a Scottish cohort. Neurology, 2017; 10.1212/WNL.0000000000003559 DOI: 10.1212/WNL.0000000000003559

Are pomegranates really the superfood we’ve been led to believe will counteract the aging process? Up to now, scientific proof has been fairly weak. And some controversial marketing tactics have led to skepticism as well. A team of scientists from EPFL wanted to explore the issue by taking a closer look at the secrets of this plump pink fruit. They discovered that a molecule in pomegranates, transformed by microbes in the gut, enables muscle cells to protect themselves against one of the major causes of aging. In nematodes and rodents, the effect is nothing short of amazing. Human clinical trials are currently underway, but these initial findings have already been published in the journal Nature Medicine.

As we age, our cells increasingly struggle to recycle their powerhouses. Called mitochondria, these inner compartments are no longer able to carry out their vital function, thus accumulate in the cell. This degradation affects the health of many tissues, including muscles, which gradually weaken over the years.

One molecule plays David against the Goliath of aging

The scientists identified a molecule that, all by itself, managed to re-establish the cell’s ability to recycle the components of the defective mitochondria: urolithin A. “It’s the only known molecule that can relaunch the mitochondrial clean-up process, otherwise known as mitophagy,” says Patrick Aebischer, co-author on the study. “It’s a completely natural substance, and its effect is powerful and measurable.”

The team started out by testing their hypothesis on the usual suspect: the nematode C. elegans. It’s a favorite test subject among aging experts, because after just 8-10 days it’s already considered elderly. The lifespan of worms exposed to urolithin A increased by more than 45% compared with the control group.

These initial encouraging results led the team to test the molecule on animals that have more in common with humans. In the rodent studies, like with C. elegans, a significant reduction in the number of mitochondria was observed, indicating that a robust cellular recycling process was taking place. Older mice, around two years of age, showed 42% better endurance while running than equally old mice in the control group.

Before heading out to stock up on pomegranates, however, it’s worth noting that the fruit doesn’t itself contain the miracle molecule, but rather its precursor. That molecule is converted into urolithin A by the microbes that inhabit the intestine. Because of this, the amount of urolithin A produced can vary widely, depending on the species of animal and the flora present in the gut microbiome. Some individuals don’t produce any at all. If you’re one of the unlucky ones, it’s possible that pomegranate juice won’t do you any good.

For those without the right microbes in their guts, however, the scientists are already working on a solution. The study’s co-authors founded a start-up company, which has developed a method to deliver finely calibrated doses of urolithin A. The company is currently conducting first clinical trials testing the molecule in humans in European hospitals.

According to study co-author Johan Auwerx, it would be surprising if urolithin A weren’t effective in humans. “Species that are evolutionarily quite distant, such as C elegans and the rat, react to the same substance in the same way. That’s a good indication that we’re touching here on an essential mechanism in living organisms.”

Urolithin A’s function is the product of tens of millions of years of parallel evolution between plants, bacteria and animals. According to Chris Rinsch, co-author, this evolutionary process explains the molecule’s effectiveness: “Precursors to urolithin A are found not only in pomegranates, but also in smaller amounts in many nuts and berries. Yet for it to be produced in our intestines, the bacteria must be able to break down what we’re eating. When, via digestion, a substance is produced that is of benefit to us, natural selection favors both the bacteria involved and their host. Our objective is to follow strict clinical validations, so that everyone can benefit from the result of these millions of years of evolution.”

Reference: 1.Dongryeol Ryu, Laurent Mouchiroud, P?n?lope A Andreux, Elena Katsyuba, Norman Moullan, Amandine A Nicolet-dit-F?lix, Evan G Williams, Pooja Jha, Giuseppe Lo Sasso, Damien Huzard, Patrick Aebischer, Carmen Sandi, Chris Rinsch & Johan Auwerx. Urolithin A induces mitophagy and prolongs lifespan in C. elegans and increases muscle function in rodents. Nature Medicine, July 2016 DOI: 10.1038/nm.4132