Anti-Aging Effects of the Mediterranean Diet On Brain Health


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

Can Pomegranates Extend Youthful Vitality and Lifespan?


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

Plant Pigment Linked To Cognitive Performance Across Lifespan

Stem Cells

A large study of older adults links consumption of a pigment found in leafy greens to the preservation of “crystallized intelligence,” the ability to use the skills and knowledge one has acquired over a lifetime.

The nutrient is lutein and the study is reported in the journal Frontiers in Aging Neuroscience.

Humans acquire lutein through the diet, primarily by eating leafy green vegetables, cruciferous vegetables such as broccoli, or egg yolks, according to University of Illinois graduate student Marta Zamroziewicz, who led the study with Illinois psychology professor Aron Barbey. It accumulates in the brain, embedding in cell membranes, where it likely plays “a neuroprotective role,” she said.

Lutein is also available as a dietary supplement which is typically extracted from the marigold plant and taken at a dosage of 20 mg per day. Most health food stores carry lutein which is often combined with zeaxanthin another nutrient from marigolds.

“Previous studies have found that a person’s lutein status is linked to cognitive performance across the lifespan,” Zamroziewicz said. “Research also shows that lutein accumulates in the gray matter of brain regions known to underlie the preservation of cognitive function in healthy brain aging.”

The study enrolled 122 healthy participants aged 65 to 75 who solved problems and answered questions on a standard test of crystallized intelligence. Researchers also collected blood samples to determine blood serum levels of lutein and imaged participants’ brains using MRI to measure the volume of different brain structures.

The team focused on parts of the temporal cortex, a brain region that other studies suggest plays a role in the preservation of crystallized intelligence.

The researchers found that participants with higher blood serum levels of lutein tended to do better on tests of crystallized intelligence. Serum lutein levels reflect only recent dietary intakes, Zamroziewicz said, but are associated with brain concentrations of lutein in older adults, which reflect long-term dietary intake.

Those with higher serum lutein levels also tended to have thicker gray matter in the parahippocampal cortex, a brain region that, like crystallized intelligence, is preserved in healthy aging, the researchers report.

“Our analyses revealed that gray-matter volume of the parahippocampal cortex on the right side of the brain accounts for the relationship between lutein and crystallized intelligence,” Barbey said. “This offers the first clue as to which brain regions specifically play a role in the preservation of crystallized intelligence, and how factors such as diet may contribute to that relationship.”

“Our findings do not demonstrate causality,” Zamroziewicz said. “We did find that lutein is linked to crystallized intelligence through the parahippocampal cortex.”

“We can only hypothesize at this point how lutein in the diet affects brain structure,” Barbey said. “It may be that it plays an anti-inflammatory role or aids in cell-to-cell signaling. But our finding adds to the evidence suggesting that particular nutrients slow age-related declines in cognition by influencing specific features of brain aging.”

Study Reference: Marta K. Zamroziewicz, Erick J. Paul, Chris E. Zwilling, Elizabeth J. Johnson, Matthew J. Kuchan, Neal J. Cohen, Aron K. Barbey. Parahippocampal Cortex Mediates the Relationship between Lutein and Crystallized Intelligence in Healthy, Older Adults. Frontiers in Aging Neuroscience, 2016; 8 DOI: 10.3389/fnagi.2016.00297

Staying Young and Extending Life By Resetting Blood Proteins

Stem Cells

A number of studies have been done where older animals were given blood from younger animals to find out if that would increase life span. It did and also improved the health of the older animals. In a new study, scientists are trying to reverse aging in older humans by filtering bad proteins from their blood and return it to a more youthful state. This comes after a study on mice showed that the procedure had some promise. For instance there was evidence that the blood cells from the younger mice produced muscle repair in the older mice. Now researchers from California are trying to replicate the results in older people in a clinical trial. The aim of this radical approach is to alter levels of bad proteins in the blood of older people. These proteins are believed to be responsible for hampering the growth of healthy tissue. This could help in the prevention of age-related disease and possibly slow down the aging process. The study was published in the journal Nature Communications.

This is part of what we are doing with Stem Cell 100 and Stem Cell 100+. They contain compounds for instance that up regulate longevity genes and help the blood and tissues to a younger state. Of course this occurs over time.

The animal study was co-funded by Calico, which is a life extension company owned by Google. The experiment was reversed on mice with old blood infused into young mice. The results showed a reduction in new liver and brain cells in the young mice and impaired performance in strength. This gave more credibility to the original experiment. In the human trial, older blood will pass through a machine that will try to reset proteins to a healthier level in the hope that body tissues will be properly maintained thus slowing down aging.

This new study is one of many that show key molecules in the blood can alter the pace of aging in body tissue. When these proteins are at low levels the body is healthy, but as we get older these protein levels can change. The team is now considering a more practical approach to control the levels of the proteins without blood transfusions. According to one scientist, these new treatments could prevent diabetes, Alzheimer’s, and Parkinson?s disease.

Another scientist Tony Wyss-Coray, from Stanford University was not convinced by the study and pointed out that only four pairs of mice were used in the experiment. In past experiments on animals, a procedure called parabiosis was used to swap blood between animals by conjoining them surgically. In this study, scientists did not use surgery but instead transferred blood through a tube and pump controlled by a computer.

The team is now working on devices that filter blood in more advanced ways to reduce high levels of the bad proteins. This will return the proteins to more youthful levels. The key here is to remove the inhibitor molecules and then to return the filtered blood back to the recipient. This medical procedure could result in life extension that could give people an extra three decades of life without any critical illnesses. This advanced treatment could become available within 3 years.

The Berkley team is currently brainstorming for ideas on how to normalize the levels of one particular protein considered to be the inhibitor. They hope clinical trials will start within six months and start producing results within three years. Scientist could be on the verge of transforming our lives by slowing the aging process and stopping age-related diseases.

References: Justin Rebo, Melod Mehdipour, Ranveer Gathwala, Keith Causey, Yan Liu, Michael J. Conboy & Irina M. Conboy. A single heterochronic blood exchange reveals rapid inhibition of multiple tissues by old blood. Nature Communications, 2016; doi:10.1038/ncomms13363

Colon Bacteria Turn Host Genes On or Off Depending Upon Diet

Colon Bacteria

New research provides further evidence of the important role that gut microbes play in health by revealing they alter host gene expression in a diet-dependent manner. Using mice, the researchers discovered that a Western diet prevents many of the gene expression changes of a plant rich diet. This provides important and additional evidence of the importance of eating lots of fruits and vegetables.

A study of the relationship between colon bacteria, diet and the genes of the host by a team at the University of Wisconsin-Madison (UW-Madison) was published in the journal Molecular Cell.

Genes found in strips of DNA contained in chromosomes are the blueprint for making organisms and sustaining life. However, while their DNA makeup is relatively fixed, genes respond to changes in environment.

Interactions with the environment do not change the genes, but they alter their expression by switching them on and off through chemical tags on the DNA.

The complete set of genetic material contained in our genes is called the genome, and the multitude of molecules that tell the genome what to do is called the epigenome.

Our gut is home to trillions of microbes altogether, they can weigh up to 2 kilograms. They not only help to digest food via fermentation, but in the process produce molecules called metabolites that influence health and disease for instance, to improve immune function and defend against infection.

In their paper, the UW-Madison researchers explain that while we have discovered that the colonies of microbes in our digestive tract collectively termed the gut microbiota produce a myriad of metabolites that affect health and disease, the underlying molecular mechanisms are poorly understood.

For their study, the researchers used mice raised on two different diets: one rich in plant carbohydrates (mimicking a human diet rich in fruits and vegetables) and the other high in simple sugars and fats (mimicking a Western diet).

The researchers found that a small group of short-chain fatty acids metabolites produced when gut bacteria ferment nutrients from plants were communicating with the cells of the host animals through the epigenome.

One of the investigators, John M. Denu, a UW-Madison professor of biomolecular chemistry and a senior researcher at the Wisconsin Institute for Discovery, says the short-chain fatty acids, and potentially many others, are partially responsible for the communication with epigenome.

When Prof. Denu and colleagues compared the mice fed on a Western-style diet with the ones on a diet rich in plant carbohydrates, they found the Western-style diet prevents many of the epigenetic changes that occur in the plant-rich diet.

In a further set of experiments, the researchers then supplemented the diet of mice raised in a germ-free environment (so they have no gut microbiota to speak of) with the short-chain fatty acids metabolites of gut bacteria fermentation.

They found that the short-chain fatty acid supplements restored the types of epigenetic changes seen in normal mice raised on the plant-rich diet.

Prof. Denu suggests their findings help show “the collection of three short-chain fatty acids produced in the plant-based diet are likely major communicators. We see that it is not just the microbe. It’s microbial metabolism.”

He and his colleagues also note that while foods rich in fat and sugar – hallmarks of the Western diet are more easily digested, they are not necessarily a good source of nutrients for gut microbes. This results in a less diverse microbiome, and less communication with the epigenome, they suggest.

They conclude that their findings have “profound implications for understanding the complex functional interactions between diet, gut microbiota, and host health.”

Another surprising result of the study is that the communication between the gut microbiome and the host reaches beyond the colon. For example, the team found evidence of communication with cells of the liver and fatty tissue of the gut.