How Stress Harms Mitochondria

New research has shown evidence and interactions between psychological and physical health effects that involve mitochondria according to experimental studies conducted by Martin Picard of Columbia University and Bruce S. McEwen of The Rockefeller University. Mitochondria are specialized cellular structures with their own DNA and are found in nearly every type of cell in the body. Sometimes referred to as cellular ?powerhouses?, they generate signals and energy required for life. When they are not working correctly, they can cause severe diseases affecting many of the different body systems.

A total of 23 experimental studies on animals conducted by researchers around the world points to mitochondria as a potential intersection between psychosocial experiences and biological stress responses. Researchers have found that acute and chronic stress influenced specific aspects of mitochondrial function, especially in the brain. A wide range of factors including genes, diet and behavior may also influence mitochondrial vulnerability to stress. The Doctors have also outlined a conceptual framework by which mitochondria may convert the effects of psychological stress on to physical health. Evidence indicates that mitochondria sense, integrate and signal information about the environment and includes stress induced mediators which cause functional and structural recalibration of the mitochondria.

Describing the functional and structural changes that mitochondria undergo as response to chronic stress, the Doctors introduced the concept of MAL (Mitochondrial Allostatic Load). These changes may lead to widespread health effects such as increased inflammation leading to a higher risk of disease and damage to cellular DNA leading to accelerated aging. It appears that mitochondria is involved in regulating the body?s stress reactivity systems including controlling immunity, inflammation and the brain. Damage to mitochondrial DNA has been associated with a biological aging clock. Recent studies have shown that mitochondria affect the rate of aging in mammals, however it is not clear whether this is the case in humans.

Emerging evidence on the role of mitochondria and translating the effects of stress on physical health extend the reach of mind-body research into the cellular/molecular domain. The findings are particularly exciting for psychosomatic medicine with its focus on reintegrating the mind and body. The findings also represent the core foundation of current biomedical training and practice. The doctors emphasize that more research is needed to test various elements of their model in humans and to further consider the dynamic bi-directional interactions between important physiological systems and mitochondria.

Journal References:

1. Martin Picard, Bruce S. McEwen. Psychological Stress and Mitochondria: A Systematic Review. Psychosomatic Medicine, 2018; 80 (2): 141 DOI: 10.1097/PSY.0000000000000545

2. Martin Picard, Bruce S. McEwen. Psychological Stress and Mitochondria: A Conceptual Framework. Psychosomatic Medicine, 2018; 80 (2): 126 DOI: 10.1097/PSY.0000000000000544

Abstract

Objective Mitochondria are multifunctional life-sustaining organelles that represent a potential intersection point between psychosocial experiences and biological stress responses. This article provides a systematic review of the effects of psychological stress on mitochondrial structure and function.

Methods: A systematic review of the literature investigating the effects of psychological stress on mitochondrial function was conducted. The review focused on experimentally controlled studies allowing us to draw causal inference about the effect of induced psychological stress on mitochondria.

Results: A total of 23 studies met the inclusion criteria. All studies involved male laboratory animals, and most demonstrated that acute and chronic stressors influenced specific facets of mitochondrial function, particularly within the brain. Nineteen studies showed significant adverse effects of psychological stress on mitochondria and four found increases in function or size after stress. In humans, only six observational studies were available, none with experimental designs, and most only measured biological markers that do not directly reflect mitochondrial function, such as mitochondrial DNA copy number.

Conclusons: Overall, evidence supports the notion that acute and chronic stressors influence various aspects of mitochondrial biology, and that chronic stress exposure can lead to molecular and functional recalibrations among mitochondria. Limitations of current animal and human studies are discussed. Maladaptive mitochondrial changes that characterize this subcellular state of stress are termed mitochondrial allostatic load. Prospective studies with sensitive measures of specific mitochondrial outcomes will be needed to establish the link between psychosocial stressors, emotional states, the resulting neuroendocrine and immune processes, and mitochondrial energetics relevant to mind-body research in humans.

Dim Light May Shrink Your Brain

Spending too much time in dimly lit rooms and offices may actually change the brain’s structure and hurt one’s ability to remember and learn, indicates groundbreaking research by Michigan State University neuroscientists.

The researchers studied the brains of Nile grass rats (which, like humans, are diurnal and sleep at night) after exposing them to dim and bright light for four weeks. The rodents exposed to dim light lost about 30 percent of capacity in the hippocampus, a critical brain region for learning and memory, and performed poorly on a spatial task they had trained on previously.

The rats exposed to bright light, on the other hand, showed significant improvement on the spatial task. Further, when the rodents that had been exposed to dim light were then exposed to bright light for four weeks (after a month-long break), their brain capacity and performance on the task recovered fully.

The study, funded by the National Institutes of Health, is the first to show that changes in environmental light, in a range normally experienced by humans, leads to structural changes in the brain. Americans, on average, spend about 90 percent of their time indoors, according to the Environmental Protection Agency.

“When we exposed the rats to dim light, mimicking the cloudy days of Midwestern winters or typical indoor lighting, the animals showed impairments in spatial learning,” said Antonio “Tony” Nunez, psychology professor and co-investigator on the study. “This is similar to when people can’t find their way back to their cars in a busy parking lot after spending a few hours in a shopping mall or movie theater.”

Nunez collaborated with Lily Yan, associate professor of psychology and principal investigator on the project, and Joel Soler, a doctoral graduate student in psychology. Soler is also lead author of a paper on the findings published in the journal Hippocampus.

Soler said sustained exposure to dim light led to significant reductions in a substance called brain derived neurotrophic factor a peptide that helps maintain healthy connections and neurons in the hippocampus and in dendritic spines, or the connections that allow neurons to “talk” to one another.

“Since there are fewer connections being made, this results in diminished learning and memory performance that is dependent upon the hippocampus,” Soler said. “In other words, dim lights are producing dimwits.”

Interestingly, light does not directly affect the hippocampus, meaning it acts first other sites within the brain after passing through the eyes. Yan said the research team is investigating one potential site in the rodents’ brains a group of neurons in the hypothalamus that produce a peptide called orexin that’s known to influence a variety of brain functions. One of their major research questions: If orexin is given to the rats that are exposed to dim light, will their brains recover without being re-exposed to bright light?

The project could have implications for the elderly and people with glaucoma, retinal degeneration or cognitive impairments.

“For people with eye disease who don’t receive much light, can we directly manipulate this group of neurons in the brain, bypassing the eye, and provide them with the same benefits of bright light exposure?” Yan said. “Another possibility is improving the cognitive function in the aging population and those with neurological disorders. Can we help them recover from the impairment or prevent further decline?”

Reference: Joel E. Soler, Alfred J. Robison, Antonio A. N??ez, Lily Yan. Light modulates hippocampal function and spatial learning in a diurnal rodent species: A study using male nile grass rat (Arvicanthis niloticus). Hippocampus, 2017; DOI: 10.1002/hipo.22822

Stem Cells and Accelerated Healing

Adult Stem Cells

New research by a team at the University of South Carolina has discovered a way to increase the body?s ability to heal after injury. The study led by Assistant Professor of Stem Cell Biology and Regenerative Medicine, has proved that adult stem cells will enter an alert state when the body sustains an injury. These ?alerted? stem cells have a greater ability to repair and heal damaged tissues.

It is theorized that after an injury a person?s blood can produce a state of alert. Using lab mice, the researchers injected healthy mice with blood from their injured counterparts. The stem cells in the healthy mice went into a state of alert. The team then identified the enzyme Hepatocyte Growth Factor Activator (HGFA), as the chemical mechanism that signaled cells to an alert state. HGFA is always in the bloodstream but only activates when the body experiences an injury. The enzyme signals adult stem cells to enter this state of alert once an injury occurs.

The team then decided to see what would happen if an injury occurred while the adult stem cells were already in a state of alert. Healthy mice were injected with HGFA. A few days later the mice were given muscle and skin injuries. The test mice were observed to heal faster, regrow missing fur and after just nine days returned to running on exercise wheels sooner. Twenty days after the injuries, the mice that had been injected with HGFA had regenerated larger muscle fibers compared to the untreated mice.

The findings support the idea that the presence of HGFA in the bloodstream prepares the body to respond faster and more efficiently to an injury. The response was similar to how vaccines prepare the body to fight specific diseases. HGFA prepares the cells to respond to tissue damage. By ?priming? the body, you can speed the process of tissue repair and recovery.

It is hoped that in the future people may be able to use HGFA prior to engaging in activities that might result in injury including sports, surgery and even combat. HGFA may also be able to be used therapeutically for people with compromised healing abilities. And this therapeutic approach may also be of value for the elderly. As we age, the body?s ability to heal itself slows down as stem cell activity diminishes with advancing age. The team posed the concept that it might be possible to restore youthful healing by activating the HGFA pathway!

Reference: Joseph T. Rodgers, Matthew D. Schroeder, Chanthia Ma, Thomas A. Rando. HGFA Is an Injury-Regulated Systemic Factor that Induces the Transition of Stem Cells into GAlert. Cell Reports, April 2017 DOI: 10.1016/j.celrep.2017.03.066

Skin Cells Produced with Gene Activation

In a scientific first, researchers at the Gladstone Institutes turned skin cells from mice into stem cells by activating a specific gene in the cells using CRISPR technology. The innovative approach offers a potentially simpler technique to produce the valuable cell type and provides important insights into the cellular reprogramming process.

“This is a new way to make induced pluripotent stem cells that is fundamentally different from how they’ve been created before,” said author Sheng Ding, PhD, a senior investigator at Gladstone. “At the beginning of the study, we didn’t think this would work, but we wanted to at least try to answer the question: can you reprogram a cell just by unlocking a specific location of the genome? And the answer is yes.”

Pluripotent stem cells can be turned into virtually any cell type in the body. As a result, they are a key therapeutic resource for currently incurable conditions, such as heart failure, Parkinson’s disease, and blindness. They also provide excellent models to study diseases and important tools to test new drugs in human cells.

In 2006, Gladstone Senior Investigator Shinya Yamanaka, MD, PhD, discovered he could make stem cells — dubbed induced pluripotent stem cells (iPSCs) — by treating ordinary skin cells with four key proteins. These proteins, called transcription factors, work by changing which genes are expressed in the cell, turning off genes associated with skin cells and turning on genes associated with stem cells.

Building on this work, Ding and others previously created iPSCs not with transcription factors, but by adding a cocktail of chemicals to the cells. The latest study, published in Cell Stem Cell, offers a third way to turn skin cells into stem cells by directly manipulating the cells’ genome using CRISPR gene regulation techniques.

“Having different options to make iPSCs will be useful when scientists encounter challenges or difficulties with one approach,” said Ding, who is also a professor of pharmaceutical chemistry at the University of California, San Francisco. “Our approach could lead to a simpler method of creating iPSCs or could be used to directly reprogram skin cells into other cell types, such as heart cells or brain cells.”

CRISPR is a powerful tool that can precisely manipulate the genome by targeting a unique sequence of DNA. That sequence of DNA is then either permanently deleted or replaced, or it is temporarily turned on or off.

Ding’s team targeted two genes that are only expressed in stem cells and known to be integral to pluripotency: Sox2 and Oct4. Like transcription factors, these genes turn on other stem cell genes and turn off those associated with different cell types.

The researchers discovered that with CRISPR, they could activate either Sox2 or Oct4 to reprogram cells. In fact, they showed that targeting a single location on the genome was enough to trigger the natural chain reaction that led to reprogramming the cell into an iPSC.

For comparison, four transcription factors are typically used to create iPSCs using the original method. What’s more, one transcription factor typically targets thousands of genomic locations in the cell and changes gene expression at each location.

“The fact that modulating one site is sufficient is very surprising,” said Ding. “Now, we want to understand how this whole process spreads from a single location to the entire genome.”

Reference: Peng Liu, Meng Chen, Yanxia Liu, Lei S. Qi, Sheng Ding. CRISPR-Based Chromatin Remodeling of the Endogenous Oct4 or Sox2 Locus Enables Reprogramming to Pluripotency. Cell Stem Cell, 2018; DOI: 10.1016/j.stem.2017.12.001

Abstract: Generation of induced pluripotent stem cells typically requires the ectopic expression of transcription factors to reactivate the pluripotency network. However, it remains largely unclear what remodeling events on endogenous chromatin trigger reprogramming toward induced pluripotent stem cells (iPSCs). Toward this end, we employed CRISPR activation to precisely target and remodel endogenous gene loci of Oct4 and Sox2. Interestingly, we found that single-locus targeting of Sox2 was sufficient to remodel and activate Sox2, which was followed by the induction of other pluripotent genes and establishment of the pluripotency network. Simultaneous remodeling of the Oct4 promoter and enhancer also triggered reprogramming. Authentic pluripotent cell lines were established in both cases. Finally, we showed that targeted manipulation of histone acetylation at the Oct4 gene locus could also initiate reprogramming. Our study generated authentic iPSCs with CRISPR activation through precise epigenetic remodeling of endogenous loci and shed light on how targeted chromatin remodeling triggers pluripotency induction.

Deep, Restorative Sleep and Learning

A good night?s sleep makes an important contribution to our health while a poor night?s sleep has a negative effect. A new study published in the Nature Communications Journal by the University of Zurich and the Swiss Federal Institute of Technology in Zurich has discovered there is a connection between deep sleep and learning efficiency.

The researchers set out to examine how disturbed deep sleep affects the brain?s ability to learn new things. More specifically, the researchers were interested in the brain?s ability to adapt and change in response to stimuli received from the environment in the motor cortex and how it is affected by deep sleep. The motor cortex is the part of the brain that is responsible for controlling and developing motor skills. The deep sleep phase, also referred to as the slow-wave sleep phase, is key to memory processing and formation and additionally helps the brain restore itself after daytime activity.

The study included seven men and six women. All were asked to perform motoric tasks during the day followed by a night of undisturbed sleep followed by a night during which time their deep sleep was disturbed. The daytime tasks involved a variety of finger movements, and the researchers identified precisely the area of the brain responsible for learning movements. Using an electroencephalogram, the researchers monitored the brain activity while the participants slept.

On the first night following the first session of learning movements, the participants were able to sleep without disturbances. During the second night of the study, the researchers manipulated the quality of sleep. They focused on the motor cortex while disrupting deep sleep therefore studying the impact poor, disturbed sleep has on the neuroplasticity associated with practicing new movements. None of the participants knew their deep sleep was being tampered with. To them, quality of sleep was identical both nights.

Researchers then studied each participant?s ability to learn new movements. The participants learning performance was at its highest in the morning as expected. However, as the day progressed, more and more mistakes were made which again was as expected.
What the researchers found after a restorative night?s sleep was the participants learning efficiency spiked again. However, following the night of disturbed, manipulative sleep, the learning efficiency did not improve as significantly and the participant?s performance was as low in the morning as it was on the evening of the previous day.

According to the researchers, during manipulated deep sleep the neuron?s synapses did not rest which would normally occur during deep sleep. Our synapses get excited during the day as response to a variety of stimuli throughout each day. With sleep, these synapses restore themselves and activity normalizes. Without a restorative period of time, the synapses stay maximally excited for too long a period. This state inhibits neuroplasticity which means learning new things is no longer possible. Learning efficiency was saturated in the strongly excited area of the brain which inhibited learning new motor skills.

To further ensure they had located the right area of the brain responsible for deep sleep, the researchers conducted the experiment again this time assigning the same tasks as in the first study, but this time manipulated a different region of the brain. There was no change in the results of the participant?s performance.

The study revealed that poor sleep keeps the brain?s synapses excited by blocking the brain?s ability to learn. This is the first study to reveal the connection between deep sleep and learning efficiency. According to Reto Huber, Professor at the University Children?s Hospital in Zurich, the significance of the study also helped provide valuable information and insight into many diseases that manifest in sleep as well. The hope is that specific areas of the brain associated with a variety of diseases can be manipulated.

Reference: Sara Fattinger, Toon T. de Beukelaar, Kathy L. Ruddy, Nicole Wenderoth, Reto Huber; Deep sleep maintains learning efficiency of the human brain. Nat. Commun. 8, 15405 doi: 10.1038/ncomms15405 (2017)

Stand Up for Longer Telomeres

During the past few years a number of studies have been published showing that sitting for long periods of time may decrease lifespan and contribute to other health problems. Now new research has studied the opposite side of this. Instead of measuring only the negative effects of prolonged sitting the scientists measured the benefits of standing. Interestingly it turns out that standing contributes to longevity and longer telomeres!

Research conducted by a team at the Karolinska Hospital in Sweden found that decreasing the amount of time elderly people spend sitting protects the DNA. Additionally, standing was associated with longer telomeres. As many of our readers know telomeres are caps which protect the end of chromosomes and the genetic code inside them. They are important for cell division and also ensure the genetic code is passed on to new cells. Telomeres are compared to the plastic tip at the end of shoelaces which protect the shoelace. Each time a cell divides, the telomeres are shortened. When telomeres become too short, cell division will stop. These shorter telomeres are indicators of disease, aging and early death. We can have as many as 8000 – 10,000 base pairs of telomeres when we are born. Every time a cell divides it loses base pairs of telomeres. As people age the number decreases to 5000 or less at which time cells become senescent and can no longer reproduce. Senescent cells also may malfunction and start producing free radicals and other toxins that can damage adjacent cells.

Dr. Mai-Lis Hellenius who led the Karolinska team, observed 49 predominantly overweight and sedentary adults, all in their late 60?s. Half of the group took part in a six month exercise regime while the other half did not take part in any physical activity. Blood was taken from each individual at the beginning of the six months and then at the end of the six months. The groups were assessed using a diary, questionnaire and pedometer to measure the total number of footsteps taken each day. The group who reduced their time spent sitting and increased their exercise were associated with telomere lengthening. The other less active group, exhibited shortened telomeres. The reduction in sitting time was of the greatest importance than in an increase in exercise time. While exercise indicates an overall healthier profile, the most significant factor appears to be home much time people spend sitting.

Dr. Joan Vernikos, former director of NASA?s Life Sciences, has observed that when astronauts returned from space they had lost muscle tissue and had experienced other damage to this health. Their sedentary lifestyle while in space contributed to a host of health issues another indicator that sitting for long periods of time was damaging to a person?s overall health and aging processes.

Stand up more and live longer! A sedentary lifestyle increases risk of death. Standing will contribute to better posture, increased energy and a lower risk for a host of serious diseases. So take a standing break as often as possible. If you have a desk job consider getting sit/stand desk which allows for raising the height to periodically work from a standing position. Another option is to set a timer and take a walking break for a few minutes every half hour or so. This also applies to any sitting whether watching television or prolonged driving. Get up and stretch, pace around or go outside and take a breath of fresh air! Protect your DNA and your telomeres by standing up for health!

Reference: Per Sj?gren, Rachel Fisher, Lena Kallings, Ulrika Svenson, G?ran Roos, Mai-Lis Hell?nius; Stand up for health?avoiding sedentary behaviour might lengthen your telomeres: secondary outcomes from a physical activity RCT in older people. Br J Sports Med Published Online First: 03 September 2014. doi: 10.1136/bjsports-2013-093342

Does Caloric Restriction Slow Down Aging in Humans?

It has been known for decades that caloric restriction significantly increases lifespan and health span in animals. Limiting food intake of mice, worms, and flies starting from birth lengthens their lifespan by 30% or more. Even more significant is that maximum lifespan increases not just the average. Of course there is no ethical or practical way to decrease calorie intake of humans during an entire lifetime so a different approach was needed. Instead of measuring actual lifespan scientists looked at the rate of biological aging in a group of 145 calorie restricted volunteers over a period of two years.

Research analysis of the data obtained through a trial study known as ?CALERIE? has shown evidence that suggests caloric restriction may benefit life span by slowing down biological aging in humans. One of the hallmarks of biologic aging is the deterioration of the human body?s systems over time. It has been known that caloric restriction hinders the aging process in animals at the physiological level. If biological aging can be slowed down through dietary caloric restriction in humans, it may be possible to prevent or slow down a variety of age-related diseases and disabilities. While chronological aging increases the same for everyone, biological aging will occur faster in some humans and slower in others.

The CALERIE study is the first study to gauge the effects of caloric restriction in human beings in a randomized setting. With population aging and the threat of an increase in disability and disease, the new field of ?geroscience? is responding to the challenge by studying and devising therapies known as ?geroprotective? therapies to assist in the extension of healthy life years.

The CALERIE study conducted by The National Institute of Aging, consisted of 220 individuals with 145 randomly restricted to a 12% caloric restriction over the 2 year course of the study, while the other 75 were allowed to maintain their existing caloric intake. Biological age for all participants was calculated according to their chronological age as well as taking into consideration biomarkers that gauge liver, kidney, metabolic system, immune system and cardiovascular functions. In addition, systolic blood pressure, cholesterol and hemoglobin levels were accounted for. At the beginning of the study the average chronological age was 38 years with an average biological age of 37 years.

At the one-year follow-up, there was an average biological age increase of 0.11 years in the group that were placed on caloric restriction. The group that was allowed to continue with their normal dietary intake indicated an average biological age increase of 0.71 years. The significant difference between the 2 groups indicated caloric restriction did slow down the rate of biological aging.

It is well known that overeating can lead to a variety of health issues that can shorten life span. Studies have shown that caloric restriction with proper nutrition reduces reactive oxygen species in the body. By restricting calories, the levels of hormones and lipid metabolites are changed and energy metabolism is altered and all of these can help lower the risk for most degenerative diseases related to aging. It also appears that caloric restriction provides a benefit to the processes of autophagy which is the way in which cells remove damaged components and replace them with new replacement parts. Research has shown that over time some specific types of damaged cellular components can contribute to damage and age-related decline to the body?s machinery. Caloric restriction is believed to have a protective effect on cells which may help cells better use antioxidants to help avoid damage caused by free radicals.

Caloric restriction has been shown to be associated with longevity and is the single non-genetic and non-pharmaceutical strategy currently shown to provide not only healthy benefits, but also slow down the biological aging process and the diseases associated with it. It is plausible that caloric restriction could be as dramatic as gains and benefits associated with exercise!

Reference: Daniel W Belsky, Kim M Huffman, Carl F Pieper, Idan Shalev, William E Kraus; Change in the Rate of Biological Aging in Response to Caloric Restriction: CALERIE Biobank Analysis; The Journals of Gerontology: Series A, Volume 73, Issue 1, 12 December 2017, Pages 4?10

Reversing Aging By Restoring Stem Cells

The stem cells found within the average adult human are capable of restoring dying cells while also fixing damaged tissue. Nothing is safe from the aging process, though, and as we get older we begin to lose the very same stem cells that once kept our bodies in functional condition. But there could be a way around that: new stem cell research has revealed a nutrient sensing pathway called TOR can be subdued in order to prevent or restore such loses. TOR plays a key role in the aging process and is largely responsible for the loss of stem cells in the human body.

The research examining the relationship between stem cells and TOR, published in the journal Cell Stem Cell, was carried out at the Buck Institute for Research on Aging in California, as well as at Stanford University. Samantha Haller, Ph.D. led the work at Buck Institute, which started with fruit flies before advancing to mice; a move made due to the similar traits shared by both. At Stanford, meanwhile, researchers also worked with mice.

The mice at Buck Institute were put on varying schedules of rapamycin treatment. Rapamycin, also known as Sirolimus, is a drug used to prevent the rejection of kidney transplants. In this study, it was used to suppress the effects of TOR. According to Buck professor and senior author Heinrich Jasper, Ph.D., rapamycin was able to successfully maintain and restore stem cells regardless of the age of the mouse. One mouse in the study was around 15 months old, which roughly equates to a 50-year-old human.

?In every case we saw a decline in the number of stem cells, and rapamycin would bring it back,? said Jasper.

When stem cell division occurs, a ?daughter? cell is created that then proliferates into new cells that can repair the damaged tissue. The process is always asymmetrical, meaning one cell will become a repair cell while the other remains a stem cell. When rapamycin is introduced, the stem cells are recovered ? though Jasper notes the current work done by Buck and Stanford is unable to confirm how, exactly, the cells are restored. It could be a simple replenishment of cells, or that the stem cells are creating two daughter cells instead of one during the division process. It could be another process altogether that the researchers have yet to uncover.

?It?s all about maintaining a balance between stem cell renewal and differentiation,? said Jasper. ?It?s easy to see how a loss of adult stem cells might accrue over a lifetime and accelerate with aging. We are excited to have a means of rescuing stem cells, boosting their ability to maintain healthy tissue.?

Going forward, Jasper explains that researchers will be focusing on better understanding TOR and how it governs stem cells, specifically asking questions like ?Is there a chronic increase in TOR over a lifetime, or is activation stronger in aging animals? What happens downstream of TOR??

It was an exciting year for research involving stem cells and aging: back in July, scientists were able to slow the aging process in mice using stem cells. The Cedars-Sinai Heart Institute revealed in August that stem cells from younger hearts could reverse the aging process in humans.

Some, like SENS Research Foundation co-founder Aubrey de Grey, believe we?re on the verge of fully understanding aging, and it?s becoming increasingly likely that stem cells will play a key role in that enlightenment.

Keep Your Brain 11 Years Younger With Leafy Green Vegetables

Stem Cells

While cognitive abilities naturally decline with age, eating one serving of leafy green vegetables a day may aid in preserving memory and thinking skills as a person grows older, according to a study by researchers at Rush University Medical Center in Chicago. The study results were published in the December 20, issue of Neurology, the medical journal of the American Academy of Neurology.

“Adding a daily serving of green leafy vegetables to your diet may be a simple way to help promote brain health,” said study author Martha Clare Morris, ScD, a nutritional epidemiologist at Rush. “There continues to be sharp increases in the percentage of people with dementia as the oldest age groups continue to grow in number. Effective strategies to prevent dementia are critically needed.”

The study results suggest that people who ate one serving of green, leafy vegetables had a slower rate of decline on tests of memory and thinking skills than people who rarely or never ate them. The study results also suggest that older adults who ate at least one serving of leafy green vegetables showed an equivalent of being 11 years younger cognitively.

960 older adults completed food questionnaires and received annual cognitive assessments

The study enlisted volunteers already participating in the ongoing Rush Memory and Aging Project, which began in 1997 among residents of Chicago-area retirement communities and senior public housing complexes. A “food frequency questionnaire” was added from 2004 to February 2013, which 1,068 participants completed. Of them, 960 also received at least two cognitive assessments for the analyses of cognitive change.

This study involved these 960 people, who at the study start were an average age of 81 years old and did not have dementia. They had their thinking and memory skills tested every year and were followed for an average of 4.7 years. The participants also completed the food frequency questionnaire, which assessed how often and how many half-cup servings they ate of either spinach; kale/collards/greens; or a one-cup serving of lettuce/salad.

The study divided the participants into five groups based on how often they ate green leafy vegetables, and compared the cognitive assessments of those who ate the most (an average of about 1.3 servings per day) and those who ate the least (0.1 servings per day).

Overall, the participants’ scores on the thinking and memory tests declined at a rate of 0.08 standardized units per year. Over 10 years of follow-up, the rate of decline for those who ate the most leafy greens was slower by 0.05 standardized units per year than the rate for those who ate the least leafy greens. This difference was equivalent to being 11 years younger in age, according to Morris.

More research needed in younger and minority populations

The results remained valid after accounting for other factors that could affect brain health, such as seafood and alcohol consumption, smoking, high blood pressure, obesity, education level and amount of physical and cognitive activities.

Psychological Traits of People Over 90 Years of Age

Italian Centenarians

In remote Italian villages nestled between the Mediterranean Sea and mountains lives a group of several hundred citizens over the age of 90. Researchers at the University of Rome La Sapienza and University of California San Diego School of Medicine have identified common psychological traits in members of this group.

The study, publishing in International Psychogeriatrics, found participants who were 90 to 101 years old had worse physical health, but better mental well-being than their younger family members ages 51 to 75.

“There have been a number of studies on very old adults, but they have mostly focused on genetics rather than their mental health or personalities,” said Dilip V. Jeste MD, senior author of the study, senior associate dean for the Center of Healthy Aging and Distinguished Professor of Psychiatry and Neurosciences at UC San Diego School of Medicine. “The main themes that emerged from our study, and appear to be the unique features associated with better mental health of this rural population, were positivity, work ethic, stubbornness and a strong bond with family, religion and land.”

There were 29 study participants from nine villages in the Cilento region of southern Italy. The researchers used quantitative rating scales for assessing mental and physical health, as well as qualitative interviews to gather personal narratives of the participants, including topics such as migrations, traumatic events and beliefs. Their children or other younger family members were also given the same rating scales and additionally asked to describe their impressions about the personality traits of their older relatives.

“The group’s love of their land is a common theme and gives them a purpose in life. Most of them are still working in their homes and on the land. They think, ‘This is my life and I’m not going to give it up,'” said Anna Scelzo, first author of the study with the Department of Mental Health and Substance Abuse in Chiavarese, Italy.

Interview responses also suggested that the participants had considerable self-confidence and decision-making skills.

“This paradox of aging supports the notion that well-being and wisdom increase with aging even though physical health is failing,” said Jeste, also the Estelle and Edgar Levi Chair in Aging and director of the Sam and Rose Stein Institute for Research on Aging at UC San Diego.

Some direct quotes from the study’s interviews include:

?”I lost my beloved wife only a month ago and I am very sad for this. We were married for 70 years. I was close to her during all of her illness and I have felt very empty after her loss. But thanks to my sons, I am now recovering and feeling much better. I have four children, ten grandchildren and nine great-grandchildren. I have fought all my life and I am always ready for changes. I think changes bring life and give chances to grow.”

?”I am always thinking for the best. There is always a solution in life. This is what my father has taught me: to always face difficulties and hope for the best.”

?”I am always active. I do not know what stress is. Life is what it is and must be faced … always.”

?”If I have to say, I feel younger now than when I was young.”

“We also found that this group tended to be domineering, stubborn and needed a sense of control, which can be a desirable trait as they are true to their convictions and care less about what others think,” said Scelzo. “This tendency to control the environment suggests notable grit that is balanced by a need to adapt to changing circumstances.”

The researchers plan to follow the participants with multiple longitudinal assessments and compare biological associations with physical and psychological health.

“Studying the strategies of exceptionally long-lived and lived-well individuals, who not just survive but also thrive and flourish, enhances our understanding of health and functional capacities in all age groups,” said Jeste.

Reference: Anna Scelzo, Salvatore Di Somma, Paola Antonini, Lori P. Montross, Nicholas Schork, David Brenner, Dilip V. Jeste. Mixed-methods quantitative?qualitative study of 29 nonagenarians and centenarians in rural Southern Italy: focus on positive psychological traits. International Psychogeriatrics, 2017; 1 DOI: 10.1017/S1041610217002721

Abstract: This was a study of positive psychological traits in a group of rural Italians aged 90 to 101 years, and their children or other family members.

Mixed-methods quantitative (standardized rating scales) and qualitative (semi-structured interviews) study.

Study participants? homes in nine villages in the Cilento region of southern Italy.

Twenty-nine nonagenarians and centenarians and 51 family members aged 51?75 years, selected by their general practitioners as a part of a larger study called CIAO (Cilento Initiative on Aging Outcomes).

We used published rating scales of mental and physical well-being, resilience, optimism, anxiety, depression, and perceived stress. Qualitative interviews gathered personal narratives of the oldest-old individuals, including migrations, traumatic events, and beliefs. Family members described their impressions about the personality traits of their older relative.

Participants age ?90 years had worse physical health but better mental well-being than their younger family members. Mental well-being correlated negatively with levels of depression and anxiety in both the groups. The main themes that emerged from qualitative interviews included positivity (resilience and optimism), working hard, and bond with family and religion, as described in previously published studies of the oldest old, but also a need for control and love of the land, which appeared to be unique features of this rural population.

Exceptional longevity was characterized by a balance between acceptance of and grit to overcome adversities along with a positive attitude and close ties to family, religion, and land, providing purpose in life.

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