Everything Old Can Get Youth Again?

Old human cells rejuvenated with stem cell technology

Source:     Stanford Medicine
Summary:    Old human cells return to a more youthful and vigorous state after being induced to briefly express a panel of proteins involved in embryonic development, according to a new study.

Stem cells illustration (stock image). | Credit: © nobeastsofierce / stock.adobe.com
Stem cells illustration (stock image).
Credit: © nobeastsofierce / Adobe Stock

Old human cells return to a more youthful and vigorous state after being induced to briefly express a panel of proteins involved in embryonic development, according to a new study by researchers at the Stanford University School of Medicine.

The researchers also found that elderly mice regained youthful strength after their existing muscle stem cells were subjected to the rejuvenating protein treatment and transplanted back into their bodies.

The proteins, known as Yamanaka factors, are commonly used to transform an adult cell into what are known as induced pluripotent stem cells, or iPS cells. Induced pluripotent stem cells can become nearly any type of cell in the body, regardless of the cell from which they originated. They’ve become important in regenerative medicine and drug discovery.

The study found that inducing old human cells in a lab dish to briefly express these proteins rewinds many of the molecular hallmarks of aging and renders the treated cells nearly indistinguishable from their younger counterparts.

“When iPS cells are made from adult cells, they become both youthful and pluripotent,” said Vittorio Sebastiano, PhD, assistant professor of obstetrics and gynecology and the Woods Family Faculty Scholar in Pediatric Translational Medicine. “We’ve wondered for some time if it might be possible to simply rewind the aging clock without inducing pluripotency. Now we’ve found that, by tightly controlling the duration of the exposure to these protein factors, we can promote rejuvenation in multiple human cell types.”

Sebastiano is the senior author of the study, which will be published online March 24 in Nature Communications. Former graduate student Tapash Sarkar, PhD, is the lead author of the article.

“We are very excited about these findings,” said study co-author Thomas Rando, MD, PhD, professor of neurology and neurological sciences and the director of Stanford’s Glenn Center for the Biology of Aging. “My colleagues and I have been pursuing the rejuvenation of tissues since our studies in the early 2000s revealed that systemic factors can make old tissues younger. In 2012, Howard Chang and I proposed the concept of using reprogramming factors to rejuvenate cells and tissues, and it is gratifying to see evidence of success with this approach.” Chang, MD, PhD, is a professor of dermatology and of genetics at Stanford.

Exposure to proteins:        Researchers in Sebastiano’s laboratory make iPS cells from adult cells, such as those that compose skin, by repeatedly exposing them over a period of about two weeks to a panel of proteins important to early embryonic development. They do so by introducing daily, short-lived RNA messages into the adult cells. The RNA messages encode the instructions for making the Yamanaka proteins. Over time, these proteins rewind the cells’ fate — pushing them backward along the developmental timeline until they resemble the young, embryonic-like pluripotent cells from which they originated.

During this process the cells not only shed any memories of their previous identities, but they revert to a younger state. They accomplish this transformation by wiping their DNA clean of the molecular tags that not only differentiate, say, a skin cell from a heart muscle cell, but of other tags that accumulate as a cell ages.

Recently researchers have begun to wonder whether exposing the adult cells to Yamanaka proteins for days rather than weeks could trigger this youthful reversion without inducing full-on pluripotency. In fact, researchers at the Salk Institute for Biological Studies found in 2016 that briefly expressing the four Yamanaka factors in mice with a form of premature aging extended the animals’ life span by about 20%. But it wasn’t clear whether this approach would work in humans.

Sarkar and Sebastiano wondered whether old human cells would respond in a similar fashion, and whether the response would be limited to just a few cell types or generalizable for many tissues. They devised a way to use genetic material called messenger RNA to temporarily express six reprogramming factors — the four Yamanaka factors plus two additional proteins — in human skin and blood vessel cells. Messenger RNA rapidly degrades in cells, allowing the researchers to tightly control the duration of the signal.

The researchers then compared the gene-expression patterns of treated cells and control cells, both obtained from elderly adults, with those of untreated cells from younger people. They found that cells from elderly people exhibited signs of aging reversal after just four days of exposure to the reprogramming factors. Whereas untreated elderly cells expressed higher levels of genes associated with known aging pathways, treated elderly cells more closely resembled younger cells in their patterns of gene expression.

When the researchers studied the patterns of aging-associated chemical tags called methyl groups, which serve as an indicator of a cell’s chronological age, they found that the treated cells appeared to be about 1½ to 3½ years younger on average than untreated cells from elderly people, with peaks of 3½ years (in skin cells) and 7½ years (in cells that line blood vessels).

Comparing hallmarks of aging:    Next they compared several hallmarks of aging — including how cells sense nutrients, metabolize compounds to create energy and dispose of cellular trash — among cells from young people, treated cells from old people and untreated cells from old people.

“We saw a dramatic rejuvenation across all hallmarks but one in all the cell types tested,” Sebastiano said. “But our last and most important experiment was done on muscle stem cells. Although they are naturally endowed with the ability to self-renew, this capacity wanes with age. We wondered, Can we also rejuvenate stem cells and have a long-term effect?”

When the researchers transplanted old mouse muscle stem cells that had been treated back into elderly mice, the animals regained the muscle strength of younger mice, they found.

Finally, the researchers isolated cells from the cartilage of people with and without osteoarthritis. They found that the temporary exposure of the osteoarthritic cells to the reprogramming factors reduced the secretion of inflammatory molecules and improved the cells’ ability to divide and function.

The researchers are now optimizing the panel of reprogramming proteins needed to rejuvenate human cells and are exploring the possibility of treating cells or tissues without removing them from the body.

“Although much more work needs to be done, we are hopeful that we may one day have the opportunity to reboot entire tissues,” Sebastiano said. “But first we want to make sure that this is rigorously tested in the lab and found to be safe.”

Other Stanford co-authors are former postdoctoral scholar Marco Quarta, PhD; postdoctoral scholar Shravani Mukherjee, PhD; graduate student Alex Colville; research assistants Patrick Paine, Linda Doan and Christopher Tran; Constance Chu, MD, professor of orthopaedic surgery; Stanley Qi, PhD, assistant professor of bioengineering and of chemical and systems biology; and Nidhi Bhutani, PhD, associate professor of orthopaedic surgery.

Researchers from the Veterans Affairs Palo Alto Health Care System, the University of California-Los Angeles and the Molecular Medicine Research Institute in Sunnyvale, California, also contributed to the study.

The research was supported by the National Institutes of Health (grants R01 AR070865, R01 AR070864, P01 AG036695, R01 AG23806, R01 AG057433 and R01 AG047820), the Glenn Foundation for Medical Research, the American Federation for Aging Research and the Department of Veterans Affairs.

Sarkar, Quarta and Sebastiano are co-founders of the startup Turn Biotechnologies, a company that is applying the technology described in the paper to treat aging-associated conditions. Rando is a member of the scientific advisory board.


Story Source::    Materials provided by Stanford Medicine. Original written by Krista Conger. Note: Content may be edited for style and length.


Journal Reference:

  1. Tapash Jay Sarkar, Marco Quarta, Shravani Mukherjee, Alex Colville, Patrick Paine, Linda Doan, Christopher M. Tran, Constance R. Chu, Steve Horvath, Lei S. Qi, Nidhi Bhutani, Thomas A. Rando, Vittorio Sebastiano. Transient non-integrative expression of nuclear reprogramming factors promotes multifaceted amelioration of aging in human cells. Nature Communications, 2020; 11 (1) DOI: 10.1038/s41467-020-15174-3

Cite This Page:

Stanford Medicine. “Old human cells rejuvenated with stem cell technology.” ScienceDaily. ScienceDaily, 24 March 2020. <www.sciencedaily.com/releases/2020/03/200324090007.htm>.
from:    https://www.sciencedaily.com/releases/2020/03/200324090007.htm

Caffeine, Inflammation, & Longevity

Caffeine may counter age-related inflammation

A chronic inflammatory process that occurs in some, but not all, older people may trigger cardiovascular problems, a new Stanford study shows. Part of the solution might be found in a cup of coffee.

Jan 16 2017

Man standing in front of kids on a swing set

Mark Davis and his colleagues studied blood samples and a variety of data from more than 100 clinical trial participants and found a link between chronic inflammation and the chronic diseases that accompany aging.
Steve Fisch

Stanford University School of Medicine scientists have unearthed a connection between advancing age, systemic inflammation, cardiovascular disease and caffeine consumption.

Extensive analysis of blood samples, survey data and medical and family histories obtained from more than 100 human participants in a multiyear study has revealed a fundamental inflammatory mechanism associated with human aging and the chronic diseases that come with it.

The study, published online Jan. 16 in Nature Medicine, implicates this inflammatory process as a driver of cardiovascular disease and increased rates of mortality overall. Metabolites, or breakdown products, of nucleic acids — the molecules that serve as building blocks for our genes — circulating in the blood can trigger this inflammatory process, the study found.

The study also provides evidence that caffeine and its own metabolites may counter the action of these circulating nucleic-acid metabolites, possibly explaining why coffee drinkers tend to live longer than abstainers.

“More than 90 percent of all noncommunicable diseases of aging are associated with chronic inflammation,” said the study’s lead author, David Furman, PhD, a consulting associate professor at the Stanford Institute for Immunity, Transplantation and Infection. More than 1,000 papers have provided evidence that chronic inflammation contributes to many cancers, Alzheimer’s disease and other dementias, cardiovascular disease, osteoarthritis and even depression, he said.

“It’s also well-known that caffeine intake is associated with longevity,” Furman said. “Many studies have shown this association. We’ve found a possible reason for why this may be so.”

Mark Davis, PhD, a professor of microbiology and immunology and the director of the Stanford Institute for Immunity, Transplantation and Infection, shares senior authorship of the study with Benjamin Faustin, PhD, a cell biologist at the University of Bordeaux in France. Davis is also a Howard Hughes Medical Institute investigator.

Caffeine link

“Our findings show that an underlying inflammatory process, which is associated with aging, is not only driving cardiovascular disease but is, in turn, driven by molecular events that we may be able to target and combat,” said Davis, who holds the Burt and Marion Avery Family Professorship.

Notably, this inflammatory mechanism was found to be activated only in some, but not all, of the older study participants. Those in whom it was relatively quiescent tended to drink more caffeinated beverages. Laboratory experiments revealed that the mechanism was directly countered by caffeine and associated compounds.

Coffee cup in the midst of coffee beans

The researchers also found that the inflammatory mechanism was dampened among older participants who tended to drink more caffeinated beverages, such as coffee.
Marian Weyo/Shutterstock

The investigators made this discovery using data gathered from the Stanford-Ellison cohort, a long-term program begun 10 years ago by Davis and study co-author Cornelia Dekker, MD, professor of pediatric infectious diseases, to study the immunology of aging. In that program, healthy participants ages 20-30 and another group older than 60 were monitored annually via surveys, blood draws and reviews of their medical histories.

For the new study, the researchers compared blood drawn from older versus younger study participants to see which genes tended to be more highly activated in older people. They zeroed in on two clusters of genes whose activity was associated with the production of a potent circulating inflammatory protein called IL-1-beta. The genes within each cluster appeared to work in coordination with one another.

The researchers also looked at two particular groups of older participants: One with high activation of one or both inflammatory gene clusters, and the other with one or both clusters exhibiting low activation. On reviewing these individuals’ medical histories, the scientists learned that nine of the 12 subjects with high cluster activity had high blood pressure, compared with only one of the 11 subjects with low cluster activity. Follow-up studies by study co-author Francois Haddad, MD, a clinical associate professor of cardiovascular medicine, revealed that individuals in the “high” group were much more likely to have stiff arteries — a risk factor for cardiovascular complications — than those in the “low” group.

Furthermore, those in the low group were eight times as likely as those in the high group to report having at least one close family member who had lived to age 90 or older. Not only that, but participants in the high group who were older than 85 in 2008 were substantially more likely to have died by 2016 than were those in the low group. The high group’s blood also showed signs of increased activity of free radicals, which can harm cells, compared with the low group’s blood. The high group also had elevated concentrations of IL-1-beta, as well as of several nucleic-acid breakdown products that can be produced by free-radical action.

The researchers found that incubating a type of immune cell with two of those nucleic-acid metabolites boosted activity in one of the gene clusters, resulting in increased IL-1-beta production. When injected into mice, the substances triggered massive systemic inflammation, along with high blood pressure. In addition, immune cells infiltrated and clogged the animals’ kidneys, increasing renal pressure substantially.

How caffeine may affect longevity

Intrigued by the correlation between older participants’ health, gene-cluster activation and self-reported rates of caffeine consumption, the researchers followed up and verified that blood from the group with low cluster activity was enriched for caffeine and a number of its metabolites, compared with blood from the group with high cluster activity. (Examples of these metabolites are theophylline, also found in tea, and theobromine, which abounds in chocolate.)

Incubating immune cells with caffeine and its breakdown products along with the inflammation-triggering nucleic acid metabolites substantially prevented the latter from exerting their powerful inflammatory effect on the cells.

What we’ve shown is a correlation between caffeine consumption and longevity.

“That something many people drink — and actually like to drink — might have a direct benefit came as a surprise to us,” said Davis, who noted that the study did not prove a causal link. “We didn’t give some of the mice coffee and the others decaf. What we’ve shown is a correlation between caffeine consumption and longevity. And we’ve shown more rigorously, in laboratory tests, a very plausible mechanism for why this might be so.”

Other Stanford co-authors are postdoctoral scholars Junlei Chang, PhD, Christopher Bohlen, PhD, and Gabriela Fragiadakis, PhD; former graduate student Matthew Spitzer, PhD; life science research associate Edward Ganio; assistant professor of anesthesia, perioperative and pain medicine Brice Gaudilliere, MD, PhD; professor of microbiology and immunology Garry Nolan, PhD; and professor of hematology Calvin Kuo, MD, PhD.

Researchers from the Sidra Medical and Research Center in Qatar, the French National Institute of Health and Medical Research and the University of North Carolina also co-authored the study.

The study was funded by the National Institute of Allergy and Infectious Diseases (grant U19AI090019) and the Ellison Medical Foundation.

Stanford’s Department of Microbiology and Immunology also supported the work.

from:    https://med.stanford.edu/news/all-news/2017/01/caffeine-may-counter-age-related-inflammation-study-finds.html

Dr. Steven Farmer on 65

Sixty-Five

By Dr. Steven Farmer

November 26th, 2013 Be the first to comment

Peaceful Forest Large

On January 11 of this year I turned 65. This is the part where you’re supposed to say or think, “Wow! He doesn’t look that old.” Sure don’t feel that old. At least most of the time! The “I” that I am feels ageless-that part of me that will ultimately dance into eternity once my physical body meets its expiration date.

However, a few weeks before my actual birthday, I got into a funk about that number. I kept getting announcements in the mail about Medicare and supplemental insurance, which I knew nothing about. Yet with every piece of mail I got, it threw the reality of it right in my face. The number itself and the encroaching birthday became specters lurking nearby, haunting and taunting me, ready to jump out at me around every corner. In spite of knowing that I was very healthy, loved, and had a great life-and I didn’t feel old at all-I realized there was something about that number that touched on a belief deeply ingrained in me. After all, weren’t people supposed to retire at that age?

After pondering this major life transition for a couple of weeks and hearing my guides tell me loud and clear that my work here isn’t finished and won’t be for at least another 20 years or more, I had to make some choices as to how I viewed myself in relation to this passage. With the help of a men’s group with which I’m involved, it came down to one thing. I can metaphorically commit to death, and be morose for the rest of my life. Or I can surrender mind, heart, and body to the reality of my age and commit to life.

I shared this with the group, and with their love and support, deeply affirmed this commitment. Stating it out loud and being very clear lifted my spirits immediately and the phrase I used, “I commit to life” continues to be a guiding mantra for this new era I’ve now entered. What it means to me is to be as fully present as possible, to continue to allow myself to evolve, and most importantly listen to and heed the voice of Spirit in whatever way it shows up.

Okay, so on Saturday January 4, I went with my stepfather Richard to get his daughter Victoria from Disneyland. We were gone for a couple hours and when we got home, I opened the door and there was Serena, our nine year old, eyes as wide as a bug’s! Glancing just past her there were quite a few people that I knew sitting in the living room. Then I saw the balloons and the decorations. It quickly sank in. This was a surprise party for me! And thank God we came back earlier than expected and Jesseca’s father had forgotten to let her know that we were on the way so that there was nobody jumping out from behind couches and doors to yell, “surprise!” Very grateful for that!

Most of my extended family was there as were two couples that were close to both Jesseca and myself. It was a very warm feeling and I felt very appreciative of everyone taking the day to share with me. After singing Happy Birthday to me, the gifts were presented. I had asked three of my nieces, all sisters, to sing for me on my birthday (which of course I thought was a week away). Jordan, Sydney, and Paris, ages 16,13, and 11, all sang one of my all time favorites “In My Life,” then Sydney did a solo of another favorite, “Hallelujah.” My heart melted with my love for these girls and their expression of their love for me. I went to my office in back of the house to get something and when I walked in, my eyes were drawn to a walking stick sitting in the corner. It was my Irish great-great grandfather’s shillelagh (She-lay-lee). This unassuming oak walking stick, waist high, with black and reddened mottling covered with a smooth veneer of polish, the luster still glowing in spite of its age, called to me with the voices of my ancestors. I was inspired to bring it into the house and a ceremony emerged.

I described the shillelagh as a representation of the ancestors of my lineage, and since most of the people there were also my blood relatives, they too shared the lineage. Everyone was already in a circle in the living room. I described how I would pass the shillelagh around and requested that each person while holding this sacred piece of wood give me a blessing as a birthday gift. In turn, I would offer them a blessing in exchange. It was a heart-filled ceremony and the blessings filled the air with love and gratitude that was palpable. Food for the heart and soul.

Following the ceremony as I sat quietly in the corner rocking chair I surveyed the room, looking at all these incredible people to whom I was related, either by blood or by a different kind of kinship. The world was right and I was glad to be alive and be sixty-five. I am committed to Life, I am committed to Live.

from:    http://www.earthmagic.net/shamanic-journey/sixty-five/

Magnesium & Your Health

Magnesium’s Importance Far Greater Than Previously Imagined

4th January 2013

By Sayer Ji

Contributing writer for Wake Up World

Calcium deficiency is a common nutritional concern, but how many folks consider the vital importance of magnesium in human health and disease?

New research published in the journal BMC Bioinformatics indicates that magnesium’s role in human health and disease is far more significant and complicated than previously imagined.

While it is well known that all living things require magnesium, and that it is found in over 300 enzymes in the human body, including those enzymes utilizing or synthesizing ATP (the molecular unit of currency for energy transfer), the new studied titled, “3,751 magnesium binding sites have been detected on human proteins,” indicates that a deficiency of magnesium may profoundly affect a far wider range of biological structures than previously understood.[i]

The proteome, or entire set of proteins expressed by the human genome, contains well over 100,000 distinct protein structures, despite the fact that there are believed to be only 20,300 protein-coding genes in the human genome.

The discovery of the “magneseome,” as its being called, adds additional complexity to the picture, indicating that the presence or absence of adequate levels of this basic mineral may epigenetically alter the expression and behavior of the proteins in our body, thereby altering the course of both health and disease.

Indeed, modern medicine and nutrition fixates primarily on calcium deficiency (due, in part, to the WHO’s highly unscientific definition of osteoporosis), even in the face of accumulating peer-reviewed research indicating that excess calcium consumption can greatly increase cardiac morbidity and mortality.

Magnesium Research

Research relevant to magnesium has been accumulating for the past 40 years at a steady rate of approximately 2,000 new  studies a year. Our database project has indexed well over 100 health benefits of magnesium thus far.  For the sake of brevity, we will address seven key therapeutic applications for magnesium as follows:

  • Fibromyalgia: Not only is magnesium deficiency common in those diagnosed with fibromyalgia,[ii] [iii] but relatively low doses of magnesium (50 mg), combined with malic acid in the form of magnesium malate, has been clinically demonstrated to improve pain and tenderness in those to which it was administered.[iv]
  • Atrial Fibrillation: A number of studies now exist showing that magnesium supplementation reduce atrial fibrillation, either by itself, or in combination with conventional drug agents.[v]
  • Diabetes, Type 2: Magnesium deficiency is common in type 2 diabetics, at an incidence of 13.5 to 47.7% according to a 2007 study.[vi]   Research has also shown that type 2 diabetics with peripheral neuropathy and coronary artery disease have lower intracellular magnesium levels.[vii] Oral magnesium supplementation has been shown to reduce plasma fasting glucose and raising HDL cholesterol in patients with type 2 diabetes.[viii] It has also been shown to improve insulin sensitivity and metabolic control in type 2 diabetic subjects.[ix]
  • Premenstrual Syndrome: Magnesium deficiency has been observed in women affected by premenstrual syndrome.[x] It is no surprise therefore  that it has been found to alleviate premenstrual symptoms of fluid retention,[xi] as well as broadly reducing associated symptoms by approximately 34% in women, aged 18-45, given 250 mg tablets for a 3-month observational period.[xii] When combined with B6, magnesium supplementation has been found to improve anxiety-related premenstrual symptoms.[xiii]
  • Cardiovascular Disease and Mortality: Low serum magnesium concentrations predict cardiovascular and all-cause mortality.[xiv]  There are a wide range of ways that magnesium may confer its protective effects. It may act like a calcium channel blocker,[xv] it is hypotensive,[xvi] it is antispasmodic (which may protect against coronary artery spasm),[xvii] and anti-thrombotic.[xviii] Also, the heart muscle cells are exceedingly dense in mitochondria (as high as 100 times more per cell than skeletal muscle), the “powerhouses” of the cell,” which require adequate magnesium to produce ATP via the citric acid cycle.
  • Migraine Disorders: Blood magnesium levels have been found to be significantly lower in those who suffer from migraine attacks.[xix] [xx] A recent Journal of Neural Transmission article titled, “Why all migraine patients should be treated with magnesium,” pointed out that routine blood tests do not accurately convey the true body magnesium stores since less than 2% is in the measurable, extracellular space, “67% is in the bone and 31% is located intracellularly.”[xxi] The authors argued that since “routine blood tests are not indicative of magnesium status, empiric treatment with at least oral magnesium is warranted in all migraine sufferers.” Indeed, oral magnesium supplementation has been found to reduce the number of headache days in children experiencing frequent migranous headaches, [xxii] and when combined with l-carnitine, is effective at reducing migraine frequency in adults, as well.[xxiii]
  • Aging: While natural aging is a healthy process, accelerated aging has been noted to be a feature of magnesium deficiency,[xxiv] especially evident in the context of long space-flight missions where low magnesium levels are associated with cardiovascular aging over 10 times faster than occurs on earth.[xxv] Magnesium supplementation has been shown to reverse age-related neuroendocrine and sleep EEG changes in humans.[xxvi] One of the possible mechanisms behind magnesium deficiency associated aging is that magnesium is needed to stabilize DNA and promotes DNA replication. It is also involved in healing up of the ends of the chromosomes after they are divided in mitosis.[xxvii]

Best Sources of Magnesium In The Diet

The best source of magnesium is from food, and one way to identify magnesium-containing foods are those which are green, i.e. chlorophyll rich. Chlorophyll, which enable plants to capture solar energy and convert it into metabolic energy, has a magnesium atom at its center. Without magnesium, in fact, plants could not utilize the sun’s light energy.

Magnesium, however, in its elemental form is colorless, and many foods that are not green contain it as well. The point is that when found complexed with food cofactors, it is absorbed and utilized more efficiently than in its elemental form, say, extracted from limestone in the form of magnesium oxide.

The following foods contain exceptionally high amounts of magnesium. The portions described are 100 grams, or a little over three ounces.

  • Rice bran, crude (781 mg)
  • Seaweed, agar, dried (770 mg)
  • Chives, freeze-dried (640 mg)
  • Spice, coriander leaf, dried (694 mg)
  • Seeds, pumpkin, dried (535 mg)
  • Cocoa, dry powder, unsweetened (499 mg)
  • Spices, basil, dried (422 mg)
  • Seeds, flaxseed (392 mg)
  • Spices, cumin seed (366 mg)
  • Nuts, brazilnuts, dried (376 mg)
  • Parsley, freeze-dried (372 mg)
  • Seeds, sesame meal (346 mg)
  • Nut, almond butter (303 mg)
  • Nuts, cashew nuts, roasted (273 mg)
  • Soy flour, defatted (290 mg)
  • Whey, sweet, dried (176 mg)
  • Bananas, dehydrated (108 mg)
  • Millet, puffed (106 mg)
  • Shallots, freeze-dried (104 mg)
  • Leeks, freeze-dried (156 mg)
  • Fish, salmon, raw (95 mg)
  • Onions, dehydrated flakes (92 mg)
  • Kale, scotch, raw (88 mg)

Fortunately, for those who need higher doses, or are not inclined to consume magnesium rich foods, there are supplemental forms commonly available on the market. Keep in mind, for those who wish to take advantage of the side benefit of magnesium therapy, namely, its stool softening and laxative properties, magnesium citrate or oxide will provide this additional feature.

For those looking to maximize absorption and bioavailability magnesium glycinate is ideal, as glycine is the smallest amino acid commonly found chelated to magnesium, and therefore highly absorbable.

from:    http://wakeup-world.com/2013/01/04/magnesiums-importance-far-greater-than-previously-imagined/

On Maintaining Brain Health As One Ages

Maintain Your Brain: The Secrets to Aging Success

ScienceDaily (Apr. 27, 2012) — Aging may seem unavoidable, but that’s not necessarily so when it comes to the brain. So say researchers in the April 27th issue of the Cell Press journal Trends in Cognitive Sciences based on counterintuitive evidence that it is what you do in old age that matters when it comes to maintaining a youthful brain rather than what you did earlier in life.

“Although some memory functions do tend to decline as we get older, several elderly show well-preserved functioning and this is related to a well-preserved, youth-like brain,” says Lars Nyberg, Professor of Neuroscience at Umeå University in Sweden.

Education won’t save your brain — PhDs are as likely as high school dropouts to experience memory loss with old age, the researchers say. Don’t count on your job either. Those with a complex or demanding career may enjoy a limited advantage, but those benefits quickly dwindle after retirement. Engagement is the secret to success. Those who are socially, mentally and physically stimulated reliably show greater cognitive performance with a brain that appears younger than its years.

“There is quite solid evidence that staying physically and mentally active is a way towards brain maintenance,” Nyberg says.

The researchers say this new take on successful aging represents an important shift in focus for the field. Much attention in the past has gone instead to understanding ways in which the brain copes with or compensates for cognitive decline in aging. The research team now argues for the importance of avoiding those age-related brain changes in the first place. Genes play a role, but life choices and other environmental factors, especially in old age, are critical.

Elderly people generally do have more trouble remembering meetings or names, Nyberg says. But those memory losses often happen later than many often think, after the age of 60. Older people also continue to accumulate knowledge and to use what they know effectively, often to very old ages.

“Taken together, a wide range of findings provides converging evidence for marked heterogeneity in brain aging,” the scientists write. “Critically, some older adults show little or no brain changes relative to younger adults, along with intact cognitive performance, which supports the notion of brain maintenance. In other words, maintaining a youthful brain, rather than responding to and compensating for changes, may be the key to successful memory aging.”

from:    http://www.sciencedaily.com/releases/2012/04/120427163335.htm