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News flashes are posted here frequently to keep you up-to-date with the latest advances in health and longevity. We have an unparalleled track record of breaking stories about life extension advances.

 

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June 30, 2010

Study suggests longevity effect for female hormones

Study suggests longevity effect for female hormonesAt the 26th annual meeting of the European Society of Human Reproduction and Embryology held in Rome, Dr Noriko Kagawa of the Kato Ladies Clinic in Tokyo reported a rejuvenating effect in old mice who received transplants of younger ovaries.

Dr Kagawa and her colleagues removed both ovaries from 140 day old mice and transplanted them into mice that were older than 525 and had become infertile. Not only did the older mice resume normal reproductive cycles, but they survived significantly longer than untreated animals, which normally live an average of 548 days. A second experiment involving the transplantation of one ovary provided similar results.

"All the mice in both experiments that had received transplants resumed the normal reproductive behavior of young mice,” Dr Kagawa reported. “Normally, old mice stay in the corner of the cage and don't move much, but the activity of mice that had had ovarian transplants was transformed into that of younger mice and they resumed quick movements. Furthermore, the lifespan of the mice who received young ovaries was much longer than that of the control mice: the mice that had received two ovaries lived for an average of 915 days, and the mice that had received one ovary, for an average of 877 days. The newest of our data show the life span of mice that received transplants of young ovaries was increased by more than 40%.”

Although the reasons for the extension in life span observed in this study are unknown, Dr Kagawa suggests that the transplants stimulate the continuation of normal hormonal function.

"Women who have ovarian tissue frozen at young ages, perhaps because they are about to embark on cancer treatment, can have their young ovarian tissue transplanted back when they are older,” she said.” Normally we would be doing this simply to preserve their fertility or to expand their reproductive lifespan. However, our mice experiment suggests that this might also improve overall longevity. Further research has to be conducted before we can know whether or not this is the case."

June 28, 2010

Resveratrol could halt age-related macular degeneration

Resveratrol could halt age-related macular degenerationAn article appearing in the July, 2010 issue of the American Journal of Pathology describes the discovery of researchers at Washington University School of Medicine in St Louis of a protective effect for resveratrol against uncontrolled blood vessel growth (angiogenesis) in the eye that leads to such sight-robbing diseases as age-related macular degeneration and retinopathy.

“A great deal of research has identified resveratrol as an antiaging compound, and given our interest in age-related eye disease, we wanted to find out whether there was a link,” stated senior investigator Rajendra S. Apte, MD, PhD. “There were reports on resveratrol’s effects on blood vessels in other parts of the body, but there was no evidence that it had any effects within the eye.”

Dr Apte and colleagues evaluated the effects of resveratrol in the eyes of mice that develop abnormal blood vessels in the retina following laser treatment. The compound was found to prevent as well as reduce abnormal blood vessel growth via the eukaryotic elongation factor-2 kinase regulated pathway, which is different than the mechanism involved in resveratrol’s effect on aging. “We have identified a novel pathway that could become a new target for therapies,” Dr Apte announced. “And we believe the pathway may be involved both in age-related eye disease and in other diseases where angiogenesis plays a destructive role."

Dr Apte noted that if resveratrol were to be tried in humans, it would need to be given in the form of a supplement because of the high doses needed to be effective. “This could potentially be a preventive therapy in high-risk patients,” he predicted. “And because it worked on existing, abnormal blood vessels in the animals, it may be a therapy that can be started after angiogenesis already is causing damage."

June 25, 2010

Resveratrol neutralizes toxic Alzheimer’s peptides

Resveratrol neutralizes toxic Alzheimer’s peptidesIn the May 28, 2010 issue of the Journal of Biological Chemistry Professor Peter M. Tessier and his associates at Rensselaer Polytechnic Institute in Troy, New York report their finding of an ability for resveratrol, a compound that occurs in red wine, to neutralize improperly folded isoforms of amyloid-beta 1-42, a peptide linked with Alzheimer’s disease.

Improperly folded peptides accumulate in plaques in the brain that damage brain cells. For the current research, Dr Tessier’s team induced amyloid-beta 1-42 peptide to assemble into 5 arrangements, three of which were demonstrated to be toxic to human cells. Administration of resveratrol resulted in remodeling of the 3 toxic arrangements into a form that was not toxic, while not affecting the other isoforms. "The surprise is that this molecule can target some of these packing arrangements that are toxic and rearrange them into packing arrangements that are not toxic,” Dr Tessier stated. “For those forms that are nontoxic, it doesn't change them.”

"We've shown how resveratrol has very interesting selectivity to target and neutralize a select set of toxic peptide isoforms," he remarked. "Because resveratrol picks out the clumps of peptides that are bad and leaves alone the ones that are benign, it helps us to think about the structural differences between the peptide isoforms."

"We have two things that look very similar, but one is toxic and the other isn't," Dr Tessier added. "What is it that makes the bad one bad and the good one good?"

This question suggests the need for a future study, according to Dr Tessier, which will help further the understanding of Alzheimer’s disease.

June 23, 2010

Large clinical trial confirms efficacy of omega-3 fatty acid against depression unaccompanied by anxiety

Large clinical trial confirms efficacy of omega-3 fatty acid against depression unaccompanied by anxietyIn the largest clinical trial to date to examine the effect of an omega-3 fatty acid on major depression, researchers at the Université de Montréal demonstrated that a fish oil supplement containing a high amount of eicosapentaenoic acid (EPA) was associated with a reduction in major depression among patients who did not also have anxiety disorders.

On June 15, 2010 in the Journal of Clinical Psychiatry, Dr François Lespérance of the Université de Montréal’s Centre de Recherche du Centre Hospitalier and his colleagues reported the findings of a double-blinded, randomized trial conducted from October, 2005 through January, 2009 in 8 Canadian clinics. The trial included 432 adults experiencing a major depressive episode lasting at least 4 weeks. Participants were assigned to 8 weeks of a supplement providing 1,050 milligrams EPA and 150 milligrams DHA per day or a placebo. Depressive symptoms were self-evaluated at the beginning of the study and at 1, 2, 4 and 8 weeks.

Supplementing with fish oil had only a small effect over placebo at the study’s conclusion, however, when those with co-existing anxiety were removed from the analysis, the effect of supplementation was similar to that of antidepressant drugs. The authors suggest that the lack of significance of the effects observed when those with anxiety were included in the analysis could be due to insufficient dosage or treatment time.

"Despite significant progress in neuroscience over the past two decades, depression is difficult to treat," Dr Lespérance observed. Concerning the use of alternative treatments for the condition, he noted that "Many of these treatments have not been adequately evaluated. That is why it was important to assess the efficacy of omega-3, one of the most popular alternative approaches."

June 21, 2010

Vitamin D deficiency found in multiple rheumatic diseases

Vitamin D deficiency found in multiple rheumatic diseasesStudies presented on June 18, 2010 at the Annual Congress of the European League Against Rheumatism held in Rome reveal the presence of deficient levels of vitamin D across a range of rheumatic diseases.

In a study conducted in England, vitamin D levels were obtained for 90 patients with inflammatory joint disease, osteoporosis or unexplained myalgia (muscle pain that may be associated with nutritional deficiency), and 90 control subjects with chronic lower back pain. In those with rheumatic conditions, vitamin D levels were 58 percent lower than those of the control group.

An Italian study found that among 1,191 patients with rheumatoid arthritis, 25-hydroxyvitamin D levels were deficient at less than 20 nanograms per liter in over half of those not using vitamin D supplements and in 33 percent of patients who supplemented with at least 800 international units (IU) per day. However, another study conducted in Italy which involved 100 participants with inflammatory and noninflammatory autoimmune disease found that only 29 percent reached desirable levels of serum 25-hydroxyvitamin D after supplementation with 800 to 1000 IU per day for 6 months. "The results of our study show that daily 800-1,000 IU supplementation is not sufficient to normalize vitamin D levels in patients with rheumatologic or bone conditions," stated first author Dr Pier Paolo Sainaghi of the Immuno-Rheumatology Clinic at A. Avogadro University of Eastern Piedmont in Novara, Italy.

"We have seen in studies that vitamin D deficiency is common in patients with a range of rheumatic diseases, and our results have confirmed this using several clinically accepted measures of disease activity," remarked Dr. L. Idolazzi of the University of Verona who coauthored the second study. "What we need to see now is a range of long term studies, which examine the clinical response of patients to vitamin D supplementation."

June 18, 2010

Ninety percent of strokes associated with 10 risk factors

Ninety percent of strokes associated with 10 risk factorsIn an article published online on June 18, 2010 in The Lancet, Martin J. O’Donnell of McMaster University and colleagues estimate that 10 risk factors are collectively responsible for 90 percent of all strokes.

The INTERSTROKE study follows the INTERHEART study, which determined that 9 modifiable risk factors were responsible for the majority of heart attacks worldwide. “The INTERSTROKE study is the first large standardised case-control study of risk factors for stroke in which countries of low and middle income were included, and where all cases completed a brain scan (usually a CT scan),” the authors announce.

In phase I of the current study, 3,000 patients with a first stroke were compared with 3000 controls from 22 countries in order to establish traditional and emerging risk factors for stroke among nations of varying income.

The INTERSTROKE investigators identified the following risk factors as accounting for 90 percent of the population attributable risk for stroke: high blood pressure, smoking, waist to hip ratio (abdominal obesity), diet, physical activity, lipids, diabetes, alcohol intake, stress and depression, and heart disorders including atrial fibrillation. When stroke was evaluated according to type, all risk factors were related to ischemic stroke, and hypertension, smoking, waist to hip ratio, diet, and alcohol were significant for hemorrhagic stroke, caused by bleeding in the brain.

The authors note that each factor’s individual population attributable risk, which is the difference in the rate of a condition between an exposed population and an unexposed population, do not add up to the overall population attributable risk for all factors combined, because many people have more than one risk factor. When the risk factors were examined independently, high blood pressure was found to be the most important.

The authors conclude that targeted interventions could substantially reduce the world’s stroke burden.

June 16, 2010

Higher B6 levels associated with reduced lung cancer risk

Higher B6 levels associated with reduced lung cancer riskThe June 16, 2010 issue of the Journal of the American Medical Association published the results of an analysis which found protective effects for vitamin B6 and the amino acid methionine against the risk of developing lung cancer.

"B vitamins, including folate, as well as related enzymes in the 1-carbon pathway, are essential for DNA synthesis and methylation," the authors write in their introduction. "The 1-carbon metabolism process is complex and involves multiple interactions between B vitamins, homocysteine, and methionine, which in turn are required for generation of S-adenosylmethionine, an essential component of methylation reactions. Deficiencies in B vitamins may increase the probability of DNA damage and subsequent gene mutations, and may influence gene expression via aberrant methylation patterns."

The study included 385,747 men and women enrolled in the European Prospective Investigation into Cancer and Nutrition study, which recruited participants from 1992 to 2000. Blood samples obtained during this time period were analyzed for methionine and vitamins B2, B6, folate and B12.

From enrollment until 2006, 899 cases of lung cancer were diagnosed. These cases were matched by gender and other factors with 1,770 control subjects. A reduction in lung cancer risk was associated with increasing serum levels of vitamin B6 as well as methionine. Those whose vitamin B6 level was among the top one-fourth of participants had a 66 percent lower risk of developing lung cancer than those whose levels were among the lowest fourth. A protective benefit was also observed for high folate levels in smokers.

The lower risk of lung cancer in association with increased serum vitamin B6 observed in the study is consistent with results of studies of colorectal cancer, however, these and other studies have not investigated the effect of serum methionine levels. "If our observations regarding serum methionine, B6, or both are shown to be causal, identifying optimum levels for reducing future cancer risk would appear to be appropriate," the authors write.

June 14, 2010

Reducing oxygen could improve organ preservation

Reducing oxygen could improve organ preservationIn an article published online on May 12, 2010 in the journal Molecular Biology of the Cell, biologist Mark B. Roth, PhD of Fred Hutchinson Cancer Research Center and his colleagues report that yeast and roundworm embryos are more able to survive freezing when put in a state of suspended animation by reducing oxygen consumption.

Subsequent to the media coverage of several cases of humans who recovered from severe prolonged hypothermia, Dr Roth sought to investigate the role that anoxia-induced suspended animation might play in hypothermia survival. In the current research, Dr Roth, along with Jesse Goldmark and Kin Chan, showed that roundworm embryos and several strains of S. cerevisiae yeast underwent a dramatic decrease in viability associated with cell cycle dysregulation when exposed to low temperatures. However, when the yeast and roundworms were first transitioned to a state of suspended animation by depriving them of oxygen, survival dramatically improved.

"We have found that extension of survival limits in the cold is possible if oxygen consumption is first diminished," Dr Roth stated. "Our experiments in yeast and nematodes suggest that organs may last longer outside the body if their oxygen consumption is first reduced before they are made cold."

"There are many examples in the scientific literature of humans who appear frozen to death,” he noted. “They have no heartbeat and are clinically dead. But they can be reanimated. Similarly, the organisms in my lab can be put into a state of reversible suspended animation through oxygen deprivation and other means. They appear dead but are not."

"When an organism is suspended its biological processes cannot do anything wrong," Dr Roth added. "Under conditions of extreme cold, sometimes that is the correct thing to be doing; when you can't do it right, don't do it at all."

June 11, 2010

How polyphenols inhibit prostate cancer growth

How polyphenols inhibit prostate cancer growthScientists in Toulouse, France report the discovery of a mechanism for polyphenols from tea and wine in reducing prostate cancer growth, in an article published online on June 3, 2010 in the journal FASEB.

Olivier Cuvillier and his colleagues evaluated the effects of the green tea polyphenol epigallocatechin gallate (EGCG), a tea polyphenol mixture, resveratrol or grapevine extract in cultured prostate cancer cell lines. They found that the compounds impeded prostate cancer cell growth via inhibition of the cell signaling sphingosine kinase-1/sphingosine 1-phosphate (SphK1/S1P) pathway.

In an experiment with mice implanted subcutaneously with human prostate cancer tumors, injection with resveratrol, grape vine extract or EGCG beginning 10 days after implantation reduced average tumor volume and intratumoral SphK1 activity compared with animals that were injected with a control substance. A similar effect on tumor volume was observed in an experiment with mice given EGCG or tea polyphenols in their drinking water beginning on the day in which the tumors were implanted.

"Not only does SphK1/S1P signaling pathway play a role in prostate cancer, but it also plays a role in other cancers, such as colon cancer, breast cancer, and gastric cancers," FASEB Journal editor-in-chief Gerald Weissmann, MD remarked. "Even if future studies show that drinking red wine and green tea isn't as effective in humans as we hope, knowing that the compounds in those drinks disrupt this pathway is an important step toward developing drugs that hit the same target."

"The profound impact that the antioxidants in red wine and green tea have on our bodies is more than anyone would have dreamt just 25 years ago," he added. "As long as they are taken in moderation, all signs show that red wine and green tea may be ranked among the most potent 'health foods' we know."

June 9, 2010

Multinutrient supplement improves men’s mental stress levels

Multinutrient supplement improves men’s mental stress levelsIn an article published online on May 8, 2010 in the journal Psychopharmacology, researchers from Newcastle-upon-Tyne, England report that a multivitamin and mineral supplement consumed daily for a month improved mental fatigue and stress levels in middle-aged men.

Crystal Haskell and colleagues at Brain, Performance and Nutrition Research Centre at Northumbria University conducted a double-blinded trial of 215 healthy men aged 30 to 55 who were engaged in fulltime employment with its resultant mental fatigue and stress. Participants received one tablet daily of a multinutrient supplement containing low amounts of vitamins B1, B2, B3, B5, B6, B12 and C, biotin, folic acid, calcium, magnesium and zinc or a placebo for 33 days. Prior to and following the last day of treatment, subjects completed questionnaires concerning mood states, perceived stress and general health. Further testing assessed cognitive performance and task-related modulation of mood and fatigue, as well as cognitive performance while walking on a treadmill.

Among participants who received the vitamin/mineral supplement, perceived stress, general health and vigor improved compared to the placebo group, as well as mental fatigue levels and cognitive function. The authors remark that while it is not possible to identify the mechanism of action given the multiple components of the supplement, possible mechanisms include a reduction in homocysteine, improved integrity and synthesis of neurotransmitters, DNA, protein and phospholipids; antioxidant effects, and specific benefits provided by the minerals included in the formula.

“In general, few studies have assessed the cognitive performance effects of vitamins/minerals in healthy, nonelderly cohorts,” the authors write. “Taken together with previous results showing beneficial effects of vitamin/mineral supplementation in healthy children and adults, these findings further suggest that augmenting vitamin/mineral levels in healthy, normal populations may provide beneficial effects in terms of brain function.”

June 7, 2010

Supplemental choline during pregnancy may benefit offspring later in life

Supplemental choline during pregnancy may benefit offspring later in lifeThe June 2, 2010 issue of Behavioral Neuroscience published the findings of researchers at Cornell University which suggest a protective effect for choline against the development of middle-age neurodegeneration in Down syndrome patients when the nutrient is consumed by their mothers during pregnancy. Down syndrome results is characterized by mental retardation, physical anomalies and early dementia due to brain neuron atrophy similar to that found in men and women with Alzheimer’s disease.

The experiment utilized a mouse model of Down syndrome in which some of the mice were born from mothers provided with a normal diet during 3 weeks of pregnancy and 3 weeks of lactation, and others were born from mice given a diet that contained 4.5 times more choline. Normal mice not bred to develop Down syndrome were given similar regimens. At 6 months of age, the mice offspring were tested on impulsivity, emotional control, attention span and other abilities.

While Down syndrome mice born to mothers that received choline became more agitated after making errors compared to normal mice, those that received choline showed improvement. "We found that supplementing the maternal diet with additional choline resulted in dramatic improvements in attention and some normalization of emotion regulation in a mouse model of Down syndrome," lead author and professor of nutritional sciences and psychology Barbara Strupp stated. "I'm impressed by the magnitude of the cognitive benefits seen in the Down syndrome-model mice. Moreover, these are clearly lasting cognitive improvements, seen many months after the period of choline supplementation."

The study is the first to evaluate the effects of maternal choline supplementation in a rodent model of Down syndrome. "Although the precise mechanism is unknown, these lasting beneficial effects of choline observed in the present study are likely to be limited to increased intake during very early development," Dr Strupp noted.

June 4, 2010

Chili peppers burn off fat

Chili peppers burn off fatAn article published in the June 4, 2010 issue of the Journal of Proteome Research reports that capsaicin, the compound responsible for the heat sensation experienced when eating chili peppers, reduces weight gain and white adipose (fat) tissue formation in rats.

Capsaicin has known anti-inflammatory and antioxidant actions. The compound has been shown to help prevent weight gain by lowering food intake and reducing adipose tissue weight, and has been linked to thermogenesis, the body's process of burning fat in the production of heat. In the current study five week old rats were fed a high fat diet and given saline or capsaicin dissolved in saline for nine weeks. An additional group of animals received normal diets.

At the end of the experiment, animals that received the high fat diet combined with capsaicin gained 8 percent less weight and had less adiposity than the group that received the high fat diet without capsaicin. Examination of white adipose tissue found a significant reduction in the size of lipid droplets in the capsaicin-fed group. Additionally, the scientists identified 10 up-regulated and 10 down-regulated proteins, most of which are associated with lipid metabolism and redox regulation. Furthermore, capsaicin was found to affect genes involved in obesity, including genes associated with thermogenesis, respiratory chain function, and fat oxidation.

"Comparative proteome analysis of a rat model of diet-induced obesity allowed us to outline possible pathways involved in the response to capsaicin," the authors write. "Proteins identified here are involved in cellular functions that include lipid metabolism, redox processes, and signal and energy transduction. Some of these have already been linked to human obesity, suggesting that the newly identified proteins might also have importance in obesity and that they should be further investigated."

 

June 2, 2010

CDP-choline helps protect against alcohol-induced birth defects

CDP-choline helps protect against alcohol-induced birth defectsA report published in Cell Death and Disease describes research conducted at the Medical College of Georgia which suggests a protective effect for CDP-choline against the programmed cell death (apoptosis) of neural crest cells that takes place in fetal alcohol syndrome, a condition that occurs when mothers consume alcohol early in pregnancy. Damage to the neural crest, a tissue complex that develops from neuroepithelial cells at the end of the first month of pregnancy, results in injury to the brain’s protective covering known as meninges. This injury causes a decrease in the production of TGF-beta-1 (a growth factor that is necessary for bone and brain development) which, in turn, leads to brain and skull damage.

"You get a snowball effect,” explained coauthor Dr Erhard Bieberich, who is a biochemist at the Medical College of Georgia Schools of Graduate Studies and Medicine. “The neural crest is damaged, the meninges doesn't develop properly and tissue like bone and brain that are regulated by the meninges don't develop properly either.”

The current research suggests that this damage is due to apoptosis (programmed cell death) induced by ceramide, a lipid that is activated by alcohol. An experiment with cultured mouse embryo neural crest cells incubated with alcohol detected high levels of ceramide along with a five-fold increase in apoptotic cells. A significant increase in neural crest cell apoptosis was also observed in the embryos of pregnant mice that were given alcohol.

When the researchers incubated neural crest cells with alcohol as well as CDP-choline, ceramide and apoptosis were reduced. Future research will seek to determine whether CDP-choline can rescue these cells from damage after alcohol exposure. "Ceramide can be bad or good," Dr Bieberich remarked. "Hopefully we can rescue some of the cells by triggering or signaling the back reaction."

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