What's Hot

What's Hot

August 2007

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

What's Hot Archive

August 31, 2007

In the very old, longevity genes' effects outweigh those of harmful genes

The August 31, 2007 issue of Public Library of Science journal PLoS Computational Biology published the finding of researchers at the Albert Einstein College of Medicine of Yeshiva University in New York that the longevity genes of people who survive to advanced ages are able to protect them against the effects of harmful gene variants.

Professor Aviv Bergman and his associates examined data from 305 Ashkenazi Jews over the age of 95 who enrolled in the university's Longevity Genes Project in 1998. The project's goal is to evaluate longevity-conferring genes in a relatively genetically homogenous population. Four hundred-eight unrelated Ashkenazi Jews and 430 children of centenarians served as controls. Participants were divided into groups representing those in their fifties, sixties, seventies, etc., and the prevalence of 66 genetic markers present in 36 aging-associated genes was determined from DNA samples.

While some disease-related variants were increased in the oldest groups of Ashkenazi Jews, longevity-associated genes were also increased, and became more prevalent with each decade of life. In particular, a favorable variant of the cholesterol ester transfer protein (CETP) gene helped reduce the negative effect of the lipoprotein A [Lp(a)] gene.

“We hypothesized that people living to 100 and beyond must be buffered by genes that interact with disease-causing genes to negate their effects,” Dr Bergman stated. "These results indicate that the frequency of deleterious genotypes may increase among people who live to extremely old ages because their protective genes allow these disease-related genes to accumulate.”

“This study shows that our approach, which was inspired by a theoretical model, can reveal underlying mechanisms that explain seemingly paradoxical observations in a complex trait such as aging,” he added. “So we’re hopeful that this method could also help uncover the mechanisms—the gene interactions—responsible for other complex biological traits such as cancer and diabetes.”

—D Dye

August 29, 2007

Garlic fights brain cancer

A report published in the September, 2007 issue of Cancer, an American Cancer Society journal, revealed the discovery of researchers at the Medical University of South Carolina that organo-sulfur compounds occurring in garlic have the ability to combat glioblastoma, a brain cancer that carries a poor prognosis.

Associate professor of Neurosciences and Neurology Swapan Ray, PhD, along with Arabinda Das, PhD and Naren L. Banik, PhD examined the effect of diallyl sulfide, diallyl disulfide, and diallyl trisulfide from garlic on two human glioblastoma cell cultures. While all of the compounds triggered self-destruction (apoptosis) in the cancerous cells, diallyl trisulfide had the strongest effect. Although garlic has antioxidant properties, the apoptosis observed in this study was found to be the result of reactive oxygen species produced by the garlic-derived compounds within the glioblastoma cells.

"This research highlights the great promise of plant-originated compounds as natural medicine for controlling the malignant growth of human brain tumor cells," Dr Ray stated. "More studies are needed in animal models of brain tumors before application of this therapeutic strategy to brain tumor patients."

To obtain the maximum benefit from consuming garlic, Dr Ray suggested cutting and peeling fresh cloves and letting them sit fifteen minutes before cooking with or consuming them, to allow sufficient time for the release of allinase, an enzyme that produces garlic's anticancer compounds.

"Our basic studies will eventually be translated to clinics for patient care," predicted Dr Banik. "We may have to wait several years before its application to humans, but the significance of this discovery is enormous. The benefits from this research to brain cancer patients will bring great satisfaction to researchers and clinicians who are trying to find a successful treatment for this devastating cancer."

—D Dye

August 27, 2007

Diet helps irresponsible cells get into recycling

A report published online in the journal Rejuvenation Research revealed a new mechanism by which calorie restriction extends life. In research conducted at the University of Florida, Stephanie Wohlgemuth, PhD and colleagues discovered that the technique improves the cells' ability to recycle damaged parts, which helps maintain efficient energy production.

In the current research, 22 young and old rats received a nutritious low-calorie diet or were allowed to eat as much as they wanted, and were evaluated for changes in proteins responsible for degrading damaged cell parts by autophagy.

“Cell survival is dependent upon the ability of the cell to reduce and recycle by a mechanism called autophagy,” explained senior author William Dunn, Jr, PhD. “When a cell is under stress, autophagy is turned on to clean up the cell by removing damaged cellular components, while recycling building blocks necessary to rebuild the cell. It’s there to protect the cell. But in aged cells, they’re basically not able to adjust to stress as well.” The team found that the stress of a low calorie diet increased autophagy in older rats 120 percent above levels observed in those allowed to consume an unlimited amount of food. Younger animals were not effected.

By providing a greater understanding of how calorie restriction extends life, the researchers hope their work will assist in the development of drugs that mimic the technique in humans. “What if we bypass the caloric restriction and find a way of increasing autophagy" Dr Dunn asked. “That is, instead of starving yourself you can find another way of enhancing autophagy that will allow the enhanced removal of various damaged organelles that accumulate in aged cells.”

“Autophagy is a housekeeping mechanism that keeps cells free of damaged and thereby detrimental mitochondria and other toxic materials while recycling their building blocks — nutrients needed by the cell,” Dr Wohlgemuth stated. "So if that process is maintained with age – or even increased – that can only be beneficial.”

—D Dye

August 24, 2007

Vitamin E doses used in clinical trials may be too low

A report published online on July 4, 2007 in the journal Free Radical Biology and Medicine concluded that insufficient doses of vitamin E could be the reason for disappointing results obtained in some clinical trials which sought to confirm the protective effect of the vitamin against heart attack suggested by epidemiologic and animal studies.

Using an assay they developed to measure F2-isoprostanes formed by oxidative stress, researchers at Vanderbilt University Medical Center determined that it took 16 weeks for a 3200 international unit (IU) daily dose of vitamin E to suppress oxidative stress in participants at risk of cardiovascular disease. This amount of vitamin E is approximately four times as much as doses used in the majority of clinical trials. In another group of subjects, at least 1600 IU was needed to result in a significant reduction in F2-isoprostanes.

The findings identify the flaw in earlier trials that failed to use doses of vitamin E that provided an antioxidant effect sufficient to protect against cardiovascular disease. In decades of vitamin E research, the study is the first to conclusively determine the dose at which the vitamin can be considered an antioxidant drug.

“All of these studies were designed in a way that they never assessed the ability of the dose of vitamin E tested to effectively reduce oxidant stress,” remarked study coauthor Jason Morrow, MD , who is Vanderbilt's chief of the Division of Clinical Pharmacology. “It was clear that large doses – and doses in excess of what all clinical studies had used – were necessary.”

"In the design of clinical trials, one needs to have good surrogate biochemical markers,” he noted. He suggests that F2-isoprostane measurement “really ought to be incorporated into studies assessing disease prevention by antioxidants in general.”

—D Dye

August 22, 2007

Cranberries boost drug efficacy in ovarian cancer treatment

The national meeting of the American Chemical Society was the site of a presentation on August 21, 2007, by Ajay P. Singh, PhD, and Nicholi Vorsa, PhD of Rutgers University of the finding that an extract of cranberries augmented the effect of platinum chemotherapy on ovarian cancer cell cultures. Platinum drugs such as Paraplatin are commonly used to treat ovarian cancer, however, cells develop resistance to the compounds, necessitating higher doses which increase side effects.

Doctors Singh and Vorsa, along with colleagues at Brown University, treated cultures of platinum drug-resistant ovarian cancer cells with varying concentrations of an extract of a commercially available cranberry drink, and exposed them to Paraplatin. An additional group of cells was treated with Paraplatin only.

They found that cells treated with cranberry extract became up to six times more sensitized to Paraplatin than those treated with the drug alone. A reduction in the growth and spread of some cancer cells was also observed in cultures treated with cranberry. The maximum amount of extract used was the human equivalent of a cup of cranberry juice.

The researchers believe that A-type proanthocyanidins that are unique to cranberries may be responsible for the effects found in the study. Based on the findings of other research, the compounds appear to work by binding to and blocking tumor promoter proteins in ovarian cancer cells, rendering them more vulnerable to the effects of the drugs. They hope to identify the most active anticancer fractions in the cranberry extract as well as the optimal dose.

“For the first time, we have shown in our in vitro studies that cranberry extracts can sensitize resistant human ovarian cancer cell lines,” Drs Singh and Vorsa noted. “This has opened up exciting possibilities for therapeutic intervention associated with platinum therapy.”

—D Dye

August 20, 2007

Colorful compounds cancel cancer

Research presented on August 19, 2007 at the national meeting of the American Chemical Society held in Boston added more evidence to the growing body of knowledge concerning the cancer fighting ability of compounds known as anthocyanins that give red, violet, and blue plants their color.

Ohio State University assistant professor of food science Monica Giusti reported the results of her work in which the effect of various extracts containing anthocyanins were tested on cultured human colon cancer cells. Using extracts from grapes, radishes, purple corn, chokeberries, bilberries, purple carrots, and elderberries, and other plants, Dr Giusti's team determined the amount needed from each to decrease the growth of the cancer cells by half. They found that purple corn extract was the most potent of the extracts tested, followed by chokeberry and bilberry. Radish extract was the least potent. However, by adding an extra sugar or acid molecule, the researchers were able to alter the pigments' structures, making them more potent. In additional research, the team discovered that anthocyanins from radish and black carrots reduced cancer cell growth from 50 to 80 percent, however, anthocyanins from purple corn and chokeberries completely stopped the cancer growth as well as killing 20 percent of the cancerous cells. And in studies with rats, anthocyanins from bilberries and chokeberries reduced the signs of colon tumors by 70 and 60 percent compared to animals that did not received the compounds, suggesting a protective effect against gastrointestinal cancers.

“All fruits and vegetables that are rich in anthocyanins have compounds that can slow down the growth of colon cancer cells, whether in experiments in laboratory dishes or inside the body,” Dr Giusti stated. “These foods contain many compounds, and we're just starting to figure out what they are and which ones provide the best health benefits."

—D Dye

August 17, 2007

Over a third of the world’s deaths attributed to pollution

In an article published online on July 31, 2007 in the journal Human Ecology, researchers from Cornell University estimate that 40 percent of the world’s deaths are caused by pollution of the air, water and soil, which, combined with population growth, increase the susceptibility of 3.7 billion people to disease and malnourishment.

Professor of ecology and agricultural sciences David Pimentel, along with a team of Cornell graduate students reviewed data from over 120 published reports concerning the effects of population growth, malnutrition and environmental degradation on human diseases. They found that the percentage of the world's population experiencing malnutrition has increased from 20 percent in 1950 to 57 percent of the current population of 6.5 billion. Malnutrition not only is directly responsible for deaths, but renders humans susceptible to respiratory infections, malaria, and many other potentially fatal diseases.

Lack of clean water is responsible for the death of 1.2 to 2.7 million people per year due to waterborne infections. Air pollution is estimated to take approximately 3 million lives per year, due to cancer, birth defects, immune system defects, and other diseases caused by exposure to smoke and various chemicals. Urban crowding, combined with a lack of sanitation, increases exposure to epidemics such as influenza and measles, over 5 million annually.

Contamination of the soil and erosion spreads microbes and toxins, resulting in additional disease and death. Global warming and changes in biological diversity increase the ability of exotic species to invade new areas, resulting in the re-emergence of some diseases as major threats, and the creation of new ones.

"A growing number of people lack basic needs, like pure water and ample food," Dr Pimental concluded. "They become more susceptible to diseases driven by malnourishment, and air, water and soil pollutants."

—D Dye

August 15, 2007

Metformin slows growth of tumors lacking p53

The July, 2007 issue of Cancer Research published the results of research conducted at the University of Pennsylvania School of Medicine which determined that metformin, a drug commonly used for diabetes, destroys tumor cells lacking a regulatory gene known as p53, which acts as a tumor suppressor. The gene is estimated to be lost in over half of all human cancers.

Studies have found that diabetics who use metformin have a lower risk of cancer and mortality within a given period than those who don't use the drug. In research funded by the National Cancer Institute, University of Pennsylvania Professor of Cancer Biology and Medicine Craig B. Thompson MD and colleagues injected human colon cancer cells with normal p53 into one side of mice and the same cells lacking p53 into the other side. After four days, the mice received daily injections of metformin or saline. The dose of metformin administered in the study was equivalent to that used by human diabetics.

At the end of the four week treatment period there was no difference among the animals in the size of tumors with normal p53, however, tumors lacking p53 in mice that received metformin were half the size of those in the saline-injected animals. The team discovered that the drug instructs cells to switch metabolic pathways from oxidative phosphorylation, the most energy efficient pathway, to a stress related one used when the cells are deficient in oxygen, glucose or other nutrients. Normally when p53 is absent, the cells are not able to perform the switch. “Without p53, if we force cells to live on alternative substrates, they can’t do it,” explained Dr Thompson .

He announced, “This is the first time you can show that tumor growth is impaired by a diabetes drug. It is specific for tumors that lack p53, which is the most common mutation in human cancer.”

—D Dye

August 13, 2007

Grapes, soy, kudzu improve menopausal symptoms

The Sex and Gender in Cardiovascular-Renal Physiology and Pathophysiology conference sponsored by the American Physiological Society featured a presentation by J. Michael Wyss of the University of Alabama on his work entitled “The Role of Estrogens and Polyphenols in Hypertension and Diabetes.” As a part of his presentation, Dr Wyss discussed the ability of plant derived polyphenols from grapes, soy and kudzu to help treat postmenopausal memory loss, high blood pressure and diabetes. The conference was held August 9-12, 2007 in Austin, Texas.

A research team led by Dr Wyss, who is a physiologist with the Department of Cell Biology at University of Alabama at Birmingham, found that administration of grape polyphenols to laboratory animals was associated with a lower incidence of working and reference memory errors, indicating that both short-term and long-term memory were improved. They also tested their hypothesis that grapeseed derived polyphenols lower salt-sensitive hypertension by administering the compound to young rats whose estrogen levels were depleted by removal of their ovaries. The study found a reduction in arterial pressure in animals that received the polyphenols for ten weeks, which may be due to the compounds' antioxidant effect. This benefit was also found in similar research conducted by Dr Wyss using soy derived polyphenols.

In research utilizing the ubiquitous southeastern vine kudzu, rats placed on a high salt diet were protected from the rise in blood pressure that normally occurs by administration of the root. Polyphenols from kudzu also lower glucose, insulin and leptin in animal models.

“It is unlikely that these polyphenols could eventually provide effective stand-alone therapy for postmenopausal women," Dr Wyss stated, "But in the future they may provide effective adjunct therapy that complements the use of lower doses of traditional pharmaceutical compounds."

—D Dye

August 10, 2007

Vitamin B1 deficiency implicated in diabetic vascular complications

An article published online on August 4, 2007 in the journal Diabetologia concluded that a deficiency of thiamin (vitamin B1) may be the culprit behind the vascular complications of diabetes, one of the most significant problems associated with the disease. Vascular complications of diabetes include heart disease and stroke, as well as microvascular complications such as kidney disease, retinopathy and neuropathy.

Professor Paul Thornalley and associates at the University of Warwick in England compared the red blood cell and plasma thiamin levels of 20 healthy volunteers with 26 individuals with type 1 diabetes and 48 type 2 diabetics. Red blood cell transketolase, which is reduced in thiamin deficiency, and markers of metabolic control and vascular dysfunction were also measured.

The team found that type 1 diabetics had a 76 percent lower, and type 2 diabetics a 75 percent lower plasma thiamin level compared to nondiabetic participants. This deficiency had not been previously discovered among diabetics through the use of the conventional method of evaluating thiamin status by measuring red blood cell levels of transketolase. The normal levels of transketolase found in diabetics were discovered to be the result of an increase in the activity of two thiamin transporter proteins that help transport thiamin into red blood cells as a result of reduced levels of the vitamin.

Low thiamin levels in diabetics were determined to be the result an increased rate of removal of thiamine from the blood into the urine. Renal clearance of the vitamin was in increased 24 fold among type 1 diabetics, and 16 fold in type 2. The decreased availability of thiamin was associated with greater levels of soluble vascular adhesion molecule-1, a marker of vascular complications.

The researchers suggest that future studies evaluate thiamin and its derivatives to correct low plasma concentrations of the vitamin and prevent and/or reverse vascular complications.

—D Dye

August 8, 2007

Green tea may be effective against inflammatory skin conditions

The August 18, 2007 edition of Experimental Dermatology published a report that described the finding of researchers at the Medical College of Georgia that green tea could be effective when applied topically to skin afflicted by inflammatory disorders such as psoriasis and dandruff.

"Psoriasis, an autoimmune disease, causes the skin to become thicker because the growth of skin cells is out of control," explained lead researcher Dr Stephen Hsu, who is an oral biologist at the Medical College of Georgia's School of Dentistry and Maxillofacial Pathology. "In psoriasis, immune cells, which usually protect against infection, instead trigger the release of cytokines, which causes inflammation and the overproduction of skin cells."

In the current study, Dr Hsu and colleagues explore the molecular pathways influenced by green tea extract in an animal model of inflammatory skin disease. They discovered that green tea regulates the expression of a protein known as caspase-14 which controls the skin cells' life cycle. "That marker guides cells by telling them when to differentiate, die off and form a skin barrier," Dr Hsu stated. "In people with psoriasis, that process is interrupted and the skin cells don't die before more are created and the resulting lesions form."

Dr Shu hopes that his team's research with green tea will contribute to a treatment that has less side effects than current treatments for inflammatory skin conditions. "The traditional treatment of ultraviolet light and medication, while it can control the lesions and be used long term, may cause squamous cell carcinoma – the second most common form of skin cancer," he said. "Some of the most effective anti-dandruff shampoos also have carcinogens in them. While the U.S. Food and Drug Administration allows that in small amounts, the bottom line is that we don't know the long-term effects of using those products continuously."

—D Dye

August 6, 2007

Osteoarthritis symptoms improved by glycine

Researchers at the Cellular Metabolism Institute in Tenerife and the Department of Biochemistry and Molecular Biology of the University of Granada have found that the amino acid glycine is helpful in alleviating the symptoms of osteoarthritis, and could be used to treat physical injuries or other conditions related to structural weakness such as osteoporosis. Osteoarthritis or arthrosis is the most common osteoarticulary condition, which occurs when cartilage degenerates until bone is exposed, resulting significant pain and impaired mobility. Although the disease is often treated with nonsteroidal anti-inflammatory drugs, there is presently no cure.

Doctor Patricia de Paz Lugo at the Cellular Metabolism Institute along with doctors Enrique Meléndez Hevia, David Meléndez Morales and José Antonio Lupiáñez Cara studied the effect of a glycine supplement on 600 subjects between the ages of 4 to 85 with osteoarthritis, osteoporosis, or physical injuries. Participants were administered 5 grams glycine in the morning and 5 grams in the evening. In all cases, symptoms significantly improved. “Therefore, we concluded that many degenerative diseases such as arthrosis can be treated as deficiency diseases due to the lack of glycine, since supplementing a diet with this amino acid leads to a notable improvement in symptomology without the need to take pain-killers," Dr de Paz Lugo stated.

Glycine is an amino acid used by the body in protein synthesis, and is found in fish, meat and dairy products. Although glycine is classified as a non-essential amino acid, meaning that it is not necessary to obtain by dietary means, the team's research indicates that glycine should be considered essential since the body's capacity to synthesize it is limited. They conclude that glycine leads to a general improvement over time, in most cases often between two weeks and four months, in osteoarthritis and other conditions of the body's mechanical structure.

—D Dye

August 3, 2007

Higher vitamin D levels associated with reduced rectal cancer risk

The July 31, 2007 issue of British Journal of Cancer published an article by researchers at the Japanese National Cancer Center which concluded that vitamin D may have a protective effect against rectal cancer.

The team utilized data from The Japan Public Health Center-based Prospective Study, an ongoing study of life-style related diseases in men and women aged 40 to 69. Questionnaires concerning medical history, diet, and other factors were completed by the participants upon enrollment. Blood samples were collected and later analyzed for 25-hydroxyvitamin D concentrations. The current study included 14,004 men and 24,369 women, among whom 256 cases of colon cancer and 119 cases of rectal cancer were identified over the 11.5 year average follow-up period.

Although the researchers did not find an association between the risk of colorectal cancer and vitamin D levels, when cancer of the rectum was separately analyzed, a significant protective effect was observed. Men whose vitamin D levels were among the lowest 25 percent of participants had 4.6 times the risk of rectal cancer than that of the remaining 75 percent. When men whose cancer was diagnosed during the first two years of follow-up were excluded from the analysis, those whose vitamin D levels were lowest still experienced more than double the disease risk. Women in the lowest 25 percent of vitamin D intake had 2.7 times the risk of rectal cancer than those whose intake was higher, regardless of whether those diagnosed in the first two years were included.

The authors suggest that differences between vitamin D's effect on colon and rectal cancer may be caused by the variance of vitamin D receptor expression between the sites. Populations other than Japanese men and women may have different risks.

—D Dye

August 1, 2007

Coenzyme Q10 improves endothelial function in heart disease patients

A report published online on July 19, 2007 in the European Heart Journal described the finding of Italian researchers that administering coenzyme Q10 (coQ10) to men and women with ischemic heart disease resulted in improvements in endothelial relaxation and greater levels of extracellular superoxide dismutase (SOD), an antioxidant enzyme that has been found to be reduced in the vasculature of individuals with coronary heart disease. Endothelium-bound extracellular SOD levels have been correlated with endothelial-mediated dilation, a biomarker of vascular function.

Luca Tiano of Polytechnic University of the Marche in Ancona, Italy and associates randomized 33 men and 5 women with coronary artery disease to receive 100 milligrams coQ10 three times per day or a placebo for one month. Participants received brachial artery endothelium-dependent vasodilation assessment, cardiopulmonary exercise testing, and measurement of endothelium-bound extracellular SOD upon enrollment and at the study's conclusion.

Supplementation with 300 milligrams coQ10 increased plasma levels four-fold in subjects that received it. In the 33 participants that completed the study, endothelium-dependent relaxation and endothelium-bound extracellular SOD were greater among those that received coQ10 than the placebo group, with increased benefits shown by those whose initial extracellular SOD levels were lowest, rendering them more prone to oxidative stress. Cardiopulmonary exercise test findings also improved in participants that received coQ10.

The researchers suggest that the improvements could be related to coQ10's involvement in energy production, or the counteraction of nitric oxide oxidation by coQ10, which would increase the compound's availability. (Nitric oxide is known to promote vascular dilation.) They recommend additional studies to determine how the effects observed in the current trial correlate with clinical benefits.

—D Dye

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