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.
Calcium, vitamin D intake associated with increased weight loss in dieters
An article published online on September 1, 2010 in the American Journal of Clinical Nutrition reports an analysis of a trial of overweight men and women which found that a greater intake of dairy calcium and higher serum vitamin D levels after 6 months of a dietary intervention predicted an increased likelihood of weight loss.
Danit R. Shahar of Ben-Gurion University of the Negev in Israel and colleagues evaluated data from 322 participants in the Dietary Intervention Randomized Controlled Trial, which included men and women who were aged 40 to 65 with a body mass greater than 27 upon enrollment, or who were diagnosed with type 2 diabetes or heart disease. Subjects were assigned to a low fat diet, a low carbohydrate diet, or a Mediterranean diet for two years. Serum vitamin D levels were measured upon enrollment and at 6 months, and calcium intake from was dairy quantified.
Participants whose initial serum 25-hydroxyvitamin D levels were lowest had a higher body mass index on average at the beginning of the trial. Those who had the highest dairy calcium intake, equal to 580 milligrams calcium at 6 months, lost 12 pounds by the end of the two year study, while those whose intake was lowest averaged 7 pounds of weight loss. An increase in serum vitamin D at 6 months was also associated with greater weight loss.“It was known that overweight people had lower levels of serum vitamin D but this is the first study that actually shows that serum vitamin D increased among people who lost weight,” remarked Dr Shahar. “This result lasted throughout the two years that the study was conducted, regardless of whether they were on a low-carb, low fat or Mediterranean diet."
Gamma-tocotrienol inhibits pancreatic tumors in mice
Experiments conducted at The University of Texas MD Anderson Cancer Center in Houston, reported online on September 23, 2010 in the journal Cancer Research, demonstrated that gamma-tocotrienol helped suppress pancreatic tumor growth as well as render tumors more sensitive to gemcitabine, one of two drugs approved to treat the disease.
In their introduction to the article, Bharat B. Aggarwal and colleagues note that the transcription factor nuclear factor-kappaB (NF-kB) has been associated with cell proliferation, invasion, angiogenesis, metastasis, antiapoptosis and chemoresistance in multiple tumors. Gamma-tocotrienol, one of the eight members of the vitamin E family, has been shown to inhibit the activation of NF-kB in several cancer cell lines, in addition to suppressing the proliferation of a variety of tumor cells.
In tests using four cultured pancreatic cancer cell lines, gamma-tocotrienol suppressed the proliferation of all lines, with higher doses and longer exposures producing a greater benefit. Administration of a 50 micromole dose of gamma-tocotrienol resulted in almost complete suppression of tumor cell proliferation. The vitamin was found to inhibit NF-kB activation and proteins involved with inflammation, in addition to sensitizing the cells to gemcitabine.
The researchers then tested the effects of gamma-tocotrienol and gemcitabine alone and in combination in a mouse model of human pancreatic cancer. Oral gamma-tocotrienol administered alone was shown to inhibit tumor growth, a finding that is a first, according to the authors. As was demonstrated in the cultured cell experiments, gamma-tocotrienol enhanced the tumor-fighting ability of gemcitabine. Gamma-tocotrienol alone was found to suppress NF-kB activation, and further suppressed NF-kB in gemcitabine-treated tissues.
“Our study is the first report to suggest that gamma-tocotrienol can enhance the apoptotic effect of gemcitabine in various pancreatic cancer cell lines in vitro,” the authors announce. “Our findings suggest that gamma-tocotrienol can inhibit the growth of human pancreatic tumors and sensitize them to gemcitabine by suppressing of NF-κB-mediated inflammatory pathways linked to tumorigenesis.”
Extra years gained by combined lifestyle improvements comparable to nonsmoking status in women
Maintaining normal weight, having a low waist-hip ratio, exercising, never have been exposed to second-hand smoking, and consuming high amounts of fruit and vegetables were associated with a reduced risk of total and cause-specific mortality in women over a 9 year period according to a report published online in the journal PLoSMedicine on September 14, 2010.
Researchers from Vanderbilt University, Shanghai Cancer Institute, and the U.S. NCI evaluated data from 71,243 women aged 40 to 70 years upon enrollment in the Shanghai Women’s Health Study. Subjects in the current analysis were those who reported never having smoked or regularly consuming alcohol. Lifestyles were scored on the basis of the following factors: normal weight, low waist to hip ratio, daily exercise, no exposure to spousal smoking and increased daily fruit and vegetable intake.
Over the 9.1 year average follow-up period, 775 women died from cardiovascular disease and 1,351 from cancer. Compared with women who reported none of the lifestyle factors, those who had 4 to 5 factors had a 43 percent lower risk of dying of any cause, a 71 percent lower risk of dying of cardiovascular disease, and a 24 percent lower risk of cancer mortality. Lifestyle-associated reductions in premature death were similar among those with and without preexisting conditions and in subjects both younger and older than age 55.
“To our knowledge, this is the first large prospective cohort study specifically designed to quantify the combined impact of lifestyle-related factors on mortality outcomes among lifetime nonsmokers and nonalcohol drinkers,” the authors write. “Results show that lifestyle factors other than active smoking and alcohol drinking have a major combined impact on mortality on a scale comparable to the effect of smoking as the leading cause of death in most populations.”
Bile acid extends yeast lifespan
A bile acid formed in mammals could help increase lifespan, according to a study described in the July, 2010 issue of the journal Aging.
In their introduction to the article, the authors note that in aging yeast, a caloric restricted diet or the administration of certain small molecules extend lifespan by targeting specific signaling pathways. By screening over 19,000 small molecules, researchers at Concordia University in Montreal identified certain bile acids as having longevity-enhancing benefits in yeast, with lithocholic acid (LCA) providing the greatest benefit.
"Our findings imply that LCA extends longevity by targeting two different mechanisms," explained first author Alexander Goldberg, who is a doctoral student at Concordia. "The first takes place regardless of the number of calories and involves the day-to-day or housekeeping proteins. The second system occurs during calorie-restriction and involves stressor proteins. Regardless of their triggers both of these mechanisms work to suppress the pro-aging process.”
"Although we found that LCA greatly extends yeast longevity, yeast do not synthesize this or any other bile acid found in mammals," noted senior author Vladimir Titorenko. "It may be that yeast have evolved to sense bile acids as mildly toxic molecules and respond by undergoing life-extending changes."
"Although we have an overall idea how LCA works to extend longevity in yeast, we still need to determine if this is the case for other species," he added. "We do know from previous studies, however, that bile acids are beneficial to health and longevity. For example, they have shown to accumulate in the serum of long living mice and play a role in improving rodent liver and pancreatic function."
"This leads us to believe that bile acids have potential as pharmaceutical agents for the treatment of diabetes, obesity and various metabolic disorders, all of which are age-related," Dr Titorenko concluded. "They may indeed offer hope for a healthy aging life."
Current evaluations of aging populations fail to take into account improvements in life expectancy and disability rates
An article appearing in the September 10, 2010 issue of the journal Science concludes that gloomy forecasts of the impact of the growing proportion of older individuals worldwide are based on outdated methods of assessment.
Current methods include measures of the portion of the population over the age of 65 and the "old age dependency ratio", which calculates the number of people dependent on others when they reach 65 years of age. "Those measures are based on fixed chronological ages, and this can generate misleading results," explained coauthor Dr Warren C. Sanderson of the International Institute for Applied Systems Analysis in Austria and Stonybrook University. "When using indicators that assume fixed chronological ages, it's assumed that there will be no progress in factors such as remaining life expectancies and in disability rates. But many age-specific characteristics have not remained fixed and are not expected to remain constant in the future."
Alternate methods include the prospective old age dependency ratio, which is arrived at by dividing the number of people in age groups with life expectancies of 15 or fewer years by the number of people at least 20 years of age in age groups with life expectancies greater than 15 years, and the adult disability dependency ratio, which is the number of adults at least 20 years old with disabilities divided by the number those without them.
"If we apply new measures of aging that take into account increasing life-spans and declining disability rates, then many populations are aging slower compared to what is predicted using conventional measures based purely on chronological age," noted Sergei Sherbov of the Vienna Institute of Demography, who coauthored the article.
Ability to manufacture DHA absent in Alzheimer’s disease patients’ livers
A report published on September 8, 2010 in the journal PLoS ONE reveals the discovery of researchers at the University of California, Irvine of an inability of the livers of Alzheimer’s disease patients to produce the omega-3 fatty acid docosahexaenoic acid (DHA). The polyunsaturated fatty acid is contained in fish oil and the algae they feed on and is made in the liver from molecules contained in plants and other foods. Studies of Alzheimer’s patients’ brain tissue have found significantly reduced levels of DHA.
Louise Turner Arnold Chair in the Neurosciences and director of the University of California, Irvine Center for Drug Discovery Daniele Piomelli and his associates compared postmortem liver tissue from Alzheimer’s disease patients and those who did not have the disease. They found that while livers derived from those who had Alzheimer’s did not produce DHA, the defect did not occur in tissue from nondiseased patients.
"We all know Alzheimer's is a brain disease, but our findings – which were totally unexpected – show that a problem with liver fat metabolism can make people more vulnerable," Dr Piomelli commented. "They also suggest a reason why clinical trials in which Alzheimer's patients are given omega-3 fatty acids to improve cognitive skills have had mixed results."
"Additionally, we found that the greater the amount of Alzheimer's-related cognitive problems experienced in life by the patients, the lower were their liver DHA levels," stated coauthor and project scientist in pharmacology, Giuseppe Astarita. "So we do see a connection."
"Our research isn't advocating that liver metabolism is a key to Alzheimer's," Dr Piomelli added. "The factors causing the disease are many and complex, but we feel this is another piece in the Alzheimer's puzzle."
EPA shows promise for metabolic syndrome
An article published online on September 1, 2010 in the journal Diabetes revealed the discovery of researchers in Japan of an antiobesity effect for the omega-3 fatty acid eicosapentaenoic acid (EPA) in a study of mice given diets containing a high amount of fat and sugar (sucrose). Western diets containing high amounts of fat and sugar have been implicated in metabolic syndrome, a cluster of symptoms that increase the risk of diabetes.
In their introduction to the article, the authors remark that visceral fat is a key factor in the development of metabolic syndrome, and that enhanced production of fat by the liver and fatty liver disease also play a role in the condition. In four experiments, male mice were fed a high fat diet or a high fat/high sucrose diet with or without the addition of EPA for 4 to 20 weeks. While obesity developed in those that received the high fat diet as well as those that received the high fat/high sucrose diet, liver lipogenic enzymes increased, the development of fatty liver was more severe and hyperinsulinemia developed more rapidly in the latter group. Eicosapentaenoic acid added to the high fat, high sucrose diet resulted in reduced weight gain and obesity-associated elevations in blood glucose and insulin, while it had no effect on obesity in mice given high fat diets. The authors suggest that suppression of enhanced hepatic fat production contributes to EPA’s antiobesity effect.
“This study is the first demonstration that the antiobesity effect of EPA in high fat/high sucrose-induced obesity is associated with the suppression of hepatic lipogenesis and steatosis,” the authors announce. “Because the metabolic syndrome is often associated with hepatic lipogenesis and steatosis, the data of this study suggest that EPA is suited for the treatment of the metabolic syndrome.”
Melatonin linked with cancer protection
The results of a study conducted by Professor Abraham Haim and colleagues at the Center for Interdisciplinary Chronobiological Research of the University of Haifa in Israel adds new evidence to an association between light at night and an increased risk of cancer due to light-induced suppression of the hormone melatonin.
Previous research conducted by Dr Haim found that men and women who reside in areas in which there is greater night-time exposure to artificial light have an increased risk of prostate and breast cancer. Suppression of melatonin, a hormone released by the pineal gland in response to darkness, was hypothesized to be the cause of the finding.
For the current research, the team injected mice with cancerous cells and divided them to receive one of the following daily regimens: exposure to 16 hours of light and 8 hours of darkness, the same regimen plus melatonin, exposure to 8 hours of light and 16 hours of darkness, or the same regimen plus a one-half hour interval of light exposure during the 16 dark hours.
At the end of the study, cancerous tumors in the mice that experienced 8 hours of light and 16 hours of uninterrupted darkness averaged 0.85 cubic centimeters in size, while those exposed to the half hour interval of light had tumors that averaged 1.84 cubic centimeters. Tumors averaged 5.92 cubic centimeters among mice that were exposed to 16 hours of light, yet those treated with melatonin had tumors that averaged 0.62 cubic centimeters, as well as lower rates of mortality compared to untreated mice.
“Light pollution as an environmental problem is gaining awareness around the world, and the World Health Organization’s International Agency for Research on Cancer (IARC) has already classified working the night shift as a higher grade of cancer risk,” the researchers note.
Veggie variety protects puffers
An article published online on August 31, 2010in the journal Cancer Epidemiology, Biomarkers & Prevention revealed the finding of a large collaboration of European researchers that consuming a variety of vegetables provides a protective benefit against lung cancer. Editorial board member Steven Hecht, PhD believes this study is one of the first to evaluate the effect of diversity rather than quantity of fruit and vegetable consumption in lung cancer risk.
Frederike L. Buchner of the National Institute of Public Health and the Environment in the Netherlands and colleagues evaluated data from 452,187 participants in the ongoing European Prospective Investigation into Cancer and Nutrition (EPIC) study. Diet and lifestyle questionnaires provided intake information on 14 commonly consumed fruits and 26 vegetables.
Over an average of 8.7 years of follow-up, 1,613 subjects were diagnosed with lung cancer. The team uncovered a reduction in lung cancer risk associated with intake of a greater variety of vegetables among current smokers, and a lower risk of squamous cell carcinoma of the lung associated with increased variety of vegetable and fruit intake, also mainly in smokers.
H. Bas Bueno-de-Mesquita, MD, MPH, PhD, who is project director of cancer epidemiology at the Netherlands’ National Institute for Public Health and the Environment, remarked that “they cannot exclude that these results can still be explained by smoking.”
“Although quitting smoking is the most important preventive action in reducing lung cancer risk, consuming a mix of different types of fruit and vegetables may also reduce risk, independent of the amount, especially among smokers” he added. “Fruits and vegetables contain many different bioactive compounds, and it makes sense to assume that it is important that you not only eat the recommended amounts, but also consume a rich mix of these bioactive compounds by consuming a large variety."