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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.
What's Hot Archive
May 12, 2008
Lutein and DHA supplementation may aid in the prevention of macular degeneration
 A study described in the May, 2008 issue of the American Journal of Clinical Nutrition concluded that supplementing with lutein and docosahexaenoic acid (DHA) may help prevent the development of age-related macular degeneration (AMD) by increasing macular pigment optical density. Lutein and zeaxanthin are the main components of macular pigment, which helps protect the macula of the eye from the oxidative damage believed to play a role in the AMD's development.
Researchers at Tufts University in Boston assigned 57 women aged 60 to 80 to one of the following daily supplement regimens: 800 milligrams DHA, 12 milligrams lutein with 0.5 milligrams zeaxanthin, DHA plus lutein with zeaxanthin, or a placebo. Macular pigment optical density was measured before and after the four month treatment period. Blood levels of the nutrients, as well as serum HDL, LDL, VLDL and lipoprotein subfraction levels were measured at the beginning of study, and at two and four months.
In all non-placebo groups, nutrient levels were higher at two and four months than at the beginning of the study. DHA supplementation resulted in central increases of macular pigment density, while lutein was associated with eccentric increases. The combination of lutein and DHA did not result in a greater total increase in macular pigment density than either nutrient alone.
Although total cholesterol, HDL, LDL, and VLDL concentrations did not appear to be influenced by lutein or DHA in this study, lipoprotein subfractions were found to be different in the two groups that received DHA compared to the placebo group. Because lipoproteins transport lutein in the blood, DHA, through its alterations of the lipoprotein profile, could help decrease the risk of macular degeneration by increasing lutein transport into the macula. "The interactions of various factors, including effects of DHA on lipoprotein subclasses, warrant investigation in a longitudinal manner," they conclude.
—D Dye
May 09, 2008
Flavonoids fight Alzheimer's peptide in mouse model
 A report published in online on April 10, 2008 in the Journal of Cellular and Molecular Medicine revealed that luteolin, a flavonoid found in some fruits and vegetables, helps reduce amyloid-beta peptide levels in a mouse model of Alzheimer's disease and in mouse cell cultures. Amyloid beta is a sticky substance that forms the neurotoxic plaques found in the brains of Alzheimer's disease patients. Most researchers believe that amyloid beta is responsible for the Alzheimer's disease process, although other factors may play a causative role.
Following positive findings using cultured mouse neurons, Jun Tan, PhD of the University of South Florida in Tampa and colleagues administered luteolin to mice programmed to develop Alzheimer's disease and found that the animals had lower soluble amyloid beta levels than those that did not receive luteolin. Mice treated with luteolin also experienced a reduction in glycogen synthase kinase 3 (GSK-3) activity, an enzyme whose dysregulation has been implicated in amyloid beta and neurofibrillary tangle development, both characteristics of Alzheimer's disease.
Oral administration of diosmin, a glycoside of a flavonoid structurally similar to luteolin, also resulted in reduced amyloid beta levels in this strain. The researchers found that the flavonoids target presenilin-1, a brain protein linked to Alzheimer's disease.
“These flavonoids are widely available in natural foods and it appears that they may be used in purified form as therapeutic agents," observed senior author Terrence Town, PhD, who is a research scientist with the departments of Neurosurgery and Biomedical Sciences at Cedars-Sinai Medical Center in Los Angeles. "The compounds have few if any side effects and are naturally occurring in citrus fruits. They also can be found as dietary supplements in health food stores.”
—D Dye
May 07, 2008
Genes aren't everything
 An article published in the July, 2007 issue of the Journal of Gerontology (Biological Sciences) reported that one of the longest lived men in the world, who died at the age of 114, did not have the expected genetic mutations related to longevity and healthy bones, despite maintaining good health and a strong skeletal structure up to the end of his life.
In their introduction to the article, Adolfo Diez-Perez and his colleagues at the Universidad Autonòma de Barcelona in Spain observe that "Aging induces loss of bone density and quality resulting in a progressive incidence of fragility fractures with significant morbidity and mortality." Dr Diez-Perez's team evaluated the bone quality and genetics of a 113-year-old man who resided in a small town on the Spanish island of Menorca in the Mediterranean Sea. The man's 101 year old step-brother, 81 and 77 year old daughters, and 85 year old nephew were included in the research.
Although the man's bones were in excellent condition and he had no history of fracture, the researchers found no mutations in the KLOTHO gene, which is related to longevity and bone mineral density levels. The step-brother, nephew, and one daughter also failed to show any KLOTHO mutations. Additionally, no mutations in the LRP5 gene, associated with variations in bone mass, were found in the subject or his family.
The authors remark that the man had maintained his independence and intellect, had no history of disease, and, until the age of 102, had worked outdoors and cycled every day. Without ruling out the possibility of other genetic mutations related to longevity, Dr Diez-Perez's team believe that the subject's long life span may be due to the Mediterranean diet consumed on the island, combined with the island's climate, regular physical activity, and low stress levels.
—D Dye
May 05, 2008
Giving infants extra iron questioned
 A study conducted by the University of Michigan found that nonanemic infants who received a formula that provided 12 milligrams of iron, the standard amount contained in American iron fortified formulas, had a tendency to experienced developmental delays in later in childhood.
Four hundred ninety-four Chilean children who did not have iron deficiency anemia were randomized to receive formulas that provided 2.3 milligrams or 12 milligrams iron per liter between the ages of 6 and 12 months. The children were followed until the age of 10, and will be re-evaluated at age 16. Tests of cognitive and visual-motor development showed that children who received the high iron formula had a tendency to lag behind those that received the low iron formula. Although the majority in the high iron group were not negatively affected, those in the top 5 percent of blood hemoglobin levels experienced the worst outcome. (Hemoglobin is a pigment in red blood cells that contains iron.)
Iron is routinely supplemented to infants because it is believed that their rapid growth diminished the amount of the mineral in their bodies. Breast feeding is recognized to supply adequate iron until the ages of 4 to 6 months. Although the mineral is essential to human life, too much iron can have adverse effects.
"Our results for 25 years of research show problems with lack of iron. For us to find this result is a big deal, it's really unexpected," stated lead researcher Dr. Betsy Lozoff, who is a research professor at the University of Michigan's Center for Human Growth and Development. "I thought that behavior and development would be better with the 12 mg formula."
"At this point there's no basis for changing practice, but It's really important that we have continued research on this issue," she added.
—D Dye
May 02, 2008
Large study links obesity and inflammation to heart failure
 The May 6, 2008 issue of the Journal of the American College of Cardiology reported the latest findings from the Multiethnic Study of Atherosclerosis (MESA) that obesity is associated with prolonged inflammation of the heart which can lead to congestive heart failure.
The current analysis, conducted by cardiology specialists at Johns Hopkins University in collaboration with other researchers, involved 6,814 MESA participants who were 45 to 84 years of age upon recruitment between 2000 and 2002. MESA researchers plan to follow the subjects until 2012.
Of the 79 participants who developed congestive heart failure after a median follow-up time of four years, 44 percent were obese. Obese subjects had higher levels of inflammatory proteins interleukin-6, fibrinogen and C-reactive protein compared with nonobese participants. Near doubling of interleukin 6 levels was associated with an 84 percent greater risk of developing heart failure, and near tripling of C-reactive protein with a 36 percent greater risk than those with lower levels. The researchers also found a link between elevated inflammation-associated proteins and metabolic syndrome.
“Our results showed that when the effects of other known disease risk factors - including race, age, sex, diabetes, high blood pressure, smoking, family history and blood cholesterol levels - were statistically removed from the analysis, inflammatory chemicals in the blood of obese participants stood out as key predictors of who got heart failure,” stated lead researcher João Lima, MD, who is a professor of medicine and radiology at the Johns Hopkins University School of Medicine.
Study coauthor Hossein Bahrami, MD added, “The basic evidence is building the case that inflammation may be the chemical route by which obesity targets the heart, and that inflammation may play an important role in the increased risk of heart failure in obese people, especially those with the metabolic syndrome.”
—D Dye
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