Studies Show Creatine May Be Effective for Older Men, Muscle Rehabilitation, Huntington's Disease

SASKATOON, Saskatchewan--Researchers from various parts of the world reported that creatine supplementation may increase lean tissue mass in men with a mean age of 70, speed up recovery in those suffering from muscle atrophy and benefit people with Huntington's disease. In the December Medicine and Science in Sports and Exercise (33, 12:2111-7, 2001) (www.ms-se.com), researchers at the University of Saskatchewan gave 30 men in a randomized, double blind study .3 g/d of creatine for every 1 kg of body weight. Both groups resistance trained three times per week for 12 weeks, going through three sets of 10 repetitions for 12 different exercises, including leg and bench presses. The creatine group had significantly higher scores after researchers measured average power, lean tissue mass and fat mass. In addition, the study's authors found that supplementation improved leg strength and endurance.

In the October issue of The Journal of Physiology (536, 2:625-33, 2001) (www.jphysiol.org), researchers reported that oral creatine taken during leg immobilization and rehabilitation may reverse atrophy faster when compared to placebo. In a double blind trial using 22 healthy volunteers, a cast was used to immobilize each subject's right leg for two weeks. Half of the subjects received creatine (gradually decreasing from 20 g/d to 5 g/d) and the other half took a placebo. Lack of movement decreased the cross-sectional area of the quadriceps in both groups, and after three sessions per week for 10 weeks of knee-extension exercises, the creatine group experienced more of an increase in the cross-sectional area of their quadriceps and a quicker return to maximum knee extension power than the placebo group.

A new study sponsored by the National Institutes of Health (NIH) and which began in October is investigating the safety and tolerability of creatine supplementation for subjects with Huntington's disease, a progressive and fatal neurological disorder. Because creatine has been shown to exhibit neuroprotective attributes in animal models, scientists believe that it may benefit the disease by relieving oxidative stress, inhibiting apoptotic neuronal death and reducing huntingtin aggregation (a protein product of the gene involved in the disease). Researchers also hope to see if creatine supplementation (8 g/d) can reverse the weakness and muscle mass loss that is usually associated with the illness. More information on this study can be found at www.clinicaltrials.gov.

Mixed Reviews for Mistletoe Extract and Cancer

CONGERS, N.Y.--In the December HSR's "Annual Research Review," an incorrect study was cited in the study titled "Mistletoe Extract May Not Benefit Melanoma Patients." The study that should have been cited was by the same author, Alexander Eggermont, M.D., Ph.D., and was also presented at the American Society of Clinical Oncology in May 2001. In this trial, the European Organization for Research and Treatment of Cancer (EORTC) conducted adjuvant therapy trials with melanoma patients at high risk of cancer recurrence after surgery.

A total of 830 patients were put into randomized groups and were studied for a median of 5.5 years. The patients were either given interferon alpha-2b (IFN2b) every other day or IFNy or mistletoe extract for one year.

The researchers found that node-positive patients on the mistletoe treatment had a higher incidence of brain metastasis and a lower incidence of having a disease-free interval and overall survival rate.

However, in a larger scale study with 10,226 cancer patients, mistletoe extract was found to improve the survival time of supplemented individuals with various types of cancer (Altern Ther Health Med, 7, 3:57-78, 2001) (www.alternative-therapies.com). In nonrandomized and randomized matched-pair studies, 1,668 patients were treated with mistletoe extract (Iscar^® by Weleda) while 8,475 did not take any type of mistletoe product.

In the nonrandomized, matched-pair study, mean survival time in the mistletoe groups was approximately 40-percent longer compared to the control groups; in the two randomized matched-pair studies, similar results were found, according to the study's authors, led by Ronald Grossarth-Maticek, M.D., Ph.D.

Melatonin Shows Promise as Alzheimer's Treatment

INDIANAPOLIS--Melatonin may have the potential to treat Alzheimer's disease because of its capacity to reduce the development of a protein complex that is a hallmark of the disease. The results of this in vitro study were published in the American Chemical Society's Biochemistry (40, 49:14995-5001, 2001) (http://pubs.acs.org/journals/bichaw).

Researchers from the Indiana University School of Medicine added melatonin to animal and human cell cultures that contained the building blocks of abnormal brain amyloid fibrils as well as human apoE4--a protein associated with strong risk for developing Alzheimer's. "Inheritance of apoE4 is a strong risk factor for the development of late-onset sporadic Alzheimer's," the researchers wrote. "Several lines of evidence suggest that apoE4 promotes formation of beta-sheet structures and amyloid fibrils. Deposition of amyloid fibrils is a critical step in the development of [the disease]."

Researchers reported that the addition of melatonin to brain cells in the presence of apoE inhibited fibril formation more effectively than with melatonin alone. This result was, however, structure-dependent upon melatonin and not related to melatonin's antioxidant properties.

"Our results clearly demonstrate the ability of melatonin to inhibit the process of forming the 'signature' amyloid protein bundles seen in Alzheimer's disease," said Miguel Pappolla, M.D., a study researcher. "This activity attributed to the 'indole' structure of melatonin appears to be specific. These exciting findings, however, mandate much more research before we can convincingly state melatonin can halt or prevent Alzheimer's disease." This study was supported by a grant from the National Institute on Aging (www.nia.nih.gov).

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