What's Hot

June 2001

What's Hot Archive

June 29, 2001

Model of calorie restriction demonstrates slower cancer growth

In a mathematical model of cancer growth created by David Eichler, PhD of Ben Gurion University in Be'er Sheva Israel, it was predicted that undernutrition creates a state in which cancer cells' growth is limited. In the study, published in the June 7, 2001 issue of Journal of Theoretical Biology, sole author Dr Eichler simulated how cell populations grow while competing for a limited number of calories. While normal cells multiplied at a slower rate, faster growing cells such as cancer cells did not survive.

Dr. Eichler told the Life Extension Foundation, "I believe that many tumors consume far more energy and other nutrients than normal cells. It is just a general principle that growth requires energy and material, so rapid growth ought to require even more per unit time than normal growth." Dr. Eichler theorizes that if cellular proliferation is hampered by a slowed response to a nutritional deficiency, under competitive conditions this slowed proliferation is a survival advantage. Because cancer cells replicate faster than healthy cells and have greater caloric needs, minimizing calories can improve the survival of individuals with cancer by starving tumors.

Research has shown that obesity and unhealthy dietary patterns are associated with an increased incidence of cancer in humans. In laboratory studies, animals on calorie restriction regimens have fewer tumors and live longer. It remains now for clinical trials to validate calorie restriction as method of preventing and combating this and other dreaded diseases.

June 27, 2001

Hypothermia now in use in heart attack patients

As part of a nationwide study evaluating the efficacy and safety of hypothermia for heart attack patients, Rush-Presbyterian-St Luke's Medical Center in Chicago are asking heart attack patients admitted to the Emergency Department to participate by allowing the administration of a device that cools the core body temperature of the patient to 89 degrees Fahrenheit.

The purpose of the new therapy, called the Radiant Medical SetPoint Endovascular Temperature Management System, is to decrease the amount of tissue damage caused by heart attack. Patients admitted within six hours of experiencing chest pain who have their heart attack confirmed by electrocardiogram, and who consent to the treatment, will have a balloon catheter inserted into the femoral artery which administers cool saline for thirty minutes. Patients concomitantly receive a mild sedative to prevent shivering. After thirty minutes, the patient's core temperature reaches 89 degrees which is the temperature researchers believe is necessary to prevent further damage. The skin remains warm, preventing discomfort. The total time needed for the cooling procedure is an hour and a half, followed by a three hour period at the lower temperature before warming is initiated by the device.

After a thirty-day period, participants will be given an angiogram to determine the amount of tissue damage that has occurred. Because heart-attack induced ischemia can cause permanent damage, the procedure should demonstrate a significant amount of protection. If animal studies are an accurate predictor of the benefits we can expect in humans, the procedure could help a tremendous number of people. Rush Cardiac Catheterization Laboratories Director, Dr Gary Schaer stated, "Tests on animals have shown that circulating a cool saline solution within a long balloon catheter placed in the inferior vena cava, can reduce body temperature and diminish the amount of heart tissue damage by as much as 90 percent."

June 25, 2001

Oral contraceptives increase bone loss; calcium may prevent it

Although one might assume that both estrogen and exercise increase bone density, reserachers at Purdue University have found that in young women who exercise and take oral contraceptives, bone loss is increased compared to women who do not exercise or those who do not use oral contraceptives. Research published in the June 2001 issue of Medicine and Science in Sports and Exercise funded by the National Institutes of Health studied a group of women aged eighteen to thirty for two years. The participants were divided into oral contraceptive users and nonusers, and randomized into a group that exercised three times per week or a non-exercising group. The control group of sedentary women lost bone density, whereas this was prevented in the exercisers, but the researchers found that women who used oral contraceptives and exercised lost more bone density in the hip and spine than the nonexercisers. However, three women exercising and taking oral contraceptives maintained their bone density, and these three had adequate calcium levels.

Study head and coauthor Connie Weaver, Professor of Foods and Nutrition at Purdue commented, "The study showed that, overall, exercise had positive affects on whole body bone mineral content for everyone. Only the spine and hip were compromised if subjects who were on oral contraceptives exercised, and only then if calcium intakes were inadequate. . . This negative interaction is very scary because we want women to exercise for all kinds of beneficial reasons. But we don't want bone, especially of the hip, to be compromised because that's the worst kind of fracture you can have. . . . If you're going to be on birth control pills and exercise, you have to get enough calcium. You either need to get calcium through foods - and that could be dairy or fortified foods, such as juices or cereals - or you need to supplement."

June 22, 2001

Elevated homocysteine associated with increase in all-cause mortality

Homocysteine is an amino acid which is a toxic byproduct of methionine metabolism, and is now recognized as a important marker cardiovascular disease risk. The July issue of the American Journal of Clinical Nutrition will feature the results of a prospective cohort study showing that elevated plasma homocysteine is associated with an increase in all-cause mortality. The study examined data obtained from 2,127 men and 2,639 women between the ages of sixty-five and sixty-seven who were enrolled as part of a Norwegian national cardiovascular screening program between 1992 and 1993, and who were followed for a four years. The participants had their plasma homocysteine levels determined at the study's onset, as well as other cardiovascular disease risk factors. Subjects were also asked to complete questionnaires on symptoms, risk factors, lifestyle and diet, and were divided into two groups consisting of high and low cardiovascular risk. During follow-up 162 men and 97 women died, and causes of death were obtained from death certificates. Deaths were categorized as cardiovascular, malignant, violent, or other causes.

A strong correlation was found between death from all causes and elevated homocysteine levels. Participants with the highest homocysteine levels in the high risk group experienced at 21% increase in all-cause mortality compared to 9% in the low risk group. An unexpected finding was a strong association between homocysteine levels and noncardiovascular deaths, which was significant regardless of cardiovascular disease risk status. The study authors concluded that for every 5 micromole per liter increase in plasma homocysteine there is a 49% increase in all-cause mortality, and they stress that homocysteine should be looked at as more than just a cardiovascular risk factor. An editorial in the same issue recommends widespread screening of homocysteine levels in middle-aged and older individuals to identify those for whom folic acid supplementation might be of help.

June 20, 2001

Lutein helps prevent atherosclerosis

Research published in the June 19 2001 issue of Circulation: Journal of the American Heart Association has found that the carotenoid lutein may help prevent the buildup of atherosclerotic plaque in the wall of the arteries of the neck that can lead to stroke. The study examined 480 men and women participants in the Los Angeles Atherosclerosis Study who had no history of stroke or heart disease. Participants received ultrasound examinations of their carotid arteries to determine thickness resulting from plaque buildup and had blood levels of lutein determined at the onset of the study and at eighteen months. Individuals with the highest levels of lutein experienced an average of a 0.004 millimeter increase in arterial wall thickness over the course of the study, whereas those with the lowest levels had an increase averaging 0.021 millimeters.

In the second part of the study the researchers cultured human arterial cells and exposed them to several combinations of lutein and low density lipoprotein, the form of cholesterol believed to be responsible for atherosclerosis. Lutein exerted a protective effect against LDL-induced inflammation in a dose-dependent manner.

The third part of the study consisted of administering lutein to mice and comparing the size of their atherosclerotic lesions to that of a control group who did not receive lutein supplementation. The mice receiving lutein experienced a reduction of 43% in the size of the lesions.

Study coauthor James Dwyer, PhD, professor of preventive medicine at the University of Southern California stated, "Scientific knowledge of the long-term effects of diet on cardiovascular disease is still rudimentary, but there is mounting evidence that increased intake of vegetables and fruits is protective against cardiovascular disease. . . . The importance of our findings concerning lutein and atherosclerosis is that we may have identified one of the many components of vegetables that account for the protective effects of vegetables."

June 18, 2001

Latest research shows Alzheimer's plaques may be caused by free radicals

It is commonly believed that the amyloid plaques that exist in the brains of Alzheimer's disease patients contribute to the oxidative damage and inflammation observed that destroys brain cells. In a study partly funded by the National Institute on Aging, published in the June 15 2001 issue of The Journal of Neuroscience, researchers from the University of Pennsylvania have demonstrated that oxidative damage caused by free radicals precedes the formation of amyloid plaques. Ninety-five percent of the brain is composed of lipids, which are subject to peroxidation.

The researchers used a mouse genetically engineered to rapidly produce the amyloid-beta characteristic of Alzheimer's disease and a control group of mice, and measured a marker of lipid peroxidation at various points between the ages of four and eighteen months. The transgenic mice showed higher urinary, plasma and brain levels of the marker of lipid peroxidation from eight months of age onward. At twelve months of age, these mice experienced a surge in amyloid beta production, and had oxidative damage levels 200% higher than controls. Although amyloid beta is known to create free radicals, because lipid peroxidation preceded amyloid formation in this study it appears to have a causative effect.

Study coauthor Domenico Practico MD, of the University of Pennsylvania School of Medicine Department of Pharmacology commented, "This opens a lot of interesting hypotheses for therapeutics. If you reduce oxidative stress in these animals very early, when they are very young, can you prevent the formation of amyloid? And by how much? We know Vitamin E, which is an antioxidant, can temporarily slow the progression of AD for some patients. What we don't yet know is what will happen if we suppress, reduce or delay oxidative stress over the long run."

June 15, 2001

Low vitamin B6 associated with elevated C-reactive protein

Data from 891 survivors of the Framingham Heart Study revealed that C-reactive protein, or CRP, a blood marker of increased heart disease risk, is associated with low levels of vitamin B6. This association was independent of plasma homocysteine levels, which are conversely associated with B6 levels. The research, published in the June 12 2001 issue of Circulation, Journal of the American Heart Association, analyzed blood samples drawn from each subject for CRP, plasma homocysteine, folate, vitamin B12, and pyridoxal-5'-phosphate, the biologically active form of vitamin B6. Dietary intake of vitamin B6 was determined through the use of food-frequency questionnaires. The subjects were divided into two groups consisting of those with normal CRP and those with CRP values of 6 milligrams or greater per liter. The two groups did not vary significantly in regard to age, sex, plasma folate, plasma vitamin B12 or vitamin B6 intake. The percentage of those with hypertension, diabetes and coronary heart disease was also similar for each group.

Analysis of the data showed that the group with elevated C-reactive protein had significantly lower levels than the normal CRP group, even after adjustment for total homocysteine levels. Because dietary intake of vitamin B6 was similar for both groups, the low plasma levels in the elevated CRP group could not be attributed to low intake, nor were they caused by increased breakdown of the vitamin. Since it is known that low vitamin B6 levels are associated with other diseases involving inflammation such as rheumatoid arthritis, the researchers hypothesized that pyridoxal-5'-phosphate is acting as a coenzyme for inflammation-related functions, and that low levels reflect higher utilization. They recommend additional studies to determine whether inflammation-associated declines in pyridoxal-5'-phosphate are involved in the cascade of metabolic events related to some diseases.

June 13, 2001

Breast cancer and HRT study may be misleading

Within days of the publication of an article in the Journal of the National Cancer Institute entitled, "Hormone Replacement Therapy Has No Adverse Effect on Cancer Recurrence and Mortality in Women with Breast Cancer", news headlines across the world were proclaiming that hormone replacement therapy (HRT) was safe for breast cancer survivors. Yet, given what we know concerning estrogen's role in breast cancer, is it really safe? Vinton C Vint MD, coauthor of the book, How to Prevent Breast Cancer, told the Life Extension Foundation, "The title of the article is extremely irresponsible and shortsighted. This alone shows how strong the psychological bias for HRT is among physicians and medical researchers."

Dr Vint enumerated the following points:

"1. The editorial writer noted that the follow-up of the HRT users was 'relatively short,': only 3.7 years for recurrence. This time frame is extremely short for breast cancer biology.

2. The editorial writer also notes that a 'healthy user' effect might have been in play. Note that the control groups not on HRT were not matched for lifestyle, alcohol, smoking, diet, exercise, body mass index, education, supplement usage, etc. Only age, stage of cancer, and year of diagnosis were used. Dr John Lee has stated on numerous occasions that most HRT studies are misleading, without carefully selected matched controls, because women chosen to be placed on HRT tend to be much healthier, have healthier lifestyles, be better educated, and be much more proactive with regards to their health, than women most doctors chose not to put on HRT. This little known fact alone plays a tremendous part in the vast majority of the early 'positive' reports of HRT on cardiovascular disease, dementia, and the playing down of induction of cancers of the ovaries, endometrium and breasts. A subset of healthier women will be expected to have an overall lower mortality from all causes.

3. Note that there was no stratification of the breast cancers into types and subtypes, especially estrogen receptor positive and negative. One would expect ER- breast cancers not to be less influenced by HRT, while the converse would be expected for ER+ breast cancers.

4. Note that the women receiving HRT had an increased rate of breast cancer in their previously noncancer-involved breast. If this doesn't tell women HRT significantly ups the risk for breast cancer, nothing will. It is to be hoped that women and their physicians will approach hormone replacement therapy with or without a previous diagnosis of breast cancer with caution, and that they not be swayed by premature pronouncements of its safety."

"It is to be hoped that women and their physicians will approach hormone replacement therapy with or without a previous diagnosis of breast cancer with caution, and that they not be swayed by premature pronouncements of its safety."

June 11, 2001

Yet another fruit with cancer-fighting properties

Almost every week, the discovery of disease fighting properties of a new fruit or vegetable is revealed. Diets high in fruits and vegetables have been shown to play a role in the prevention of heart disease, cancer and other conditions. An abstract presented at the 2000 annual Food Technology meeting revealed that mangoes have anticancer properties beyond those conferred by their natural carotenoid content. Researchers at the University of Florida in Gainesville tested several dilutions of an organic extract of mangoes and an aqueous extract in which the carotenoids were removed on an in vitro model of cancer consisting of 3T3 mouse cells treated with a carcinogen. The cells were incubated with the mango extracts for a period of three to six weeks before being examined for transformation into cancer cells. Although both extracts inhibited cancer cell formation, the water-soluble compound was found to be ten times as potent in inhibiting the formation of cancer cells than the carotenoid-containing extract, demonstrating the presence of an as yet unknown compound in mangoes responsible for this benefit. The researchers believe that the known anticancer properties of carotenoids were responsible for the cancer-inhibiting effects of the organic extract.

Study coauthor Sue Percival PhD, of the department of Food science and Human Nutrition at the University of Florida, summarized, "We did a study with cells in culture and found that mangoes were able to inhibit the formation of cancerous-type cells. The water soluble portion was about 10 times more effective." The researchers conclude that mango consumption may be beneficial in reducing the risk of some cancers.

June 8, 2001

Selenium deficiency could contribute to flu epidemics

A study published in the June 2001 issue of the Federation of American Societies for Experimental Microbiology (FASEB) journal revealed a serious consequence of selenium deficiency. Selenium is a trace mineral that acts as an antioxidant and is deficient in some diets, although in some areas the soil provides sufficient amounts.

A University of North Carolina Chapel Hill research team fed mice diets that had normal or deficient selenium levels, then exposed them to a mild strain of human influenza virus. The mice deficient in selenium experienced greater and longer lasting lung inflammation than the mice fed normal diets, comparable to the difference between severe and mild pneumonia, a difference that can be life-threatening. The researchers then analyzed the viruses for mutations and found that the virus isolated from the low selenium group had a number of mutations, which can render the virus more likely to spread. Melinda A Beck, associate professor of pediatrics and nutrition at the University of North Carolina schools of medicine and public health elaborated, "We believe our latest findings are both important and potentially disturbing because they suggest nutritional deficiencies can promote epidemics in a way not appreciated before. Here we looked at flu virus because it hospitalizes more than 100,000 people each year in the United States alone. But what we found conceivably could be true for any RNA virus -- cold virus, AIDS virus and Ebola virus. . . . Once the mutations have occurred, even mice with normal nutrition are more susceptible to the newly virulent strain. This work, in conjunction with our earlier work with coxsackievirus, shows that specific nutritional deficiencies can have a profound impact on the genome of RNA viruses. Poor nutritional status may contribute to the emergence of new viral strains and might promote epidemics."

"It might be that any kind of oxidative stress to the host produces a similar effect, but we won't know that for sure until we look at other antioxidants," she observed.

June 5, 2001

Vitamin C and lipoic acid toxic to cancer cells

A study published in the British Journal of Cancer showed that vitamin C administered in an in vitro model of cancer caused the death of cancer cells. The addition of lipoic acid provided a synergistic effect.

Researchers acting on experimental and clinical evidence that vitamin C increases survival in cancer patients and inhibits tumor growth utilized a tumor model to test the anticancer effects of varying concentrations of vitamin C as well as combinations of vitamin C with phenyl ascorbate, (a lipophilic vitamin C analog), vitamin K3, two forms of lipoic acid and doxorubicin, a chemotherapy drug. To discover whether the effective concentrations were achievable in humans, the researchers experimentally infused a cancer patient volunteer with varying amounts of vitamin C to determine peak plasma concentrations.

Ascorbic acid alone was found to increase the percentage of apoptotic and necrotic cells in the cancer model, but the high concentration necessary may not always be attainable by intravenous vitamin C infusion. However, the addition of lipoic acid synergized with vitamin C to a point at which significant death of tumor cells could occur at concentrations readily achievable by IV (30 to 60 grams). The tumor cell-killing effect of vitamin C was additively enhanced by phenyl ascorbate and vitamin K3.

One of the concerns in regard to antioxidant consumption concomitant with chemotherapy is that antioxidant nutrients will protect the tumor cells from the drug's tumoricidal effects. With doxorubicin, low doses of vitamin C appeared to protect cells from the effect of the drug, while high doses increased its tumoricidal efficacy.

One of vitamin C's mechanisms of action in combating cancer is that of a pro-oxidant, with high concentrations of vitamin C producing hydrogen peroxide at a level that kills tumor cells. Other mechanisms include enhanced immune response, strengthening of the extracellular matrix against tumor cell invasion and a reduction in the severity of cachexia.

June 4, 2001

Genetic mechanisms for ginkgo's benefits discovered

The herb ginkgo biloba has been tested in clinical trials in the form known as EGb761, an extract containing 24% flavone glycosides, 6% terpene lactones, and other constituents. A study published in the May 29 2001 issue of the Proceedings of the National Academy of Sciences sought to determine the effect of ginkgo on genetic expression by administering a diet containing EGb761 to ten rats and a low flavonoid diet to ten controls, and conducting high density oligonucleotide microarrays of the hippocampus and cortex of their brains. The microarrays looked for changes of an amplitude of three fold or more in genetic transcription of the mice receiving ginkgo.

After four weeks the hippocampi and cortices of the mice were removed and analyzed. Of the mice receiving ginkgo, ten genes were found to be upregulated by a factor of three-fold or more, one in the hippocampus and the rest in the cortex. The hippocampal gene encoded transthyretin, a protein involved in the transport of the thryoid hormone thyroxin, which, with other thyroid hormones, is involved in the regulation of brain cell proliferation. Transthyretin has been shown to sequester amyoid-beta, (the protein found in the brains of Alzheimer's disease patients) and prevent its aggregation. Two other upregulated genes were responsible for proteins that form and breakdown the neurofibrillary tangles that are characteristic of Alzheimer's. Additionally, a cortical gene involved in the formation of nerve synapses and neural circuitry was upregulated, which further demonstrates ginkgo's ability to enhance neurologic function.

The study's authors found it interesting that another gene impacted by ginkgo increased growth hormone in the brain's cortex. Although growth hormone is mainly known for its effects on muscle and bones, the brain possesses receptors for growth hormone, and growth hormone deficiency can cause cognitive impairment and negatively impact mood.

This is the first study to elucidate the mechanisms of ginkgo's protective effects in the brain. The authors suggest further studies to investigate what effects the changes caused by ginkgo have on overall brain function.

June 1, 2001

Diabetes incidence lower in nutritional supplement users

The May 1 2001 issue of the American Journal of Epidemiology published a study in which participants in the first National Health and Nutrition Examination Survey conducted from 1971 to 1975 were followed up in order to determine the incidence of diabetes and its relationship to supplement taking. The study examined data from 9,573 participants whose ages ranged from twenty-five to seventy-four years at the beginning of the study. Participants were asked at the baseline and at follow-up (from 1982 to 1993) if they were regular or irregular users of supplements, and regular users were asked to report the supplements they were using. One thousand ten individuals developed diabetes during the follow up period. Of participants who reported using supplements within thirty days of their baseline interview, 21.4% were diagnosed with the disease, compared to 33.5% of those who did not report using supplements, with men having the lower risk. Similar results were observed among those who reported both regular and irregular supplement use, with regular supplement users having a slightly lower incidence. Those reporting regular supplement use both at baseline and follow up experienced a significant reduction in risk.

The author of the study noted that vitamin and mineral supplements containing iron or supplemented with additional iron did not significantly increase diabetes risk. Because iron is a prooxidant and oxidation may be involved in the development of diabetes, an increase in the incidence of diabetes might have been expected in iron supplement users. Those who used iron supplements alone without other supplements experienced a slightly higher risk of diabetes than nonsupplement users.

This study is one of the few that link vitamin use to a lower risk of diabetes. With the incidence of the disease on the rise, the author urges the exploration of new approaches to prevention, and suggests the judicious use of vitamins as possibly playing a role.

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