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Showing posts from September, 2009

Fighting a Losing War That Must Be Won

Once the “war on cancer” was declared in 1971 by Congress, researchers have sought to defeat it (1), but after losses of many knights in shining armor, a newfound respect has come around for this dragon of a disease (1). In the 1990s and 2000s, however, a new sense of hope had come about. “End cancer by the year 2015” was the message shared in 2003 by Andrew C. von Eschenbach, MD, director of the National Cancer Institute (NCI). And although he’s had many critics saying it couldn’t be done, others joined him in saying it could. Just two years afterward, in 2005, NCI modified it’s lofty goal to a softer “alleviate pain, suffering and death associated with cancer” (2). The change meant a new direction of “controlling” but not “curing” the disease . The same year, 2005, one Eschenbach supporter put forward a plan for a victory (3). His name was Mikhail V Blagosklonny, MD, PhD, and his approach was by combining strategies that target cancerous cells directly while protecting normal cells i

Anti-Soy Fiction

I just read a citizen's petition to FDA by Gail Elbek calling for the removal of soy because of antinutrients (trypsin inhibitors and phytates) and endocrine disruptors. Gave me a bit of a laugh, but I expect it will scare a lot of unwitting people. The outrageous claims Ms. Elbek makes are not grounded in any science. Soy phytotoxicity is going to “kill our children”? Please. I’m not about to throw out my soy milk, tofu and soy sauce. What’s next? Spinach. Spinach contains a lot of phytates. Many raw foods like raw soybeans contain all sorts of anti-nutrients, but that’s why we dehull, cook, or ferment these raw foods. Most anti-nutrients are eliminated just by the processing. There is a point to be made about high amounts of concentrated phytoestrogens (soy isoflavones) in a few dietary supplements, which are often marketed to women as natural hormonal therapy. These are basically drugs of which we don’t know enough about. The research is still out on whether or not they’re benef

Boron and Disease

Boron's ability to induce sex hormone levels give it a role preventing chronic disease. For example, adequate dietary boron may potentially reduce risk of lung cancer (1). The effects also explain why boron supplementation may support bone density guarding against osteoporosis (2). However, caution should be exercised before supplementation with boron. Greater estrogen levels due to boron supplementation may potentially increase risk of breast cancer (1;2). Thus, boron should not be taken by women with high risk of breast cancer or who've had breast cancer. Reference List 1. http://www.pccnaturalmarkets.com/health/2813008/ 2. http://www.osteopenia3.com/Boron-Osteoporosis.html

Nickel toxicity

Nickel is a known carcinogen. When in the diet in toxic amounts it contributes to oxidative stress, just as mercury and cadmium do, by reducing glutathione thereby interfering with cell membrane integrity and increasing lipid peroxidation (1). The oxidative damage, like from free iron or copper, can cause DNA damage (2). Reference List 1. Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem 2005;12:1161-208. 2. Tkeshelashvili LK, Reid TM, McBride TJ, Loeb LA. Nickel induces a signature mutation for oxygen free radical damage. Cancer Research; 53, 4172-4174, September 15, 1993.

Flouride and the World

As one travels around the world, especially in developing countries, the state of oral health stands out as an issue that needs attention. Fluoride treatment of drinking water can be an important step in improving oral health (1), but some populations may find it's not necessary because they may already be consuming adequate or even too much fluoride daily. Careful review of fluoride exposure must be evaluated region by region before deciding to treat local water with fluoride (2). According to the World Health Organization (WHO), flouride intake can vary depending fluoride already in water, on diet and other variables such as local pollution (2). Areas of greater volcanic activity, for example, tend have highest concentrations of fluoride in groundwater (2). The act of tea drinking can provide significant amounts of fluoride (1). In parts of China where high-fluoride coal is burned, the ash that pollutes crops may be providing fluoride (2). And in Tanzania, the use of contaminated

Molybdenum and Gout

A young electrician with a painful gouty arthritis in 2005 became the first case observed of occupational exposure of toxic amounts of molybdenum (1). Molybdenum is an activator of xanthine oxidase, which oxidizes xanthine producing uric acid (2). Too much produced hyperuricemia (1). The electrician can be thankful that his doctors found the cause of the gout because of previous men afflicted with gout by having consumed 10 to 15 mg of molybdenum daily (3;4). Tolerable uptake limits are set at 2 mg (2). Reference List 1. Selden AI, Berg NP, Soderbergh A, Bergstrom BE. Occupational molybdenum exposure and a gouty electrician. Occup Med (Lond) 2005;55:145-8.2. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.3. http://lpi.oregonstate.edu/infocenter/minerals/molybdenum/ 4. http://www.crnusa.org/safetypdfs/027CRNSafetyMolybdenum.pdf

Manganese as a Neurotoxin

Toxicity of manganese is more common than its deficiency (1), which unfortunately cause damage to the brain. Manganese appears to cause neurogeneration by activating microglia and causing them to release neurotoxins such as reactive oxygen and nitrogen species, which produce oxidative damage (2). The neurotoxins are also thought to possibly alter influence of neurotransmitters such as dopamine or gamma-aminobutyric acid (GABA) (1). According to a studies on non-human primates exposed to high doses of manganese, the mineral can lead to deficits in working memory performance and even induce an increase of beta-amyloid production linking manganese to Alzheimer's disease (3;4). Reference List 1. Anderson JG, Fordahl SC, Cooney PT, Weaver TL, Colyer CL, Erikson KM. Manganese exposure alters extracellular GABA, GABA receptor and transporter protein and mRNA levels in the developing rat brain. Neurotoxicology 2008;29:1044-53. 2. Zhang P, Wong TA, Lokuta KM, Turner DE, Vujisic K, Liu B.

Mutagenic Metals

The biochemical mechanism by which metals are mutagenic is by their effects on DNA. The main pathway shared by iron, copper, chromium, vanadium and cobalt is by redox-cycling reactions and mercury, cadmium and nickel by depleting glutathione and bonding to sulfihydryl groups (1). Free iron, in particular, can cause oxidative damage on DNA that can cause cancer in the spleen (2). Arsenic, in particular binds directly to critical thiols producing DNA damage (1). Cadmium interferes with and inhibits DNA repair (3;4). Reference List 1. Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem 2005;12:1161-208. 2. Wu X, Kannan S, Ramanujam VM, Khan MF. Iron release and oxidative DNA damage in splenic toxicity of aniline. J Toxicol Environ Health A 2005;68:657-66. 3. Slebos RJ, Li M, Evjen AN, Coffa J, Shyr Y, Yarbrough WG. Mutagenic effect of cadmium on tetranucleotide repeats in human cells. Mutat Res 2006;602:92-9. 4. Giaginis C, Gatzidou E, Theocharis S. DNA

Ca and Mg balance

Calcium (Ca) and magnesium (Mg) are non-heavy metals with the same valence charge that are both critical for physiologic function, yet overlap each other in their mechanisms. For example, they both use the same transport systems in kidney competing with each other for absorption. They also oppose one another in blood coagulation, smooth muscle contraction and PTH release. The relationship between Ca and Mg is important as it promotes a balance in given biological systems for proper function of the body. Deficiency either mineral could result in an improper balance leading to problems.

Vanadium treatment of type 2 diabetes enhanced by organic ligands

Vanadyl ions can act in an insulin-like manner in the body. Thus, when taken orally they may potentiate insulin’s effects, which can potentially improve situations of type 2 diabetes (1). Bioavailability of vanadyl compounds, however, can depend on whether of organic or inorganic nature (2). The organic bis-ligand oxovanadium appear to be far more bioavailable and efficacious than inorganic vanadyl sulfate (2). According to a couple of trials performed earlier this year in Canada, the organic version taken in doses of 10-90mg has no adverse effects (2). Further, it was found to help reduce fasting blood glucose levels and improves glucose tolerance (2). Reference List 1. Conconi MT, DeCarlo E, Vigolo S et al. Effects of some vanadyl coordination compounds on the in vitro insulin release from rat pancreatic islets. Horm Metab Res 2003;35:402-6. 2. Thompson KH, Lichter J, LeBel C, Scaife MC, McNeill JH, Orvig C. Vanadium treatment of type 2 diabetes: a view to the future. J Inorg Bioc

Life Depends on Arsenic?

As Gropper, Smitth and Groff tell it, arsenic "conjures an image of toxicity" unlike any other ultratrace mineral (1), but there are good things that come of arsenic and its story is worth discussion. Without arsenic, DNA synthesis couldn't happen. This is because arsenic is needed for normal metabolism. Specifically, the mineral is required for forming and using methyl groups to S-adenosylmethionine (SAM) (1). SAM is used for methylation to form DNA compounds (1). Arsenic, in fact, may have once been part of DNA itself. The mineral is very similar to phosphorus, which is currently the backbone of nucleic acids. Because this is is so it has been suggested that arsenic may have served as an alternate element early on, although not possible in modern biochemistry (3). According to scientists Felisa Wolfe-Simon, Paul Davies and Ariel Anbar, there may even be possibility that organisms may still be using arsenic in their DNA today, but simply not yet found (3). Reference List

Estrogen & Osteoporosis

Estrogen appears to directly influence bone turnover. Its mechanism is byacting on estrogen receptors in bone cells (1). The hormone influencesvitamin D metabolism by increasing conversion of 25-hydroxyvitamin D(25OHD) to 1,25-(0H)2D as it does in birds (2). The increase of 1,25-(0H)2D then enhances calcium absorption in the bones(2). Estrogen, thereby, contributes to bone density by slowing down boneloss and its absence can lead to lower bone density and predispose forosteoporosis (1;2). This biochemistry supports evidence that already exists that estrogenreplacement therapy (ERT) combined with adequate calcium and vitamin Dintake as well as exercise may help prevent osteoporosis (3;4). Despite the effects, however, I have the same opinion about using long-term estrogen replacement therapy (ERT) in postmenopausal women for osteoporosis as I do about estrogen for reducing risk of cardiovascular disease in postmenopausal women. While there are benefits outlined suggesting that future re

Chromium and Glucose Tolerance

Because of chromium’s known ability to potentiate action of insulin, an adequate chromium status is important especially for people with diabetes, insulin resistance and hypoglycemia to maintain glycemic control (1;2). According to an evaluation of 15 randomized clinical trials, amounts of about 200 mcg per day appear to improve use of glucose (3). In addition, a placebo-controlled trial of 180 Chinese patients found that doses at 200 mcg and as high as 1,000 mcg of chromium taken per day lowered blood glucose levels by 15-19% (3). Dose may depend on form of chromium since one form may be more bioavailable than another. Chromium picolinate appears to be the most bioavailable and, thus, the most potent (3). The amount of chromium taken, however, should not exceed 1,000 mcg per day due to potential toxicity (1). Chromium picolinate, in addition, should not be taken in amounts over 600 mcg because of association with renal failure and hepatic dysfunction (1). Reference List 1. Groppe

Chromium nicotinate, but not picolinate may improve body composition

Advertisements that suggest chromium picolinate may help consumers lose fat or gain muscle mass are largely overstated. A double-blind, randomized, placebo-controlled 12-week trial in 2001 found that chromium picolinate offered moderately obese women participating in an exercise program no significant changes to body composition, resting metabolic rate, plasma glucose, serum insulin, plasma glucagon, serum C-peptide or serum lipid concentrations (1). The 2001 study’s results supported at least three previous studies of which had also shown that chromium picolinate had been ineffective in changing body composition in obese women, in military personnel and in weight-lifting football players (2-4). A 12-week randomized, placebo-controlled trial in 2008 combined chromium picolinate with conjugated linoleic acid and evaluated effects on body composition changes of young, overweight women for 12 weeks (5).; still, no significant changes were found (5). Lastly, because of chromium’s known eff

Selenium and Prostate Cancer

Prostate cancer has been associated with low serum selenium concentration. To investigate the mechanisms by which selenium affects gene expression prostate tissue, researchers set out to measure activity of glutathione peroxidase in men with relatively high serum selenium concentration (1). The researchers measured serum selenium concentration in 98 men using atomic absorption spectrometry. Afterward, 12 men were selected for having the highest serum selenium concentration and another 12 were identified as having the lowest serum selenium concentration. Fresh prostate tissue samples were taken of the selected men to measure selenium concentration and glutathione peroxidase activity. The study, which was published in July 2007, reported a positive correlation found between a higher serum selenium concentration and a prostate tissue concentration. However, there was no significant increase of glutathione peroxidase activity associated with the higher concentration of selenium concentrati

DHA May Assist in Preventing Alzheimer's Disease

Summary: Complementary preventive therapy for Alzheimer’s disease should include DHA for its biochemical implications, especially in apoE4-genotype obese-diabetic patients. DHA mechanisms involve reducing adiposity and secretions, improving insulin sensitivity, guarding against oxidative stress, and guarding against beta-amyloid plaque, neurofibrillary tangles and advanced glycation end-products. Background: Urgent Call for Alzheimer’s Disease Preventive Therapies Foresight warns that the present epidemic of obesity and diabetes in the United States of America will lead to future medical epidemics and among them will be Alzheimer’s disease (AD), the most common neurodegenerative disease seen in aging. AD is seriously debilitating and at present time has no cure. Current treatments are limited to cholinesterase inhibitors to improve function of signaling pathways in memory, but are not intended to prevent or slow further brain damage. Preventive strategies are currently being studied to