Every substance, medication, & supplement can be a nutrient or it can be a poison, depending upon the rate of administration, route of administration, and amount of administration.
Never go cheap when getting your medicines or supplements. Do your own research, insist on pharmaceutical grade, assayed products. If you can’t get a direct look at the data, look for a more reputable source. The difference between the top of the line, quality nutraceutical and a cheap knock-off is a few pennies per day. Get the best quality that you can reasonably afford.
Restoration of health and a sense of well-being should be the principal goal of medicine. Due to the way that the practice of medicine has evolved, attention has been paid largely to the treatment of illness and injury, (sometimes referred to allopathic medicine,) and less to the prevention of disease.
The science of anti-aging medicine focuses on the restoration of health, which can be viewed as being entirely different from the treatment of disease. In reality, both types of medicine have the same goal, but the approach is what makes them different. This approach is sometimes referred to as “holistic.”
That focus involves the restoration of balance within the body, that is, provision of medication, nutrient, and hormone with the end-point being a healthy level with restoration of healthy function.
This end-point is not defined by ‘population normals,’ but by that amount and that ratio that is healthy for the individual. It is this the philosophical point that separates the allopathic practitioner from the allopathic practitioner.
Williams C, Kingwell BA, Burke K, McPherson J, Dart AM. Folic acid supplementation for 3 wk reduces pulse pressure and large artery stiffness independent of MTHFR genotype. Am J Clin Nutr. Jul 82(1):26-31, 2005.
BACKGROUND: Folic acid reduces plasma homocysteine and may be an important therapy for preventing cardiovascular disease. A key mechanism may be the reduction of arterial stiffness.
OBJECTIVE: The effect of folic acid supplementation on blood pressure and large artery stiffness was examined in relation to methylenetetrahydrofolate reductase (MTHFR) genotype.
DESIGN: Forty-one asymptomatic men with normal or high-normal ambulatory blood pressure (systolic: >130 to 80 to participated. The study had a randomized, placebo-controlled, double-blind, crossover design that incorporated 3-wk treatments with 5 mg folic acid/d or matching placebo; each treatment was separated by a 4-wk washout phase.
RESULTS: Folic acid reduced brachial pulse pressure by 4.7 +/- 1.6 mm Hg (P < 0.05) without changing mean arterial pressure. Systemic arterial compliance increased by 0.15 +/- 0.03 mL/mm Hg (P < 0.05) after folic acid treatment but did not change after placebo treatment. These responses did not significantly correlate with either homocysteine or folate plasma concentrations. MTHFR genotype CC homozygotes (without the 677C–>T polymorphism) with normal blood pressure had a larger reduction in homocysteine concentrations in response to folic acid than did T allele carriers. Blood pressure and arterial stiffness responses were independent of MTHFR genotype.
CONCLUSION: Folic acid is a safe and effective supplement that targets large artery stiffness and may prevent isolated systolic hypertension.
BACKGROUND: Endothelial dysfunction and arterial stiffening are commonly observed in type 2 diabetes. These abnormalities might be secondary to increased plasma concentrations of homocysteine. We sought to determine whether oral folic acid supplementation, by lowering homocysteine levels, enhanced endothelial function and reduced arterial stiffness in type 2 diabetes.
METHODS: Twenty-six type 2 diabetic patients (age 56.5 +/- 0.9 years, diabetes duration 5.5 +/- 0.6 years, means +/- SEM) with no history of cardiovascular disease received 5 mg/d of oral folic acid or placebo for 4 weeks in a double-blind, randomized controlled, parallel group trial. The following parameters were measured before and after treatment: 1) endothelial function (forearm arterial blood flow during local intra-arterial administration of endothelium-dependent [acetylcholine 1.5, 4.5, and 15 microg/min] and endothelium-independent [sodium nitroprusside 1, 2, and 4 microg/min] vasodilators); and 2) carotid-radial and carotid-femoral pulse wave velocity.
RESULTS: Folic acid reduced plasma homocysteine concentrations and enhanced endothelium-dependent vasodilatation during each acetylcholine infusion rate (mean and 95% confidence interval post versus pretreatment differences in forearm arterial blood flow ratio between the infused and control arm +0.19 (0.03-0.35), P < .01; +0.39 (0.02-0.81), P < .05; and +0.40 (0.09-0.89), P < .05, respectively). Endothelium-independent vasodilatation and pulse wave velocity were not affected. No significant changes in forearm arterial blood flow and pulse wave velocity were observed in the placebo group. Multiple regression analysis showed that changes in folic acid, but not homocysteine, concentrations independently described changes in maximal endothelium-dependent vasodilatation.
CONCLUSIONS: Short-term oral folic acid supplementation significantly enhances endothelial function in type 2 diabetic patients, independent of homocysteine lowering.[/fusion_toggle][fusion_toggle title="The importance of early folate status" open="no"]Muskiet FA. The importance of (early) folate status to primary and secondary coronary artery disease prevention.Reprod Toxicol. 2005 Sep-Oct;20(3):403-10.
Folate, methionine, betaine, choline, zinc and Vitamins B(12), B(6) and B(2) are involved in one-carbon metabolism, which includes S-adenosylmethionine (SAM) substrated methylation. Inadequate enzyme activities and imbalances of substrates and cofactors in one-carbon metabolism, together referred to as the ‘methyldietary’ constituents, may cause homocysteine and S-adenosylhomocysteine accumulation. Hyperhomocysteinemia is associated with many disorders including coronary artery disease (CAD). CAD at adult age is also associated with low birth weight-induced ‘programming’, which prepares for unfavorable postpartum conditions and carries the potential of transgenerational transmission. CAD risks of hyperhomocysteinemia and ‘programming’ might find a common biochemical basis in epigenetics, which, among others, operates via SAM-substrated methylation of DNA and histones. Folic acid-responsive global and locus-specific hypomethylation were found in hyperhomocysteinemia and CAD. Currently, there is
no hard evidence that folic acid supplementation of CAD patients is beneficial or that improved folate status in pregnancy prevents CAD in the offspring at adult age. The folate RDA as derived from CAD primary prevention might require embracement of the assumption that ‘what nutritional measures are best for CAD patients are most probably best for the general population’. We have no
knowledge on the optimal ‘methyldiet’ balance on which our genome has become adapted during millions of years of evolution and on which our genome consequently functions best. More insight may derive from the study of methyldietary constituents and soft endpoints such as plasma homocysteine and gene methylation, in healthy, pregnant and non-pregnant, subjects and CAD patients and in populations with high and low CAD risks and those consuming diets more closely related to our ancient diet. Folic acid supplementation is obviously unnecessary at sufficient intake of naturally occurring folates, implying that continuing efforts should aim at meeting the recommendations by making the right choice of food products, that are either or not folate-enriched by genetic modification.
Kuo HK, Yen CJ, Bean JF. Levels of homocysteine are inversely associated with cardiovascular fitness in women, but not in men: data from the National Health and Nutrition Examination Survey 1999-2002. J Intern Med. 2005 Oct;258(4):328-35.
OBJECTIVES:Cardiovascular fitness represents the ability of active skeletal muscle to utilize oxygen during aerobic exercise. Elevated homocysteine, causing tissue injury by such mechanisms as oxidative stress, endothelial damage, and protein homocysteinylation, is associated with increased risk of cardiovascular disease, dementia and osteoporotic fracture. However, the association between elevated homocysteine and cardiovascular fitness has not been reported.
DESIGN: Population-based cross-sectional study.
SETTING: National Health and Nutrition Examination Survey from 1999 to 2002 in the USA.
SUBJECTS: A total of 1444 noninstitutionalized adults aged 20–49 years with reliable measures of cardiovascular fitness and non-missing values in homocysteine. Main outcome measures. Cardiovascular fitness, estimated maximal oxygen uptake or VO(2)max (mL kg(-1) min(-1)), was obtained by a submaximal exercise test. Levels of homocysteine were measured by the Abbott homocysteine assay, a fully automated fluorescence polarization immunoassay method and were natural-log-transformed due to right skewness.
RESULTS. After adjustment for age, race and body mass index, there was a 0.70 mL kg(-1) min(-1) decrease (P=0.033) in the estimated VO(2)max for each standard deviation (SD) increase in the natural-log-transformed homocysteine level for women. Additional adjustment of hypertension, diabetes, smoking status, alcohol intake, use of lipid-lowering agents, physical activity, self-report health condition, as well as levels of folate, vitamin B(12), creatinine, C-reactive protein, total cholesterol and haemoglobin seemed to influence the association. In the fully adjusted model, we observed a 1.18 mL kg(-1) min(-1) decrease (P=0.003) in the estimated VO(2)max for each SD increase in the natural-log-transformed homocysteine level in women. There was no association between cardiovascular fitness and homocysteine levels in men.
CONCLUSION. High homocysteine levels were inversely associated with cardiovascular fitness in women, but not in men. The results suggest that homocysteine levels are important indicators of exercise tolerance amongst women and may be useful in targeting female individuals requiring endurance intervention to prevent loss of cardiovascular fitness and function.[/fusion_toggle][fusion_toggle title="Insulin and endothelial function improvements after folate and B12 therapy" open="no"]Setola E, Monti LD, Galluccio E, et al:Insulin resistance and endothelial function are improved after folate and vitamin B12 therapy in patients with metabolic syndrome: relationship between homocysteine levels and hyperinsulinemia. Eur J Endocrinol. 2004 Oct;151(4):483-9.
OBJECTIVE: The purpose of this study was (a) to study whether a folate and vitamin B12 treatment, aimed at decreasing homocysteine levels, might ameliorate insulin resistance and endothelial dysfunction in patients with metabolic syndrome according to the National Cholesterol Education Program-Adult Treatment Panel-III criteria and (b) to evaluate whether, under these metabolic conditions, there is a relationship between hyperhomocysteinemia and insulin resistance.
DESIGN AND METHODS: A double-blind, parallel, identical placebo-drug, randomized study was performed for 2 months in 50 patients. Patients were randomly allocated to two groups. In group 1, patients were treated with diet plus placebo for 2 months. In group 2, patients were treated with diet plus placebo for 1 month, followed by diet plus folic acid (5 mg/day) plus vitamin B12 (500 microg/day) for another month.
RESULTS: In group 2, folate treatment significantly decreased homocysteine levels by 27.8% (12.2+/-1.2 vs 8.8+/-0.7 micromol/l; P<0.01). A significant decrement was observed for insulin levels (19.9+/-1.7 vs 14.8+/-1.6 microU/ml; P<0.01) accompanied by a 27% reduction in the homeostasis model assessment levels. A positive relationship was found between the decrement of homocysteine and insulin levels (r=0.60; P<0.002). In parallel, endothelial dysfunction significantly improved in the treated group, since post-ischemic maximal hyperemic vasodilation increased by 29.8% and cGMP by 13.6% while asymmetrical dimethylarginine levels decreased by 21.7%. On the contrary, in group 1 patients, treated with placebo, no changes were shown in any of the variables.
CONCLUSIONS: Folate and vitamin B12 treatment improved insulin resistance and endothelial dysfunction, along with decreasing homocysteine levels, in patients with metabolic syndrome, suggesting that folic acid has several beneficial effects on cardiovascular disease risk factors.[/fusion_toggle][fusion_toggle title="Alzheimer's prevention with folic acid and pregnenolone" open="no"]Ravaglia G, Forti P, >Maioli F, Martelli M, Servadei L, Brunetti N, Porcellini E, Licastro F. Homocysteine and folate as risk factors for dementia and Alzheimer disease. Am J Clin Nutr. 2005
BACKGROUND: In cross-sectional studies, elevated plasma total homocysteine (tHcy) concentrations have been associated with cognitive impairment and dementia. Incidence studies of this issue are few and have produced conflicting results.
OBJECTIVE: We investigated the relation between high plasma tHcy concentrations and risk of dementia and Alzheimer disease (AD) in an elderly population. DESIGN: A dementia-free cohort of 816 subjects (434 women and 382 men; mean age: 74 y) from an Italian population-based study constituted our study sample. The relation of baseline plasma tHcy to the risk of newly diagnosed dementia and AD on follow-up was examined. A proportional hazards regression model was used to adjust for age, sex, education, apolipoprotein E genotype, vascular risk factors, and serum concentrations of folate and vitamin B-12.
RESULTS: Over an average follow-up of 4 y, dementia developed in 112 subjects, including 70 who received a diagnosis of AD. In the subjects with hyperhomocysteinemia (plasma tHcy > 15 mumol/L), the hazard ratio for dementia was 2.08 (95% CI: 1.31, 3.30; P = 0.002). The corresponding hazard ratio for AD was 2.11 (95% CI: 1.19, 3.76; P = 0.011). Independently of hyperhomocysteinemia and other confounders, low folate concentrations.
There is a lot of interesting data coming out with regards to control of the aging process. Unfortunately, there is even more garbage being written, as well. This is a tricky area of medicine/nutrition.
The beta-amyloid peptide (Abeta) is centrally related to the pathogenesis of Alzheimer’s disease (AD) and is potently neurotoxic to central nervous system neurons. The neurotoxicity of Abeta has been partially related to the over activation of glutamatergic transmission and excitotoxicity. Taurine is a naturally occurring beta-amino acid present in the mammalian brain. Due to its safety and tolerability, taurine has been clinically used in humans in the treatment of a number of non-neurological disorders. Here, we show that micromolar doses of taurine block the neurotoxicity of Abeta to rat hippocampal and cortical neurons in culture. Moreover, taurine also rescues central neurons from the excitotoxicity induced by high concentrations of extracellular glutamate. Neuroprotection by taurine is abrogated by picrotoxin, a GABA(A) receptor antagonist. GABA and muscimol, an agonist of the GABA(A) receptor, also block neuronal death induced by Abeta in rat hippocampal and cortical neurons. These results suggest that activation of GABA(A) receptors protects neurons against Abeta toxicity in AD-affected regions of the mammalian brain and that taurine should be investigated as a novel therapeutic tool in the treatment of AD and of other neurological disorders in which excitotoxicity plays a relevant role.
van Guldener C, >Stehouwer CD. Diabetes mellitus and hyperhomocysteinemia. Semin Vasc Med. Feb;2(1):87-95, 2002
Patients with diabetes mellitus are prone to cardiovascular disease and risk factors presumably unrelated to diabetes, such as hyperhomocysteinemia, may be involved in the atherothrombotic process in these subjects. Plasma homocysteine levels are usually normal in diabetes, although both lower and higher levels have been reported. This has been ascribed to hyperfiltration and renal dysfunction or low folate status, respectively. Insulin resistance does not appear to be a major determinant of plasma homocysteine level. Hyperhomocysteinemia has been associated with microalbuminuria and retinopathy in type 1 and type 2 diabetes. In patients with type 2 diabetes, plasma homocysteine concentration has also been shown to be related to macrovascular disease and death. This relation seems to be stronger in diabetics than in subjects without diabetes. The underlying pathophysiological mechanism of this increased vascular risk remains unexplained but may relate to worsening of endothelial dysfunction or structural vessel properties. Because homocysteine and diabetes have an apparent synergistic negative vascular effect, patients with diabetes are good candidates for screening and treatment with folic acid until the results of ongoing clinical trials are available.
Ukraintseva SV, Arbeev KG, Michalsky AI, et al:: Antiaging treatments have been legally prescribed for approximately thirty years. Ann N Y Acad Sci. Jun;1019:64-9, 2004.
There is an interesting divergence between the achievements of geriatrics and gerontology. On the one hand, during the last 30 years physicians in many developed countries have successfully prescribed several medicines to cure various symptoms of senescence. On the other hand, the influence of such medicines on human life span practically has not been studied. The most common of the relevant medicines are nootropic piracetam, gamma-aminobutyric acid (GABA), selegiline, Ginkgo biloba, pentoxifylline, cerebrolysin, solcoseryl, ergoloid, vinpocetin, sertraline, and estrogens, among others. Available data from human clinical practices and experimental animal
studies indicate that treatments with these drugs improve learning, memory, brain metabolism, and capacity.
Some of these drugs increase tolerance to various stresses such as oxygen deficit and exercise, stimulate the regeneration of neurons in the old brain, and speed up the performance of mental and physical tasks. This means that modern medicine already has “antiaging” treatments atits disposal.
However, the influence of such treatments on the mean and maximal life span of humans, and on the age trajectory of a human survival curve has been poorly studied. The increase in human life expectancy at birth in the second half of the last century was mostly caused by the better survival at the old and oldest old rather than at the young ages. In parallel, the consumption of brain protective and regenerative drugs has been expanding in the elderly population. We provide evidence in support of the idea that the consumption of medicines exerting antiaging properties may contribute to the increase in human longevity.
Biswas SK, McClure D, Jimenez LA, Megson IL, Rahman I. Curcumin induces glutathione biosynthesis and inhibits NF-kappaB activation and interleukin-8 release in alveolar epithelial cells: mechanism of free radical scavenging activity. Antioxid Redox Signal. Jan-Feb;7(1-2):32-41, 2005.
Oxidants and tumor necrosis factor-alpha (TNF-alpha) activate transcription factors such as nuclear factor-kappaB (NF-kappaB), which is involved in the transcription of proinflammatory mediators, including interleukin-8 (IL-8). Curcumin (diferuloylmethane) is a naturally occurring flavonoid present in the spice turmeric, which has a long traditional use as a chemotherapeutic agent for many diseases. We hypothesize that curcumin may possess both antioxidant and antiinflammatory properties by increasing the glutathione levels and inhibiting oxidant- and cytokine-induced NF-kappaB activation and IL-8 release from cultured alveolar epithelial cells (A549).
Treatment of A549 cells with hydrogen peroxide (H2O2; 100 microM) and TNF-alpha (10 ng/ml) significantly increased NF-kappaB and activator protein-1 (AP-1) activation, as well as IL-8 release. Curcumin inhibited both H2O2- and TNF-alpha-mediated activation of NF-kappaB and AP-1, and IL-8 release. Furthermore, an increased level of GSH and glutamylcysteine ligase catalytic subunit mRNA expression was observed in curcumin-treated cells as compared with untreated cells. Curcumin interacted directly with superoxide anion (O2*-) and hydroxyl radical (*OH) as shown by electron paramagnetic resonance, quenching the interaction of the radicals with the spin trap, Tempone-H. This suggests that curcumin has multiple properties: as an oxygen radical scavenger, antioxidant through modulation of glutathione levels, and antiinflammatory agent through inhibition of IL-8 release in lung cells.
Experiments have shown that chronic nicotine administration caused oxidative damage in various organs by increasing lipid peroxidation products and decreasing the activity of endogenous antioxidants. The aim of this study was to investigate the effects of taurine treatment on nicotine-induced oxidative changes in rat thoracic aorta and heart and to explore the possible mechanisms of action. Male Wistar albino rats (200-250 g) were injected with nicotine hydrogen bitartrate (0.6 mg/kg; i.p.) or saline for 21 days. Taurine was administered (50 mg/kg; i.p.) alone or along with nicotine injections. After decapitation, the thoracic aorta and heart tissues were excised.
The aorta was used for in vitro contractility studies or stored along with the heart samples for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content. Tissue samples were also examined histologically. Serum samples were stored for the measurement of MDA, GSH and lactate dehydrogenase (LDH) activity. Chronic nicotine treatment impaired both the contraction and relaxation responses of the aortic rings to phenylephrine and acetylcholine, respectively. It increased lipid peroxidation, MPO levels and tissue collagen content of bothaorta and heart samples. Taurine supplementation to nicotine-treated animals reversed the contractile dysfunction and restored the endogenous GSH levels and
decreased high lipid peroxidation and MPO activities in both tissues. These data suggest that taurine supplementation effectively attenuates the oxidative damage because of chronic nicotine administration possibly by its antioxidant effects.
Metallothioneins (MTs) are a class of ubiquitously occurring low molecular weight cysteine- and metal-rich proteins containing sulfur-based metal clusters. The conservation of these clusters in an increasing number of three-dimensional structures of invertebrate, vertebrate and bacterial MTs signifies theimportance of this structural motif. In the postgenomic era, it is becoming increasingly clear that MTs fulfil different functions.
Increasing body of evidence show that diverse functions of the mammalian MT-1/MT-2 isoforms including involvement in zinc homeostasis, protection against heavy metal toxicity and oxidative damage are related to their clusters. In contrast, the biological properties of the brain-specific MT-3 isoform implythat the clusters in this protein play a structural role. The recent highlights of MT research are the subject of this review.
Pandi-Perumal SR, Zisapel N, Srinivasan V, Cardinali DP: Melatonin and sleep in aging population.
The neurohormone melatonin is released from the pineal gland in close association with the light-dark cycle. There is a temporal relationship between the nocturnal rise in melatonin secretion and the ‘opening of the sleep gate’ at night. This association, as well as the sleep promoting effect of exogenous melatonin, implicates the pineal product in the physiological regulation of sleep. Aging is associated with a significant reduction in sleep continuity and quality. A decreased production of melatonin with age is documented in a majority of studies.
Diminished nocturnal melatonin secretion with severe disturbances in sleep/wake rhythm has been consistently reported in Alzheimer’s disease (AD). A recent survey on the effects of melatonin in sleep disturbances, including all age groups, failed to document significant and clinically meaningful effects of exogenous melatonin on sleep quality, efficiency and latency. However, in clinical trials involving elderly insomniacs and AD patients suffering from sleep disturbances exogenous melatonin has repeatedly been found to be effective in improving sleep. The results indicate that exogenous melatonin is more effective to promote sleep in the presence of a diminished production of endogenous melatonin. A MT(1)/MT(2) receptor analog of melatonin (ramelteon) has recently been introduced as a new type of hypnotics with no evidence of abuse or dependence.
Cohen PG: Aromatase, adiposity, aging and disease. The hypogonadal-metabolic-atherogenic-disease and aging connection. Med Hypotheses. 2001 Jun;56(6):702-8.
In males, aging, health and disease are processes that occur over physiologic time and involve a cascade of hormonal, biochemical and physiological changes that accompany the down-regulation of the hypothalamic-anterior pituitary-testicular axis. As aging progresses there are relative increases of body fat and decreases in muscle mass. The increased adipose tissue mass is associated with the production of a number of newly generated factors.
These include aromatase, leptin, PAI-1, insulin resistance, and the dyslipidemias, all of which can lead to tissue damage. Fatty tissue becomes the focal point for study as it represents the intersection between energy storage and mobilization. The increase in adipose tissue is associated with an increase in the enzyme aromatase that converts testosterone to estradiol and leads to diminished testosterone levels that favor the preferential deposition of visceral fat. As the total body fat mass increases, hormone resistance develops for leptin and insulin. Increasing leptin fails to prevent weight gain and the hypogonadal-obesity cycle ensues causing further visceral obesity and insulin resistance.
The progressive insulin resistance leads to a high triglyceride-low HDL pattern of dyslipidemia and increased cardiovascular risk. All of these factors eventually contribute to the CHAOS Complex: coronary disease, hypertension, adult-onset diabetes mellitus, obesity and/or stroke as permanent changes unfold. Other consequences of the chronic hypogonadal state include osteopenia, extreme fatigue, depression, insomnia, loss of aggressiveness and erectile dysfunction all of which develop over variable periods of time.
Baulieu EE, Robel P, Fellous A, Duchossoy Y, Fontaine-Lenoir V, David S. MAPREG: toward a novel approach of neuroprotection and treatment of Alzheimer’s disease. J Mol Neurosci. 2004;24(1):63-5.
MAPREG (microtubule-associated protein/neurosteroidal pregnenolone) is a start-up company that was created in October 2000. Its acronym recalls the basic discovery (Murakami et al., 2000) from which drug(s) will hopefully be developed that are useful for neuroprotection and repair in conditions such as post-traumatic and postischemic lesions, as well as defects proper to normal aging and neurodegenerative diseases, that is, principally Alzheimer’s disease.
Pregnenolone, the main steroid synthesized from cholesterol in the nervous system (therefore, a neurosteroid), binds specifically with high affinity (> or = 40 nM) to microtubule-associated protein 2 (MAP2), a protein family involved in the assembly and stabilization of microtubules made from tubulin alpha and beta polymers, and in the bundling of several microtubules by MAP2 projection arms. Pregnenolone binding increases MAP2-induced microtubule polymerization, when purified tubulin and MAP2 are coincubated in GTP containing buffer at 37 degrees C. Therefore, MAP2 can be considered as a receptor for a novel mechanism of steroid action.
The underlying principle and its potential pharmacological consequences are described in an INSERM patent (FR 0003430; March 17, 2000). MAPREG has established its own laboratory in a space rented to Bicetre hospital, near the research building of INSERM, where two of the main founders of the company (Drs. E. Baulieu and P. Robel) work. The company has been quite successful, largely thanks to the support of ISOA (attributed in October 2002). A lead compound (pregnenolone derivative) was tested and patented by MAPREG early in 2003 (FR 0300507; January 17, 2003). Activities and results reported at the ISOA meeting on Oct. 2, 2003, include in vitro basic studies, in vitro and in vivo neuroprotection trials in rodent systems, and studies with human cells and an AD transgenic mouse model. Copyright 2004 Humana Press Inc.
21;1038(2):123-31.Previously, it has been shown that taurine exerts its protective function against glutamate-induced neuronal excitotoxicity through its action in reducing glutamate-induced elevation of intracellular free calcium, [Ca2+]i. Here, we report the mechanism underlying the effect of taurine in reducing [Ca2+]i. We found that taurine inhibited glutamate-induced calcium
influx through L-, P/Q-, N-type voltage-gated calcium channels (VGCCs) and NMDA receptor calcium channel.
Surprisingly, taurine had no effect on calcium influx through NMDA receptor calcium channel when cultured neurons were treated with NMDA in Mg2+-free medium. Since taurine was found to prevent glutamate-induced membrane depolarization, we propose that taurine protects neurons against glutamate excitotoxicity by preventing glutamate-induced membrane depolarization, probably through its effect in opening of chloride channels and, therefore, preventing the glutamate-induced increase in calcium influx and other downstream events.
ABOUT THE STUDY
In the retrospective study, researchers from the University of Massachusetts, Harvard University and the University of Iowa examined the diets of 1,057 women who reported PMS symptoms and 1,068 who did not. They found that…
Women who consumed nearly twice the recommended daily allowance (RDA) of vitamin D (the RDA for vitamin D is 400 international units, or IU) — the equivalent of seven or more cups of milk — were 40% less likely to experience PMS than women who consumed the vitamin D equivalent of one cup or less of milk daily.
Women who took in one-and-one-half times the RDA of calcium (RDA is approximately 1,000 mg depending on your age) the equivalent of four-and-one-half or more cups of milk) were 30% less likely to experience PMS than women who consumed the calcium equivalent of less than half a cup of milk daily.
These results were reported in the June 12, 2005, issue of Archives of Internal Medicine.
WHAT THIS MEANS TO YOU
the study makes clear some kind of association between vitamin D, calcium, magnesium and PMS, the diary format of the study does not appropriately isolate each element to show causation. So what does that mean and what should you do?According to Wendy Vannoy, ND, a naturopathic physician in Portland, Oregon, women often don’t get enough calcium and vitamin D — two nutrients that are especially critical during the childbearing years.
Since milk and other dairy products are not necessarily the best sources of calcium, Daily Health News contributing editor Andrew L. Rubman, ND, suggests other good dietary sources of calcium, such as broccoli, spinach, collard greens and turnip greens. As far as vitamin D is concerned, it’s actually one of the easiest vitamins to get — only 10 to 15 minutes a day outdoors in the sunshine
will enable your body to manufacture all of this vitamin you need. For more on vitamin D’s vital role, see Daily Health News, June 17, 2003.
If you’re not taking in sufficient nutrients (and most of us don’t), Dr. Vannoy recommends taking a good daily multivitamin along with a calcium/magnesium supplement. (The magnesium will help with the absorption of the calcium.) Dr. Vannoy has found that getting proper nutrition combined with regular sleep and exercise can significantly reduce PMS symptoms for many women.