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George seems too much worried to umbalance a natural condition, but I insist in saying that at the recommended doses it might be only a waste of money at worst.BTW George, I am still waiting for your comments on the 'Shanghai report' and the engineers versus docs issue...where everything started from, last August.When you get bored of vitamin intoxication issues, of course.ikod
One serious problem with cod liver oil is the total collapse of the cod sticks and the cod fishing industry – it is in no position to try to satisfy new and expanding markets for its products. This, if nothing else, demands that in the long run only a synthetic substitute for cod liver oil could be sustainably sold to an expanding marketplace.George
Whether our elderly relatives need vitamin B12 or not,to keep their brain in good shape is still a matter ofdebate. Negative reports prevailed in the past, nowtimes are changing a bit.This is a positive report from Israel.I find it sharp and encouraging indeed...If only a few patients respond to a treatment, we haveto identify their 'size and shape', instead of throwingthe whole research in the garbage bin.Neuropsychology of vitamin B12 deficiency in elderly dementia patients and control subjects.Osimani A, Berger A, Friedman J, Porat-Katz BS, Abarbanel JM.Kaplan Hospital, Rehovot, Israel and the Department of Behavioral Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel.Cobalamin deficiency may cause cognitive deficits and even dementia. In Alzheimer's disease, the most frequent cause of dementia in elderly persons, low serum levels of vitamin B12, may be misleading. The aim of this work was to characterize the cognitive pattern of B12 deficiency and to compare it with that of Alzheimer's disease. Nineteen patients with low levels of vitamin B12 were neuropsychologically evaluated before treatment and a year later. Results were compared with those of 10 healthy control subjects. Final results suggest that there is a different pattern in both diseases. Twelve elderly patients with dementia improved with treatment. Seven elderly demented patients did not improve; they deteriorated after 1 year although their levels of cobalamin were normal. Analysis of the initial evaluation showed that the 2 groups of patients had a different neuropsychological profile. The group that improved had initially more psychotic problems and more deficits in concentration, visuospatial performance, and executive functions. They did not show language problems and ideomotor apraxia, which were present in the second group. Their memory pattern was also different. These findings suggest that cobalamin deficiency may cause a reversible dementia in elderly patients. This dementia may be differentiated from that of Alzheimer's disease by a thorough neuropsychological evaluation.J Geriatr Psychiatry Neurol. 2005 Mar;18(1):33-8.http://content.answers.com/main/content/img/McGrawHill/Encyclopedia/images/CE734300FG0010.gif
If the combination of foodstuff we eat from time to time is correct, thanks to our family traditions and culture, for example, we probably won't have any deficiency problem from the cradle to the end of our life.
We conclude that the average concentrations of Cu, Mg and Na in vegetables and the average concentrations of Cu, Fe and K in fruit available in the UK have decreased significantly between the 1930s and the 1980s.
May I be so bold and hark back somewhat to the original question about wether we need supplements or not? For I think there is also another important issue here to consider which has not been addressed.Quote from: Iko mentionedIf the combination of foodstuff we eat from time to time is correct, thanks to our family traditions and culture, for example, we probably won't have any deficiency problem from the cradle to the end of our life.That would indeed be great but we also have to take into account that much produce (veg & fruit)seem to have 'lost' quite a bit of their mineral/vitamin content vs e.g. 70 years ago.
Attention News/Assignment/Health Editors: Vitamin D Deficiency Drains $9 billion From Canadian Health Care System Vitamin D Society Declares November 'Vitamin D Awareness Month' in Canada KELOWNA, BC, Oct. 31 /CNW/ - Research this year has left no doubt thatvitamin D deficiency - which affects an estimated 97 per cent of Canadians inthe winter - is nothing less than a Canadian crisis and a worldwide problem. This is why Canada's Vitamin D Society is recognizing the month ofNovember as the world's first Vitamin D Awareness Month.... For more information on vitamin D visit: - www.vitaminDsociety.org - www.vitamindcouncil.com - www.Direct-ms.org. - www.sunarc.org
BONE, HOOF, JOINT & MUSCLES COD LIVER OILThis non-heating oil for energy and mobility is high in fish Omega 3 & 6 essential oils (strictly speaking it is only suitable for carnivores as we do not often see horses fishing!) but it has been used for many years as an additive to equine feeds. Any oil helps lubricate the joints of veterans of any species and Cod Liver Oil also promotes a sleek coat and healthy skin as well as nutritional support for bones and hooves. Quality: ******* Health Cod Liver Oil is 100% pure and contains no heavy metals, it is important to find out if a cheaper version does.Feeding: 10 to 20ml (20ml is about 1 tablespoon) per 100kg bodyweight (16.2hh is about 500kg) best divided between 2 feeds daily. Feed the lower rate for general maintenance and the higher for pregnant or lactating mares, breeding stallions, young stock and very hard working animals (eg. racehorses & highly competitive animals) 1Lt will last a general maintenance 500kg horse about 20 days and a high category 500kg horse about 10 days.more from: http://www.pegasushealth.com/productinfo.php?product_id=48http://www.pegasusfirstaid.com.au/images/snuggle.jpg
********* COD LIVER OIL is a high energy oil which is palatable to all animals. The oil is derived from a cod's liver (fish), making it a pure natural product. It contains two essential fatty acids and important stabilised vitamins A and D. It is also widely known for its nutritional and therapeutic value and is used extensively on thoroughbred studs, racing, trotting and greyhound establishments and for birds.VITAMIN A is an essential nutrient for all horses, dogs and cattle. It is necessary for general growth, bone formation and for the formation of visual purple in the eye. A deficiency of it leads to drying of mucous membranes, which makes them more susceptible to bacterial invasion. This also results in increased susceptibility to diseases in the respiratory tract. For females, during gestation and lactation, there is an increased need for vitamin A. For animals that are fed a high concentration of dry, prepared diets, vitamin A is essential as it may be lost during the food processing.Suggested Dose Rates: Large Animals ie. horses, cattle Age Small Animals ie. dogs, cats 15 ml Baby 1 ml 30 ml Yearling 3 ml 60 ml Adult 5 ml VITAMIN D is important for growth of bones and teeth and it ensures the bodies right utilisation of calcium and phosphorus. A daily intake of ******** COD LIVER OIL will provide your animal with a fine healthy coat and skin. Animals housed and rugged are not able to intake natural vitamin D derived from the sunlight. Cod Liver Oil with vitamin D and two essential fatty acids helps overcome this deficiency.more from: http://www.equinade.com/products/facts-cod_liver_equinade.html ...it's for the birds!http://www.seapets.co.uk/gallery/healthybird-thumb.jpg
CoEnzyme Q10 protects nerve cellsCoEnzyme Q10 has shown the ability to protect nerve cells and potentially lower the risk of various degenerative diseases.Cells in the brain and nervous system depend on optimal mitochondrial function for energy. A research study published in the journal Neurobiology of Disease showed that oxidative stress causes mitochondria to produce excessive free radicals, leading to nerve cell damage and destruction. Due to its function in the mitochondrial energy process and its role as an antioxidant, researchers evaluated CoEnzyme Q10 for its ability to protect nerve cells.The results of this study revealed that CoEnzyme Q10 inhibits the production of free radicals by the mitochondria and stabilizes the mitochondrial membrane when nerve cells are subjected to oxidative stress. CoEnzyme Q10 may therefore have a potential benefit in reducing the risk of various neurodegenerative diseases.Neurobiol Dis. 2005 Apr;18(3):618-27
Statins Inhibit Coenzyme Q10 SynthesisSince coenzyme Q10 (CoQ10) and cholesterol are both synthesized from the same substance, mevalonate, statin drugs (Lipitor, Zocor, etc) also inhibit the body's synthesis of coenzyme Q10. This is not a "side effect," of statins, but a direct, inherent function of the drugs.In fact, the use of statins can decrease the body's synthesis of coenzyme Q10 by as much as 40%!
The widespread use of statin drugs is of special concern because they can lower the endogenous levels of Coenzyme Q10, the naturally-occurring form of ubiquinone in humans. Ubiquinone is widely recognized as an essential component of energy metabolism in the electron-transfer system in mitochondrial membranes. At physiological concentrations it is also recognized as an effective lipid-soluble antioxidant. It is one of the end products of the mevalonate pathway where dolichol (a component of animal membranes) and cholesterol are synthesized. Both ubiqionone and dolichol are released by the liver cells into the blood circulation, but in much lower concentrations than that of cholesterol.Ghirlanda et al(2) reported in a double-blind, placebo-controlled study a decrease of 50-54% of CoQ10 levels in the statin treatment groups, and similar results were reproduced by Watts et al(3).Bliznakov and Wilkins reviewed studies of the effect of statins on the biosynthesis of Coenzyme Q10 and the clinical implication of CoQ10 deficiency.(4) The authors report that lovastatin, pravastatin and simvastatin lower the endogenous levels of Coenzyme Q10, as CoQ10 shares the common biosynthetic pathway with cholesterol.Considering that Coenzyme Q10 is essential for mitochondrial function and antioxidant activity, and since oxidative mechanisms are important in atherogenesis, it can be assumed that a reduction in CoQ10 level may compromise coronary atherosclerosis despite optimal reduction in cholesterol levels by the use of statin drugs.Furthermore, the reduction of ubiquinone levels might be associated with myopathy, a rare adverse effect associated with statin drugs. This "metabolic" myopathy is related to ubiquinone deficiency in muscle cell mitochondria, disturbing normal cellular respiration and causing adverse effects such as rhabdomyolysis, exercise intolerance, and recurrent myoglobinuria.(5)It has also been suggested that CoQ10 deficiency can cause mitochondrial encephalomyopathies related to a primary or secondary ubiquinone deficient status, or even to an altered function of ubiquinone in the respiratory chain.(6) It is important to emphasize that Coenzyme Q10 supplementation does not interfere with the cholesterol-lowering effect of statin drugs(7) and therefore may be considered for all patients using such medications for an extended period of time.Recognizing the importance of dietary supplementation with vitamins (E, C, B6, folate), and essential nutrients (CoQ10, L-arginine, propionyl L-carnitine) as an adjunct in the treatment of cardiovascular disease, we should pay attention to the potential adverse effect of drug-induced nutrient depletion affecting the aforementioned nutrients.Pharmaceutical companies that market statin drugs should consider including the described CoQ10 potential depletion in their drug information materials provided to physicians and pharmacists, and they should encourage patients to consult their physician and pharmacist for appropriate supplementation.Integration of nutritional medicine in the clinical practice of medicine can benefit for our patients using prescription medications for disease management and treatment.
do we actually need vitamin suppliments? you see in boots for instance, a whole range of suppliments with a lot aimed at children.do children need suppliments?I can see a case for them in more deprived countries where a balanced diet may not be possible.
Quote from: paul.fr ink=topic=7032.msg72885#msg72885 date=1174976505do we actually need vitamin suppliments? you see in boots for instance, a whole range of supplements with a lot aimed at children.do children need supplements?I can see a case for them in more deprived countries where a balanced diet may not be possible. If you do your homework, you will find supplements out there that aren't full of chemicals that are man made. You have to eat pounds and pounds of food these days to get the equivalent of a good supplement, due to the over-processing and soil depletion. It can be done but personally I can't eat that much.
do we actually need vitamin suppliments? you see in boots for instance, a whole range of supplements with a lot aimed at children.do children need supplements?I can see a case for them in more deprived countries where a balanced diet may not be possible.
...talking about garlic and 'kitchen medicine'...Quote from: iko on 03/10/2007 09:57:51Curcumin as "Curecumin": From kitchen to clinic.Goel A, Kunnumakkara AB, Aggarwal BB.Gastrointestinal Cancer Research Laboratory, Department of Internal Medicine, Charles A. Sammons Cancer Center and Baylor Research Institute, Baylor University Medical Center, Dallas, TX, United States.Although turmeric (Curcuma longa; an Indian spice) has been described in Ayurveda, as a treatment for inflammatory diseases and is referred by different names in different cultures, the active principle called curcumin or diferuloylmethane, a yellow pigment present in turmeric (curry powder) has been shown to exhibit numerous activities. Extensive research over the last half century has revealed several important functions of curcumin. It binds to a variety of proteins and inhibits the activity of various kinases. By modulating the activation of various transcription factors, curcumin regulates the expression of inflammatory enzymes, cytokines, adhesion molecules, and cell survival proteins. Curcumin also downregulates cyclin D1, cyclin E and MDM2; and upregulates p21, p27, and p53. Various preclinical cell culture and animal studies suggest that curcumin has potential as an antiproliferative, anti-invasive, and antiangiogenic agent; as a mediator of chemoresistance and radioresistance; as a chemopreventive agent; and as a therapeutic agent in wound healing, diabetes, Alzheimer disease, Parkinson disease, cardiovascular disease, pulmonary disease, and arthritis. Pilot phase I clinical trials have shown curcumin to be safe even when consumed at a daily dose of 12g for 3 months. Other clinical trials suggest a potential therapeutic role for curcumin in diseases such as familial adenomatous polyposis, inflammatory bowel disease, ulcerative colitis, colon cancer, pancreatic cancer, hypercholesteremia, atherosclerosis, pancreatitis, psoriasis, chronic anterior uveitis and arthritis. Thus, curcumin, a spice once relegated to the kitchen shelf, has moved into the clinic and may prove to be "Curecumin".Biochem Pharmacol. 2007 Aug 19;
Curcumin as "Curecumin": From kitchen to clinic.Goel A, Kunnumakkara AB, Aggarwal BB.Gastrointestinal Cancer Research Laboratory, Department of Internal Medicine, Charles A. Sammons Cancer Center and Baylor Research Institute, Baylor University Medical Center, Dallas, TX, United States.Although turmeric (Curcuma longa; an Indian spice) has been described in Ayurveda, as a treatment for inflammatory diseases and is referred by different names in different cultures, the active principle called curcumin or diferuloylmethane, a yellow pigment present in turmeric (curry powder) has been shown to exhibit numerous activities. Extensive research over the last half century has revealed several important functions of curcumin. It binds to a variety of proteins and inhibits the activity of various kinases. By modulating the activation of various transcription factors, curcumin regulates the expression of inflammatory enzymes, cytokines, adhesion molecules, and cell survival proteins. Curcumin also downregulates cyclin D1, cyclin E and MDM2; and upregulates p21, p27, and p53. Various preclinical cell culture and animal studies suggest that curcumin has potential as an antiproliferative, anti-invasive, and antiangiogenic agent; as a mediator of chemoresistance and radioresistance; as a chemopreventive agent; and as a therapeutic agent in wound healing, diabetes, Alzheimer disease, Parkinson disease, cardiovascular disease, pulmonary disease, and arthritis. Pilot phase I clinical trials have shown curcumin to be safe even when consumed at a daily dose of 12g for 3 months. Other clinical trials suggest a potential therapeutic role for curcumin in diseases such as familial adenomatous polyposis, inflammatory bowel disease, ulcerative colitis, colon cancer, pancreatic cancer, hypercholesteremia, atherosclerosis, pancreatitis, psoriasis, chronic anterior uveitis and arthritis. Thus, curcumin, a spice once relegated to the kitchen shelf, has moved into the clinic and may prove to be "Curecumin".Biochem Pharmacol. 2007 Aug 19;
Curcumin seems to be a real 'panacea' these days...Think of the massive impact on our lives and societysevere brain injuries have, either from strokes orheavy head traumas.Dietary curcumin counteracts the outcome of traumatic brain injury on oxidative stress, synaptic plasticity, and cognition.Wu A, Ying Z, Gomez-Pinilla F. Dept. Physiological Science, Univ.of California at Los Angeles, 621 Charles E. Young Drive, 90095, USA.The pervasive action of oxidative stress on neuronal function and plasticity after traumatic brain injury (TBI) is becoming increasingly recognized. Here, we evaluated the capacity of the powerful antioxidant curry spice curcumin ingested in the diet to counteract the oxidative damage encountered in the injured brain. In addition, we have examined the possibility that dietary curcumin may favor the injured brain by interacting with molecular mechanisms that maintain synaptic plasticity and cognition. The analysis was focused on the BDNF system based on its action on synaptic plasticity and cognition by modulating synapsin I and CREB. Rats were exposed to a regular diet or a diet high in saturated fat, with or without 500 ppm curcumin for 4 weeks (n = 8/group), before a mild fluid percussion injury (FPI) was performed. The high-fat diet has been shown to exacerbate the effects of TBI on synaptic plasticity and cognitive function. Supplementation of curcumin in the diet dramatically reduced oxidative damage and normalized levels of BDNF, synapsin I, and CREB that had been altered after TBI. Furthermore, curcumin supplementation counteracted the cognitive impairment caused by TBI. These results are in agreement with previous evidence, showing that oxidative stress can affect the injured brain by acting through the BDNF system to affect synaptic plasticity and cognition. The fact that oxidative stress is an intrinsic component of the neurological sequel of TBI and other insults indicates that dietary antioxidant therapy is a realistic approach to promote protective mechanisms in the injured brain.Exp Neurol. 2006 Feb;197(2):309-17. http://www.imlawfirm.com/photos/brain-injury.jpghttp://www.onlinewellnessworld.com/images/brain-injury-lawyer.jpghttp://www.goodshepherdrehab.org/photos/brain-injury-rehab2.jpgNeuroprotective effect of curcumin in middle cerebral artery occlusion induced focal cerebral ischemia in rats.Thiyagarajan M, Sharma SS.Dept.Pharmacol.Toxicol., Natl.Inst.Pharmaceutical Edu. and Res.Sector 67, S.A.S. Nagar-160 062, Punjab, India. Free radical induced neuronal damage is implicated in cerebral ischemia reperfusion (IR) injury and antioxidants are reported to have neuroprotective activity. Several in vitro and in vivo studies have proved the antioxidant potential of curcumin and its metabolites. Hence, in the present study the neuroprotective potential of curcumin was investigated in middle cerebral artery occlusion (MCAO) induced focal cerebral IR injury. 2 h of MCAO and 22 h of reperfusion resulted in the infarct volume of 210.39 +/- 31.25 mm3. Administration of curcumin 100 and 300 mg/kg, i.p. 30 min. after MCAO produced 37.23 +/- 5.10% and 46.39 +/- 10.23% (p < 0.05) reduction in infarct volume, respectively. Ischemia induced cerebral edema was reduced in a dose dependent manner. Curcumin at 300 mg/kg, i.p. produced 50.96 +/- 6.04% reduction in edema (p < 0.05) volume. Increase in lipid peroxidation after MCAO in ipsilateral and contralateral hemisphere of brain was observed, which was reduced by curcumin (300 mg/kg, i.p.)-treatment. Decrease in superoxide dismutase and glutathione peroxidase activity was observed in ipsilateral hemisphere of MCAO animal. Curcumin-treatment (300 mg/kg, i.p.) prevented IR injury mediated fall in glutathione peroxide activity. Peroxynitrite measured using rhodamine123 fluorescence and anti-nitrotyrosine immunofluorescence indicated increased peroxynitrite formation after IR insult. Curcumin-treatment reduced peroxynitrite formation and hence the extent of tyrosine nitration in the cytosolic proteins. These results suggest the neuroprotective potential of curcumin in cerebral ischemia and is mediated through its antioxidant activity.Life Sci. 2004 Jan 9;74(:969-85.Soon curcumin preparations will be quite commonin any Intensive Care Unit of this Planet anda heady scent of curry will invade all thehospitals and rehabilitation facilities.Maybe.