Thiamine, or vitamin B1, is used by the body to neutralize and/or excrete toxic heavy metals that inevitably find their way into food, water, and air. Proof of this function is provided in a study published by Derrick Lonsdale (a link to his paper is found in the references to the entry on thiamine at Wikipedia).
Unfortunately, the vitamin B1 in almost every multivitamin and B-complex vitamin is either thiamine mononitrate or thiamine hydrochloride. The body’s ability to absorb these two forms of thiamine is limited to about 2 mg per dose (see David Bender, “The Nutritional Biochemistry of the Vitamins”, an authoritative text on vitamins). Any thiamine mononitrate or hydrochloride in excess of about 2 mg exits the body into the toilet entrained with the solids (no wonder side effects from thiamine supplements are unknown!). There is another class of thiamine molecules called allithiamines. The ability of the body to absorb allithiamines is unlimited. A 150 mg capsule of an allithiamine delivers almost the entire 150 mgs into the bloodstream. I recommend that multivitamin manufacturers consider formulating their multivitamins with a mixture of thiamine mononitrate/hydrochloride and allithiamines.
Lonsdale studied the effect of allithiamine supplements on a group of autistic children. If I understood the paper correctly (see the reference in the Wikipedia entry on thiamine), the results were fantastic. Several children were transformed from severely autistic to non-autistic after 60 days of treatment. The children were screened for heavy metals before, during, and after the treatment. A surprising result from the study was a linkage between arsenic and autism. Lonsdale seemed at a loss to explain a source of arsenic that could be associated with the observed dramatic rise in autism in recent years. I can help. The average U.S. coal contains 24 ppm arsenic (just search “arsenic in coal” on google for a USGC fact sheet). If just 10% of this arsenic escapes into the atmosphere as arsine and other arsenic containing gasses, this provides a source of more than 2000 tons/year of arsenic, year after year after year. The vaporized arsenic rains down out of the sky, contaminating air, food, and water.
Affordable technology exists to cut heavy metals emissions from coal fired electric power plants by a factor of one hundred. I do not believe that scientists or the public clearly understand the connection between rising rates of children requiring special education services and heavy metals emissions from coal-fired power plants. If/when the connection is clearly established, I’m confident the problem will be swiftly resolved. In the meantime, I recommend that all parents provide their children with vitamin C, niacin, and multivitamin supplements. I also recommend that parents of children receiving special education services follow the example of Lonsdale and treat their children with 150 mg allithiamine supplements (the most readily available supplement goes by the name benfotiamine) for 60 days.
Steve – have you had a chance to review these 2 studies showing Vitamin C decreases mitochondria function? This to me does not mean Vitamin C supplementation should be avoided, but that perhaps we need far less than thought.
1: Am J Clin Nutr. 2008 Jan;87(1):142-9. Links
Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance.Gomez-Cabrera MC, Domenech E, Romagnoli M, Arduini A, Borras C, Pallardo FV, Sastre J, Viña J.
Department of Physiology, Faculty of Medicine, University of Valencia, Valencia, Spain.
BACKGROUND: Exercise practitioners often take vitamin C supplements because intense muscular contractile activity can result in oxidative stress, as indicated by altered muscle and blood glutathione concentrations and increases in protein, DNA, and lipid peroxidation. There is, however, considerable debate regarding the beneficial health effects of vitamin C supplementation. OBJECTIVE: This study was designed to study the effect of vitamin C on training efficiency in rats and in humans. DESIGN: The human study was double-blind and randomized. Fourteen men (27-36 y old) were trained for 8 wk. Five of the men were supplemented daily with an oral dose of 1 g vitamin C. In the animal study, 24 male Wistar rats were exercised under 2 different protocols for 3 and 6 wk. Twelve of the rats were treated with a daily dose of vitamin C (0.24 mg/cm(2) body surface area). RESULTS: The administration of vitamin C significantly (P = 0.014) hampered endurance capacity. The adverse effects of vitamin C may result from its capacity to reduce the exercise-induced expression of key transcription factors involved in mitochondrial biogenesis. These factors are peroxisome proliferator-activated receptor co-activator 1, nuclear respiratory factor 1, and mitochondrial transcription factor A. Vitamin C also prevented the exercise-induced expression of cytochrome C (a marker of mitochondrial content) and of the antioxidant enzymes superoxide dismutase and glutathione peroxidase. CONCLUSION: Vitamin C supplementation decreases training efficiency because it prevents some cellular adaptations to exercise.
2) Moderate exercise up-regulates the expression of antioxidant genes and of transcription factors for mitochondrial biogenesis. Oral antioxidants administration prevents it
Gomez-Cabrera, Maria Carmen ; Domenech, Elena ; Borras, Consuelo ; Pallardo, Federico Vicente ; Vina, Jose ;
1. Departamento de Fisiologia, Universidad de Valencia, Valencia, Spain. 2. Universidad Catolica de Valencia, Valencia, Spain.
Search Medline for articles by:
Vina, J
Pallardo, FV
Borras, C
Domenech, E
Gomez-Cabrera, MC
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Exhaustive exercise generates excessive amounts of oxidative free radicals (Sastre et al, 1992) that overwhelm cellular antioxidant defences and may cause tissue damage (Gomez-Cabrera et al, 2003). They may, however, constitute signals to regulate muscle cell function. Accordingly, there is considerable interest in the potential of these mediators to regulate muscle adaptation to exercise. This is one of the oldest postulates in the field, dating back to the suggestion that free radicals produced in exercising muscle might stimulate mitochondrial biogenesis (Davies et al, 1981) and the expression of genes for antioxidant enzymes. Moderate exercise increases lifespan in humans but this may be due to other healthy habits of the exercising population. The aim of this study is to elucidate the role of the free radicals generated in moderate physical exercise, in the expression of antioxidant genes and of transcription factors for mitochondrial biogenesis. Twenty male wistar rats were randomly divided into four groups: sedentary controls (n=5), exercised (n=5), exercised treated with 500 mg/Kg of vitamin C (n=5) and exercised treated with 32 mg/Kg of allopurinol (n=5). Allopurinol acts as an antioxidant because it inhibits xanthine oxidase, an important generator of free radicals in exercise (Gomez-Cabrera et al, 2003). The experimental protocol was approved by the Committee on Ethics in Research of the Faculty of Medicine Valencia. Where indicated animals were subjected to moderate exercise training (10, 17, 24 and 26 m/min for 5, 10, 10 and 20 min. each, five days a week during three weeks). Rats were anesthetized with 50 mg/kg sodium pentobarbithal by i.p. injection and gastrocnemius muscle was obtained by quick removal. Rats were killed by an ovedose of the anesthetic. Our results, using quantitative Real-Time RT-PCR, show that moderate exercise significantly up-regulates the expression of antioxidant enzymes associated with longevity, such as Mn-SOD (3.5-fold change, P<0.0001) and GPx (3.4-fold change, P<0.0001). We also found that moderate exercise up-regulated the expression of NRF-1 (14-fold change, P<0.0001) that is a key transcriptional activator of nuclear genes encoding mitochondrial enzymes and Tfam (30-fold change, P<0.0001), which stimulates mitochondrial DNA transcription and replication. However, supplementation with vitamin C or allopurinol during training prevented all of these adaptations. Significance was determined by ANOVA followed by Tukey test relative to sedentary controls after normalization to GAPDH. We conclude that oral antioxidant supplementation is very likely to be useful before competition when exercise is likely to be exhaustive, and damaging (Gomez-Cabrera et al, 2003), but not when training.
Sastre J et al. (1992). Am J Physiol 263, R992-995. Gomez-Cabrera MC et al. (2003). JAMA 289, 2503-2504. Davies KJA et al.(1981). Arch Biochem Biophys 209, 539-554.
My e-mail is BMC273@aol.com if you want to contact me. Thanks!
Brian