Heavy Metal Detox
Upon arising: freshly squeezed juice of ½ lemon in glass of room temperature water
Breakfast
½ cup lowfat ricotta cheese, 1 tsp. flaxseed oil, figs or berries
1-2 omega-3 eggs, ½ melon or 1 orange
Flaxmeal muffin made with dried coconut, 1 fruit
6 ounces sugar-free yogurt, 1 cup raspberries
Lunch and Dinner
Tahini and unsweetened jam sandwich, or almond butter and jam on wheat-free bread
Sardines, large green salad, flax oil or sugar-free dressing
Grilled (unprocessed) cheese sandwich, wheat-free bread, chili w/pinto beans
Tuna salad, assorted raw vegetables, sauerkraut
6 ounces salmon, steamed greens, 1 cup black eyed peas, miso soup
6 ounces broiled organic liver, roasted vegetables, diced beets
4 oz. Flank steak, baked sweet potatoes, large green salad with flax oil dressing
4 oz. Roasted turkey, steamed broccoli, dandelion greens
Snacks
Organic raw veggies, 1 piece organic fruit, diced beets, fresh coconut,
sliced bananas with dried coconut
Avoid
Alcohol, Tylenol (acetaminophen) coffee, soft drinks, processed meats, hydrogenated oils, sunflower, safflower, corn oils, processed foods high in salt
Beverages
Tomato juice and 8 oz. freshly prepared beet juice 1-2x per day
Green drinks: Green Magma, Kyogreen, or Green Kamut: (1 tsp. 1-3x day in water)
Herbal Teas: Chamomile, Dandelion root and leaf, Green Tea
Suggestions and Goals
To gradually remove toxic metals with minimal inconvenience for the patient. Removing them too quickly can cause aggressive behavior, irritability, and depression. Removing them gradually will not cause this.
Supplements
Vitamin C1,000-5,000 mg
Phosphatidyl Choline1,000-3,000 mg (2-6 Tbsp. PC 55% Granules)
Lipoic Acid100-600 mg
N-Acetyl-Cysteine1,000 mg
Leucine1,000 mg
Vitamin E400 IUs
B Complex50 mg
Selenium400 mcg
Taurine1-3 grams
Zincas per ZTT
For Lead Removal:
Allithiamine (fat soluble B1)50-100 mg
Research Review
Higher Vitamin C Levels Associated with Lower Lead Levels
CONTEXT: Some animal studies suggest that orally administered ascorbic acid may chelate lead and decrease the risk of the toxic effects of lead. However, results from several small studies in humans have yielded inconclusive evidence of a beneficial effect of ascorbic acid on lead toxicity. OBJECTIVE: To examine the relationship between serum ascorbic acid levels and prevalence of elevated blood lead levels. DESIGN, SETTING, AND PARTICIPANTS: Cross-sectional analysis of a probability sample of the US population enrolled in the Third National Health and Nutrition Examination Survey, 1988-1994 (4213 youths aged 6- 16 years and 15365 adults aged > or =17 years) without a history of lead poisoning. MAIN OUTCOME MEASURES: Elevated and log blood lead levels by serum ascorbic acid level. RESULTS: A total of 22 youths (0.5%) and 57 adults (0.4%) had elevated blood lead levels (defined as > or =0.72 micromol/L [15 microg/dL]) and > or =0.97 micromol/L [20 microg/dL], respectively). After controlling for the effects of age, race, sex, income level, and dietary energy, fat, calcium, iron, and zinc intake, youths in the highest serum ascorbic acid tertile had an 89% decreased prevalence of elevated blood lead levels compared with youths in the lowest serum ascorbic acid tertile (odds ratio, 0.11; 95% confidence interval, 0.04-0.35; P for trend = .002). Adults in the highest 2 serum ascorbic acid tertiles had a 65% to 68% decreased prevalence of elevated blood lead levels compared with adults in the lowest serum ascorbic acid tertile (P for trend = .03). As a continuous predictor, serum ascorbic acid level was independently associated with decreased log blood lead levels among adults (P.001), but not among youths (P=.14). CONCLUSIONS: Our data suggest that high serum levels of ascorbic acid are independently associated with a decreased prevalence of elevated blood lead levels. If these associations are related causally, ascorbic acid intake may have public health implications for control of lead toxicity.1
Selenium Protects Against Cadmium Exposure
Total superoxide dismutase (total SOD), copper zinc containing superoxide dismutase (CuZn SOD), and manganese superoxide dismutase (Mn SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione- S-transferase (GST) activities as well as ascorbic acid (AsA), and vitamin E (vit E) concentrations were analysed in the liver of rats exposed to cadmium (15 mg Cd/day/kg), selenium (7 micrograms Se/day/kg), and to cadmium+selenium (15 mg Cd + 7 micrograms Se/day/kg), and in control animals. Cadmium caused a decrease of total SOD, Mn SOD, CAT and GSH-Px but an increase of GST activity in the liver of rats. Contrary to cadmium, selenium caused a significant increase of the activity of these enzymes except for GSH-Px. By concomitant exposure to both cadmium and selenium, the toxic effects of cadmium on the activity of mentioned enzymes we abolished. In all exposed groups, the activity of enzyme glutathione-S-transferase was enhanced, indicating its increased role in prevention of lipid peroxidation. Cadmium decreased the concentration of AsA and increased the concentration of vitamin E in the liver, while selenium increased the concentration of both vitamins. However, by concomitant administration of cadmium and selenium, these changes were diminished and tended to reach control values.2
Toxic Metals Block Vitamin D Metabolism
Vitamin D increases intestinal calcium and phosphate absorption. Not so well known, however, is that vitamin D stimulates the co-absorption of other essential minerals like magnesium, iron, and zinc; toxic metals including lead, cadmium, aluminum, and cobalt; and radioactive isotopes such as strontium and cesium. Vitamin D may contribute to the pathologies induced by toxic metals by increasing their absorption and retention. Reciprocally, lead, cadmium, aluminum, and strontium interfere with normal vitamin D metabolism by blocking renal synthesis of 1,25-dihydroxyvitamin D. This is the first review of the role of the vitamin D endocrine system in metal toxicology.3
Vitamin E Succinate Protects Against Cadmium Exposure
Rat hepatocyte suspensions were exposed to toxic concentrations of cadmium (Cd) in the presence and absence of unesterified alpha- tocopherol (T) or alpha-tocopheryl succinate (TS). The exogenous administration of TS completely protected hepatocytes from Cd-induced injury and lipid peroxidation. However, hepatocytes exposed to T were not protected from the toxic manifestations of cadmium even though this treatment resulted in a rapid marked accumulation of cellular T. The rate of cadmium uptake by hepatocytes was not significantly altered by exogenous TS or T treatment. These studies indicate that TS cytoprotection against Cd toxicity results not from alterations in Cd uptake or the accumulation of T but rather from the cellular presence of the intact TS molecule. The data also indicate that the depletion of cellular T is not the critical cellular event that is responsible for Cd-induced injury. Instead it appears that TS possess unique cytoprotective properties that intervene in the critical cellular events that lead to Cd toxicity. Thus, TS administration represents a promising new strategy for the mechanistic study and prevention of tissue damage resulting from Cd exposure.4
Lipoic Acid Protects Against Cadmium Exposure
The suitability of DL-alpha-lipoic acid (LA) to serve as an antidote in cadmium (Cd) toxicity in rat hepatocytes was investigated. Isolated hepatocytes were exposed to 200 and 450 microM Cd in the presence of 0.2, 1.0 and 5.0 mM LA, respectively. After 30 min of incubation various criteria of cell viability were monitored. Lipoic acid markedly diminished Cd uptake. Concomitantly, Cd-induced membrane injury, as reflected by the leakage of aspartate aminotransferase and sorbitol dehydrogenase (SDH) was decreased. Moreover, LA protected against intracellular toxic responses to Cd, such as a decrease in cellular SDH activity, a decrease in cellular acid soluble thiols, especially in total glutathione, a decrease in cellular urea and an increase in thiobarbituric acid (TBA) reactants, as a measure of lipid peroxidation. Most protective effects were seen in hepatocytes challenged with the lower Cd concentration and coincubated with 5 mM LA. In contrast, at 450 microM Cd even the highest LA concentration applied either did only reverse Cd-effects incompletely (SDH-response, TBA-reactants) or did not protect at all (Cd uptake, enzyme leakage, loss of glutathione). The data indicate that DL-alpha-lipoic acid serves as a protective tool against Cd-induced membrane damage and cell dysfunction in hepatocytes. This stands as long as Cd exposure is low enough to permit interaction with LA prior to interaction with cell structures.5
The Effects of Cadmium Toxicity
Cadmium has been shown to manifest its toxicity in human and animals by mainly accumulating in almost all of the organs and kidney is the main target organ where it is concentrated mainly in cortex. Environmental exposure of cadmium occurs via food, occupational industries, terrestrial and aquatic ecosystem. At molecular level, cadmium interferes with the utilization of essential metals e.g. Ca, Zn, Se, Cr and Fe and deficiencies of these essential metals including protein and vitamins, exaggerate cadmium toxicity, due to its increased absorption through the gut and greater retention in different organs as metallothionein (Cd-Mt). Cadmium transport, across the intestinal and renal brush border membrane vesicles, is carrier mediated and it competes with zinc and calcium. It has been postulated that cadmium shares the same transport system. Cadmium inhibits protein synthesis, carbohydrate metabolism and drug metabolizing enzymes in liver of animals. Chronic environmental exposure of cadmium produces hypertension in experimental animals. Functional changes accompanying cadmium nephropathy include low molecular weight proteinuria which is of tubular origin associated with excess excretion of proteins such as beta 2 microglobulin, metallothionein and high molecular weight proteinuria of glomerular origin (excretion of proteins such as albumin IgG, transferrin etc.). Recent data has shown that metallothionein is more nephrotoxic to animals. Cadmium is also toxic to central nervous system. It causes an alterations of cellular functions in lungs. Cadmium affects both humoral and cell mediated immune response in animals. Cadmium induces metallothionein in liver and kidney but under certain nutritional deficiencies like protein-calorie malnutrition and calcium deficiency, enhanced induction and greater accumulation of cadmium metallothionein has been observed.6
The Biochemistry of Lead
At the levels to which human beings are exposed in the workplace as well as in the general environment, lead has been shown to be a toxic element in most of its chemical forms, whether it is inhaled or ingested in water or food. The four main sources of contamination of food are soil, industrial pollution, agricultural technology and food processing. Reasonable quantities of the metal can be stored by humans in a relatively inert form in bone; lead has an affinity for bone and acts by replacing calcium. Gastrointestinal lead absorption and retention, the major pathway of lead intake, has been shown to vary widely depending on the chemical environment of the gastrointestinal lumen, age and iron stores (nutritional status of the subject). Studies in animals have shown that certain substances bind lead and increase its solubility, thus enhancing its absorption. These dietary components consist of sodium citrate, ascorbate, amino acids, vitamin D, protein and fat, and lactose. Data suggest a three-compartmental pool for lead metabolism: (1) blood; (2) soft tissue (hair, nails, sweat, salivary, gastric, pancreatic and biliary secretions); and (3) skeleton. Lead absorption occurs primarily in the duodenum where lead enters the epithelial mucosal cells. The total bodily amount of lead does not affect lead absorption; lead does not have a feedback mechanism which limits absorption. In the adult rat, lead absorption from the intestinal lumen appears to proceed by both active transport and passive diffusion. Bile is an important route of excretion in the gut.7
1. Simon JA, Hudes ES. Relationship of ascorbic acid to blood lead levels [see comments]. Jama 1999;281(24):2289-93.
2. Ognjanovic B, Zikic RV, Stajn A, Saicic ZS, Kostic MM, Petrovic VM. The effects of selenium on the antioxidant defense system in the liver of rats exposed to cadmium. Physiol Res 1995;44(5):293-300.
3. Moon J. The role of vitamin D in toxic metal absorption: a review. J Am Coll Nutr 1994;13(6):559-64.
4. Fariss MW. Cadmium toxicity: unique cytoprotective properties of alpha tocopheryl succinate in hepatocytes. Toxicology 1991;69(1):63-77.
5. Muller L. Protective effects of DL-alpha-lipoic acid on cadmium-induced deterioration of rat hepatocytes. Toxicology 1989;58(2):175-85.
6. Nath R, Prasad R, Palinal VK, Chopra RK. Molecular basis of cadmium toxicity. Prog Food Nutr Sci 1984;8(1-2):109-63.
7. DeMichele SJ. Nutrition of lead. Comp Biochem Physiol A 1984;78(3):401-8.
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