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Get the Lead Out

 

These are the symptoms of lead poisoning—do they look familiar? Chronic infection in children, loss of appetite, weight loss, chronic fatigue, cramps, insomnia, alopecia (hair loss), colic and abdominal pain, indigestion, constipation, nausea, headache, weakness, metallic taste, anemia, pre-eclampsia, miscarriage, sterility, kidney damage leading to elevated blood pressure, peripheral neuritis, arthritis, anxiety, mood swings, nightmares, hyperactivity, aggressiveness, delinquent and disruptive behavior, depression, mental retardation, delirium, coma, and death. General cognitive, verbal, and perceptual abilities decrease as lead in the system increases. These brain functions are impaired by lead significantly reducing zinc, copper, and iron in the brain, interfering with the zinc, copper, and iron-dependent enzymes that regulate mental processes. Lead also interferes with calcium, magnesium, and zinc, the sedative elements, leading to convulsions. Hyperactivity and epilepsy are among the first presenting symptoms of lead poisoning.

 

Addition of silicofluoride to the water of many communities causes people to absorb more lead. The lead blocks the action of calcium atoms in fostering the production of neurotransmitters in the brain—such as dopamine and serotonin. As a result, mental processes are seriously interfered with, and nerve reactions throughout the body depressed ... this sort of toxicity is shown by research to play a role in epileptic seizures and other convulsions.” [Ref: Fluoridation and Truth Decay, 1974, p.93]  We will pick up the lead thread following the abstracts.

 

In one study, after seven months of fluoride treatment, the protein content of brain with fluorosis decreased, and the total brain phospholipid content (the stuff brains are made of) decreased by 10% and 20% in the 30 and 100-ppm fluoride groups, respectively. The main species of phospholipid influenced by fluorosis were phosphatidylethanolamine, phosphatidylcholine (both found plentifully in lecithin), and Phosphatidylserine. The results demonstrate that the contents of phospholipid and ubiquinone (CoQ-10) are modified in brains affected by chronic fluorosis and these changes of membrane lipids could be involved in the pathogenesis of this disease. Most physicians do not recognize fluoridation’s adverse health effects, but they are documented in blind and double-blind studies. Allergy, hypersensitivity, gastrointestinal, and skin irritation are known side effects of fluoride ingestion. It impairs memory and concentration and causes lethargy, headache, depression, and confusion. Fluoride accumulates in human and animal pineal glands where it impairs melatonin production. The toxicity of fluoride is increased in people with inadequate nutrition (substandard vitamin-mineral-amino intake, especially iodine, the only thing known to remove it from the body), or who are immune-compromised (e.g., diabetics, renal disease, etc.). When inorganic fluoride compounds combine with gastric HCl, hydrofluoric acid is formed which exerts an irritating action upon the mucous of the stomach and the upper gastrointestinal tract. All these effects can be antagonized by giving calcium and magnesium combined (50 mg/kg each). Rather than giving such a rediculously high amount of these minerals, you must remove all fluoride from your drinking and bath water (or neutralize it with borax as outlined elsewhere in this paper), toothpaste, and prepared breakfast cereals that (due to use of fluoridated water in manufacturing) have up to three times as much fluoride as is legal for drinking water. Supplementing the above-mentioned phospholipids may be wise.

 

These two abstracts are quoted in full because of their import:

 

A hypothalamic digoxin-mediated model for autism.

Ravikumar Kurup a1 and Parameswara Achutha Kurup a2

A1 Department of Neurology, Medical College Hospital, Trivandrum, Kerala, India

A2 Metabolic Disorders Research Center, Trivandrum, Kerala, India

 

Abstract:

The isoprenoid pathway and its metabolites—digoxin (similar to digitalis – both from the fox glove plant), dolichol (long-chain, unsaturated, isoprenoid alcohols found within the mitochondria) and ubiquinone (CoQ-10)--were assessed in autism. The isoprenoid pathway and digoxin status was also studied for comparison in individuals of differing hemispheric dominance to determine the role of cerebral dominance in the genesis of autism. There was an upregulation of the isoprenoid pathway as evidenced by elevated HMG CoA reductase activity (a liver enzyme that produces cholesterol - indicating an excess) in autism. Digoxin, an endogenous Na+-K+ ATPase inhibitor secreted by the hypothalamus, was found to be elevated and RBC membrane Na+-K+ ATPase activity was reduced in autism (reducing energy generation). Membrane Na+-K+ ATPase inhibition can result in increased intracellular Ca2+ and reduced magnesium levels (an excitotoxic condition). Hypothalamic digoxin can modulate conscious and subliminal perception and its dysfunction may lead to autism. (This excess) Digoxin can also preferentially upregulate tryptophan transport over tyrosine resulting in increased levels of depolarizing tryptophan catabolites—(that includes) serotonin, quinolinic acid (NMDA agonist), strychnine (blocks glycinergic inhibitory transmission), and nicotine and decreased levels of hyperpolarizing tyrosine catabolites--dopamine, noradrenaline, and morphine--contributing to membrane Na+-K+ ATPase inhibition. Increased nicotine levels can produce increased dopaminergic transmission in the presence of low dopamine levels. NMDA excitotoxicity could result from hypomagnesemia induced by membrane Na+-K+ ATPase­inhibition and quinolinic acid, an NMDA agonist, acting on the NMDA receptor (as an excitotoxin). (This) Hypomagnesemia and increased dolichol level can affect glycoconjugate metabolism and membranogenesis leading on to disordered synaptic connectivity in the limbic allocortex and defective presentation of viral antigens and neuronal antigens contributing to autoimmunity and viral persistence (common in autism) important in the pathogenesis (development of disease). Membrane Na+-K+ ATPase inhibition can produce immune activation, a component of autoimmunity. Mitochondrial dysfunction consequent to altered calcium/magnesium ratios and reduced ubiquinone levels can result in increased free-radical generation and reduced free-radical scavenging and defective apoptosis leading to abnormal synaptogenesis (look this one up on Google). Autism can thus be considered a syndrome of hypothalamic, digoxin hypersecretion consequent to an upregulated isoprenoid pathway. The biochemical patterns including hyperdigoxinemia observed in autism correlated with those obtained in right hemispheric chemical dominance. Right hemispheric chemical dominance is a predisposing factor for autism. END

 

This note is of interest here: Many proteins pertinent to normal cell physiology are glycosylated (have sugars attached), and variations in their glycosylation pattern often lead to changes in their function. Most major diseases are associated with a change in the glycosylation pattern of a central protein structure. These diseases (e.g., cancer, rheumatoid arthritis, heart disease, diabetes, infectious diseases and neurodegenerative diseases) directly involve glycoconjugates. Acidic glycohydrolases sequentially cleave sugar molecules off the glycoproteins (probably to meet their varying needs) and excrete them in small amounts in normal urine, but in increased amounts in individuals with diabetes and/or renal (and probably other) disease. - John S. Axford, BS, MD, FRCP

 

Hypothalamic digoxin deficiency in obsessive-compulsive disorder and Tourette’s syndrome

Int J Neurosci 2002 Jul;112(7):797-816, Kurup RK, Kurup PA.

Department of Neurology, Medical College Hospital, Trivandrum, Kerala, India.

 

Abstract

The isoprenoid pathway related cascade was assessed in 15 patients with obsessive-compulsive disorder (OCD) and Tourette’s syndrome (TS). The pathway was also assessed in right hemispheric dominant, left hemispheric dominant, and bi-hemispheric dominant individuals to assess whether hemispheric dominance has any correlation with these disease states. The levels of serum digoxin, HMG CoA reductase activity, and dolichol were found to be decreased in OCD and Tourette’s syndrome as well as in left hemispheric dominant individuals with a corresponding increase in RBC Na(+)-K+ ATPase activity, serum ubiquinone, and magnesium levels. There was an increase in tyrosine and its catabolites, and a reduction in tryptophan and its catabolites in the serum (possibly reducing niacin and serotonin). The total and individual glycosaminoglycan (GAG) fractions, carbohydrate residues of glycoproteins, and the concentration of glycolipids decreased in the serum. The activity of GAG degrading enzymes and glycohydrolases were decreased. The RBC membrane glycoconjugates (glycoproteins, glycolipids, oligosaccharides, polysaccharides, proteoglycans) were increased while the membrane cholesterol:phospholipid ratio was decreased. The activity of free-radical scavenging enzymes increased while the concentration of free radicals decreased significantly. On the other hand, there was hyperdigoxinemia and the reverse biochemical patterns in those with right hemispheric dominance (as stated in the previous abstract). Membrane Na(+)-K+ ATPase stimulation can result in decreased intracellular Ca2+ and increased magnesium levels. Increased levels of dopamine can lead to a tic syndrome, while reduced levels of serotonin and increased dopamine can both lead to obsessive-compulsive disorder. A decrease in fucose and sialo-ligands (two vital sugars), (along with) increased immunosuppressive morphine levels, decreased T-cell calcineurin (an iron-zinc enzyme also called protein phosphatase 2B) signal transduction related to decreased intracellular calcium, reduced free radical production, and altered presentation of bacterial glycoconjugate antigens can lead to a hypoimmune response and recurrent respiratory infection in OCD patients. OCD and Tourette’s syndrome are associated with left hemispheric chemical dominance. END

 

Thus, we see that an excess of digoxin contributes to autism and possibly high cholesterol, whereas a lack contributes to OCD, Tourette's, and possibly low cholesterol (a serious condition affecting hormone production and possibly the formation of cancer). The Fox Glove plant is too poisonous to recommend as an herbal, but it seems that a doctor could administer Digoxin to these suffering children who show a lack. It would appear that chelation of lead, diligent removal of all fluoride exposure and its removal from the body with a high intake of iodine and borax, action to increase serotonin and decrease dopamine, treatment of copper-zinc imbalances, and a supplement of Advanced Ambrotose complex to provide the missing sugars, would be very productive in overcoming OCD, tics, and Tourette's; whereas, action to reduce serotonin and increase dopamine (by a supplement of tyrosine or a nicotine patch), treatment of a copper-zinc imbalance, and a supplement of CoQ-10, magnesium, and Ambrotose AO to provide for the missing sugars and antioxidants would be indicated in Autism not commingled with OCD/Tourette's. 

 

A challenge test for lead will only reveal what is in the blood, and blood tests may be nil. Lead is quickly stored in tissue, bone, and brain, and only found in testing if something has stirred it up. The best test for lead is hair analysis, often reading 10 times higher than in the blood. Nevertheless, it may take a year or more of nutritional therapy before lead is released from tissue storage and becomes detectable on hair tests. During chelation, it may appear to all be gone, only to be released from another reservoir and show high readings again a year later! It is of importance to note that children retain up to 50% of lead ingested, probably 5 times higher than adults, and they retain much more of that ingested between meals or with high fat or low casein diets, or when iron deficient. Lead can displace manganese and copper, both required for optimal adrenal function. Lead and fluoride are frequently associated with hypothyroidism, impairing the uptake of iodine by the thyroid. Lead is frequently associated with low zinc levels, and this low zinc is frequently associated with hypoglycemia and hypothyroidism. A low calcium/phosphorus ratio causes more lead to be incorporated into the skeleton, and adequate calcium, magnesium, zinc, vitamins B and C, and alginate must be present to eliminate lead. Since too much phosphorus interferes with calcium absorption, do not take your calcium supplements or high calcium foods with soft drinks or orange juice. Additionally, fluorine, chlorine, and bromine can and will, if given half a chance, replace iodine in any and all chemical reactions. “We even reverse hypothyroidism by simply getting rid of the lead poisoning.”—Dr. Garry Gordon, MD.

 

Additionally, today's “bromine problem” is particularly insidious because it causes “hidden hypothyroidism,” a condition in which “brominated thyroid” masquerades as thyroid hormone, fooling your doctor and robbing you of this energy-producing hormone. That’s right; excess bromine could be producing a “false read.”

 

If any heavy metal readings are “high normal” or more, they must be detoxified—preferably by nutritional means (see my Chapter “Heavy Metals Poisoning?” from my Electronic Book “Self-help to Good Health” ($29.95 US). Reducing lead from “high normal” will remove a number of the above listed symptoms. Do not use the chelators DMPS or high dose DMSA as these will likely further damage the gut, and they will impair Phase I liver enzyme function causing a further buildup of toxins. They (especially DMPS) can also further damage the sulfur oxidation system by draining the body of copper, molybdenum, zinc, and other mono-oxidase Phase I liver catalysts. The Physician’s Desk Reference™ documents that DMSA can cause neutropenia as a side effect. Neutropenia is a deficiency in neutrophil cells, the immune cells that kill foreign organisms, like fungus. Under no circumstances use DMPS and then Tylenol™ for pain. Tylenol™ toxicity from such a combination is a very real danger.

 

EDTA may not be the best choice for chelating mercury, or for removing lead, for it removes 8 to 12 essential minerals (EDTA and the dithiol complexing agents have affinities for Cu, Zn, Mn, Cr and Mo, and can indirectly result in Mg depletion), and it only chelates what is in the blood and on arterial walls. It does not reach into the body tissues, and by removing calcium, it encourages deposition of lead. In addition, studies have found that use of EDTA by patients with high levels of mercury can cause serious side effects, so calcium EDTA should be used only when mercury levels have been found to be low. Nevertheless, Dr. Boyd Haley says EDTA “in excess” totally prevents toxicity of cadmium, lead, and copper, though it does make mercury more toxic. “Toxicity of Hg2+ is synergistically increased by the presence of other heavy metals such as Pb2+, Cu2+, Ag2+, Zn2+, etc. For example, an LD-1 kill rate of Pb2+ added to an LD-1 of Hg2+ gave a solution with an LD-100. If it were additive, it would have been and LD-2 solution. Now, consider what would happen if you added EDTA to this mixture of Pb2+ and Hg2+. The EDTA would chelate the Pb2+ removing its synergistic toxicity, which is major. Also, the EDTA could make the Hg2+ more toxic. However, the increase in Hg2+ toxicity caused by EDTA would be much less than the decrease in toxicity caused by removal of the Pb2+ by EDTA. Therefore, even though I know that EDTA cannot be expected to pull Hg2+ off protein thiol groups (a covalent bond), it could reduce the ‘effective toxicity’ of Hg2+ by removing Pb2+, Cd2+, etc., freeing up reduced glutathione to bind and remove Hg2+.”

 

It seems to me that there are safer ways to remove lead, cadmium, and copper, and thus minimizing the toxicity of mercury. For example, in addition to the nutrients listed above, battery manufacturers found zinc with vitamin C very helpful. While using 2000 mg vitamin C and 60 mg zinc, the blood level of lead dropped 25% in 24 weeks, even as they continued working in the high-lead atmosphere. (This much vitamin C and zinc should be balanced with 8 mg copper - unless copper toxic - and 20 mg manganese.) Vitamin B1, 50–100 mg (in form of a B–complex supplement), detoxifies lead also. One urgent reason to remove these heavy metals is the fact that they harbor bacteria, viruses, and yeast and protect them from antibiotics!

 

Alpha Lipoic Acid (ALA) is a medium-chain, fatty acid that is a powerful antioxidant, soluble in both water and fat, and an effective metals chelator. It regenerates both vitamins C and E, keeping them effective longer. A deficiency of lipoic acid results in reduced muscle mass, brain atrophy, failure to thrive, and increased lactic acid and pyruvate accumulation. Supplemental ALA enhances glutathione production, and regenerates glutathione and CoQ10 giving cells a double dose of antioxidant protection. It inputs nutrients (glucose) into the cells to improve the mitochondrial function (so those suffering hypoglycemia may find it lowers blood sugar adversely) and increases plasma ascorbate, plasma sulfur, and T-helper lymphocytes/T-helper-suppressor cell ratios. A supplement seems desirable, but do not use more than one milligram per pound of body weight in any one serving (it may be better to use only half that). Its short half-life indicates it should be taken several times a day. If any adverse responses are observed, cut that amount in half. Alpha-lipoic acid is very safe at these recommended dosages, although occasionally it causes mild stomach upset, and in rare cases it can trigger an allergic skin rash (detoxication?). If you experience any of these reactions, reduce the dose or stop taking the supplement. It is reported that large amounts can significantly alter thiol (sulfur) metabolism, distribution, and excretion—significantly increasing plasma cysteine levels, and by increasing bile excretion of glutathione, it may result in depletion of the liver stores of glutathione. Opioids have been shown to decrease hepatic glutathione also. This lack of GSH will seriously affect the availability of the thyroid hormones T3 and T4, and of the enzyme, aconitase that is dependent upon glutathione. A deficiency of aconitase will allow citric and aconitic acids to build up.

 

The human body can make enough alpha lipoic acid to prevent a recognizable deficiency disease, though not enough to perform all its functions. The optimal level of alpha lipoic acid varies with each person depending on biochemical differences, lifestyle, exercise, and how much oxidative stress they experience. The requirement of NADH and NADPH as cofactors in the cellular reduction of alpha-lipoic acid to dihydrolipoate in various cells and tissues has been reported. These cofactors can be lacking and block effectiveness of ALA. Certain diseases, environmental conditions, and age can cause a deficiency in lipoic acid, and thus the body often doesn’t make enough to meet all its metabolic and antioxidant needs.

 

When sugar is metabolized in the production of energy, it is converted into pyruvic acid. An enzyme complex that contains lipoic acid, niacin, and thiamine breaks down the pyruvate. Pyruvic acid can be elevated for a number of reasons, but mercury is notorious for interfering with the mitochondrial, pyruvate dehydrogenase complex, where it binds to and deactivates the lipoic acid coenzyme, resulting in elevated pyruvic acid. Since the human body tends to have only the minimum amount of alpha lipoic acid to prevent recognizable disease, supplementation may help improve energy metabolism. This is particularly applicable in people with lower than normal levels, for example, individuals with diabetes, liver cirrhosis, heart disease, mercury toxicity, and HIV.

 

Nevertheless, there is compelling scientific evidence that high and constant doses of lipoic acid have the potential to seriously disrupt a number of key minerals including copper, zinc, and molybdenum, possibly elevating copper or zinc to potentially toxic levels. More than the recommended amounts will compete excessively with biotin, creating a deficiency of this vital B-complex vitamin. It may also impair a vital enzyme, Carboxylase. It is thought to deplete copper stores of the liver and distribute it to other tissues, creating a potential toxicity. Do not use ALA if known to have high (or low) levels of these minerals, or high levels of cysteine. Large supplemental amounts can also deplete the liver of vital glutathione, defeating the very thing for which it is being used. A German study reports that six months of lipoic acid causes a vitamin B12 deficiency [M Siepmann, W Kirch]. It decreases lipoic acid serum levels of vitamin B12 [Aktuelle Neurologie, 2000, Vol 27, Iss 1, pp 33-35. www.drmirkin.com/diabetes/8310.html]. It would thus be wise to supplement vitamin B12, molybdenum, and biotin with the lipoic acid. It might be helpful to supplement reduced (hydrogenated) glutathione, except where there is high cysteine. One of the concerns is the capacity of ALA to chelate mercury. If one has high levels of methyl-mercury (inorganic mercury from fish), ALA can hurt. This freed mercury will attach to available selenium. Unless adequate selenium is being supplemented, the mercury may not be promptly excreted, and a selenium deficiency could be induced. Hepatic GSH is a primary substrate for organic-Hg clearance from the human; and intraneuronal GSH participates in various protective responses against Hg in the CNS.

 

Many of the “backfires” from using DMPS indicate a loss of the sulfur-oxidizing enzyme “sulfite oxidase”, a molybdenum-histidine containing enzyme, and a dose dependent reduction of cellular, low-weight thiols including that vital antioxidant glutathione. This will compound the PST/sulfate problem. Antibiotics should be avoided for the same reason, and steroids will do more harm than any long-term good. Giving steroids might reduce the rate of demyelination, if that exists, or “cool” an inflamed gut, but giving steroids can also further disrupt the immune function and exacerbate an underlying infection such as HHV-6 or blood-brain-barrier, localized measles. Save the drugs until all else recommended herein fails (it won’t).

 

The best detoxifier of all in this instance is glutathione, but don’t take the glutathione precursors that contribute directly to the cysteine pool. L-cysteine, ALA, and whole glutathione do this. N-Acetyl-L-Cysteine (NAC) produces glutathione, and it is a mercury chelator in its own right. It should completely clear the body within 24 hours if it is not utilized in making glutathione (according to published pharmokinetics study). NAC does not contribute directly to cysteine toxicity unless you take massive amounts of it. Around 600 mg/day (adult) stands to benefit without significantly increasing risk of cysteine toxicity. NAC should not be used initially or by itself with anyone suspected of having a significant body burden of mercury. Like alpha-lipoic acid, cysteine and cystine, NAC can bind with mercury and carry it across cell membranes. NAC is also a good culture medium for yeast, like its parent molecule, cysteine.

 

Build glutathione and “cool” the inflamed gut and the autoimmune response with A----------®, or A----------t® by M--------------h™. In addition, P--------S and S----------T by M------------h™ supplies plant sterols that removes mercury. Investigators have revealed that phytosterols block the development of tumors in colon, breast, and prostate glands. The mechanisms by which this occurs are not well understood, but we do know that phytosterols appear to alter cell membrane transfer in tumor growth and reduce inflammation. PLUS and Ambrotose® also remove lead. PLUS, Ambrotose®, and Phyt•Aloe® protect against organic solvents as well as heavy metals. I should note that Phyt•Aloe® bears several high sulfur, phenol-content vegetables, and may be contraindicated for some PST kids, or to those allergic to any of these foods, and it may be an irritant to Crohn’s or Celiac Disease until bowel function is improved (use Ambrotose® and PLUS for marvelous improvements in bowel function).

 

Dr. Yoshiaki Omura discovered that the leaves of the coriander plant (Cilantro) could accelerate the excretion of mercury, lead, and aluminum from the body. He had been treating patients for an eye infection called trachoma (granular conjunctivitis), which is caused by the microorganism Chlamydia trachomatis. Following the standard treatment with antibiotics, Dr. Omura found that the patients’ symptoms would clear up initially, and then recur within a few months. He experienced similar difficulties in treating viral related problems like Herpes Simplex types I & II and Cytomegalovirus infection. (Does this recurrent infection sound familiar?) Dr. Omura found those organisms seemed to hide and flourish in areas of the body where there were concentrations of heavy metals like mercury, lead, and aluminum. Somehow, the organisms were able to use the toxic metals to protect themselves from the antibiotics! (It is interesting to note: “Oral antibiotics inhibit excretion of mercury”—James B. Adams, Professor Chemical and Materials Engineering, Arizona State University.)

 

Dr. Omura noticed the mercury level in the urine increased after patients consumed a healthy serving of Vietnamese soup containing Chinese parsley, better known as cilantro, or coriander, since it comes from the leaves of the coriander plant. Further testing revealed that eating cilantro also increased urinary excretion of lead and aluminum. When cilantro was used concurrently with antibiotics or natural anti-viral agents and/or fatty acids like EPA with DHA, the above infections could be eliminated for good. (Acupnct Electrother Res. 95:20 (3-4): 195-229.) Further testing with those who had high levels of mercury following amalgam removal, showed that, without the help of any chelation agents, cilantro was able to remove the mercury in two to three weeks. (Acupunct Electrother Res 96;21 (2): 133-60.) I think this removed only the free mercury from the amalgam removal in this short time, however, Cilantro Extract has been shown in clinical trials and research to mobilize mercury, tin, and other toxic metals stored in the brain and spinal cord, and it moves them rapidly out of those tissues. This is a revolutionary discovery and makes cilantro the first known substance that mobilizes mercury from the Central Nervous System (CNS). Dr. Amy Yasko, ND, has discovered that even when all mercury has been removed by extensive DMSA usage, when she drops the viral load, mercury comes pouring out, confirming Dr. Omura’s experience.

 

Be aware that mercury readings from the hair or blood will only reflect a current or recent exposure within approximately three months, or the body’s active detoxification of mercury. A negative reading may be meaningless.

 

In addition to soup, one may use a Cilantro Pesto:

            1 clove of garlic;

            1/2 cup of almonds, cashews, or other nuts;

            1 cup packed fresh cilantro leaves;

            2 tablespoons lemon juice;

            6 tablespoons olive oil.

 

Put the cilantro and olive oil in blender, and process until the cilantro is chopped. Add the rest of the ingredients, and process to a lumpy paste. (You may need to add a touch of hot water and scrape the sides of the blender.) You can change the consistency by altering the amount of olive oil and lemon juice, but keep the 3:1 ratio of oil to juice. (It freezes well, so you can make several batches at once.)

 

Cilantro is a very popular herb in Mexican cooking, and due to their large Mexican populations it is easy to find anywhere from Texas to California. In other areas, you may need to visit an Oriental market or specialty supermarket where is may be called Chinese parsley.

 

Dr. Klinghardt suggests making this “pesto” to increase your intake of cilantro:

 

Start with fresh, organic cilantro and wash it thoroughly. Place the cilantro in a blender, along with water, sea salt and olive oil. Blend the ingredients until creamy. Dr. Klinghardt recommends taking 1-3 tablespoons of this cilantro pesto, three times daily with meals. For those suffering from neurological problems, such as Alzheimer’s, or brain “fogginess” and difficulty concentrating, the pesto may be taken more often, he says.

 

The best form of cilantro is a tincture available from Dragon River™ (505-583-2348) www.dragonriverherbals.com. The dose is one dropper applied on the wrists and rubbed in twice a day. The tincture is also particularly useful for any joint pain, and could be rubbed on the joint that is hurting as an alternative. You can also augment the tincture with using the herb. It is not as potent, but certainly will add to the program. However, like with chlorella, many people are sensitive to oral cilantro. So, if you develop any nausea or discomfort after eating cilantro, do not use it orally.

 

Garlic is one of the best chelators, and Kyolic™ aged garlic (800-421-2998) is a deodorized form that concentrates its chelating ability to 200 times that of a fresh garlic clove. It is shown to increase fecal excretion of mercury to 400%, and to completely protect blood cells against high levels of lead. It provides large amounts of selenium (prevents recycling of mercury into the system), germanium, and sulfur. The liquid extracts of garlic are said to contain less sulfites. Cilantro, garlic, selenium (selenomethionine), zinc, copper, manganese, magnesium, calcium, NAC, and glutathione are all effective mercury chelators, and I.V. vitamin C has been helpful in preventing brain fog. I would play it safe, and skip chlorella.

 

 

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