Vitamin B12, Drinking Water Fluoridation, and Alzheimer’s Dementia (AD)
Joseph G. Hattersley – November 2002
1,505 words
Introduction. An estimated 2.3 million Americans now have the condition. Prevalence doubles every five years after the age of 60, increasing from 1 percent among 60- to 64-years-old up to 40% of those aged 85 years and older. These statistics suggest there will be between 5 and 7 million Alzheimer’s patients over the next 10 years. Nursing home care costs about $47,000 per patient annually, a huge burden on the healthcare system. It is interesting to consider what proportion of AD may be related to undernutrition.

I. On vitamin B12. John V. Dommisse, MD, practicing medicine in Tucson, Arizona, has confirmed   that Alzheimer’s disease appears to result from too-low serum vitamin B12; its repletion succeeds despite other risk factors. “Most cases of Alzheimer’s dementia are actually missed B12 deficiency cases because of the too-low normal range for B12.”1 U.S. clinical laboratories regard 200 pg/ml (trillionths of a gram per milliliter) as the lower range of normal. That low limit was set with hematologic criteria, not neuropsychiatric criteria, which have now become much more critical.

	The normal range for serum B12 should be 600 to 2,000 pg/ml. In Japan the “normal” range is 500-1,300 pg/ml; this may explain why Japan has such a low rate of Alzheimer’s dementia, compared to the United States. Mammals including humans are born with serum levels about 2,000 pg/ml, which gradually decline throughout life.1  Below 550 to 600 pg/ml, deficiencies start to appear in the cerebrospinal fluid.  On the basis here suggested, nearly all elderly must be B12 deficient.

	When deficiency is recognized (serum level below 200 pg/ml), just as in the case of the [pernicious anemia] dementia, the neuropathy may well have become irreversible. Psychiatric manifestations can occur without anemia or macrocytosis.  The procedure can reverse 75 percent of B12 deficiency dementias, when discovered early enough. The neurological and cerebral manifestations of B12 deficiency require dosages larger, and over a longer time, than to reverse hematologic effects.

	High-dose vitamin B12 might well prevent Alzheimer’s disease. 2,000 to 2,500 ug sublingually after breakfast and supper works as successfully as monthly to quarterly one-milliliter IM injection -- apparently by a non-intrinsic factor mechanism. Inexpensive tablets of that size are available at American health food stores, IM vials from pharmacies by prescription. Compliance was better using oral intake -- patients didn’t always get to the doctor’s office for their injections in a timely manner.

	About as difficult technically as pushing a pin into a ripe orange, IM can be very economical if a patient can self-administer or spouse can administer and re-use the syringe (as I do at age 79: hydroxycobalamin twice a week.). I sterilize the needle and the top of the vial with isopropyl alcohol before and after but minimize skin contact. Such solvents are dangerously toxic.

	B12 deficiency can cause depression,      bipolar-1 disorder (manic depressive) and more commonly bipolar-2 (cyclothymic personality).   Psychotic forms of depression have been particularly associated with B12 deficiency; it has also been linked to paranoid psychoses and chronic fatigue syndrome;   weakened immunity leading to susceptibility to cancer and recurrent infections; asthma, disrupted sleep/wake rhythms, environmental illness, low stress tolerance, osteoporosis, AIDS, premature aging, and multiple sclerosis  -- as well as increasing risk of cardiovascular disease and much more by hindering remethylation of homocysteine into methionine. In numerous cases, violent behavior disappeared.     The findings conflict with conventional drug-oriented psychiatrists' self-serving assumption that the brain, like some sort of black box, is unaffected by diet and environment. What other single measure offers at least a degree of protection against so much? And at such low cost?

	Causes of B12 deficiency include excessive long-term use of antibiotics and other drugs to mask symptoms; oral antibiotics destroy the "good" bugs in the gut as well as the "bad," ruining absorption. B12 deficiency, common with folate deficiency in dementia,  worsens with folate deficiency. Other possible causes of dementia: subclinical hypothyroidism,    zinc deficiency and copper toxicity, often from copper in water pipes; chronic overuse of antacids, both OTC and prescribed. Excessive use of alcohol promotes vitamin excretion. Mercury was found in the brains of 83 randomly chosen accident victims with amalgam fillings. 

Dr. Dommisse does not reveal the proportion of his patients who are thyroid deficient, drink fluoridated water, have extensive dental amalgams, take Ibuprofen, etc. Correcting each/all of these sources of B12 deficiency seems unlikely to effect permanent reversal of dementia unless B12 is repleted and maintained at high level. This seems to do the trick, regardless. 
	
	Possible mechanisms for spinal cord and peripheral nerve effects include axonal degeneration and demyelination of insulating nerve sheaths. Deana found low levels of neurotransmitters in the brains of B12-deficient rats. A University of Kentucky study found impaired G-protein signaling and proposed a feed-forward cycle of progressive neuronal dysfunction, related to phosphoinositide signaling. “Spector has hypothesized that idiopathic (Alzheimer’s) dementia is a brain-vitamin-deficiency state due to inadequate transport of vitamins from the blood across the choroid plexus (the ‘blood brain barrier’) and into the cerebrospinal fluid -- the only source of these nutrients for the brain.” McCaddon and Kelly, using sources they cite,      have proposed a somewhat different mechanism.
	
	“The only question now is what proportion of cases of mood-disorder is caused by B12-deficiency and what percentage is idiopathic. Almost all of Dommisse’s uni- and bipolar patients have had B12 levels in the lowest one third of the so called normal (to prevent pernicious anemia) range, levels which he now regards as deficient (for adequate affective, cognitive and other mental functions). When their levels have been raised to the highest one third of that ‘normal’ range, every one of those patients has done and felt better. In some cases who came out of their depression or mood-swing disorder, this was the only new or different treatment they received. When such patients’ affective disorder has got worse, their B12 level had again dropped. Dr. Chris Reading of Australia now thinks in most cases of ‘intractable depression’ a subtle B12, or other nutrient, or thyroid hormone, deficiency has been missed.” 
	
	Little research is published about all this because of the “heavy pharmaceutical industry sponsorship of research and teaching in medical schools. Career-track academicians have realized, if they want to fulfill their ambitions, they have to eschew nutritional research for that of drugs.”1 
	
	Jonathan Wright and other physicians use B12 injections -- “for anyone over 60 who doesn't feel very, very well” -- in an individualized program of sensible nutrition: minimize white flour and white sugar, avoid margarine and other trans fatty acids- and excitotoxins-  containing processed foods. They use multivitamins and other B vitamins as well as folate.
	
	What is the risk of overdose? Patients of Dr. H.L Newbold in New York City injected themselves three times daily with triple-strength doses of B12 (9,000 ug per day) indefinitely. Their serum B12 levels reached 200,000 pg/ml and more, but none had any significant side effects. Dr. Dommisse prefers hydroxycobalamin to cyanocobalamin. A person taking the latter might over a period of years accumulate a toxic amount of cyanide and possibly damage vision. Methylcobalamin, according to one source, might be risky for schizophrenic patients.
	
“It is hard not to justify therapeutic trials when testing is several times more expensive than injections. A part of medicine is shifting from treating a disease with one agent to correcting a metabolic pathway and thereby treating and preventing a wide variety of diseases.”

	Regarding neurotoxicity of vitamin B6, Dr. Dommisse suggests some B12 may help. Russell Jaffe, MD, PhD, found that pharmaceutical grade pyridoxine hydrochloride (PN) totally avoided neurotoxic side effects. Volunteers took 200 to 2,000 mg/day for as long as two years. Vitamin Research Products. 3579 US Hwy 50E, Carson City NV 89701. 1-800-877-2447; 1-702-884-1300. www.vrp.com. VRP also offers pyridoxal phosphate, PLP (also called P5P), the active form the body uses. About 15 percent of patients cannot convert PN from supplements into PLP. They can supplement PLP; about one-tenth as much suffices. Others may offer pharmaceutical-grade vitamins.

II. On fluoridated water. J.A. Varner and associates studied laboratory rats to learn whether alum (aluminum sulfate) would combine with fluoride and penetrate the blood-brain barrier.  Water supply facilities frequently add alum to clarify drinking water; aluminum is neurotoxic to humans and animals. “And there is no substance as biochemically active in the human organism as fluoride.” 

Eighty percent of the rodents died; they also suffered significant kidney and brain damage. The dose of fluoride and alum used was similar to that in artificially fluoridated drinking water -- even without the excessive levels of fluoride getting into people from other sources and the extraordinary toxicity of the witches’ brew used in most American fluoridation. Pharmaceutical grade sodium fluoride (NaF) is used in about 10% of American fluoridation, and likely close to 100% overseas in the few countries that use it. Ninety percent of US and probably Canadian fluoridation uses fertilizer or aluminum plant wastes rich in arsenic, uranium-238, mercury, dioxins, etc., and often up to 400 milligrams of lead per liter. About 20 percent of the mixture is highly acidic silicofluorides.
	
“Striking parallels were seen between aluminum-induced alterations in cerebral blood vessels associated with Alzheimer’s disease and other forms of presenile dementia. The Varner study confirmed results of their two previous studies. It may take 2-3 years for the National Toxicology Program to act upon the USEPA request for further research.” 

AD is observed in 30- to 40-year old Canadians who consume fluoridated water. “A number of people in Seattle, WA, between the ages of 40 and 60 with symptoms associated with early-onset Alzheimer’s (memory loss, confusion, difficulty concentrating) and pains in kidneys and back – symptoms of chronic fluoride poisoning – after two to three months of avoiding all sources of fluorine (particularly water and toothpaste), were restored to full functioning.”

Many assume that the genetic risk of Alzheimer’s disease is “hard-wired,” making the disease inevitable. “But any inherited disease or trait that has a serious impact on fitness must fade over time, because the genes that spell it out will be passed on to fewer and fewer individuals. Therefore, common illnesses with severe fitness costs are unlikely to have a genetic cause.”

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