Vitamin B12 for Alzheimer's Disease

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Vitamin B12 for Alzheimer's Disease
Townsend Letter for Doctors and Patients, May 2006 by Joseph G. Hattersley


It is interesting to consider what proportion of Alzheimer's dementia (AD) may result from under-nutrition, (1) especially when it seems that there may be an easy, low-cost, perfectly safe, nutritional way that may allow people to avoid a miserable illness that many people consider worse than death. Some people might say, "That's too good to be true!" In fact, an at-home nutritional program, using a lot of vitamin B12 may indeed prevent and virtually eliminate AD. An early launch of the treatment soon after first warning symptoms start could even turn off the process.

Confusion, difficulty concentrating, loss of memory, marked changes in personality that can lead to outbursts of violence, hallucinations, wandering away, and early death all characterize Alzheimer's dementia. An estimated 2.3 million Americans now have AD. Prevalence doubles every five years after the age of 60, increasing from one percent among those 60 to 64 up to 40% among those aged 85 years and older. Nursing home care costs about $47,000 per AD patient annually, and this figure is rising steadily, putting a huge burden on the health care system. The disease is also terrible for the patients' caregivers. In what experts are calling "a looming public health disaster," statistics suggest there will be between five and seven million Alzheimer's patients over the next ten years. (2)

Let's start with a little background. Mammals, including humans, are born with serum levels of vitamin B12 at about 2,000 pg/ml (picograms--i.e., trillionths of a gram, per milliliter). The level declines throughout human life owing to practices common in Western societies. (4) Below 550 to 600 pg/ml, deficiencies start to appear in the cerebrospinal fluid. (5,6) US clinical laboratories regard 200 pg/ml as the lower range of normal. That low limit was set with hematologic criteria. But neuropsychiatric criteria, which are much higher, have become more critical.

"Most cases of Alzheimer's dementia are actually missed B12 deficiency cases, because of the too-low normal range for B12," wrote John V. Dommisse, MD in 1991 in Medical Hypotheses.

 (3) Dommisse, who practices medicine in Tucson, Arizona, has confirmed (7,8,9) that:

Alzheimer's disease appears to result from too-low serum vitamin B12, and repletion of the vitamin succeeds despite other risk factors. Repleting B12, according to Dommisse, can reverse 75% of B12 deficiency dementias when the condition is discovered early enough. (10)

Other aspects of the therapy should be noted: The neurological and cerebral manifestations of B12 deficiency require dosages larger, (11) and extending over a longer time, (12) than to those needed to reverse hematologic effects. (13) B12 therapy appears to be perfectly safe; in other words, the risk of overdose is virtually nil. Patients of Dr. H.L. Newbold in New York City injected themselves three times daily with triple-strength doses of B12 (9,000 ug/micrograms/per day) indefinitely. Their serum B12 levels reached 200,000 pg/ml (100 times the normal level found in newborn babies and higher), but none had any significant side effects. (3)

Other Conditions Benefit From B12 Replenishment

Besides Alzheimer's, B12 ("cobalamin"*) deficiency can also cause the following conditions. And when started early, replenishing B12 (i.e., restoring it to or near to levels found at birth) may often significantly improve these afflictions as well: (Note this does not mean that the following conditions will always respond to B12 supplementation or that the cause of the following conditions is always B12 deficiency ed.)

* Depression Often in mild form, depression can be one of the first clues foretelling dementia. (14-19) Chris Reading, BSc, DipAgSc, MBBS, FRANZCP, FACNEM ( of Australia concurs: "... in most cases of [not only mild but also] 'intractable depression,' a subtle B12, or other nutrient, or thyroid hormone, deficiency has been missed." (20,21) 

Psychotic depression has been particularly associated with B12 deficiency. (22) As I'll discuss later, success of B12 therapy against depression in its various forms is "probable."

* Paranoid psychoses This nutritional deficit has also been linked to paranoid psychoses, characterized by over-suspiciousness and delusions.

* Bipolar-1 disorder Bipolar-1 disorder (manic depressive), marked by alternating periods of elation and depression; and more commonly bipolar-2 (cyclothymic personality), marked by mood swings within normal limits. (24-26)

* Chronic fatigue syndrome (27-29)

* Weakened immunity Weakened immunity can occur, leading to susceptibility to recurrent infections and cancer, as well as increasing risk of cardiovascular disease, cancer, (30) and much more by a second pathway, hindering remethylation of the toxic sulfur amino acid homocysteine back into the nontoxic essential amino acid methionine. (31)

* Asthma Incomplete digestion of foods due to hypochlorhydria and low pepsin production (see below) can be involved in subsequent allergic response in asthma. (32)

* Disrupted sleep/wake rhythms (33,34)

* Environmental illness (35)

* Low stress tolerance (36)

* Osteoporosis (37)

* AIDS (Acquired ImmunoDeficiency Syndrome) (38)

* Premature aging (39)

* Multiple sclerosis (40,41) Symptoms of MS have been noted in persons with a vitamin B12 deficiency prior to evidence of megaloblastic anemia. There is a remarkable epidemiologic similarity between MS and pernicious anemia, and similar HLA (human lymphocyte antigens) are suggested for the association of the two conditions.

*violent behavior Intramuscular injection of B12 also has yielded seeming miracle cures in still other desperate illnesses. In numerous cases of patients with violent behavior, for instance, when B12 was replenished (with or without other changes in life), violent behavior disappeared. (45-49)

"The only question now," writes Dommisse, "is what proportion of cases of mood-disorder is caused by B12-deficiency and what percentage is idiopathic." Almost all of his uni-and bipolar patients have had B12 levels in the lowest one-third of the so-called normal (to prevent pernicious anemia) range, levels that 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 felt better. For some patients, who came out of their depression or mood-swing disorder, this was the only new or different treatment they received. In subsequent instances when their affective disorder worsened, B12 levels had again dropped. So, would restoring ample serum B12 levels prevent many or most of those adverse conditions? Evidence shown below, cautiously suggests Dr. Dommisse, means, "Yes, at least in the case of depression."

There is no maximum allowable age to begin B12 therapy. A friend recently told me her 90-year-old mother is beginning to think less clearly than in the past, and to feel a bit depressed. I suggested, "If your dear mother would like to stop her incipient downward slide, let her start the therapy." God never wrote on tablets of stone that 90 years of age is too old to turn one's health around and begin to make life fun again.

It is important to note that having a quality laboratory measure serum B12 is an essential part of the replenishment process. Simply supplementing B12 "in the dark" could miss the mark badly. And to really know the patient's whole picture, Sherry A. Rogers, MD, suggests the ION Panel (N.E.E.D.S.; 800-634-1380) is well worth its cost (currently, about $600). (50)

The normal range for serum B12, states Dr. Dommisse, should be defined as 600 to 2,000 pg/ml. Japan's "normal" range is 500-1,300. (51) According to Dommisse, this may explain why Japan has such a low rate of Alzheimer's dementia (52) compared to the United States. (53) By some estimates, as many as 80% of elderly American patients may share hidden B12 insufficiency. (54-56)

Also, B12 deficiency is common with folate deficiency in dementia (57-59) and worsens over time as the deficiency increases. (60) The impact was seen first on neuropsychiatric measures, where augmentation of B12 and folate materially improved scores on cognitive performance tests. (61,62)

Methods of Treatment

The most direct method for adding these megadoses of B12 is through intramuscular (IM) injection, which requires a doctor's prescription and a doctor or nurse's instruction. It is about as difficult technically as pushing a pin into a ripe orange (63) and can be economical if a patient can self-administer or a companion can administer

Another feasible approach uses inexpensive sublingual B12 at 2,500-5,000 mcg (2.5 to 5 mg), which anyone can buy at a quality health food store. Taken in that way, evidence indicates that most of the vitamin goes via the lymphatic system. Therefore, this treatment mode may yield more benefit by avoiding the digestive system. (65)

Causes of B12 Insufficiency

Several common features of modern life accelerate the decline of vitamin B12 in serum through life, including the following:

* Microwave ovens In one test, microwaving milk degenerated 30% to 40% of milk's vitamin B12 in six minutes; with conventional heating, 25 minutes of boiling was needed to depress B12 that much. (67) More importantly, the heat of microwaving destroys all the enzymes in ingested food, which are required to enable absorption and utilization of food. And so by eating microwaved food, both at home and in restaurant and take-out meals, tens of millions of Americans are making themselves increasingly vulnerable to AD, as well as to cancer.

* The Western diet B12 ingestion and stores tend to be insufficient among millions who have for decades eaten RDA-fortified, yet vitamin- and mineral-depleted, processed Western diets, which are also big sources of disease-creating free radicals. (69) Too low levels of omega-3 essential fatty acids in Western diets, harmful in many ways, must also contribute to insufficient B12 levels. (70) Omega-3 supplementation may yield its benefits largely through augmenting vitamin B12. Too-low levels of acetyl-carnitine and folic acid also appear to worsen risk of the condition. (71,72) It's worth noting that in an Alzheimer's disease mouse model, a diet rich in omega-3 essential fatty acids, specifically DHA (docosahexaenoic acid), has been shown to potentially slow or even prevent Alzheimer's disease. (73) At modest cost, we can easily ingest DHA in fish oil or [Carlson's] cod liver oil. Also worth considering is the role of trans-fatty acids (TFA) found in products labeled "zero trans-fats" with EPA approval. In a study of over 800 senior citizens, those with high TFA were twice as likely to suffer symptoms of Alzheimer's disease compared to those with the lowest TFA intake (; accessed 2/17/06).

*Hypochlorhydria.i.e. insufficient hydrochloric acid Most commonly, B12 insufficiency results directly from hypochlorhydria--insufficient hydrochloric acid (HCl) in the stomach--or by achlorhydria--no HCI at all. The acid should be concentrated enough to dissolve a nail in an hour. (77) Hypochlorhydria is likely caused by zinc/vitamin B6 deficiency (78) and a shortage of ionized calcium. (79,80) (Both deficiencies are typically present in older people.) Lack of enough pepsin or HCl in the stomach to generate the bond between B12 and its carrier protein typically shows with atrophic gastritis. (81,82) Both are also risk factors for gastric cancer. (83) Incomplete digestion of foods due to hypochlorhydria and low pepsin production also can be involved in subsequent allergic response in asthma. (84)

Intrinsic Factor, Bacteria, Cobalamid, Failure of Absorption B12 deficiency can also result from inadequate stomach secretion of the tiny open-ended protein capsules known as intrinsic factor; from presence in the gut of bacterial overgrowth; (85) from ingestion of cobalamid, a B12 antagonist; (86) or failure of absorption for other reasons. (87)

Antacids & Antibiotics Chronic overuse of antacids, both prescribed and over-the-counter (OTC), by tens of millions of elderly may also be responsible. When all the acid is mopped up daily by antacids, the B-vitamins never even get to first base. (88) For example, B12 absorption is dramatically reduced when the drug Prilosec (omeprazole), which has recently gone OTC, is used. (89,90) "A significant percentage of patients taking omeprazole are also being treated for or are at high risk of heart disease, and therefore almost all are instructed to eat a diet low in red meat (or devoid of it completely) and of animal products, which are the best source of vitamin B12. (91) Also, omeprazole reduces gastric (stomach) levels of multi-protective ascorbic acid (vitamin C), (92) still another route to cancer.**

This is another egregious example of iatrogenic disease, created by tunnel-visioned, one-organ specialists (who seldom if ever communicate with each other) using a "band-aid" approach to treatment of a symptom or test reading, oblivious to the possibly disastrous long-term effect on the patient. Other causes of B12 deficiency include excessive long-term use of antibiotics and other drugs to mask symptoms without learning and correcting their cause. Oral antibiotics destroy the trillions of "good" bugs as well as the bad in the gut, ruining absorption. (93)

* Vegan Diets (cooked diet) Many vegan (total) vegetarians have for decades consumed few if any foods containing B12. As a result, their body stores of the vitamin have gradually diminished. Forty-seven of 78 adult vegans had levels below 200 pg/ml. When they chewed a 100 ug (microgram) B12 tablet once a week, their levels promptly rose to normal. (94) Some vegans depend on sea vegetables such as arame, wakame, and some varieties of kombu, or on algae. (95) The B12 in these, although absorbed, may not be fully bio-available. (96) A recent study in the Townsend Letter provided strong evidence that a commonly consumed seaweed known as nori does, in fact, contain bio-available forms of B12. (97) Whether or not that substance is available to large numbers of vegans and whether its use would lift serum B12 levels enough is not known.

Repletion of the Vitamin Succeeds Despite Other Risk Factors.

In his study, Dr. Dommisse does not reveal, or need to know, the proportion of his patients who experience other AD risks: for example, how many are thyroid deficient, drink fluoridated water, have extensive dental amalgams, take Ibuprofen (99) (some non-steroidal anti-inflammatory drugs [NSAIDs], along with their famous multitude of adverse effects, may lower AD risk by about 50% (99)), etc. He doesn't consider the number of patients who have been exposed occupationally to electromagnetic fields, promoting formation of beta amyloid, a protein common in the brains of Alzheimer's patients. (100,101) Nor does he present any numbers showing high content of aluminum in AD patients' brains (102) from consumption of aluminum-treated drinking water (103,104) and/or from consuming a variety of everyday sources (see also the combination of aluminum-containing alum with fluoridated water*). Dommissee's study also doesn't consider the extent of melatonin use as a brain antioxidant to counteract accumulation of free radical-creating iron, (105) nor does the study look at potentially brain-damaging homocysteine in patients' serum. (106,107)

As a side note: Possible mechanisms for spinal cord and peripheral nerve effects of vitamin B12 deficiency include axonal degeneration and demyelination of insulating nerve sheaths. (108) Deana found low levels of neurotransmitters in the brains of B12-deficient rats. (109) A University of Kentucky study found impaired G-protein signaling and proposed a feed-forward cycle of progressive neuronal dysfunction, related to phosphoinositide signaling. (110) 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. (111)]

Dr. Dommisse prefers vitamin B12 as hydroxycobalamin. A person taking cyanocobalamin might over a long period of years accumulate a toxic amount of cyanide and possibly damage vision. (112) Also, methylcobalamin, widely used in Japan, is increasingly popular in the US, because it is reputed to be better absorbed. A compounding pharmacist may be able to provide methylcobalamin after a doctor prescribes it. Certain OTC sublingual preparations also provide methylcobalamin.

In Preventive Medicine Update (May 1995), Jeffrey Bland, PhD reported: "Five clinician/subscribers have sent clinical case histories. On high-dose folate/B12/B6, homocysteine levels dropped ... Also, a number of reports have come ... about patients suffering with presenile dementia or Alzheimer-like symptoms. On IM B12, their methyl malonic acid (MMA) levels, an indication of deficient B12 status, came down to normal range, and their walking, balance, gait, and perception improved. I've had reports of individuals who had lost their ability to read, start to read again; people who had not been able to look at video screens now comfortably looking at them; and two reports of people who had movement dystonia, who, after vitamin B12 therapy were able to get in the car and be transported without fear of being unable to accommodate passing scenery. So there is a wide range of very important clinical outcomes from improving folate/B12/B6 status, cutting across neurological and arterial functional status." (113)

Because the typical environmentally ill (EI) patient often has low zinc/B6 and thyroid, low chromium glucose tolerance factor (GTF), and high candida/low bifidus as well as low B12, to suggest B12 only as the only treatment would not be consistent with holistic thinking. (114) So, if high-dose B12 doesn't do the trick pretty fast, consider additional measures, keeping in mind the results of the ION Panel test, if given. (115)

Little research is published about B12 therapy for AD and other neurological diseases, Dommisse writes, because of the "heavy pharmaceutical industry sponsorship of research and teaching in medical schools. Career-track academicians have realized that, if they want to fulfill their ambitions, they have to eschew nutritional research for that of drugs." (3) The volume of published research on drugs to fight Alzheimer's disease is overwhelming. To continue their careers, the authors of these studies have a powerful financial incentive to report positive results, whether truthful or not. Yet, the best that Alzheimer's drugs can do is to conceal the symptoms for a while. The underlying cause, notably deficiency of vitamin B12, continues to worsen unabated.

In that vein, I also offer a caution on statin (cholesterol-lowering) drugs. Along with others, I exposed these high-margin products ten years ago as potential patient-killers. (116) Big Pharma is now waking up belatedly to that fact. Now pharmaceutical companies would like to promote statins as a preventative for Alzheimer's dementia. A recent CBS Evening News report quoted a University of California medical professor who is conducting new government-funded (note, not drug-maker-funded) research on statin drugs' effect on Alzheimer-susceptible patients: "We have people who have lost thinking ability so rapidly that within the course of a couple of months they went from being heads of major divisions of companies to not being able to balance a checkbook." (117,118)

Vitamin B12 therapy still faces a very real obstacle: Codex regulations, likely to go into effect in the near future, will prohibit any dose of any vitamin to be sold at much above the Recommended Dietary Allowance (RDA). For B12, the adult RDA is only 3.02 micrograms. Millions may suffer and die from this terrible B12-preventable disease if that Codex regulation is enforced.

One final note: it is important to cultivate a positive, optimistic outlook to maximize the prospect for success against such mental diseases. One should avoid a scenario akin to that in which the attending physician tells the cancer patient, "You have X months to live." Classes and groups related to AD often move in that direction, forecasting the worst outcome. In fact, I have heard of no AD awareness classes that even mention vitamin B12 therapy in a positive way. MD physicians, whose medical education omitted or put a negative spin on anything using nutrition, may be behind the structure of many such classes. What a different story it might be if instruction and awareness emphasized the usually successful measures brought out in this article. One has to ask why doctors don't at least tell the public about this seemingly magical therapy, which is available to all at trivial cost? Just think about that, and the answer becomes obvious.


Joseph G. Hattersley, MA

2209 Craig Road SE

Olympia, Washington 98503-7119 USA




1. Bland JS. Funct Med Update. August 2002.

2. Centers for Disease Control. Mortality from Alzheimer's disease--United States 1979-1987. JAMA. 1991;265(3):313-317.

3. Med Hypotheses. 1989.

4. Dommisse JV. Subtle vitamin-B12 deficiency and psychiatry: A largely unnoticed but devastating relationship? Med Hypotheses. 1991;34:131-140.

5. Regland B. Vitamin-B12 Deficiency In Dementia Disorders (Monograph/doctoral thesis, comprising six papers, with co-authors). Dept. of Psych. and Neurochem, University of Goteborg, Sweden. January 1991.

6. Ikeda T, Furuwaka Y, Mashimoto S et al. Vitamin B12 levels in serum and cerebrospinal fluid of people with Alzheimer's disease. Acta Scand Psychiatrica.. 1990;82;4:327-329.

7. Dommisse JV. Psychiatry and vitamin B12 deficiency. Kirk Hamilton, PAC, Clinical Pearls News. March 1998: Interview.

8. Dommisse JV. Subtle vitamin-B12 deficiency and psychiatry. Op. cit.

9. Spector R, Cancilla P, Damasio AR. Is idiopathic dementia a regional vitamin-deficiency state? Op. cit.

10. Roos D. Neurological complications in patients with impaired vitamin B12 absorption following partial gastrectomy (monograph/D Med Sci thesis). Supplement 69 to Acta Neurologica Scandinavica. 19, Minksgaard, Copenhagen, 1978.

11. Roos D. Neurological complications in patients with impaired vitamin B12 absorption. Idem.

12. Whitehead JA, Chosen MM. Paraphrenia and pernicious anemia. Geriatrics. 1972; May:148-158.

13. Smith ADM. Megaloblastic madness. Brit Med Jour. 1960;2:1840.

14. Ferrara A, Arieti S, English WH. Cerebral changes in the course of pernicious anemia, and their relationship to psychic symptoms. Jour of Neuropathology & Experimental Neurology. 1945;4:217.

15. Burvill PW, Jackson JM, Smith WG. Psychiatric symptoms due to vitamin-B12 deficiency without anemia. Med Jour Australia. 1969; Aug 23:388-390.

16. Levitt AJ, Joffe RT. Vitamin B12 in psychotic depression. Brit Jour Psychiatry. 1988;153:266-267.

17. Phillips SL, Kahamer KP. An unusual presentation of vitamin-B12 deficiency (letter). Amer Jour Psychiatry. 1983;145;4:529.

18. Evans DL, Edelsohn GA, Golden RN. Organic psychosis without anemia or spinal cord symptoms in patients with vitamin-B12 deficiency. Amer Jour Psychiatry. 1983;140;2:218-221.

19. Elsborg L, Hansen T, Rafaelson OJ. Vitamin-B12 concentrations in psychiatric patients. Acta Psychiatrica Scandinavica. 1979;59:145-152.

20. Reading CM. X-linked dominant manic-depressive illness: Op. cit.

21. Reading CM. Latent pernicious anemia: A preliminary report. Med Jour Australia. 1975; (Jan. 25) 1:91-94.

22. Levitt AJ, Joffe RT. Vitamin B12 in psychotic depression. Brit Jour Psychiatry. 1988;153:266-267.

23. Lindenbaum J, Healton EB, Savage DG et al. Neuropsychiatric disorders. Op. cit.

24. Reading CM. Latent pernicious anemia (letter to the editor). Med Jour Australia. 1975; March 29:430-431.

25. Zucker DK, Livingston RL, Narka R, Clayton P. B12-deficiency and psychiatric disorders: Case-report and literature review. Biological Psychiatry. 1981;16;2:197-205.

26. Van Tiggelen CJM, Peperkamp JPC, TerToolen JFW. Assessment of vitamin-B12 status in CSF. Amer Jour Psychiatry. 1984;141;1:136-137.

27. Ellis FR, Nasser S. A pilot study of vitamin-B12 in the treatment of tiredness. British Jour Nutrition. 1973; April.

28. Lindenbaum J, Healton EB, Savage DG et al. Neuropsychiatric disorders. Op. cit.

29. Reading CM. X-linked dominant manic-depressive illness: Linkage with Xg blood-group, red-green colorblindness and vitamin-B12 deficiency. Orthomolecular Psychiatry. 1979;8;2:68-77.

30. Bland JS. Functional Medicine Update. 2004; Jan.

31. McCully KS. Homocysteine theory. Development and current status. Atherosclerosis Rev. 1983;11:157-246.

32. Wright JV. Treatment of childhood asthma with parenteral vitamin B12, gastric re-acidification, and attention to food allergy, magnesium and pyridoxine: Three case reports with background and an integrated hypothesis. J Nutr Med. 1990;1:277-282.

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