B Vitamins

B Vitamins are essential nutrients. We can't make them, our cells can't burn their fuel without them, the body needs them to put together and take apart some of the most important molecules it makes and destroys. To oversimplify just a little a bit: B vitamins are to your body's biochemistry what spark plugs are to your car's engine: they catalyze the reactions that keep things going.1 When there's plenty of fresh Bs you get better mileage, your cellular engines run smooth, last longer and make less noise.

In their role as co-factors B vitamins help the body make nerves, immune cells, glands and organs and help them talk to each other. B-depleted people can have low levels of neurotransmitters and all the other specialized molecules body organs need to stay in touch with each other and work as a team.

We can become B-depleted eating modern food. B vitamins are found in everything but most of them break down easily in heat and leach out in water. They're ground away when wheat or rice are refined and turned white. Some B vitamins are even destroyed by light or alkali environments. By the time our food is harvested, processed, packaged, distributed, stored, cooked and eaten some of the B content has been lost.

For years I've observed patient after patient improving when taking extra Bs. Maybe this is because we cook our food. Our ancestors got by without fire much longer than we've had it. Heat damages B vitamins so perhaps its cooking or the way we cook and eat our food that lowers our dietary intake of the vitamins B.2

Restarting B Supplementation

If you haven't taken B vitamins for awhile there's an excellent chance your cells have been running out-of-tune. In somewhat the same way as an out-of-tune car makes more smog B-deprived cells run inefficiently and make more waste. At the same time, the body's biochemical pathways for identifying, disarming and excreting that waste - which themselves require B vitamins to function - are also impaired. Toxins - inappropriate levels of biochemical reaction byproducts - build up in the body.

When catalytic Bs are resupplied and energy returns there's an excess of these molecules waiting to be disarmed and excreted. As the body sets about this work there are two steps involved. First, the body dumps waste - usually out of storage in fat tissue - into the bloodstream. Second, usually in the Liver, the molecules are disassembled and dumped into stool for eventual disposal.

Don't be put off by the following scenario. There's an easy way to avoid it.

But in detox if the first step (dumping waste into the blood) happens faster than the second step (washing treated waste out of the body) we get sick.3 Most commonly this appears as a cold or flu, but B-induced detox crises can take many different forms including headaches, skin rashes, nausea, burning urination or emotional upsets. The body's capacity for clearing the bloodstream is being overwhelmed by the avalanche of metabolic debris set in motion by resupplying the catalysts required to break it loose.

So when one hasn't had any B vitamins in awhile, start slow. Use a liquid B4 and at first take just 1-4 drops/day (less if aged, weak, or excessively pale.) Watch for "ceiling signs" - headaches, flu symptoms, skin rashes or other signs that the body has dumped more stored waste into the bloodstream than can be gracefully eliminated. If ceiling signs appear, stop the Bs for a few days. Take hot baths and sweat (unless one's over 50 or has a heart condition, in which case check with the doctor before sweating.) When the ceiling signs pass, start the Bs again at a slightly lower dose and stay there awhile.

Once the ceiling signs have eased, or if they never came in the first place, slowly increase the B vitamin dose by a few drops every 4 or 5 days. Slowly work one's way up to the manufacturer's recommended dose (listed on the bottle); usually 1 teaspoon or tablespoon per day. Once there, switch over to taking B capsules if desired. B-50's, which have 50 mg or mcg of each of the B vitamins, will usually do the job. You can find B-50 products at any decent health-food store and many pharmacies. I usually recommend my patients take them 5-6x/week (it may not be best not to take them every single day.)

A B-50 product will give you roughly 8-10 times the currently recommended Daily Value amount of each B vitamin. There's several good reasons to do this.

First, they're relatively non-toxic. Niacin and pyridoxine are the only ones requiring caution, and B-50 products don't have enough of these two to cause problems.

Second, the Daily Values are set in such a way as to avoid frank deficieny symptoms; they're not meant to represent optimal doses, just mimimal ones.

Next, circulation in certain critical body areas is sometimes impaired or reduced (the lumbar vertebral discs and certain areas of the brain and digestive system under emotionally stressed circumstances come to mind.) Taking generous amounts of Bs helps ensure that enough is transported into areas where circulation may be poor.

Excessive amounts of Bs tend to wash out in water fairly quickly, so the body uses what it needs and discards the rest.

Last, people vary widely in their ability to absorb and metabolize B vitamins; so taking extra is cheap insurance.

One of the reasons people's need for B vitamins can vary so widely (some folks need doses tens or hundreds of times more than others) is that if we're starved of them long enough, the body can lose its ability to absorb them once they're reintroduced into the diet. This was discovered in the mid 1930s, when researchers found that dogs kept on a starvation diet for some time later required up to ten times the amount of Bs considered adequate in order to prevent pellagra symptoms.5 Further studies done on Canadian soldiers kept on a starvation diet in a Japanese prisoner of war camp showed that, after release, those who ate normal diets suffered a wide range of physical and mental problems, while those who took very large doses of nutrients improved substantially and were able to live essentially normal lives.6

B vitamins are found in all foods, but they're only found all together in flesh or dairy products and nutritional yeast.

B Vitamins and the Mind

Thiamin (B1)

Thiamin is part of several coenzymes that pull fuel into and activate the Krebs cycle - the mitochondrial furnaces in every cell that burn carbs, fats and protein and produce energy. Lack of adequate mitochondrial activity produces beri-beri, a disease in which the hands and feet swell, burn and itch while the mind slowly fails (memory loss and confusion are common symptoms.) Thiamin deficiency first appeared in great numbers during the Industrial Revolution when the falling price of mechanically-refined flour made refined products more affordable. (Thiamin, like many other valuable nutrients, is found in the coating of the seed which is ground away to make white refined grains and grain flours.)

After 1878 when the invention of steel roller grinders made thiamin deficiency affordable to the masses, beri-beri became epidemic and a frenzy of scientific activity was launched to try to determine the cause. At one point everyone thought it "proven" that the disease was transmissible, and so scientists went looking for a microbial cause. It took an accident - a new caretaker for a flock of experimental pigeons with beri-beri changed their diet to brown rice when he wasn't supposed to - and an observant researcher who wasn't afraid to go against the tide - Christiaan Eijkman - to discover beri-beri's real cause: diets of milled, refined, polished white rice.

Humans have only 25-50% of the thiamin in their brains that other mammals have.7 Thiamin-dependent processes are impaired in the brains of patients with a number of diseases involving decaying neurons. It appears that oxidizers (free radicals, excess blood sugars) find thiamine delicious and are all too ready to use it up.8

Alcohol overconsumption can produce beri-beri but in a different way: alcohol attacks intestinal tissue in such a way that it loses its ability to absorb thiamin. The psychological syndrome that results is called Wernicke-Korsakoff syndrome, which is easy to miss as its symptoms (irritability and mental confusion) are so common.9

Low thiamine levels are found in the brains of people with frontal lobe degeneration leading to dementia.10 Other studies have shown thiamin deficiency to be associated with difficulty in thinking clearly, with this effect appearing most clearly in the elderly.11,12 Thiamin supplements have improved mood13 and reaction times in young women14 and Alzheimer's patients.15 Thiamin supports the action of acetylcholine, the neurotransmitter of memory and learning.16

Riboflavin (B2)

Riboflavin's main job is to help with the chains of reactions that metabolize amino acids, fats and carbs to make energy in the mitochondria. It's also involved in the creation of fatty acids. Studies have shown a relationship between riboflavin status and cognitive ability, especially in the elderly.17,18,19 Low blood (RBC) riboflavin has been associated with mood disorders.20 A classic sign of riboflavin deficiency is sore and tender areas around the mouth and tongue. Green leafy vegetables are among the richest sources of riboflavin, but more than half the B2 in food can be lost in cooking.21 Riboflavin is helpful in some cases of migraine.22

Niacin/nicotinic acid/niacinamide (B3)

There are three forms of niacin found in the body: niacin itself, nicotinic acid and niacinamide. This vitamin is crucial for metabolizing fat, carbohydrates and protein and for synthesizing fats and steroids.23 Lack of niacin causes pellagra, a disease that used to be epidemic in the southern U.S.24 and parts of Europe, particularly where corn was a dietary staple.25 Pellagra symptoms include red, roughened skin in areas exposed to the sun, digestive problems, and loss of ability to detect the position of one's limbs in space.

The range of affective and neurological symptoms possible with niacin deficiency is broad. Emotional instability appears along with hyperactivity, hypersensitivity, depression, fatigue and anxiety. Chronic headaches may present.26 Symptoms can become quite severe - severe depression, delusions of persecution, irritability and memory loss are sometimes seen.27,28

The similarities between the mental symptoms of pellagra and schizophrenia led to much research and controversy in the 1950s and 1960s on the use of niacin for schizophrenia. Some scientists thought that, in certain people, problems with the assimilation or metabolism of niacin might create madness and respond to doses of B3 high enough to overcome the processing problem.29,30,31 Studies done to replicate these findings had mixed results.32,33 The pro-niacin camp points out that just about all of these studies attempted niacin treatment in chronic schizophrenia, and they'd only claimed success in cases of recent onset.

Effective doses can vary tremendously from person to person while controlled trials prefer to use a small range or simply a single dose level. Enough vitamin C and other co-factors must also be available,34 another consideration not always addressed in the studies that have had negative results. The original researcher who reported consistent results, Abram Hoffer, claims to have successfully treated chronic schizophrenia with individually-designed matrices of nutrients to this day.35,36

Recent work suggests that niacin's relationship to schizophrenia may be mediated through NAD (nicotinamide-adenine dinucleotide), an important brain coenzyme that helps create the large amount of energy the brain needs; it also helps detoxifies alcohol.37,38 The body can make niacin from the amino acid tryptophan if enough vitamin B6 (pyridoxine) is present.39 Niacin's fat-metabolizing action helps build and maintain cell walls.40,41 It could also be that by sparing tryptophan42 niacin supplements leave more of that serotonin-producing amino acid available to calm the brain.

The brain is a very fatty organ, cell walls are made from fat - how resilient or porous those cell walls become have a lot to do with how the brain works and therefore how well we think and feel. Niacin is involved in the construction of the insulating myelin sheaths that keep neurons from short circuiting.43 Niacin has been shown to improve short-term memory.44 Niacin in combination with other B vitamins and minerals has shown some usefulness in attention-deficit disorders.45 It also helps reduce cholesterol46 although at lower doses the effect is gradual.47

Nicotinic acid can cause the release of histamine; this can be dangerous to people with stomach ulcers and asthma.48 Large doses of niacin can also cause liver toxicity.49 As usual, it's always best to start small and increase dose slowly.

However people who have been B3-deprived for long periods of time may need very large amounts of niacin to keep them free from symptoms once the niacin is resupplied to them - up to 60 times the normal amount!50 Interventions with aggressively pharmacological doses of vitamins like this should obvious be only attempted with medical supervision. Niacin at normal doses (DV=10 mg.) should pose no problem ... although again if one has not supplemented for years if ever it's always smart to start with very low doses and work one's way up.

Biotin

Biotin in the brain is concentrated in the hippocampus,51a brain region that controls both hearing52 and memory. Lack of the active forms of biotin cause clumsiness and deafness.53,54

Biotin is important for cell growth and fatty acid production, and like the other Bs for synthesis and the oxidation of proteins, carbohydrates and fats into energy. Biotin is also important for the assimilation of other B vitamins in the gut, where it's produced by the friendly bacteria that live there. Overuse of antibiotics can kill off those friendly bacteria causing biotin deficiency. Eating excessive egg whites will too - egg whites contain a protein called avidin, which binds with biotin and makes it unavailable. Biotin deficiencies have been associated with depression, hair loss and insomnia, but there hasn't been much research in these areas.

Pantothenic Acid

Pantothenic acid is another B vitamin involved in the metabolism of fats, proteins and carbs. It helps convert choline into acetycholine, the memory and attention neurotransmitter.55,56 The adrenals use pantothenic acid along with vitamin C and cholesterol to make glucocorticoids, a group of hormones that help us adapt to stress but which in excess can also slowly wear us out.57 Volunteers fed a diet low in pantothenic acid became emotionally unstable, irritable and depressed. Other studies found that both animals and humans could withstand more physical and emotional stress after large doses of pantothenic acid.58 Like other B vitamins, pantothenic acid is found in the coating of the wheat seed (the part that's ground off to make white flour.) At least half the B5 is lost when flour is ground and bleached white,59 although in some commercial "enriched" flours a certain amount of B5 is added back in.

Pyridoxine (B6)

Pyridoxine is required for a number of enzymes involved in metabolizing protein. One set of enzymes prepares amino acids to be burned for fuel, another set helps in the synthesis of GABA (calming, filtering), serotonin (relaxation), norepinephrine (focused awareness) and histamine (allergic inflammation.) It's also involved in the conversion of tryptophan to niacin.60 Because it's so important to protein utilization the amount we need varies according to how much protein there is in our diets.

Freezing destroys 15-70% of the B6 in vegetables, 50-90% is lost in the milling of grains, and a number of drugs, including birth control pills, can create B6 deficiencies.61,62

Pyridoxine is an important catalyst of the process that creates brain energy. It's been found useful in some cases of depression63,64 particularly pre-menstrual depression.65 It's also been attempted as a treatment for ADHD with some success.66,67,68 and even autism.69,70 Some nutrition-oriented physicians use it as a treatment of choice for allergies, especially allergies affecting behavior.71 Overdoses of pyridoxine have been shown to create numbness and tingling in the hands and feet.72,73 One would have to work at it to create an overdose (1 gm/day or total lifetime intake above 1,000 gms).74 Doses in substantial multiples of the RDA (2mg./day) are quite safe; doses above a few hundred milligrams/day should only be taken under a physician's supervision.

Folic Acid

DNA is made by stringing nucleic acids together. Folic acid is essential to the process by which nucleic acids are themselves made. As a result, folic acid is essential to the processes by which cells grow, divide and reproduce themselves.75

Folic acid becomes biopterin - part of the hydroxylases, enzymes that make serotonin (relaxation) from tryptophan and dopamine (motivation), adrenaline (fear/fight) and noradrenaline (attention) from tyrosine and phenylalanine.76 Folic acid therefore helps us relax, focus and complete our tasks. Folic acid has been shown to improve some resistant depressive patients' response to Prozac.77 Low folic acid levels have been found in depressed people in the U.S.78

Perhaps folic acid's most critical function is to convert the dangerous molecule homocysteine into harmless methionine. Homocysteine buildup has long been known to be associated with heart attacks. It damages the delicate cells that line our arteries by oxidizing them. These damaged bits of artery then attract and oxidize more fat flowing by in the blood while stimulating the growth of smooth muscle, plaque and repair-attempting collagens - all of which narrow arteries, reduce blood flow, and set the stage for blockage - heart attack and stroke.79

More recently, homocysteine accumulations are been connected to declines in cognitive function, including some cases of Alzheimer's disease,80,81,82 although not all researchers agree.83,84 It makes sense that clogging the arteries of the brain would impair blood supply and ultimately affect the brain's ability to process information. Homocysteine levels tend to be higher in diets rich in refined carbs and animal products . . . staples of modern diets.85

Cobalamin (B12)

While there's still debate about niacin's role in mental health86 there's less debate about cobalamin. It's required for DNA synthesis - growth, blood formation, fat and carb metabolism depend on B12, as does the nervous system. All B12 comes from animals - plants only have it when they're contaminated by bugs or bacteria. Adult vegetarians who avoid eggs and cheese can take years to show the effects of B12 deficiency because the body stores B12 for years. Folic acid in plentiful supply will also mask the effects of B12 deficiency for some time in grownups. Children will often show the effects of B12 deprivation within a few years because they haven't yet had time to store B12 in their tissues.87

B12 deficiency symptoms usually begin with numbness and tingling in the hands and feet, clumsiness and a loss of the ability to feel vibration.88 Eventually the central nervous system becomes involved and all mental processes are damaged: slowness, forgetfulness, aggressive or depressed behavior can progress to hallucinations, visions and other delusional symptoms.89,90

B12 is required, along with folic acid, to turn artery-rotting homocysteine into harmless methionine.91 While the relationship between homocysteine and behavior is still being defined, the relationship between B12 deficiency and psychological disorders is better-documented.92,93 B12 deficiency is associated with the various dementias we typically associate with very old people.94,95 Some elderly digestive tracts seem to develop difficulty assimilating B1296 and this mild preclinical deficiency can be involved in some cases of cognitive decline.

1 For the analogy to really hold, the spark plugs would also have to help the factory make the car in the first place by helping the workers read and understand the instructions, while going on to help them create what the instructions call for . . . but now it's not a simple, easy-to-digest analogy anymore.
2 As well as the heat in processing: dairy products, for example, are pasteurized to sterilize them. Pasteurization uses high heat to kill off microbes in milk.
3 There are schools of medical thought which consider the idea of accumulating and cleansing body toxins unscientific. Perhaps this is true; the wide variety of exposures and idiosyncratic responses to environmental and endogenous toxins makes it hard to pin down a precise definition for the word. As a clinical matter, though, a naturopathic physician gets to deal with toxicity every day. Helping patients clean their bodies produces consistently positive results, as long as certain precautions are taken (like making the treatment dosages highly individualized.) My own view is that more mainstream researchers, needing to use standardized dosages in their studies, frequently miss this cleansing effect of B vitamins, mistaking it for toxic or dangerous reactions to the B vitamins themselves. Of course this doesn't apply to pyridoxine (B6) and niacin (B3), both of which have well-documented toxic effects when taken in inadvisably large amounts.
4 Make sure you get a liquid B complex that contains all the B vitamins. Some health food store clerks, hearing that you want a liquid B, will assume that you want liquid B12, which is only one B vitamin. As always, read the small print.
5 Philpott, William et al. 2000. Brain Allergies. Los Angeles: Keats. 74.
6 Ibid.
7 Bettendorff, L. et al. 1996. Thiamin, thiamin phosphates, and their metabolizing enzymes in human brain. Journal of Neurochemistry. 66(1):250-258.
8 Gibson, G.E. 2002. Interactions of oxidative stress with thiamine homeostasis promote neurodegeneration. Neurochemistry International. 40(6):593-504.
9 Zubaran, C. et al. 1997. Wernicke-Korsakoff syndrome. Postgraduate Medical Journal. 73(855):27-31.
10 Bettendorff, L. et al. 1997. Low thiamine diphosphate levels in brains of patients with frontal lobe degeneration of the non-Alzheimer's type. Journal of Neurochemistry. 69(5):2005-2010.
11 Eininger, J. 1997. Thiamin and cognitive impairment. Journal of the American College of Nutrition. 16(1):96-98.
12 Bates, C.J. 1997. Nutrition and cognitive function in the elderly. American Journal of Clinical Nutrition. 66(2):449-450.
13 Benton, D. et al. 1995. Vitamin supplementation for 1 year improves mood. Neuropsychobiology. 32(2):98-105.
14 Benton, D. et al. 1997. Thiamine supplementation mood and cognitive functioning. Psychopharmacology (Berlin). 129(1):66-71
15 Meador, K. et al. 1993. Preliminary findings of high-dose thiamine in dementia of Alzheimer's type. Journal of Geriatric Psychiatry and Neurology. 6(4):222-229. 16 Ibid.
17 Goodwin, J.S. et al. 1983. Association between nutritional status and cognitive functioning in a healthy elderly population. Journal of the American Medical Association. 21:2917-2921.
18 Tucker, D.M. et al. 1990. Nutrition status and brain function in aging. American Journal of Clinical Nutrition. 52(1):93-102.
19 Heseker, H. et al. 1995. Interaction of vitamins with mental performance. Bibliotheca nutritio et dieta. 52:43-55.
20 Carney, M.W. 1982. Thiamine, riboflavin and pyridoxine deficiency in psychiatric in-patients. British Journal of Psychiatry. 141:271-272
21 Agte V., et al. 2002. Vitamin profile of cooked foods: how healthy is the practice of ready-to-eat foods? International Journal of Food Sciences and Nutrition. 53(3):197-208.
22 Bigal, M.E. et al. 2002. New migraine preventive options: an update with pathophysiological considerations. Revista do Hospital das Clinicas Sao Paulo. 57(6):293-298.
23 Kanarek. R. and Marks-Kaufman, R. 1991. Nutrition and Behavior. New York: Reinhold. 43-44.
24 Etheridge, E.W. 1972. The Butterfly Caste: A social History of Pellagra in the South. Westport, CT: Greenwood.
25 Ibid. 42-43.
26 Frostig, J.P., Spies, T.D. 1940. The initial syndrome of pellagra and associated deficiency diseases. American Journal of Medical Science. 199:268.
27 Rao, B.S.N. and C. Gopalan. 1984. Niacin, In Present Knowledge in Nutrition, ed. R.E. Olson et al. Washington DC: Nutrition Foundation. 319-331.
28 Robinson, C and Lawler, M. 1982. Normal and Therapeutic Nutrition. New York: MacMillan.
29 Hoffer, A.H, and Osmond, M.J. 1957. Treatment of schizophrenia with nicotinic acid and nicotinamide. Journal of Clinical and Experimental Psychopathology. 18:131-158.
30 Pauling, L. 1968. Orthomolecular psychiatry. Science. 160:265-271.
31 Denson, R. 1962. Nicotinamide in the treatment of schizophrenia. Diseases of the Nervous System. 23:167-172.
32 Ashby, W.R., Collings, G.H., Bassett, M. 1960. The effects of nicotinamide and placebo on the chronic schizophrenic. Journal of Medical Science. 106:1555-1559.
33 Greenbaum, C. 1970. An evaluation of niacinamide in the treatment of childhood schizophrenia. American Journal of Psychiatry. 127:129-132.
34 Pfeiffer, C et al. 1975. Copper, zinc, manganese, niacin and pyridoxine in the schizophrenias. Journal of Applied Nutrition. 27(2,3):1139.
35 Hoffer, A. 2002. Editorial: schizophrenic patients: a historical overview. Journal of Orthomolecular Medicine. 17(2):67.
36 Hoffer, A. 2002. Treating chronic schizophrenic patients. Journal of Orthomolecular Medicine. 17(1):25.
37 Philpott, Ibid. 75.
38 Gibson, G.E., Blass, B.P. 1985. Oxidative metabolism and acetylcholine synthesis during acetylpyridine treatment. Neurochemical Research 10(4):453-467.
39 Peters, J.C. 1991. Tryptophan nutrition and metabolism: an overview. Advances in Experimental Medicine and Biology. 294:345-358.
40 Fenton, W.S. et al. 2000. Essential fatty acids, lipid membrane abnormalities, and the diagnosis and treatment of schizophrenia. Biological Psychiatry. 47(1):8-21.
41 Basilio, C.M. 1987. The effect of nicotinic acid on the depressent action of ethanol and pentobarbital. Alcohol and Alcoholism. 22(4):395-400.
42 Since the body makes niacin from tryptophan, taking supplemental niacin will reduce the need for the body to do its own conversion. This leaves more tryptophan available for other purposes, like making serotonin, the calming, centering neurotransmitter.
43 Nakashima, Y., Suzue, R. 1984. Effect of 3-acetylpyridine on the content of myelin in the developing rat brain. Journal of Nutritional Science and Vitaminology (Tokyo). 30(5):411-451.
44 Loriaux, S.M. 1985. The effects of nicotinic acid and xanthinol nicotinate on human memory in different categories of age. A double blind study. Psychopharmacology (Berlin). 87(4):390-395.
45 Brenner, A. 1982. The effects of megadoses of selected B-complex vitamins on children with hyperkinesis: Controlled studies with long-term follow-up. Journal of Learning Disabilities. 15:258-264.
46 Carlson, L.A. 2005. Nicotinic acid: the broad-spectrum lipid drug. A 50th anniversary review. Journal of Internal Medicine. 258(2):94-114.
47 Denke, M.A. 2005. Diet, lifestyle and nonstatin trials: review of time to benefit. American Journal of Cardiology. 96(5A):3F-10F.
48 Lipton, M.A. et al. 1979. Vitamins, megavitamin therapy, and the nervous system. In Nutrition and the Brain. Wurtman and Wurtman, eds. New York: Raven Press. 183-264.
49 Alhadeff, L et al 1984. Toxic effects of water-soluble vitamins. Nutrition Reviews. 42:33-40.
50 Philpott. Ibid. 74.
51 Wang, H., Pevsner, J. 1999. Detection of endogenous biotin in various brain tissues: novel functions in the hippocampus and implications for use in avidin-biotin technology. Cell Tissue Research. 296(3):511-516.
52 Heller, A.J. et al. 2002. Localization of biotinidase in the brain: implications for its role in hearing loss in biotinidase deficiency. Hearing Research. 173(1-2);62-68.
53 Tsao, C.Y., Kien, C.L. 2002. Complete biotinidase deficiency presenting as reversible progressive ataxia and sensorineural deafness. Journal of Child Neurology. 17(2):146.
54 Wolf, B. et al. 1983. Phenotypic variation in biotinidase deficiency. Journal of Pediatrics. 103(2):233-237.
55 Rivera-Calimlim, L. et al. 1988. Effects of ethanol and pantothenic acid on brain acetylcholine synthesis. British Journal of Pharmacology. 95(1):77-82.
56 Spector, R. 1986. Pantothenic acid transport and metabolism in the central nervous system. American Journal of Physiology. 250(2Pt2):R292-297.
57 Fidanaza, A et al. 1981. Panthenol and glucocorticoids. Bollettino della Societa italiana di biologia sperimentale. 58(18):1869-1872.
58 Philpott, Ibid. 77.
59 Schroeder, H.A. 1971. Losses of vitamins and trace minerals resulting from processing and preservation of foods. American Journal of Clinical Nutrition. 24(5):562-573.
60 Kanarek, Ibid. 47.
61 McCormick, D. 1988. Vitamin B6. in Modern Nutrition in Health and Disease, 7th ed. Shils, M.E. and Young, V.R., eds. Philadelphia: Lean and Febiger: 376-382.
62 Robinson, C. H., Lawler, M.R. 1982. Normal and Therapeutic Nutrition. New York: MacMillan.
63 Bell, I.R. et al. 1991. B complex vitamin patterns in geriatric and young adult inpatients with major depression. Journal of the American Geriatric Society. 39(3):252-257.
64 Bell, I.R., et al. 1992. Low thyroxine levels in female psychiatric inpatients with riboflavin deficiency: implications for folate-dependent methylation. Acta psychiatrica Scandinavica. 85(5):360-363.
65 Bassler, K.H. 1988. Megavitamin therapy with pyridoxine. International Journal of Vitamin and Nutrition Research. 58:105-118.
66 Coleman, M. et al. 1979. A preliminary study of the effect of pyridoxine administration in a subgroup of hyperkinetic children: a double-blind crossover. Biological Psychiatry. 14:741-751.
67 Brenner, A. 1982. The effects of megadoses of selected B-complex vitamins on children with hyperkinesis: Controlled studies with long-term followup. Journal of Learning Disabilities. 15:258-264.
68 Bhagavan, H.N. et al. 1975. The effect of pyridoxine hydrochloride on blood serotonin and pyridoxal phosphate contents in hyperactive children. Pediatrics. 55(3):437-441.
69 Rimland, B. et al. 1978. The effect of high doses of vitamin B6 on autistic children: a double-blind crossover study. American Journal of Psychiatry. 135(4):472-475.
70 Which makes one wonder if it might be helpful in cases of Asperger's syndrome, the social awkwardness characteristic of certain high-functioning autistics.
71 Philpott, W. Ibid. 76
72 Albin, R.L. et al. 1987. Acute sensory neuropathy-neuronopathy from pyridoxine overdose. Neurology. 37:1729-1732.
73 Schaumburg, H.J. et al. 1983. Sensory neuropathy from pyridoxine abuse. New England Journal of Medicine. 309:445-448.
74 Bendich, A., Cohen, M. 1990. Vitamin B6 safety issues. Annals of the New York Academy of Science. 585:321-330.
75 Kanarek, R. Ibid. 52-53.
76 Braverman, Eric. 1987. The Healing Nutrients Within. New Canaan: Keats. 9.
77 Fava, M. et al. 1997. Folate, vitamin B12, and homocysteine in major depressive disorder. American Journal of Psychiatry. 154(3):426-428.
78 Morris, M.S. et al. 2003. Depression and folate status in the US Population. Psychotherapy and Psychosomatics. 72(2):80-87.
79 McCully, K.S. 1998. Homocysteine, folate, vitamin B6, and cardiovascular disease. Journal of the American Medical Association. 279(5):392-393.
80 Miller, A.L. 2003. The methionine-homocysteine cycle and its effects on cognitive diseases. Alternative Medicine Review. 8(1):7-19
81 Leblhuber, F. et al. 2000. Hyperhomocysteinemia in dementia. Journal of Neural Transmission.107(12):1469-1474.
82 Delport, R. 2000. Hyperhomocyst(e)inemia, related vitamins and dementias. The Journal of Nutrition, Health and Aging. 4(4):195-196.
83 Ravaglia, G. et al. 2000. Elevated plasma homocysteine levels in centenarians are not associated with cognitive impairment. Mechanisms of Ageing and Development.121(1-3):251-261.
84 Ravaglia, G. et al. 2000. Blood homocysteine and vitamin B levels are not associated with cognitive skills in healthy normally ageing subjects. Journal of Nutrition, Health and Aging. 4(4):218-222.
85 Berrino, F. 2002. Western diet and Alzheimer's disease. Epidemiologia e prevenzione. 26(3): 107-115.
86 Some would say the debate's long over, but get several in a room and disagreements about who lost and who won would break out promptly.
87 Kanarek, R. Ibid. 50-51.
88 Savage, D.G., Lindenbaum, J. 1995. Neurological complications of acquired cobalamin deficiency: clinical aspects. Bailliere's Clinical Haematology. (8)3:657-678.
89 Herbert V., Coleman N. 1988. Folic acid and vitamin B12. in Modern Nutrition in Health and Disease, 7th ed. Shils, M.E., Young, V.R., eds. Philadelphia: Lea and Febiger. 376-382. cited in Kanarek, R. Ibid.
90 Lindenbaum, J. et al. 1988. Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. New England Journal of Medicine. 318(26):1720-1728.
91 Bottiglieri, T. 1996. Folate, vitamin B-12, and neuropsychiatric disorders. Nutrition Reviews. 54(12):382-390.
92 Lindenbaum, J. et al. 1988. Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. New England Journal of Medicine. 318(26):1720-1728.
93 Kristensen, M.O. et al. 1993. Serum cobalamin and methylmalonic acid in Alzheimer's dementia. Acta Neurologica Scandinavica. 87(6):475-481.
94 Delport, R. Ibid.
95 Which isn't to say that relatively younger ones can't become demented themselves . . . especially with B vitamin deficiencies . . .
96 Carmel, R. 1997. Cobalamin, the stomach, and aging. American Journal of Clinical Nutrition. 66(4):750-759.