Vitamins & minerals

B vitamins

Vitamin C

The newborn brain may be particularly vulnerable to vitamin C deficiency, which has been found in rodent studies to lead to a marked decrease in the number of brain cells in the hippocampus. Although there is no clear evidence that vitamin C supplements on their own improve memory or brain function in adults, two large studies of older adults have found that taking both vitamin C and vitamin E supplements significantly reduced the risk of Alzheimer's. Other indications suggest the efficacy of these vitamins may depend on whether they are taken in through food or through supplements (food is better), and whether the individual has the "Alzheimer's gene" (better not to).

Vitamin D

Vitamin E

It's been proposed that vitamin E might help prevent Alzheimer's, because of the role that oxidative stress plays in the development of the disease. Vitamin E is an antioxidant. It has been found in cultured cell studies that vitamin E does help protect against the effects of oxidative stress, and results in significantly fewer neurons dying. At the level of the organism, results are not so clearcut. One study of older adults found those eating the most vitamin E-rich foods had a lower risk of developing Alzheimer's, provided they didn't have the 'Alzheimer's gene'. Supplements did not have the same effect. Another, larger, study found that those with high intakes of vitamins E and C were less likely to develop Alzheimer's, regardless of gene status. This was especially true for smokers.


Research indicates that choline is a crucial ingredient in a pregnant woman's diet, for brain development in the fetus. Among older adults, choline, particularly in conjunction with omega-3 fatty acids and uridine (not available from food), has been found to improve memory in those cognitively impaired. Top sources of choline are eggs, peanuts, and meat. Fish and soy are also good sources. A choline food database is available at:



Research with rats indicates that increasing magnesium levels in the brain improves learning and memory, apparently through its effects on synaptic density and plasticity. Unfortunately, traditional supplements have little effect on magnesium levels in the brain, but the researchers developed a new compound that was effective. Magnesium deficits are common in the population of industrialized countries, and increase with age. Good sources of magnesium are dark green leafy vegetables (such as spinach), some nuts (almonds and cashews are particularly good), beans, seeds and whole unrefined grains (especially buckwheat). See here for a list of magnesium-rich foods.


Zinc has been linked to cognitive and motor function in very young children and adults, and one small study has found zinc supplements improved cognition, especially attention, in adolescents, who are particularly at risk of zinc deficiency. Red meats, fish and grains are good sources of zinc.

See the article on Mempowered

A two-year study which involved metabolic testing of 50 people, suggests that Alzheimer's disease consists of three distinct subtypes, each one of which may need to be treated differently. The finding may help explain why it has been so hard to find effective treatments for the disease.

The subtypes are:

  • Inflammatory, in which markers such as C-reactive protein and serum albumin to globulin ratios are increased.
  • Non-inflammatory, in which these markers are not increased but other metabolic abnormalities (such as insulin resistance, hypovitaminosis D, and hyper-homocysteinemia) are present. This tends to affect slightly older individuals than the first subtype: 80s rather than 70s.
  • Cortical, which affects relatively young individuals (typically 50s- early 70s) and appears more widely distributed across the brain than the other subtypes, showing widespread cortical atrophy rather than marked hippocampal atrophy. It typically presents with language and number difficulties first, rather than memory loss. Typically, there is an impaired ability to hold onto a train of thought. It is often misdiagnosed, typically affects people without a family history of Alzheimer's, who do not have an Alzheimer's-related gene, and is associated with a significant zinc deficiency (Zinc is implicated in multiple Alzheimer's-related metabolic processes, such as insulin resistance, chronic inflammation, ADAM10 proteolytic activity, and hormonal signaling. Zinc deficiency is relatively common, and associated with increasing age.).

The cortical subtype appears to be fundamentally a different condition than the other two.

I note a study I reported on last year, that found different molecular structures of amyloid-beta fibrils in the brains of Alzheimer's patients with different clinical histories and degrees of brain damage. That was a very small study, indicative only. However, I do wonder if there's any connection between these two findings. At the least, I think this approach a promising one.

The idea that there are different types of Alzheimer's disease is of course consistent with the research showing a variety of genetic risk factors, and an earlier study indicating at least two pathways to Alzheimer's.

It's also worth noting that the present study built on an earlier study, which showed that a program of lifestyle, exercise and diet changes designed to improve the body's metabolism reversed cognitive decline within 3-6 months in nine out of 10 patients with early Alzheimer's disease or its precursors. Note that this was a very small pilot program, and needs a proper clinical trial. Nevertheless, it is certainly very interesting.

Bredesen, D.E. 2015. Metabolic profiling distinguishes three subtypes of Alzheimer's disease. AGING, 7 (8), 595-600. Full text at

Bredesen, D.E. 2014. Reversal of cognitive decline: A novel therapeutic program. AGING, Vol 6, No 9 , pp 707-717. Full text at

Like us, guinea pigs can’t make vitamin C, but must obtain it from their diet. This makes them a good model for examining the effects of vitamin C deficiency.

In a recent study looking specifically at the effects of prenatal vitamin C deficiency, 80 pregnant guinea pigs were fed a diet that was either high or low in vitamin C. Subsequently, 157 of the newborn pups were randomly allocated to either a low or high vitamin C diet (after weaning), creating four conditions: high/high (controls); high/low (postnatal depletion); low/high (postnatal repletion); low/low (pre/postnatal deficiency). Only males experienced the high/low condition (postnatal depletion).

Only the postnatal depletion group showed any effect on body weight; no group showed an effect on brain weight.

Nevertheless, although the brain as a whole grew normally, those who had experienced a prenatal vitamin C deficiency showed a significantly smaller hippocampus (about 10-15% smaller). This reduction was not reversed by later repletion.

This reduction appeared to be related to a significant reduction in the migration of new neurons into the dentate gyrus. There was no difference in the creation or survival of new neurons in the hippocampus.

This finding suggests that marginal deficiency in vitamin C during pregnancy (a not uncommon occurrence) may have long-term effects on offspring.

The study involved 104 healthy older adults (average age 87) participating in the Oregon Brain Aging Study. Analysis of the nutrient biomarkers in their blood revealed that those with diets high in omega 3 fatty acids and in vitamins C, D, E and the B vitamins had higher scores on cognitive tests than people with diets low in those nutrients, while those with diets high in trans fats were more likely to score more poorly on cognitive tests.

These were dose-dependent, with each standard deviation increase in the vitamin BCDE score ssociated with a 0.28 SD increase in global cognitive score, and each SD increase in the trans fat score associated with a 0.30 SD decrease in global cognitive score.

Trans fats are primarily found in packaged, fast, fried and frozen food, baked goods and margarine spreads.

Brain scans of 42 of the participants found that those with diets high in vitamins BCDE and omega 3 fatty acids were also less likely to have the brain shrinkage associated with Alzheimer's, while those with high trans fats were more likely to show such brain atrophy.

Those with higher omega-3 scores also had fewer white matter hyperintensities. However, this association became weaker once depression and hypertension were taken into account.

Overall, the participants had good nutritional status, but 7% were deficient in vitamin B12 (I’m surprised it’s so low, but bear in mind that these are already a select group, being healthy at such an advanced age) and 25% were deficient in vitamin D.

The nutrient biomarkers accounted for 17% of the variation in cognitive performance, while age, education, APOE genotype (presence or absence of the ‘Alzheimer’s gene’), depression and high blood pressure together accounted for 46%. Diet was more important for brain atrophy: here, the nutrient biomarkers accounted for 37% of the variation, while the other factors accounted for 40% (meaning that diet was nearly as important as all these other factors combined!).

The findings add to the growing evidence that diet has a significant role in determining whether or not, and when, you develop Alzheimer’s disease.

A study involving 676 children (7-9) in rural Nepal has found that those whose mothers received iron, folic acid and vitamin A supplementation during their pregnancies and for three months after the birth performed better on some measures of intellectual and motor functioning compared to offspring of mothers who received vitamin A alone. However, there was no significant benefit for those whose mothers received iron, folic acid and zinc (plus vitamin A), or multiple micronutrients.

A negative effect of adding zinc is consistent with other research indicating that zinc inhibits iron absorption. Interestingly, new “ground-breaking” research demonstrates further the complexity of iron’s effects on the body. The researcher argues that many neurodegenerative diseases (such as Alzheimer’s) are partly caused by poorly bound iron, and it is vital to consume nutrients which bind iron and prevent the production of the toxins it will otherwise produce.

Such nutrients include brightly-colored fruits (especially purple) and vegetables, and green tea.

It’s also argued that Vitamin C is only beneficial if iron is safely bound, and if it’s not, excess Vitamin C might be harmful.

Another study has come out showing that older adults with low levels of vitamin D are more likely to have cognitive problems. The six-year study followed 858 adults who were age 65 or older at the beginning of the study. Those who were severely deficient in vitamin D were 60% more likely to have substantial cognitive decline, and 31% more likely to have specific declines in executive function, although there was no association with attention. Vitamin D deficiency is common in older adults in the United States and Europe (levels estimated from 40% to 100%!), and has been implicated in a wide variety of physical disease.

A study involving 236 persons with multiple sclerosis has found that only 7% of those with secondary-progressive MS showed sufficient vitamin D in their blood, compared to 18.3% of patients with the less severe relapsing-remitting type, and that higher levels of vitamin D3 and its byproducts were associated with better scores on cognitive tests (especially reasoning and planning), and less brain atrophy and fewer brain lesions. Lower-than-normal vitamin D status is known to be associated with a higher risk of developing MS

The results were reported at the American Academy of Neurology's 62nd Annual Meeting in Toronto, April 10–17, 2010.

Seventh graders given 20 mg zinc, five days per week, for 10 to 12 weeks showed improvement in cognitive performance, responding more quickly and accurately on memory tasks and with more sustained attention, than classmates who received no additional zinc. Those who received only 10mg a day did not improve their performance. Previous studies have linked zinc nutrition to motor, cognitive and psychosocial function in very young children and adults, but this is the first study of its effect in adolescents. Adolescents are at particular risk of zinc deficiency, because they are undergoing rapid growth and often have poor eating habits. Red meats, fish and grains are good sources of zinc.

The findings were presented at Experimental Biology 2005, as part of the scientific sessions of the American Society of Nutritional Sciences.

A study of over 3,100 older men (49-71) from across Europe has found that men with higher levels of vitamin D performed consistently better in an attention and speed of processing task. There was no difference on visual memory tasks. Although previous studies have suggested low vitamin D levels may be associated with poorer cognitive performance, findings have been inconsistent. Vitamin D is primarily synthesised from sun exposure but is also found in certain foods such as oily fish.

A review described as “definitive” has concluded that there is ample biological evidence to suggest an important role for vitamin D in brain development and function, and that supplementation for groups chronically low in vitamin D is warranted. Vitamin D has long been known to promote healthy bones, but more recently has been found to have a much broader role — over 900 different genes are now known to be able to bind the vitamin D receptor. Evidence for vitamin D's involvement in brain function includes the wide distribution of vitamin D receptors throughout the brain, as well as its ability to affect proteins in the brain known to be directly involved in learning and memory and motor control. Because we receive most of our Vitamin D from sunlight (UV from the sun converts a biochemical in the skin to vitamin D), those with darker skin living in northern latitudes are particularly at risk of vitamin D deficiency. Nursing infants and the elderly are also particularly vulnerable. It has also argued that current recommendations set the recommended level of vitamin D too low. This review is the fourth in a series that critically evaluate scientific evidence linking deficiencies in micronutrients to brain function. Earlier reviews have looked at DHA, choline, and iron.

A chemical called methionine (an amino acid found in beta-amyloid) may be the source of the toxic free radicals produced by the amyloid-beta peptide. Recent studies have demonstrated that higher than normal doses of vitamin E may slow the advance of Alzheimer's in some people with late stages of the disease. The current study provides a possible explanation for this link. Vitamin E, an antioxidant, appears to work by destroying free radicals (oxidants) produced by amyloid.

The study was presented at the 2000 International Chemical Congress of Pacific Basin Societies.

Two studies have come out in favor of a diet rich in foods containing vitamin E to help protect against Alzheimer's disease. One study involved 815 Chicago residents age 65 and older with no initial symptoms of mental decline, who were questioned about their eating habits and followed for an average of about four years. When factors like age and education were taken into account, those eating the most vitamin E-rich foods had a lower risk of developing Alzheimer’s, provided they did not have the ApoE e4 allele. This was not true when vitamin E was taken as a supplement. Intake of vitamin C and beta carotene appeared protective, but not at a statistically significant level. The other study involved 5,395 people in the Netherlands age 55 and older who were followed for an average of six years. Those with high intakes of vitamins E and C were less likely to become afflicted with Alzheimer's, regardless of whether they had the gene variation. This association was most pronounced for current smokers, for whom beta carotene also seemed to be protective. A number of clinical trials are underway to further investigate these links.

Engelhart, M.J., Geerlings, M.I., Ruitenberg, A., van Swieten, J.C., Hofman, A., Witteman, J.C.M. & Breteler, M.M.B. 2002. Dietary Intake of Antioxidants and Risk of Alzheimer Disease. JAMA, 287, 3223-3229. Morris, M.C., Evans, D.A., Bienias, J.L., Tangney, C.C., Bennett, D.A., Aggarwal, N., Wilson, R.S. & Scherr, P.A. 2002. Dietary Intake of Antioxidant Nutrients and the Risk of Incident Alzheimer Disease in a Biracial Community Study. JAMA, 287, 3230-3237.

A theory that changes in fat metabolism in the membranes of nerve cells play a role in Alzheimer's has been supported in a recent study. The study found significantly higher levels of ceramide and cholesterol in the middle frontal gyrus of Alzheimer's patients. The researchers suggest that alterations in fats (especially cholesterol and ceramide) may contribute to a "neurodegenerative cascade" that destroys neurons in Alzheimer's, and that the accumulation of ceramide and cholesterol is triggered by the oxidative stress brought on by the presence of the toxic beta amyloid peptide. The study also suggests a reason for why antioxidants such as vitamin E might delay the onset of Alzheimer's: treatment with Vitamin E reduced the levels of ceramide and cholesterol, resulting in "a significant decrease in the number of neurons killed by the beta amyloid and oxidative stress.

Cutler, R.G., Kelly, J., Storie, K., Pedersen, W.A., Tammara, A., Hatanpaa, K., Troncoso, J.C. & Mattson, M.P. 2004. Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease. PNAS, 101, 2070-5.

A study involving 4,740 elderly (65 years or older) found the greatest reduction in both prevalence and incidence of Alzheimer's in those who used individual vitamin E and C supplements in combination, with or without an additional multivitamin. There was no significant benefit in using vitamin C alone, vitamin E alone, or vitamin C and multivitamins in combination.

Zandi, P.P., Anthony, J.C., Khachaturian, A.S., Stone, S.V., Gustafson, D., Tschanz, J.T., Norton, M.C., Welsh-Bohmer, K.A. & Breitner, J.C.S. 2004. Reduced Risk of Alzheimer Disease in Users of Antioxidant Vitamin Supplements: The Cache County Study. Archives of Neurology, 61, 82-88.

A guinea pig study has found that newborn guinea pigs subjected to moderate vitamin C deficiency had 30% fewer hippocampal neurons and markedly worse spatial memory than guinea pigs given a normal diet. For several reasons the neonatal brain is thought to be particularly vulnerable to even a slight lowering of the vitamin C level. Vitamin C deficiency is very common in some parts of the world, and even in wealthy nations occurs in an estimated 5-10% of the adult population.

A rat study has found that increased levels of magnesium in the brain improved many aspects of learning and memory in both young and old rats. Because it is difficult to boost brain magnesium levels with traditional oral supplements, the researchers developed a new magnesium compound, magnesium-L-threonate (MgT). The cognitive improvements were associated with an increase in synapses and improved synaptic plasticity. It’s important to note that the control rats had a normal diet which is widely accepted to contain a sufficient amount of magnesium; thus the observed effects were due to elevation of magnesium to levels higher than provided by a normal diet. It is also estimated that half the population of industrialized countries has a magnesium deficit, which increases with aging. See here for a list of magnesium-rich foods.