Vitamins & minerals - news reports

About these topic collections

I’ve been reporting on memory research for over ten years and these topic pages are simply collections of all the news items I have made on a particular topic. They do not pretend to be in any way exhaustive! I cover far too many areas within memory to come anywhere approaching that. What I aim to do is provide breadth, rather than depth. Outside my own area of cognitive psychology, it is difficult to know how much weight to give to any study (I urge you to read my blog post on what constitutes scientific evidence). That (among other reasons) is why my approach in my news reporting is based predominantly on replication and consistency. It's about the aggregate. So here is the aggregate of those reports I have at one point considered of sufficient interest to discuss. If you know of any research you would like to add to the collection, feel free to write about it in a comment (please provide a reference).

A more rigorous measurement of diet finds that dietary factors account for nearly as much brain shrinkage as age, education, APOE genotype, depression and high blood pressure combined.

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.

High daily doses of B-vitamins significantly slowed cognitive decline and brain atrophy in those with MCI, especially if they had high levels of homocysteine.

In a small study, 266 older adults with mild cognitive impairment (aged 70+) received a daily dose of 0.8 mg folic acid, 0.5 mg vitamin B12 and 20 mg vitamin B6 or a placebo for two years. Those treated with B vitamins had significantly lower levels of homocysteine at the end of the trial (high homocysteine is a known risk factor for age-related cognitive decline and dementia). Moreover, this was associated with a significantly slower rate of brain shrinkage.

However, while there were significant effects on homocysteine level, brain atrophy, and executive function, it wasn’t until results were separated on the basis of baseline homocysteine levels that we get really dramatic results.

It was the group with high homocysteine levels at the start of the study who really benefited from the high doses of B vitamins. For them, brain atrophy was cut by half, and there were clear benefits in episodic memory, semantic memory, and global cognitive function, not just executive function. Among those with high baseline homocysteine who received the placebo, significant cognitive decline occurred.

The level of B vitamins in the supplements was considerably greater than the recommended standard. However, caution must be taken in dosing yourself with supplements, because folic acid can have negative effects. Better to try and get your diet right first.

A longer and larger follow-up study is now planned, and hopefully that will tell us if such treatment can keep MCI developing into Alzheimer’s.

More evidence of the importance of adequate folate consumption for cognitive functioning at all ages.

Most research into the importance of folate and B12 levels has centered on seniors, and it does seem clear now that having adequate levels of these vitamins is important for maintaining cognitive functioning as you get older. Folic acid levels are of course also regarded as crucial when the brain is developing, which is why pregnant women are urged to take supplements, and why some countries fortify their bread with it. There is less research in the extensive ground between these two end-points.

A Swedish study involving 386 15-year-olds has now found that those in the top third of folic acid intake (more than 253 micrograms per day for girls and 335 for boys) performed significantly better on their school grades compared to those in the bottom third (less than 173 micrograms folic acid per day for girls and 227 for boys).

Interestingly, while homocysteine levels in the blood were initially significant, this association disappeared after other significant predictors (gender, smoking, and SES) were controlled for. Neither was a genotype linked to higher homocysteine levels (MTHFR 677 TT homozygosity) significantly related to academic achievement. Low folate and B12 levels are associated with higher homocysteine levels in the blood, and there is evidence that it is this increase in homocysteine that is the reason for the cognitive impairment seen in age-related cognitive decline. This finding, then, suggests that this is only one part of the story.

Sweden does not fortify flour with folic acid as the United States, Canada and Australia do. Folate is a B vitamin found particularly in citrus fruit, green leafy vegetables, whole-wheat bread, and dried beans and peas; however, they are often destroyed by cooking or processing.

The sum of school grades in 10 core subjects obtained in the final semester of compulsory 9 years of schooling was used as the measure of academic achievement

A long-running study adds to the evidence that high levels of homocysteine increase the risk of developing Alzheimer’s, and higher levels of vitamin B12 help to bring down these levels and reduce risk.

A seven-year study involving 271 Finns aged 65-79 has revealed that increases in the level of homocysteine in the blood were associated with increasing risk of developing Alzheimer’s (each micromolar increase in the concentration of homocysteine increased the risk of Alzheimer's by 16%), while increases in the level of vitamin B12 decreased the risk (each picomolar increase in concentration of B12 reduced risk by 2%). A larger study is needed to confirm this. 17 people (6%) developed Alzheimer’s over the course of the study.

Still, these results are consistent with a number of other studies showing greater risk with higher homocysteine and lower B12. High levels of vitamin B12 are known to lower homocysteine. However, studies directly assessing the effects of B12 supplements have had mixed results. Low levels of B12 are common in the elderly.

Vitamin B supplements markedly reduced brain atrophy in older adults with MCI, offering hope that they may be effective in delaying the development of Alzheimer’s.

A two-year study involving 271 older adults (70+) with mild cognitive impairment has found that the rate of brain atrophy in those taking folic acid (0.8 mg/d), vitamin B12 (0.5 mg/d) and vitamin B6 (20 mg/d), was significantly slower than in those taking a placebo, with those taking the supplements experiencing on average 30% less brain atrophy. Higher rates of atrophy were associated with lower cognitive performance. Moreover those who with the highest levels of homocysteine at the beginning of the trial benefited the most, with 50% less brain shrinkage. High levels of homocysteine are a risk factor for Alzheimer’s, and folate, B12 and B6 help regulate it.

The finding that atrophy can be slowed in those with MCI offers hope that the treatment could delay the development of Alzheimer’s, since MCI is a major risk factor for Alzheimer’s, and faster brain atrophy is typical of those who go on to develop Alzheimer’s.

A clinical trial has found improvement in verbal (but not general) memory in patients with mild Alzheimer's who drank a nutritional cocktail for 12 weeks.

A European trial involving 225 patients with mild Alzheimer's has found that those who drank Souvenaid (a cocktail of uridine, choline and the omega-3 fatty acid DHA, plus B vitamins, phosopholipids and antioxidants) for 12 weeks were more likely to improve their performance in a delayed verbal recall task. 40% of the Souvenaid group showed improved performance compared to 24% of the placebo group. Those with the mildest cases of Alzheimer’s showed the most improvement. There was no improvement on the more general ADAS-cog test. Three further clinical trials, one in the U.S. and two in Europe, are now underway.

Scheltens, P. et al. 2010. Efficacy of a medical food in mild Alzheimer's disease: A randomized, controlled trial. Alzheimer's & Dementia, 6 (1), 1-10.

A preliminary study suggests that a regime of high doses of folic acid, B12 and B6 reduces levels of homocysteine in people with mild to moderate Alzheimer’s. A larger study, recruiting 400 participants from all over the U.S., is to be undertaken to assess whether such a vitamin regime can slow the progression of Alzheimer's disease. In the meantime, it is not advised that people take high doses of these vitamins, as there are possible side-effects, including peripheral nerve damage.

[723] Bell, K., Sano M., Aisen P. S., Egelko S., Andrews H., Diaz-Arrastia R., et al. (2003).  A pilot study of vitamins to lower plasma homocysteine levels in Alzheimer disease. The American Journal of Geriatric Psychiatry: Official Journal of the American Association for Geriatric Psychiatry. 11(2), 246 - 249.

The nutrient choline is known to play a critical role in memory and brain function by positively affecting the brain's physical development through increased production of stem cells (the parents of brain cells). New research demonstrates that this occurs through the effect of choline on the expression of particular genes. The important finding is that diet during pregnancy turns on or turns off division of stem cells that form the memory areas of the brain. Developing babies get choline from their mothers during pregnancy and from breast milk after they are born. Other foods rich in choline include eggs, meat, peanuts and dietary supplements. Breast milk contains much more of this nutrient than many infant formulas. Choline is a vitamin-like substance that is sometimes treated like B vitamins and folic acid in dietary recommendations.
A choline food database is available at: www.nal.usda.gov/fnic/foodcomp.

Older news items (pre-2010) brought over from the old website

Vitamin B12 may protect the brain in old age

A five-year study of 107 older adults (61—87) has found that those who had higher vitamin B12 levels were six times less likely to experience brain shrinkage compared with those who had lower levels of the vitamin in their blood, even though none of them had vitamin B12 deficiency. Vitamin B12 is found in meat, fish and milk, and is often deficient in older people.

[516] Vogiatzoglou, A., Refsum H., Johnston C., Smith S. M., Bradley K. M., de Jager C. A., et al. (2008).  Vitamin B12 status and rate of brain volume loss in community-dwelling elderly. Neurology. 71(11), 826 - 832.

http://www.eurekalert.org/pub_releases/2008-09/aaon-vbm090208.php

B-vitamin deficiency may cause vascular cognitive impairment

A new mouse study helps clarify the association between homocysteine, folate & B12, and cognitive impairment. The study found that mice fed a diet deficient in folate and vitamins B12 and B6 demonstrated significant deficits in spatial learning and memory compared with normal mice, developed plasma homocysteine concentrations that were seven-fold higher, and showed smaller capillary length and density in blood vessels in the hippocampus. Homocysteine is produced by the breakdown of a dietary protein called methionine; B-vitamins are required to convert homocysteine back to methionine. A third group of mice were fed a diet enriched with methionine. These mice showed similar, but less pronounced effects. The findings indicate that increased levels of homocysteine, produced by low intake of folate and B vitamins, impairs cognition through microvascular changes.

[1025] Troen, A. M., Shea-Budgell M., Shukitt-Hale B., Smith D. E., Selhub J., & Rosenberg I. H. (2008).  B-vitamin deficiency causes hyperhomocysteinemia and vascular cognitive impairment in mice. Proceedings of the National Academy of Sciences. 105(34), 12474 - 12479.

Full text is available at http://www.pnas.org/content/105/34/12474.abstract
http://www.physorg.com/news139574626.html

How food affects the brain

I’ve reported on quite a lot of studies finding beneficial effects of one food or another on the brain. Now a researcher has analyzed more than 160 studies about food's effect on the brain, and here’s the bottom line. He comes out for omega-3 fatty acids, as both improving synaptic plasticity and the expression of several molecules proteins to learning and memory, as well as protecting against attention-deficit disorder, dyslexia, dementia, depression, bipolar disorder and schizophrenia. He suggests it’s better to get it from food than supplements (which is always recommended). Salmon, walnuts and kiwi fruit are all good sources. They’re still working out which fatty acids are most important, but one is definitely docosahexaenoic acid, or DHA — which like vitamin C we’re not good at making for ourselves; we have to ingest it. He also concludes that diets high in trans fats and saturated fats are bad for cognition.
Studies also support the need for folic acid (found in spinach, orange juice and yeast), which is essential for brain function, and appears to reduce age-related cognitive decline and dementia. And BDNF, important for learning and memory as well as metabolic regulation (so there’s a connection there with obesity), is helped by omega-3 fatty acids and the curry spice curcumin, and also, it seems, smaller food portions.

[1293] Gómez-Pinilla, F. (2008).  Brain foods: the effects of nutrients on brain function. Nat Rev Neurosci. 9(7), 568 - 578.

Full text is available online at www.nature.com/nrn/journal/v9/n7/abs/nrn2421.html
http://www.eurekalert.org/pub_releases/2008-07/uoc--slh070908.php

Vitamin B12, folate, and cognitive function

Confirming earlier studies, a large epidemiological study has found that older people with normal vitamin B12 status and high levels of folate had higher scores on a test of cognitive function. The study clarifies some inconsistencies in earlier research by disentangling the interaction between these factors. It appears seniors with normal levels of vitamin B12 perform better if folate level is high, but when vitamin B12 is low, high levels of folate are associated with poor cognitive performance, as well as a greater probability of anemia. There are also indications that the combination might be a factor in some other diseases.

[1443] Morris, M. S., Jacques P. F., Rosenberg I. H., & Selhub J. (2007).  Folate and vitamin B-12 status in relation to anemia, macrocytosis, and cognitive impairment in older Americans in the age of folic acid fortification. Am J Clin Nutr. 85(1), 193 - 200.

http://www.eurekalert.org/pub_releases/2007-02/tu-fab020907.php

Folic acid supplementation may improve cognitive performance

A study involving 818 older adults with raised homocysteine levels and normal vitamin B12 levels found that those given daily folic acid supplements (800 micrograms) for 3 years had lower homocysteine levels and improved cognitive performance compared to those given a placebo.

[443] Durga, J., van Boxtel M. P. J., Schouten E. G., Kok F. J., Jolles J., Katan M. B., et al. (2007).  Effect of 3-year folic acid supplementation on cognitive function in older adults in the FACIT trial: a randomised, double blind, controlled trial. Lancet. 369(9557), 208 - 216.

http://www.eurekalert.org/pub_releases/2007-01/l-fas011707.php

More evidence for value of folate for aging brains

Confirming a growing body of evidence, a study of 50-85 year old Boston-area men (members of the ongoing Normative Aging Study) found that men who obtained more folate in their diets showed significantly less of a decline in verbal fluency skills over the course of three years than did men with lower dietary folate intake. High folate levels also appeared protective against declines in spatial copying. The effects of folate were independent of its impact on homocysteine, which turned out to be more strongly associated with tests of memory. Folate is a B vitamin found particularly in leafy green vegetables and citrus fruit.

[888] Tucker, K. L., Qiao N., Scott T., Rosenberg I., & Spiro A. (2005).  High homocysteine and low B vitamins predict cognitive decline in aging men: the Veterans Affairs Normative Aging Study. Am J Clin Nutr. 82(3), 627 - 635.

http://www.eurekalert.org/pub_releases/2005-09/tu-lgv092205.php

Preventing high levels of homocysteine may protect against age-related cognitive impairment

Previous studies have found a link between high levels of homocysteine and poor cognitive performance, but it has been difficult to work out just what the association is, in view of confounding factors such as cardiovascular risk factors and levels of folate, B12, and B6, all of which play a role in high levels of homocysteine. A new analysis has disentangled these factors, and has found that, in people over 60 (but not those under 60), higher levels of homocysteine are independently associated with lower levels of cognitive performance. Similarly, higher levels of vitamin B12 are associated with higher levels of cognitive performance. The researchers suggest vitamins B12, B6, and folate taken before 60 could help protect against later cognitive impairment.

[839] Wolf, P. A., Elias M. F., Sullivan L. M., D'Agostino R. B., Elias P. K., Jacques P. F., et al. (2005).  Homocysteine and Cognitive Performance in the Framingham Offspring Study: Age Is Important. Am. J. Epidemiol.. 162(7), 644 - 653.

http://www.eurekalert.org/pub_releases/2005-09/bu-atp092705.php

Folates more effective in limiting Alzheimer's disease risk than antioxidants, other nutrients

Analysis of data from the Baltimore Longitudinal Study of Aging has revealed that those with higher intake of folates, vitamin E and vitamin B6 had a lower risk of developing Alzheimer’s. When the three vitamins were analyzed together, only folates were associated with a significantly decreased risk. Those who had at least 400mcg of folates a day (the recommended daily allowance) had a 55% reduction in risk of developing Alzheimer’s. Unfortunately, most people who reached that level did so by taking supplements, suggesting the difficulty of doing so through diet alone. Folates are abundant in foods such as liver, kidneys, yeast, fruits (like bananas and oranges), leafy vegetables, whole-wheat bread, lima beans, eggs and milk; however, they are often destroyed by cooking or processing. No association was found between vitamin C, carotenoids (such as beta-carotene) or vitamin B-12 intake and decreased Alzheimer's risk.

Corrada, M.M., Kawas,C.H., Hallfrisch,J., Muller,D. & Brookmeyer,R. Reduced risk of Alzheimer’s disease with high folate intake: The Baltimore Longitudinal Study of Aging. Alzheimer’s & Dementia, 1 (1), 11-18.

http://www.eurekalert.org/pub_releases/2005-08/uoc--fme081105.php

Moderately high homocysteine linked to Alzheimer’s risk

A study of 83 Alzheimer’s patients, 78 patients with vascular dementia, 64 stroke patients, and 71 healthy controls, found that elevated levels of homocysteine were associated with a more than five-fold increase in the risk for stroke, a nearly five-fold risk for vascualr dementia, and almost triple the risk for Alzheimer's disease. High blood levels of homocysteine have been found to be associated with an increased heart attack risk in several studies. High levels of homocysteine have been found to be associated with deficiencies in vitamin B12 and folate, and also with smoking.

McIlroy, S.P., Dynan, K.B., Lawson, J.T., Patterson, C.C. & Passmore, A.P. 2002. Moderately Elevated Plasma Homocysteine, Methylenetetrahydrofolate Reductase Genotype, and Risk for Stroke, Vascular Dementia, and Alzheimer Disease in Northern Ireland. Stroke, 33, 2351 – 2356.

http://www.eurekalert.org/pub_releases/2002-10/aha-mhh092602.php

Study links high levels of homocysteine, and folic acid or vitamin B-12 deficiencies to cognitive decline

Current estimates suggest that more than one million elderly in Europe and about 750,000 elderly in North America become cognitively impaired each year. Recent research suggests that deficiencies of folate or vitamin B-12 and elevations of plasma homocysteine (tHcy) may be partly responsible. A British study of 331 participants in a longitudinal survey found significant negative effects on cognition in the elderly subjects who had deficiencies of folic acid or vitamin B-12 and elevated tHcy. In the older group (aged 76-78), increased levels of tHcy correlated both with lower serum folate and vitamin B-12 concentrations and with lower cognitive test scores. In the younger group (aged 61-63),higher folate concentrations correlated with higher scores on one of the assessment tests, but otherwise no effects of B vitamins or tHcy were apparent.
Green leafy vegetables, citrus fruits and juices, whole wheat bread and dry beans are good sources of folate.

[899] Duthie, S. J., Whalley L. J., Collins A. R., Leaper S., Berger K., & Deary I. J. (2002).  Homocysteine, B vitamin status, and cognitive function in the elderly. Am J Clin Nutr. 75(5), 908 - 913.

Smith, A.D. 2002. Homocysteine, B vitamins and cognitive deficit in the elderly. American Journal of Clinical Nutrition, 75,785-6.

http://www.eurekalert.org/pub_releases/2002-04/ajoc-nsa041902.php

Folic acid possibly a key factor in preventing Alzheimer's disease

Experiments with mice bred with mutant genes that cause Alzheimer's disease found that those mice fed on a diet deficient in folate had fewer neurons in the hippocampus ( a brain region critical for learning and memory that is destroyed as plaques accumulate during Alzheimer’s disease), and elevated levels of homocysteine. Researchers suspect that increased levels of homocysteine in the brain caused damage to the DNA of nerve cells in the hippocampus. In the mice fed an adequate amount of folate, nerve cells in this brain region were able to repair the damage. But in those mice fed a folate-deficient diet, nerve cells were unable to repair this damage. A human study is being planned.
Green leafy vegetables, citrus fruits and juices, whole wheat bread and dry beans are good sources of folate. In the U.S., since 1998, the Food and Drug Administration has required the addition of folic acid to enriched breads, cereals, flours, corn meals, pastas, rice, and other grain products.

Kruman, I.I., Kumaravel, T.S., Lohani, A., Pedersen, W.A., Cutler, R.G., Kruman, Y., Haughey, N., Lee, J., Evans, M. & Mattson, M.P. 2002. Folic Acid Deficiency and Homocysteine Impair DNA Repair in Hippocampal Neurons and Sensitize Them to Amyloid Toxicity in Experimental Models of Alzheimer's Disease. Journal of Neuroscience, 22, 1752-1762.

http://www.eurekalert.org/pub_releases/2002-03/nioa-fap030102.php

High homocysteine levels may double Alzheimer's risk

Findings from the long-running Framingham study found people with elevated levels of homocysteine in the blood had nearly double the risk of developing Alzheimer’s disease (AD). This study is the first to tie homocysteine levels measured several years before with later diagnosis of AD and other dementias, and provides the most powerful evidence yet of the link between high homocysteine levels and AD.

Seshadri, S., Beiser, A., Selhub, J., Jacques, P.F., Rosenberg, I.H., D'Agostino, R.B., Wilson, P.W.F. & Wolf, P.A. 2002. Plasma homocysteine as a risk factor for dementia and Alzheimer's disease. The New England Journal of Medicine, 346, 476-483.

http://www.eurekalert.org/pub_releases/2002-02/nioa-hhl021202.php

Research ties vitamin B12 and folate deficiencies with Alzheimer's disease

People with low levels of B12 or folate may have a higher risk of developing Alzheimer's disease. A 3-year Swedish study of 370 people 75-years-old and older found that more than half (46 out of 78) of those diagnosed with dementia during the timeframe of the study had both low levels of vitamin B12 or folate and Alzheimer's type dementia. Low vitamin B12 and folate levels have long been observed in elderly people, and it has been theorized that this vitamin deficiency might be tied to neurological or psychiatric disorders. This study breaks new ground by connecting these deficiencies with Alzheimer's disease.
Vitamins B12 and folate (a form of water-soluble vitamin B) are found in common foods. Vitamin B12 is naturally found in animal foods including fish, milk and milk products, eggs, meat, and poultry. Leafy greens such as spinach and turnip greens, dry beans and peas, fortified cereals and grain products, and some fruits and vegetables are rich food sources of folate.

[2416] Wang, H. - X., Wahlin Å., Basun H., Fastbom J., Winblad B., & Fratiglioni L. (2001).  Vitamin B12 and folate in relation to the development of Alzheimer’s disease. Neurology. 56(9), 1188 - 1194.

http://www.eurekalert.org/pub_releases/2001-05/AAoN-RtvB-0705101.php

High homocysteine levels are associated with decreased memory capability after age 60

Recent studies have linked Alzheimer disease and dementia after multiple strokes to extremely high serum homocysteine concentrations. A survey of 1299 men and women aged 60 and over, none of who had previously had a stroke, found an independent relationship between very high homocysteine levels and poor performance on cognitive tests. The folate status of the participants was checked as folate has been shown to significantly modify homocysteine levels. Story recall was worse among subjects with a combination of low folate and high homocysteine than in those whose homocysteine levels were normal or low. Homocysteine levels increased with age and were accompanied by a comparable decline in folate status. The researchers found independent associations between the highest levels of homocysteine and poorer recall. Among subjects with the highest level of homocysteine, the odds of passing a word delayed-recall test were identical whether their folate status was high or low.

[2415] Morris, M. S., Jacques P. F., Rosenberg I. H., & Selhub J. (2001).  Hyperhomocysteinemia associated with poor recall in the third National Health and Nutrition Examination Survey. The American Journal of Clinical Nutrition. 73(5), 927 - 933.

http://www.eurekalert.org/pub_releases/2001-04/AJoC-Hhla-2504101.php

Iron

Iron-enriched baby formula improves cognitive development when infants have low iron levels, but harms development when iron levels are already high. Teenage iron levels are linked to white matter integrity in adulthood.

Iron deficiency is the world's single most common nutrient deficiency, and a well-known cause of impaired cognitive, language, and motor development. Many countries therefore routinely supplement infant foods with iron. However, a new study suggests that, while there is no doubt that such fortification has helped reduce iron deficiency, it may be that there is an optimal level of iron for infant development.

In 1992-94, 835 healthy, full-term infants living in urban areas in Chile, took part in a randomized trial to receive iron-fortified formula from 6 months of age to 12 months. A follow-up study has now assessed the cognitive functioning of 473 of these children at 10 years of age. Tests measured IQ, spatial memory, arithmetic achievement, visual-motor integration, visual perception and motor functioning.

Those who had received iron-fortified formula scored significantly lower than the non-fortified group on the spatial memory and visual-motor integration tests. Moreover, their performance on the other tests also tended to be worse, although these didn’t reach statistical significance.

There was no difference in iron level between these two groups (at age 10), and only one child had iron-deficiency anemia.

The crucial point, it seems, lies in the extent to which the infants needed additional iron. Children who had high iron levels at 6 months (5.5%, i.e. 26 infants) had lower scores at 10 years if they had received the iron-fortified formula, but those with low 6-month iron levels (18.4%; 87 infants) had higher scores at 10 years.

Further research is needed to confirm these findings, but the findings are not inconsistent with the idea that iron overload promotes neurodegenerative diseases.

In another longitudinal study, brain scans have revealed that teenage iron levels are associated with white matter fiber integrity.

The study first measured iron levels in 615 adolescent twins and siblings, and then scanned their brains when they were in their early twenties. Myelin (white matter) contains a lot of iron, so the strong correlation between teenage iron level and white matter integrity in young adulthood is not unexpected.

The correlation was stronger between identical twins that non-identical twins, suggesting a genetic contribution. Again, not unexpected — the transport of iron around the body is affected by several genes. One particular gene variant, in a gene that governs cellular absorption of transferrin-bound iron, was associated with both high iron levels and improved white matter integrity. This gene variant is found in about 12-15% of Caucasians.

The vital missing bit of information (because it wasn’t investigated) is whether this gene variant is associated with better cognitive performance. Further research will hopefully also investigate whether, while it might be better to have this variant earlier in life, it is detrimental in old age, given the suggestions that iron accumulation contributes to some neurodegenerative disorders (including Alzheimer’s).

New findings help explain why too much copper and iron are bad for your brain, and why curry is good for it.

A new study finds out why curcumin might help protect against dementia, and links two factors associated with Alzheimer’s and Parkinson’s diseases: DNA damage by reactive oxygen species (ROS), and excessive levels of copper and iron in parts of the brain. It turns out that high levels of copper or iron help generate large numbers of ROS and interfere with DNA repair.

While small amounts of iron and copper are vital, these are normally bound by proteins. However, when there’s too much, it can overwhelm the proteins and the result is "free" iron or copper ions circulating in the blood, able to initiate chemical reactions that produce reactive oxygen species. Moreover, the free copper and iron also interferes with the activity of two enzymes that repair DNA, NEIL1 and NEIL2.

However, the curry spice curcumin binds to iron and copper and was extremely effective in protecting the NEIL enzymes from the metals.

Hegde, M.L., Hegde, P.M. , Rao, K.S.J. & Mitra, S. 2011. Oxidative Genome Damage and Its Repair in Neurodegenerative Diseases: Function of Transition Metals as a Double-Edged Sword. Journal of Alzheimer's Disease , 25 (1), 183-198.

A study and a recent review suggest that while iron is important for brain health and development, whether it’s beneficial or harmful depends on the other nutrients consumed with it.

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.

Older news items (pre-2010) brought over from the old website

Iron supplements might harm infants who have enough

U.S. infant formulas typically come fortified with 12 mg/L of iron to prevent iron-deficiency anemia, although Europe generally uses a lower amount. A study of 494 Chilean children has now showed that those who received iron fortified formula in infancy at the 12 mg level used in the U.S. lagged behind those who received low-iron formula in cognitive and visual-motor development by age 10 years. While most children who received the higher level formula did not show lower scores, the 5% with the highest hemoglobin levels at 6 months showed the poorest outcome. Adversely affected children scored 11 points lower in IQ and 12 points lower in visual-motor integration. This suggests that those who are not deficient in iron are adversely affected by giving them too much. It seems likely that more than 5% of U.S. infants will have high hemoglobin levels. More research is needed to confirm this finding.

Castillo, M. & Smith, J.B. 2008. Poorer developmental outcome at 10 years with 12 mg/L iron-fortified formula in infancy. Paper presented May 5 at the Pediatric Academic Societies annual meeting in Honolulu.

http://www.eurekalert.org/pub_releases/2008-05/uom-ism043008.php

Iron-deficient infants have lower cognitive scores at 19, especially in lower socioeconomic levels

Another study has come out finding that teenagers who were iron-deficient as infants continue to lag behind their peers in cognitive test scores, with a wider gap for children at lower socioeconomic levels. The study of 185 children from an urban area in Costa Rica, found that among children from middle-class families, initial scores on cognitive tests were eight points apart, 101.2 for those with iron deficiency and 109.3 for those with sufficient iron levels, and this gap remained at eight or nine points through 19 years. However, for those in lower socio-economic classes, initial scores that were ten points apart (93.1 for iron-deficient infants and 102.8 for those with normal iron levels) had widened by 19 years to 25 points (70.4 vs. 95.3). The finding points to the snowball effect of early failure.

[1145] Lozoff, B., Jimenez E., & Smith J. B. (2006).  Double Burden of Iron Deficiency in Infancy and Low Socioeconomic Status: A Longitudinal Analysis of Cognitive Test Scores to Age 19 Years. Arch Pediatr Adolesc Med. 160(11), 1108 - 1113.

http://www.eurekalert.org/pub_releases/2006-11/jaaj-idi110206.php

Impact of iron deficiency in infancy continues into adolescence

A new study has found that teens who suffered iron deficiency as infants are likely to score lower on cognitive and motor tests, even if that iron deficiency was identified and treated in infancy. The study followed 191 children. Those who were diagnosed with severe, chronic iron deficiency when they were 12-23 months old and were treated with iron supplements, lagged behind their peers in both motor and mental measures. The difference, moreover, actually increased over time. The iron-deficient infants scored about six points lower on cognitive tests at age 1-2 years, and 11 points lower at age 15-18 years. The gap was even more pronounced for children of families with low socioeconomic status, lower stimulation in the home or mothers lower in IQ. For children with good iron status, family conditions did not seem to affect their cognitive test scores. The researcher stressed that the children were not generally malnourished. Moreover, it must be emphasized that these children received treatment for their iron deficiency, yet still showed continuing ill effects, pointing to the need to prevent the deficiency occurring in the first place.

Lozoff, B. 2004. Longitudinal Analysis of Cognitive and Motor Effects of Iron Deficiency in Infancy. Presented at the Pediatric Academic Societies' annual meeting in San Francisco May 3.

http://www.eurekalert.org/pub_releases/2004-05/uom-iis050404.htm

American Academy of Pediatrics information on iron intake for infants: http://aappolicy.aappublications.org/cgi/content/full/pediatrics;104/1/119

Even moderate iron deficiency affects cognitive performance

A new study involving 149 young women (aged 18 to 35, average age 21), has found that iron supplementation significantly improved attention, short-term and long-term memory, and performance on cognitive tasks in those who were deficient in iron, even if not classified as anemic. On the baseline test, women who were iron deficient but not anemic completed the tasks in the same amount of time as iron sufficient women of the same age, but they performed significantly worse. Women who were anemic both performed significantly worse and took longer, with length of time increasing with degree of anemia. However, 16 weeks of iron supplementation markedly improved both scores and time to complete the task.
While iron deficiency was once presumed to exert most of its deleterious effects only if it had reached the level of anemia, it has more recently become recognized that many organs show negative changes in functioning before there is any drop in iron hemoglobin concentration. Iron deficiency is thought to occur in 9 – 11% of women of reproductive age and 25% of pregnant women. In non-industrialized countries, the prevalence of anemia is over 40% in non-pregnant women and over 50% for pregnant women and children aged five to 14.

Murray-Kolb, L., Beard, J. & Whitfield, K. 2004. presented at Experimental Biology 2004, in the American Society of Nutritional Sciences' scientific program.

http://www.eurekalert.org/pub_releases/2004-04/foas-mid040404.php

U.N. prescribes nutrient-fortified foods

A new U.N. survey says the brainpower of many developing countries has diminished because of a shortage of the right vitamins. To fight the problem, the United Nations is prescribing artificially fortified foods: soy sauce laced with zinc, "super salt" spiked with iron, cooking oil fortified with vitamin A. The report claimed a lack of iron lowered children's IQs by an average five to seven points, while a deficiency in iodine cuts it 13 more points. The report was produced by the Micronutrient Initiative and the United Nations Children's Fund.
http://www.micronutrient.org/

Iron deficiency may affect maths achievement in children and teens

A U.S. national study of 5,398 children aged 6 to 16 found iron deficiency in 3% of the children overall, and 8.7% of girls aged 12 to 16 (7% without anemia). Average math scores for iron-deficient children with or without anemia were about six points lower than those with normal iron levels. Among adolescent girls, the difference in scores was more than eight points. Previous research has linked iron-deficiency anemia with lower developmental test scores in young children, but there is less information on older children and on iron deficiency without anemia. It is suggested that this finding may help explain why the female superiority in maths at younger ages reverses itself in adolescence.

Halterman, J.S., Kaczorowski, J.M., Aligne, C.A., Auinger, P. & Szilagyi, P.G. 2001. Iron Deficiency and Cognitive Achievement Among School-Aged Children and Adolescents in the United States. Pediatrics, 107 (6), 1381-1386.

http://www.pediatrics.org/cgi/content/abstract/107/6/1381

Anemia linked to impaired thinking in older adults

For older adults, anemia has long been linked to fatigue, muscle weakness and other physical ailments. But a new study suggests it may also be an independent risk factor for executive-function impairment. The study examined 364 women between 70 and 80 years old, of whom some 10% had mild anemia. Those with anemia were four to five times more likely to perform worst on the executive function tests.

[708] Chaves, P. H. M., Carlson M. C., Ferrucci L., Guralnik J. M., Semba R., & Fried L. P. (2006).  Association Between Mild Anemia and Executive Function Impairment in Community-Dwelling Older Women: The Women's Health and Aging Study II. Journal of the American Geriatrics Society. 54(9), 1429 - 1435.

http://www.eurekalert.org/pub_releases/2006-09/jhmi-aab091306.php

Other vitamins & minerals

A guinea pig study demonstrates that low levels of vitamin C during pregnancy have long-lasting effects on the child's hippocampus.

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.

A more rigorous measurement of diet finds that dietary factors account for nearly as much brain shrinkage as age, education, APOE genotype, depression and high blood pressure combined.

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 and a recent review suggest that while iron is important for brain health and development, whether it’s beneficial or harmful depends on the other nutrients consumed with it.

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 shows that older adults with low levels of vitamin D have higher levels of cognitive decline, particularly in executive function (but not attention).

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 multiple sclerosis sufferers has found very high rates of vitamin D deficiency, 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.

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.

[1407] Yesavage, J. A., & Rose T. L. (1984).  The effects of a face-name mnemonic in young, middle-aged, and elderly adults. Experimental Aging Research. 10(1), 55 - 57.

A new compound that boosts brain levels of magnesium improved many aspects of learning and memory in both young and old rats.

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.

Older news items (pre-2010) brought over from the old website

Low vitamin D levels associated with poorer cognition in older men

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 synthesized from sun exposure but is also found in certain foods such as oily fish.

[614] Casanueva, F. F., Finn J. D., Forti G., Giwercman A., Han T. S., Huhtaniemi I. T., et al. (2009).  Association between 25-hydroxyvitamin D levels and cognitive performance in middle-aged and older European men. Journal of Neurology, Neurosurgery & Psychiatry. 80(7), 722 - 729.

http://www.eurekalert.org/pub_releases/2009-05/uom-vdf051909.php

Vitamin D important in brain development and function

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.

[825] McCann, J. C., & Ames B. N. (2008).  Is there convincing biological or behavioral evidence linking vitamin D deficiency to brain dysfunction?. FASEB J.. 22(4), 982 - 1001.

http://www.eurekalert.org/pub_releases/2008-04/chr-vdi041808.php

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