You can help your brain, especially as it ages, by eating and drinking right
New research confirms the correlation between lower neighborhood socioeconomic status and lower cognitive function in older adults, and accounts for most of it through vascular health, lifestyle, and psychosocial factors.
In the last five years, three studies have linked lower neighborhood socioeconomic status to lower cognitive function in older adults. Neighborhood has also been linked to self-rated health, cardiovascular disease, and mortality. Such links between health and neighborhood may come about through exposure to pollutants or other environmental stressors, access to alcohol and cigarettes, barriers to physical activity, reduced social support, and reduced access to good health and social services.
Data from the large Women’s Health Initiative Memory Study has now been analyzed to assess whether the relationship between neighborhood socioeconomic status can be explained by various risk and protective factors for poor cognitive function.
Results confirmed that higher neighborhood socioeconomic status was associated with higher cognitive function, even after individual factors such as age, ethnicity, income, education, and marital status have been taken into account. A good deal of this was explained by vascular factors (coronary heart disease, diabetes, stroke, hypertension), health behaviors (amount of alcohol consumed, smoking, physical activity), and psychosocial factors (depression, social support). Nevertheless, the association was still (barely) significant after these factors were taken account of, suggesting some other factors may also be involved. Potential factors include cognitive activity, diet, and access to health services.
In contradiction of earlier research, the association appeared to be stronger among younger women. Consistent with other research, the association was stronger for non-White women.
Data from 7,479 older women (65-81) was included in the analysis. Cognitive function was assessed by the Modified MMSE (3MSE). Neighborhood socioeconomic status was assessed on the basis of: percentage of adults over 25 with less than a high school education, percentage of male unemployment, percentage of households below the poverty line, percentage of households receiving public assistance, percentage of female-headed households with children, and median household income. Around 87% of participants were White, 7% Black, 3% Hispanic, and 3% other. Some 92% had graduated high school, and around 70% had at least some college.
 Shih, R. A., Ghosh-Dastidar B., Margolis K. L., Slaughter M. E., Jewell A., Bird C. E., et al.
(2011). Neighborhood Socioeconomic Status and Cognitive Function in Women.
Am J Public Health. 101(9), 1721 - 1728.
Lang IA, Llewellyn DJ, Langa KM, Wallace RB, Huppert FA, Melzer D. 2008. Neighborhood deprivation, individual socioeconomic status, and cognitive function in older people: analyses from the English Longitudinal Study of Ageing. J Am Geriatr Soc., 56(2), 191-198.
Sheffield KM, Peek MK. 2009. Neighborhood context and cognitive decline in older Mexican Americans: results from the Hispanic Established Populations for Epidemiologic Studies of the Elderly. Am J Epidemiol., 169(9), 1092-1101.
Wight RG, Aneshensel CS, Miller-Martinez D, et al. 2006. Urban neighborhood context, educational attainment, and cognitive function among older adults. Am J Epidemiol., 163(12), 1071-1078.
A study involving 62 children with type 1 diabetes, of whom 33 had experienced diabetic ketoacidosis, has found those with such experience performed significantly worse on a memory test that tested their ability to recall events in association with specific details. The finding points to the importance of avoiding diabetic ketoacidosis, which is avoidable in those known to have diabetes.
 Ghetti, S., Lee J. K., Sims C. E., DeMaster D. M., & Glaser N. S.
(2010). Diabetic Ketoacidosis and Memory Dysfunction in Children with Type 1 Diabetes.
The Journal of Pediatrics. 156(1), 109 - 114.
The ongoing Memory in Diabetes (MIND) study, involving some 3,000 type 2 diabetics 55 years and older, has found that cognitive functioning abilities drop as average blood sugar levels rise. However, there was no connection between daily blood glucose levels and cognitive performance. The study adds to growing evidence that poorer blood glucose control is strongly associated with poorer memory function, that may eventually lead to mild cognitive impairment, vascular dementia and Alzheimer's disease. It is also possible that people with impaired cognitive ability are less compliant in taking medications and controlling their diabetes. Further research will test the hypothesis that improving glucose control results in improved cognitive function.
 Marcovina, S. M., Launer L. J., Cukierman-Yaffe T., Gerstein H. C., Williamson J. D., Lazar R. M., et al.
(2009). Relationship Between Baseline Glycemic Control and Cognitive Function in Individuals With Type 2 Diabetes and Other Cardiovascular Risk Factors.
Diabetes Care. 32(2), 221 - 226.
A comparison of 41 adults with diabetes and 424 adults in good health, aged between 53 and 90, has revealed that healthy adults performed significantly better than adults with diabetes on two of the five domains tested: executive functioning and speed of processing. There were no significant differences on tests of episodic and semantic memory, verbal fluency, reaction time and perceptual speed. The effect remained even when only the younger group (those below 70) were analyzed, indicating that the diabetes-linked cognitive deficits appear early and remain stable.
 Yeung, S. E., Fischer A. L., & Dixon R. A.
(2009). Exploring effects of type 2 diabetes on cognitive functioning in older adults.
Neuropsychology. 23(1), 1 - 9.
Following research showing that decreasing brain function in the area of the hippocampus called the dentate gyrus is a main contributor of normal age-related cognitive decline, an imaging study has been investigating the cause of this decreasing function by looking at measures that typically change during aging, like rising blood sugar, body mass index, cholesterol and insulin levels. The study of 240 community-based nondemented elders (average age 80 years), of whom 60 had type 2 diabetes, found that decreasing activity in the dentate gyrus only correlated with levels of blood glucose. The same association was also found in aging rhesus monkeys and in mice. The finding suggests that maintaining blood sugar levels, even in the absence of diabetes, could help maintain aspects of cognitive health. It also suggests that one reason why physical exercise benefits memory may be its effect on lowering glucose levels.
 Mayeux, R., Vannucci S. J., Small S. A., Wu W., Brickman A. M., Luchsinger J., et al.
(2008). The brain in the age of old: The hippocampal formation is targeted differentially by diseases of late life.
Annals of Neurology. 64(6), 698 - 706.
Growing evidence links diabetes to cognitive impairment. Now a small study of 16 adults (aged 50 years and older) with type 2 diabetes compared their cognitive performance on three separate occasions, fifteen minutes after consuming different meals. One meal consisted of high fat products – a danish pastry, cheddar cheese and yogurt with added whipped cream; the second meal was only water; and the third was the high-fat meal plus high doses of vitamins C (1000 mg) and E (800 IU) tablets. Researchers found that vitamin supplementation consistently improved recall scores relative to the meal alone, while those who ate the high fat meal without vitamin supplements showed significantly more forgetfulness of words and paragraph information in immediate and time delay recall tests. Those on water meal and meal with vitamins showed similar levels in cognitive performance. The finding indicates not only that diabetics can temporarily further worsen already underlying memory problems associated with the disease by consuming unhealthy meals, but also that this can be remedied by taking high doses of antioxidant vitamins C and E with the meal, suggesting that the effect of high-fat foods is to cause oxidative stress. However, this is hardly a recommended course of action, and the real importance of this finding is that it emphasizes the need for diabetics to consume healthy foods high in antioxidants, like fruits and vegetables. Of course, this is a very small study, and further replication is needed.
 Chui, M., & Greenwood C.
(2008). Antioxidant vitamins reduce acute meal-induced memory deficits in adults with type 2 diabetes.
Nutrition Research. 28(7), 423 - 429.
A rodent study sheds light on why diabetes can impair cognitive function. The study found that increased levels of a stress hormone (called cortisol in humans) in diabetic rats impaired synaptic plasticity and reduced neurogenesis in the hippocampus. When levels returned to normal, the hippocampus recovered. Cortisol production is controlled by the hypothalamic-pituitary axis (HPA). People with poorly controlled diabetes often have an overactive HPA axis and excessive cortisol.
 Stranahan, A. M., Arumugam T. V., Cutler R. G., Lee K., Egan J. M., & Mattson M. P.
(2008). Diabetes impairs hippocampal function through glucocorticoid-mediated effects on new and mature neurons.
Nature Neuroscience. 11(3), 309 - 317.
A long-running study involving 1,441 type 1 diabetics, aged 13 to 39, has demonstrated that multiple episodes of severe hypoglycaemia, though they can cause confusion, irrational behavior, convulsions and unconsciousness, do not lead to long-term loss of cognitive ability.
 The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications(DCCT/EDIC) Study Research
(2007). Long-Term Effect of Diabetes and Its Treatment on Cognitive Function.
N Engl J Med. 356(18), 1842 - 1852.
Previous research had indicated that tight blood glucose control -- achieved by taking three or more insulin injections daily – meant type 1 diabetics were three times as likely to suffer episodes of severe hypoglycemia, raising the fear that it might lead to a long-term loss of cognitive ability. Now a follow-up study provides the reassuring news that there was no link between multiple severe hypoglycemic reactions and impaired cognitive function in people with type 1 diabetes.
Jacobson, A.M. et al. 2006. Effects of Intensive and Conventional Treatment on Cognitive Function Twelve Years after the Completion of the Diabetes Control and Complications Trial (DCCT). Abstract Number 750232, presented at the American Diabetes Association's 66th Annual Scientific Sessions held in Washington, D.C, June 9—13.
A new study reveals why obese patients who have diabetes also may have problems with their long-term memory. Leptin — the so-called ‘fat’ hormone — doesn't cross into the brain to help regulate appetite in obese people. Leptin also acts in the hippocampus, suggesting that leptin plays a role in learning and memory. The new study supports this by demonstrating that mice navigated a maze better after they received leptin. Moreover, mice with elevated levels of amyloid-beta plaques (characteristic of Alzheimer's) were particularly sensitive to leptin.
 Farr, S. A., Banks W. A., & Morley J. E.
(2006). Effects of leptin on memory processing.
Peptides. 27(6), 1420 - 1425.
Age-related macular degeneration (AMD) develops when the macula, the portion of the eye that allows people to see in detail, deteriorates. An investigation into the relationship between vision problems and cognitive impairment in 2,946 patients has been carried out by The Age-Related Eye Disease Study (AREDS) Research Group. Tests were carried out every year for four years. Those who had more severe AMD had poorer average scores on cognitive tests, an association that remained even after researchers considered other factors, including age, sex, race, education, smoking, diabetes, use of cholesterol-lowering medications and high blood pressure. Average scores also decreased as vision decreased. It’s possible that there is a biological reason for the association; it is also possible that visual impairment reduces a person’s capacity to develop and maintain relationships and to participate in stimulating activities.
Chaves, P.H.M. et al. 2006. Association Between Mild Age-Related Eye Disease Study Research Group. 2006. Cognitive Impairment in the Age-Related Eye Disease Study: AREDS Report No. 16. Archives of Ophthalmology,124, 537-543.
A review of 96 papers involving 36 very large, ongoing epidemiological studies in North America and Europe looking at factors involved in maintaining cognitive and emotional health in adults as they age has concluded that controlling cardiovascular risk factors, such as reducing blood pressure, reducing weight, reducing cholesterol, treating (or preferably avoiding) diabetes, and not smoking, is important for maintaining brain health as we age. The link between hypertension and cognitive decline was the most robust across studies. They also found a consistent close correlation between physical activity and brain health. However, they caution that more research is needed before specific recommendations can be made about which types of exercise and how much exercise are beneficial. They also found protective factors most consistently reported for cognitive health included higher education level, higher socio-economic status, emotional support, better initial performance on cognitive tests, better lung capacity, more physical exercise, moderate alcohol use, and use of vitamin supplements. Psychosocial factors, such as social disengagement and depressed mood, are associated with both poorer cognitive and emotional health in late life. Increased mental activity throughout life, such as learning new things, may also benefit brain health.
Wagster M, Hendrie H, Albert M, Butters M, Gao S, Knopman DS, Launer L, Yaffe K, Cuthbert B, Edwards E. The NIH Cognitive and Emotional Health ProjectReport of the Critical Evaluation Study Committee. Alzheimer's and Dementia [Internet]. 2006 ;2(1):12 - 32. Available from: http://www.alzheimersanddementia.com/article/S1552-5260(05)00503-0/abstract?articleId=&articleTitle=&citedBy=false&medlinePmidWithoutMDLNPrefix=&overridingDateRestriction=&related=false&restrictdesc_author=&restrictDescription=&restrictName.jalz=jalz&rest
A new large-scale study supports earlier suggestions that those with a high risk for stroke within 10 years are also at risk for lowered cognitive function and show a pattern of deficits similar to that seen in mild vascular cognitive impairment. It is speculated that the reason may lie in structural and functional changes in the brain that do not rise to the level of clinical detection, and this is supported by a recent brain imaging study showing that abnormal brain atrophy is related both to higher risk of stroke and poorer cognitive ability. The probability of experiencing stroke within 10 years was calculated using weighted combinations of age, systolic blood-pressure, presence of diabetes, cigarette smoking, history of cardiovascular disease, treatment for hypertension and atrial fibrillation.
 Elias, M. F., Sullivan L. M., D'Agostino R. B., Elias P. K., Beiser A., Au R., et al.
(2004). Framingham stroke risk profile and lowered cognitive performance.
Stroke; a Journal of Cerebral Circulation. 35(2), 404 - 409.
From around age 60, "white-matter lesions" appear in the brain, significantly affecting cognitive function. But without cognitive data from childhood, it is hard to know how much of the difference in cognitive abilities between elderly individuals is due to aging. A longitudinal study has been made possible by the Scottish Mental Survey of 1932, which gave 11-year-olds a validated cognitive test. Scottish researchers have tracked down healthy living men and women who took part in this Survey and retested 83 participants. Testing took place in 1999, when most participants were 78 years old.It was found that the amount of white-matter lesions made a significant contribution to general cognitive ability differences in old age, independent of prior ability. The amount of white-matter lesions contributed 14.4% of the variance in cognitive scores; early IQ scores contributed 13.7%. The two factors were independent.Although white-matter lesions are viewed as a normal part of aging, they are linked with other health problems, in particular to circulatory problems (including hypertension, diabetes, heart disease and cardiovascular risk factors).
 Deary, I. J., Leaper S. A., Murray A. D., Staff R. T., & Whalley L. J.
(2003). Cerebral white matter abnormalities and lifetime cognitive change: a 67-year follow-up of the Scottish Mental Survey of 1932.
Psychology and Aging. 18(1), 140 - 148.
A new study takes an important step in explaining cognitive impairment in diabetics, and suggests a possible cause for some age-related memory impairment. The study assessed non-diabetic middle-aged and elderly people. Those with impaired glucose tolerance (a pre-diabetic condition) had a smaller hippocampus and scored worse on tests for recent memory. These results were independent of age or overall cognitive performance. The brain uses glucose almost exclusively as a fuel source. The ability to get glucose from the blood is reduced in diabetes. The study raises the possibility that exercise and weight loss, which help control blood sugar levels, may be able to reverse some of the memory loss that accompanies aging.
 Convit, A., Wolf O. T., Tarshish C., & de Leon M. J.
(2003). Reduced glucose tolerance is associated with poor memory performance and hippocampal atrophy among normal elderly.
Proceedings of the National Academy of Sciences of the United States of America. 100(4), 2019 - 2022.
A large-scale six-year study of people aged 40 to 70 years old found that people with diabetes and high blood pressure are more likely to experience cognitive decline. Diabetes was associated with greater cognitive decline for those younger than 58 as well as those older than 58, but high blood pressure was a risk factor only for the 58 and older group.
 Knopman, D. S., Boland L. L., Mosley T., Howard G., Liao D., Szklo M., et al.
(2001). Cardiovascular risk factors and cognitive decline in middle-aged adults.
Neurology. 56(1), 42 - 48.
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.
 de Jager, C. A., Oulhaj A., Jacoby R., Refsum H., & Smith D. A.
(Submitted). Cognitive and clinical outcomes of homocysteine‐lowering B‐vitamin treatment in mild cognitive impairment: a randomized controlled trial.
International Journal of Geriatric Psychiatry.
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).
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: www.nal.usda.gov/fnic/foodcomp
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
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.
New findings reveal that mild cognitive impairment is more likely to develop into Alzheimer’s if vascular risk factors are present, especially if untreated.
A study following 837 people with MCI, of whom 414 (49.5%) had at least one vascular risk factor, has found that those with risk factors such as high blood pressure, diabetes, cerebrovascular disease and high cholesterol were twice as likely to develop Alzheimer's disease. Over five years, 52% of those with risk factors developed Alzheimer's, compared to 36% of those with no risk factors In total, 298 people (35.6%) developed Alzheimer's.
However, of those with vascular risk factors, those receiving full treatment for their vascular problems were 39% less likely to develop Alzheimer's disease than those receiving no treatment, and those receiving some treatments were 26% less likely to develop the disease.
Treatment of risk factors included using high blood pressure medicines, insulin, cholesterol-lowering drugs and diet control. Smoking and drinking were considered treated if the person stopped smoking or drinking at the start of the study.
 Li, J., Wang Y. J., Zhang M., Xu Z. Q., Gao C. Y., Fang C. Q., et al.
(2011). Vascular risk factors promote conversion from mild cognitive impairment to Alzheimer disease.
Neurology. 76(17), 1485 - 1491.
Three more studies point to the increased risk of memory loss in older adults with cardiovascular problems.
The new label of ‘metabolic syndrome’ applies to those having three or more of the following risk factors: high blood pressure, excess belly fat, higher than normal triglycerides, high blood sugar and low high-density lipoprotein (HDL) cholesterol (the "good" cholesterol). Metabolic syndrome has been linked to increased risk of heart attack.
A new French study, involving over 7,000 older adults (65+) has found that those with metabolic syndrome were 20% more likely to show cognitive decline on a memory test (MMSE) over a two or four year interval. They were also 13% more likely to show cognitive decline on a visual working memory test. Specifically, higher triglycerides and low HDL cholesterol were linked to poorer memory scores; diabetes (but not higher fasting blood sugar) was linked to poorer visual working memory and word fluency scores.
The findings point to the importance of managing the symptoms of metabolic syndrome.
High cholesterol and blood pressure in middle age tied to early memory problems
Another study, involving some 4800 middle-aged adults (average age 55), has found that those with higher cardiovascular risk were more likely to have lower cognitive function and a faster rate of cognitive decline over a 10-year period. A 10% higher cardiovascular risk was associated not only with increased rate of overall mental decline, but also poorer cognitive test scores in all areas except reasoning for men and fluency for women.
The cardiovascular risk score is based on age, sex, HDL cholesterol, total cholesterol, systolic blood pressure and whether participants smoked or had diabetes.
Memory problems may be sign of stroke risk
A very large study (part of the REGARDS study) tested people age 45 and older (average age 67) who had never had a stroke. Some 14,842 people took a verbal fluency test, and 17,851 people took a word recall memory test. In the next 4.5 years, 123 participants who had taken the verbal fluency test and 129 participants who had taken the memory test experienced a stroke.
Those who had scored in the bottom 20% for verbal fluency were 3.6 times more likely to develop a stroke than those who scored in the top 20%. For the memory test, those who scored in the bottom 20% were 3.5 times more likely to have a stroke than those in the top quintile.
The effect was greatest at the younger ages. At age 50, those who scored in the bottom quintile of the memory test were 9.4 times more likely to later have a stroke than those in the top quintile.
Together, these studies, which are consistent with many previous studies, confirm that cardiovascular problems and diabetes add to the risk of greater cognitive decline (and possible dementia) in old age. And point to the importance of treating these problems as soon as they appear.
 Raffaitin, C., Féart C., Le Goff M., Amieva H., Helmer C., Akbaraly T. N., et al.
(2011). Metabolic syndrome and cognitive decline in French elders.
Neurology. 76(6), 518 - 525.
The findings of the second and third studies are to be presented at the American Academy of Neurology's 63rd Annual Meeting in Honolulu April 9 to April 16, 2011
http://www.eurekalert.org/pub_releases/2011-02/aaon-msl012511.php http://www.eurekalert.org/pub_releases/2011-02/aaon-hca020811.php http://www.eurekalert.org/pub_releases/2011-02/aaon-mpm020811.php
A Japanese study finds higher IQ among children who habitually eat white rice for breakfast, compared to those who eat white bread.
A number of studies have provided evidence that eating breakfast has an immediate benefit for cognitive performance in children. Now a new study suggests some “good” breakfasts are better than others.
A Japanese study of 290 healthy, well-nourished children, has revealed that those whose breakfast staple was white rice had a significantly larger ratio of gray matter in their brains, and several significantly larger regions, including the left superior temporal gyrus and bilateral caudate. Those who habitually ate white bread had significantly larger regional gray and white matter volumes of several regions, including the orbitofrontal gyri, right precentral gyrus and postcentral gyrus. Overall IQ scores, and scores on the perceptual organization subcomponent in particular, were significantly higher for the rice group.
One possible reason for the difference may be the difference in the glycemic index (GI) of these two substances; foods with a low GI are associated with less blood-glucose fluctuation than are those with a high GI. There is also a difference in fat content, with those eating white bread typically consuming more fat than those eating a rice-based breakfast. High levels of fat have been shown to reduce the expression of BDNF.
Regardless of the reason for the difference, the fact that breakfast staple type affects brain size and cognitive function in healthy children points to the importance of good nutrition during the years of brain development.
 Taki, Y., Hashizume H., Sassa Y., Takeuchi H., Asano M., Asano K., et al.
(2010). Breakfast Staple Types Affect Brain Gray Matter Volume and Cognitive Function in Healthy Children.
PLoS ONE. 5(12), e15213 - e15213.
Two recent studies suggest that caffeine is most effective in boosting your energy and alertness in small doses, and more effective for males.
A study involving 80 college students (34 men and 46 women) between the ages of 18 and 40, has found that those given a caffeinated energy drink reported feeling more stimulated and less tired than those given a decaffeinated soda or no drink. However, although reaction times were faster for those consuming caffeine than those given a placebo drink or no drink, reaction times slowed for increasing doses of caffeine, suggesting that smaller amounts of caffeine are more effective.
The three caffeine groups were given caffeine levels of either 1.8 ml/kg, 3.6 ml/kg or 5.4 ml/kg. The computerized "go/no-go" test which tested their reaction times was given half an hour after consuming the drinks.
In another study, 52 children aged 12-17 drank flattened Sprite containing caffeine at four concentrations: 0, 50 mg, 100 mg or 200 mg. Changes in blood pressure and heart rate were then checked every 10 minutes for one hour, at which point they were given a questionnaire and an opportunity to eat all they wanted of certain types of junk food.
Interestingly, there were significant gender differences, with boys drinking high-caffeine Sprite showing greater increases in diastolic blood pressure (the lower number) than boys drinking the low-caffeine Sprite, but girls being unaffected. Boys were also more inclined to report consuming caffeine for energy or “the rush”, than girls were.
Those participants who ingested the most caffeine also ate more high-sugar snack foods in the laboratory, and reported higher protein and fat consumption outside the lab.
 Howard, M. A., & Marczinski C. A.
(2010). Acute Effects of a Glucose Energy Drink on Behavioral Control.
Experimental and Clinical Psychopharmacology. 18(6), 553 - 561.
 Temple, J. L., Dewey A. M., & Briatico L. N.
(2010). Effects of Acute Caffeine Administration on Adolescents.
Experimental and Clinical Psychopharmacology. 18(6), 510 - 520.
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.
 Christian, P., Murray-Kolb L. E., Khatry S. K., Katz J., Schaefer B. A., Cole P. M., et al.
(Submitted). Prenatal Micronutrient Supplementation and Intellectual and Motor Function in Early School-aged Children in Nepal.
JAMA: The Journal of the American Medical Association. 304(24), 2716 - 2723.
 Kell, D. B.
(2010). Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson’s, Huntington’s, Alzheimer’s, prions, bactericides, chemical toxicology and others as examples.
Archives of Toxicology. 84(11), 825 - 889.
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