Nutrition and cognition

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Eating a variety of foods helps to ensure adequate nutritional intake

Food is conventionally regarded as a means to provide energy and building material within the body. Recently, the ability of food to prevent and protect against diseases has started to become recognized, mainly in relation to the effects of nutrients on molecular processes within the body.[1] Certain cells require particular nutrients to play specific roles in order to function properly, and neurons are not exempt from this.[2]

Relatively speaking, the brain consumes an immense amount of energy in comparison to the rest of the body. The mechanisms involved in the transfer of energy from foods to neurons are likely to be fundamental to the control of brain function.[1] Human bodily processes, including the brain, all require both macronutrients, as well as micronutrients.[2]

Insufficient intake of selected vitamins, or certain metabolic disorders, may affect cognitive processes by disrupting the nutrient-dependent processes within the body that are associated with the management of energy in neurons, which can subsequently affect synaptic plasticity, or the ability to encode new memories.[1]

The prevalence of specific vitamin deficiencies has become rare in most industrialized countries with the introduction of vitamin fortification in flour, cereals, and other foods. However, in many African, Asian, and Latin American countries, individuals must contend with a range of nutritionally-significant diseases that continue to be major health problems within their respective populations.[3]

Nutrients needed for memory development[edit]


Choline is an essential nutrient and its primary function within the human body is the synthesis of cellular membranes,[4] although it serves other functions as well. It is a precursor molecule to the neurotransmitter Acetylcholine which serves a wide range of functions including motor control and memory. Choline itself has also been shown to have additional health benefits in relation to memory and choline deficiencies may be related to some liver and neurological disorders.[5] Because of its role in cellular synthesis, choline is an important nutrient during the prenatal and early postnatal development of offspring as it contributes heavily to the development of the brain.

Deficiencies and treatments[edit]

Despite the wide range of foods that choline is found in, studies have shown that the mean choline intake of men, women and children are below the Adequate Intake levels.[5] It is important to note that not enough choline is naturally produced by the body, so diet is an important factor. Women, especially pregnant or lactating women, older people, and infants, are especially at risk for choline deficiency.[5] In such instances of deficiency, choline supplements or (if able) dietary changes may be beneficial. Good sources of choline include liver, milk, eggs and peanuts.[6]

B-Vitamin deficiencies and cognition[edit]

Many protein-rich foods are high in B vitamin content. Liver is an excellent source of many of the B vitamins

B vitamins, also known as the B-complex, are an interrelated group of nutrients which often co-occur in food. The complex consists of: thiamine (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5), pyridoxin (B6), folic acid (B9), cobalamin (B12), and biotin.[7] B vitamins are not synthesized in the body, and thus need to be obtained from food. B-complex vitamins are water-soluble vitamins, which means that they are not stored within the body. In consequence, the B vitamins need ongoing replenishment.[8]

It is possible to identify broad cognitive effects of certain B vitamins, as they are involved in many significant metabolic processes within the brain.[2]

Vitamin B1 (thiamine)[edit]

Vitamin B1, also known as thiamine, is a coenzyme essential for the metabolism of carbohydrates.[9] This vitamin is important for the facilitation of glucose use, thus ensuring the production of energy for the brain,[2] and normal functioning of the nervous system, muscles, and heart.[8]

Thiamine is found in all living tissues,[10] and is uniformly distributed throughout mammalian nervous tissue, including the brain and spinal cord. Metabolism and coenzyme function of the vitamin suggest a distinctive function for thiamin within the nervous system.[11]

The brain retains its thiamine content in the face of a vitamin-deficient diet with great tenacity, as it is the last of all nervous tissues studied to become depleted. A 50% reduction of thiamine stores in rats becomes apparent after only 4 days of being put on a thiamine-deficient diet. However, polyneuritic signs do not begin to appear until about 4 or 5 weeks have passed.[11] Similar results have been found in human subjects.[10]


The body has only small stores of B1; accordingly, there is risk of deficiency if the level of intake is reduced only for a few weeks.[10] Lack of thiamin causes the disease known as beriberi.[12] There are two forms of beriberi: "wet", and "dry". Dry beriberi is also known as cerebral beriberi. Characteristics of wet beriberi include prominent edema and cardiac involvement, whereas dry beriberi is mainly characterized by a polyneuritis.[11]

In industrialized nations, thiamine deficiency is a clinically significant problem in individuals with chronic alcoholism or other disorders that interfere with normal ingestion of food.[13] Thiamine deficiency within developed nations tends to manifest as Wernicke–Korsakoff syndrome.[12]

Individuals with chronic alcoholism may fall short on minimum daily requirements of thiamine in part due to anorexia, erratic eating habits, lack of available food, or a combination of any of these factors. Thiamine deficiency has been reported in up to 80% of alcoholic patients due to inadequate nutritional intake, reduced absorption, and impaired utilization of thiamine.[14] Alcohol, in combination with its metabolite acetaldehyde, interacts with thiamine utilization at the molecular level during transport, diphosphorylation, and modification processes. For this reason, chronic alcoholics may have insufficient thiamine for maintenance of normal brain function, even with seemingly adequate dietary intake.[13]


Clinical signs of B1 deficiency include mental changes such as apathy, decrease in short-term memory, confusion, and irritability.[12] Moderate deficiency in thiamine may reduce growth in young populations, in increase chronic illness in both young and middle-aged adults. In addition, moderate deficiency of thiamine may increase rates of depression, dementia, falls, and fractures in old age.[13]

The lingering symptoms of neuropathy associated with cerebral beriberi are known as Korsakoff's syndrome, or the chronic phase of Wernicke-Korsakoff's.[15] Wernicke encephalopathy is a neurological disorder resulting from a deficiency in thiamine, sharing the same predominant features of cerebral beriberi, as characterized by ocular abnormalities, ataxia of gait, a global state of confusion, and neuropathy.[13] The state of confusion associated with Wernicke's may consist of apathy, inattention, spatial disorientation, inability to concentrate, and mental sluggishness or restlessness.[9] Clinical diagnosis of Wernicke's disease cannot be made without evidence of ocular disturbance, yet these criteria may be too rigid.[16] Korsakoff's likely represents a variation in the clinical manifestation of Wernicke encephalophathy, as they both share similar pathological origin.[16]

Korsakoff's syndrome is often characterized by confabulation, disorientation, and profound amnesia.[15] Characteristics of the neuropathology are varied, but generally consist of bilaterally symmetrical midline lesions of brainstem areas, including the mammillary bodies, thalamus, periaqueductal region, hypothalamus, and the cerebellar vermis.[13][15]


Immediate treatment of Wernicke encephalopathy involves the administration of intravenous thiamine, followed with long-term treatment and prevention of the disorder through oral thiamine supplements, alcohol abstinence, and a balanced diet.[9] Improvements in brain functioning of chronic alcoholics may occur with abstinence-related treatment, involving the discontinuation of alcohol consumption and improved nutrition.[13] Wernicke's encephalopathy is life-threatening if left untreated. However, a rapid reversal of symptoms may result from prompt administration of thiamine.[10]


Fortification of flour is practiced in some countries to replace the thiamine lost during processing. However, this method has been criticized for missing the target population of chronic alcoholics, who are most at risk for deficiency. Alternative solutions have suggested the fortification of alcoholic beverages with thiamine.[10]

Ingesting a diet rich in thiamine may stave off the adverse effects of deficiency. Foods providing rich sources of thiamine include unrefined grain products, ready-to-eat cereals, meat (especially pork), dairy products, peanuts, legumes, fruits and eggs.[17]

Vitamin B3 (niacin)[edit]

Vitamin B3, also known as niacin, includes both nicotinamide as well as nicotinic acid, both of which function in many biological oxidization and reduction reactions within the body. These functions include the biochemical degradation of carbohydrates, fats and proteins. Niacin is also involved in the synthesis of fatty acids and cholesterol,[18] which are known mediators of brain biochemistry, and in effect, of cognitive function.[19]

Sufficient niacin intake is either obtained from diet, or synthesized from the amino acid tryptophan.[18]


Pellagra initially presents as dermatitis

Severe niacin deficiency typically manifests itself as the disease pellagra.[18] Synthesis of B3 from tryptophan involves vitamin B2 and B6, so deficiencies in either of these nutrients can lead to niacin deficiency. An excess of leucine, an essential amino acid, in the diet can also interfere with tryptophan conversion and subsequently result in a B3 deficiency.[20]

Pellagra is most common to populations within developing countries in which corn is the dietary staple. The disease has virtually disappeared from industrialized countries, yet still appears in India and parts of China and Africa.[18] This is in part due to the bound form of niacin that unprocessed corn contains, which is not readily absorbed into the human body. The processes involved in making corn tortillas, can release the bound niacin into a more absorbable form. Pellegra is not problematic in countries which traditionally prepare their corn in this way, but is a problem in other countries where unprocessed corn is main source of caloric intake.[21]

Though pellagra predominantly occurs in developing countries, sporadic cases of pellagra may be observed within industrialized nations, primarily in chronic alcoholics and patients living with functional absorption complications.[20]


Pellagra is classically characterized by four 4 "D's": diarrhea, dermatitis, dementia, and death.[20] Neuropsychiatric manifestations of pellagra include headache, irritability, poor concentration, anxiety, hallucinations, stupor, apathy, psychomotor unrest, photophobia, tremor, ataxia, spastic paresis, fatigue, and depression. Symptoms of fatigue and insomnia may progress to encephalophathy characterized by confusion, memory loss, and psychosis.[20]

Those afflicted with pellagra may undergo pathological alterations in the nervous system. Findings may include demylenation and degeneration of various affected parts of the brain, spinal cord, and peripheral nerves.[22]


Prognosis of deficiency is excellent with treatment. Without, pellagra will gradually progress and lead to death within 4–5 years, often a result of malnutrition from prolonged diarrhea, or complications as caused by concurrent infections or neurological symptoms. Symptoms of pellagra can be cured with exogenous administration of nicotinic acid or nicotinamide.[20]

Flushing occurs in many patients treated therapeutically with nicotinic acid,[18] and as a result, nicotinamide holds more clinical value as it is not associated with the same uncomfortable flushing. The adult dose of nicotinamide is 100 mg taken orally every 6 hours until resolution of major acute symptoms, followed with oral administration of 50 mg every 8–12 hours until skin lesions heal. For children, treatment involves oral ingestion of 10–15 mg of nicotinamide, depending on weight, every 6hours until signs and symptoms are resolved. Severe cases require 1 gram every 3–4 hours, administered parenterally.[20]

Oral nicotinamide has been promoted as an over-the-counter drug for the treatment of Alzheimer's dementia. Conversely, no clinically significant effect has been found for the drug, as nicotinamide administration has not been found to promote memory functions in patients with mild to moderate dementia of either Alzheimers', vascular, or fronto-temporal types. This evidence suggests that nicotinamide may treat dementia as related to pellegra, but administration does not effectively treat other types of dementia.[23]


The best method of prevention is to eat food rich in B3. Generally, this involves the intake of a protein-rich diet. Foods that contain high concentrations of niacin in the free form include beans and organ meat, as well as enriched grain and cereal products.[18] While niacin is present in corn and other grains, the bioavailability of the nutrient is much less than it is in protein-rich sources. Different methods of processing corn may result in a higher degree of bioavailability of the vitamin.[21]

Though treatment with niacin does little to alter the effects of Alzheimer's dementia, niacin intake from foods is inversely associated with the disease.[24]

Vitamin B9 (folic acid)[edit]

Folic acid is the most oxidized and stable form of folate, and can also be referred to as vitamin B9. It rarely occurs naturally in foods, but it is the form used in vitamin supplements as well as fortified food products.[25]

Folate coenzymes are involved in numerous conversion processes within the body, including DNA synthesis and amino acid interconversions.[25] Folate and vitamin B12 play a vital role in the synthesis of S-adenosylmethionine, which is of key importance in the maintenance and repairment of all cells, including neurons.[26] In addition, folate has been linked to the maintenance of adequate brain levels of cofactors necessary for chemicals reactions that lead to the synthesis of serotonin and catecholamine neurotransmitters.[25]

Folate has a major, but indirect role in activities which help to direct gene expression and cell proliferation. These activities occur at a greatly increased rate during pregnancy, and depend on adequate levels of folate within blood plasma.[27]

Concentrations of blood plasma folate and homocysteine concentrations are inversely related, such that an increase in dietary folate decreases homocysteine concentration. Thus, dietary intake of folate is a major determinant of homocysteine levels within the body.[28]


Folate deficiency most commonly arises from insufficient folate intake from the diet, but may also stem from inefficient absorption or metabolic utilization of folate, usually a result of genetic variation.[29] The relationship between folate and B12 is so interdependent that deficiency in either vitamin can result in megaloblastic anemia, characterized by organic mental change.[30]

The process of neural tube transformation into structures that will eventually develop into the central nervous system is known as neurulation, the success of which is dependent on the presence of folate within the body. This process begins in the human approximately 21 days after conception, and is completed by 28 days. Thus, a woman may not even be aware of her pregnancy by the time the process of neurulation is complete, potentially causing severe consequences in the development of the fetus.[25]

Functional problems in the absorption and utilization of vitamins may also play a role in folate deficiencies within the elderly.[26]


Anencephaly is the most common presentation of neural tube defects[31]

The link between levels of folate and altered mental function is not large, but is sufficient enough to suggest a causal association.[25] Deficiency in folate can cause an elevation of homocysteine within the blood,[28] as the clearance of homocysteine requires enzymatic action dependent on folate, and to a lesser extent, vitamins B6 and B12. Elevated homocysteine has been associated with increased risk of vascular events, as well as dementia.[32]

Differences lie in the presentation of megaloblastic anemia induced by either folate or B12 deficiency. Megaloblastic anemia related to deficiency in B12 generally results in peripheral neuropathy, whereas folate-related anemia often results in affective, or mood disorders.[30][33] Neurological effects are not often associated with folate-related megaloblastic anemia, although demyelinating disorders may eventually present.[30] In one study, mood disturbances were recorded for the majority of patients presenting with megaloblastic anemia in the absence of B12 deficiency.[25] In addition, folate concentrations within blood plasma have been found to be lower in patients with both unipolar and bipolar depressive disorders when compared with control groups. In addition, depressive groups with low folate concentrations responded less well to standard antidepressant therapy than did those with normal levels within plasma.[25] However, replication of these findings are less robust.[34]

The role of folic acid during pregnancy is vital to normal development of the nervous system in the fetus. A deficiency in folate levels of a pregnant woman could potentially result in neural tube disorder, a debilitating condition in which the tubes of the central nervous system do not fuse entirely.[27] NTDs are not to be confused with spina bifida, which does not involve neural elements.[25] Neural tube defects can present in a number of ways as a result of the improper closure at various points of the neural tube. The clinical spectrum of the disorder includes encephalocele, craniorachischisis, and anencephaly. In addition, these defects can also be classified as open, if neural tissue is exposed or covered only by membrane, or can be classified as closed, if the tissue is covered by normal skin.[31]

Intake of the vitamin has been linked to deficits in learning and memory, particularly within the elderly population.[25] Elderly people deficient in folate may present with deficits in free recall and recognition, which suggests that levels of folate may be related to efficacy of episodic memory.[35]


Lack of adequate folate may produce a form of dementia considered to be reversible with administration of the vitamin. Indeed, there is a degree of improvement in memory associated with folate treatment. In a 3-year longitudinal study of men and women aged 50–70 years with elevated homocysteine plasma concentration, researchers found that a daily oral folic acid supplementation of 800μg resulted in an increase in folate levels and a decrease in homocysteine levels within blood plasma. In addition to these results, improvements of memory, and information-processing speed, as well as slight improvements of sensorimotor speed were observed,[36] which suggests there is a link between homocysteine and cognitive performance.

However, while the amount of cognitive improvement after treatment with folate is correlated with the severity of folate deficiency, the severity of cognitive decline is independent of the severity of folate deficiency. This suggests that the dementia observed may not be entirely related to levels folate, as there could be additional factors that were not accounted for which might have an effect.[37]


Because neurulation may be completed before pregnancy is recognized, it is recommended that women capable of becoming pregnant take about 400μg of folic acid from fortified foods, supplements, or a combination of the two in order to reduce the risk of neural tube defects.[25] These major anomalies in the nervous system can be reduced by 85% with systematic folate supplementation occurring before the onset of pregnancy.[27]

The incidence of Alzheimer's and other cognitive diseases has been loosely connected to deficiencies in folate. It is recommended for the elderly to consume folate through food, fortified or not, and supplements in order to reduce risk of developing the disease.[26] Good sources of folate include liver, ready-to-eat breakfast cereals, beans, asparagus, spinach, broccoli, and orange juice.[38]

Vitamin B12 (cobalamin)[edit]

Also known as cobalamin, B12 is an essential vitamin necessary for normal blood formation. It is also important for the maintenance of neurological function and psychiatric health.[39] The absorption of B12 into the body requires adequate amounts of intrinsic factor, the glycoprotein produced in the parietal cells of the stomach lining. A functioning small intestine is also necessary for the proper metabolism of the vitamin, as absorption occurs within the ileum.[39]

B12 is produced in the digestive tracts of all animals, including humans.[40] Thus, animal-origin food is the only natural food source of vitamin B12[41] However, synthesis of B12 occurs in the large intestine, which is past the point of absorption that occurs within the small intestine. As such, vitamin B12 must be obtained through diet.[40]


Unlike other B vitamins which are not stored in the body, B12 is stored in the liver. Because of this, it may take 5–10 years before a sudden dietary B12 deficiency will become apparent in a previously healthy adult.[42] B12 deficiency, also known as hypocobalaminemia, often results from complications involving absorption into the body.[43]

B12 deficiency is often associated with pernicious anemia, as it is the most common cause.[44] Pernicious anemia results from an autoimmune disorder which destroys the cells that produce intrinsic factor within the stomach lining, thereby hindering B12 absorption. B12 absorption is important for the subsequent absorption of iron, thus, people with pernicious anemia often present with typical symptoms of anemia, such as pale skin, dizziness, and fatigue.[45]

Among those at highest risk for B12 deficiency are the elderly population, as 10-15% of people aged 60+ may present with some form of hypocobalaminemia. High rates of deficiency in the elderly commonly results from the decrease of functional absorption of B12, as production of intrinsic factor declines with age. However, pernicious anemia is the most common cause of B12 deficiency in North American and European populations.[41]

Those afflicted with various gastrointestinal diseases may also be at risk for deficiency as a result of malabsorption. These diseases may affect production of intrinsic factor in the stomach, or of pancreatic bile. Diseases that involve disorders of the small intestine, such as celiac disease, Crohn's disease and ileitis, may also reduce B12 absorption. For example, people with celiac disease may damage the microvilli within their small intestines through the consumption of gluten, thereby inhibiting absorption of B12 as well as other nutrients.[43]

A diet low in B12, whether voluntary or not, can also cause symptoms of hypocobalaminemia. Many rich sources of B12 come from animal meats and by-products. Populations in developing countries may not have access to these foods on a consistent basis, and as a result may become deficient in B12.[46] In addition, vegans, and to a lesser extent vegetarians, are at risk for consuming a diet low in cobalamin as they voluntarily abstain from animal sources of B12.[43] A combination of these two scenarios may increase prevalence of cobalamin deficit. For instance, B12 deficiency is problematic in India, where the majority of the population is vegetarian and the scarcity of meat consumption is common for omnivores as well.[46]


An assortment of neurological effects can be observed in 75–90% of individuals of any age with clinically observable B12 deficiency. Cobalamin deficiency manifestations are apparent in the abnormalities of the spinal cord, peripheral nerves, optic nerves, and cerebrum. These abnormalities involve a progressive degeneration of myelin,[47] and may be expressed behaviourally through reports of sensory disturbances in the extremities, or motor disturbances, such as gait ataxia. Combined myelopathy and neuropathy are prevalent within a large percentage of cases. Cognitive changes may range from loss of concentration to memory loss, disorientation, and dementia. All of these symptoms may present with or without additional mood changes.[41] Mental symptoms are extremely variable, and include mild disorders of mood, mental slowness, and memory defect. Memory defect encompasses symptoms of confusion, severe agitation and depression, delusions and paranoid behaviour, visual and auditory hallucinations, urinary and fecal incontinence in the absence of overt spinal lesions, dysphasia, violent maniacal behaviour, and epilepsy. It has been suggested that mental symptoms could be related to a decrease in cerebral metabolism, as caused by the state of deficiency.[47] All of these symptoms may present with or without additional mood changes.[41]

Mild to moderate cases of pernicious anemia may show symptoms of bleeding gums, headache, poor concentration, shortness of breath, and weakness. In severe cases of pernicious anemia, individuals may present with various cognitive problems such as dementia, and memory loss.[45]

It is not always easy to determine whether B12 deficiency is present, especially within older adults.[43] Patients may present with violent behaviour or more subtle personality changes. They may also present with vague complaints, such as fatigue or memory loss, that may be attributed to normative aging processes. Cognitive symptoms may mimic behaviour in Alzheimer's and other dementias as well.[41] Tests must be run on individuals presenting with such signs to confirm or negate cobalamin deficiency within the blood.[45]


Individuals with absorption disorders, or those who abstain from animal products should supplement their diet with B12 regularly

Patients deficient in B12 despite normal absorption functionality may be treated through oral administration of at least 6 mg of the vitamin in pill form. Patients who suffer from irreversible causes of deficiency, such as pernicious anemia or old age, will need lifelong treatment with pharmacological doses of B12. Strategy for treatment is dependent on the patient's level of deficiency as well as their level of cognitive functioning.[43] Treatment for those with severe deficiency involves 1000 mg of B12 administered intramuscularly daily for one week, weekly for one month, then monthly for the rest of the patients life. Daily oral supplementation of B12 mega-doses may be sufficient in reliable patients, but it is imperative that the supplementation be continued on a lifelong basis as relapse may occur otherwise.[45]

The progression of neurological manifestations of cobalamin deficiency is generally gradual. As a result, early diagnosis is important or else irreversible damage may occur.[39] Patients who become demented usually show little to no cognitive improvement with the administration of B12.[45]

A deficiency in folate may produce anemia similar to the anemia resulting from B12 deficiency. There is risk that folic acid administered to those with B12 deficiency may mask anemic symptoms without solving the issue at hand. In this case, patients would still be at risk for neurological deficits associated with B12 deficiency-related anemia, which are not associated with anemia related to folate deficiency.[29]


In addition to meeting intake requirements through food consumption, supplementation of diet with vitamin B12 is seen as a viable preventative measure for deficiency. It has been recommended for the elderly to supplement 50 mg a day in order to prevent deficit from occurring.[45]

Animal protein products are a good source of B12, particularly organ meats such as kidney or liver. Other good sources are fish, eggs, and dairy products.[40] It is suggested that vegans, who consume no animal meat or by-products, supplement their diet with B12. While there are foods fortified with B12 available, some may be mislabelled in an attempt to boost their nutritional claims. Products of fermentation, such as algae extracts and sea vegetables, may be labelled as sources of B12, but actually contain B12 analogues which compete for the absorption of the nutrient itself.[46] In order to get adequate amounts of the vitamin, orally administered pills or fortified foods such as cereals and soy milk, are recommended for vegans.[48]

Vitamin A deficiency and impaired memory[edit]

Vitamin A is an essential nutrient for mammals which takes form in either retinol or the provitamin beta-Carotene. It helps regulation of cell division, cell function, genetic regulation, helps enhance the immune system, and is required for brain function, chemical balance, growth and development of the Central Nervous System and vision.[49]

Learning memory[edit]

In an experiment by Chongqing Medical University pregnant rats were either plentiful in Vitamin A or were of a Vitamin A deficiency (VAD) due to their diet. The offspring of these rats were then tested in a water maze at 8 weeks old and it was found the VAD offspring had a harder time finishing the maze which helps show that these rats, even while having a deficiency from In utero, have more problems with learning memory.[50] Young rats in a separate study by the same university also showed impaired long-term potentiation in the hippocampus when they were VAD which shows neuronal impairment.[51] When the patient is VAD for too long, the effects of the damage to the hippocampus can be irreversible.[52]

Spatial memory[edit]

Vitamin A affects spatial memory most of the time because the size of the nuclei in hippocampal neurons are reduced by approximately 70% when there is a deficiency which affects a person's abilities for higher cognitive function. In a study by the University Of Cagliari, Italy, VAD rats had more trouble learning a Radial arm maze than rats who had normal levels of the vitamin. The healthy rats were able to correctly solve the maze within the 15-day training period and other rats that were once deficient but had Vitamin A restored to normal levels were also able to solve it. Here it was found that the Retinoid receptors which help transport Vitamin A were of normal function.[53]

Prevention, treatment and symptoms[edit]

Eating foods high in Vitamin A or taking dietary supplements, Retinol or Retinal will prevent a deficiency. The foods highest in Vitamin A are any pigmented fruits and vegetables and leafy green vegetables also provide beta-Carotene.[49] There can be symptoms of fat loss and a reduction of any weight gain that would be considered normal for an individual,[53] especially developmental weight gains such as in infants which would occur if the infant was deprived of Vitamin A while In utero and/or if it was deprived postnatal for an extensive period of time.[50] The deficiency can also cause conditions such as blindness or night blindness, also known as Nyctalopia. Night blindness is due to the inability to regenerate Rhodopsin in the rods which is needed in dim light in order to see properly.[49] A treatment of supplements of Retinoic acid which is a part of Vitamin A can help replenish levels and help bring learning to normal,[54] but after 39 weeks this is ineffective even if the treatment is daily because it will not bring the retinoid hypo-signalling back to normal.[52]

Relationship with zinc[edit]

Zinc is a very important part of the brain as well; many regions of the brain, such as the cerebellum, and hippocampus have neurons that contain this nutrient.[55] Zinc is needed to maintain normal Vitamin A levels in blood plasma.[49] It was found that VAD rats had lower plasma Retinol levels.[54] It also helps Vitamin A become metabolized by the Liver. However evidence suggests that when someone is deficient in both Vitamin A and zinc, memory is more improved when just Vitamin A is increased than when just zinc is increased. Of course Memory has the largest improvement when both are increased. When one of these nutrients is not balanced, the other is most likely to be affected because they rely on each other for proper functioning in learning.[55]

Aging and cognitive disease[edit]

Foods that are rich in Omega-3 fatty acids have been shown to decrease risk of getting Alzheimer's disease.[56] Omega-3 fatty acids, primarily Docosahexanoic acid (DHA), which is the most prevalent omega-3 fatty acid found in neurons, have been studied extensively for use in possible prevention and therapy of Alzheimer's disease. Some studies (cross-sectional) suggest that reduced intake or low brain levels of DHA are associated with earlier development of cognitive deficits or development of dementia, including Alzheimer's disease. Several clinical trials suggest that omega-3 fatty acid supplementation does not have significant effects in the treatment of Alzheimer's disease—which in turn may suggest that the protective benefits of omega-3 fatty acid supplementation could depend on the scope of the disease and other confounding factors.[57] A diet that is rich in antioxidants will also help get rid of free radicals in your body, which could be a cause for Alzheimer's. The buildup of Beta Amyloid plaques, a marker highly associated with Alzheimer's disease, generates cell damaging free radicals. Therefore, the role of antioxidants as protectants against Alzheimer's disease has become a hot topic of study.[58] Simple dietary modification, towards fewer highly processed carbohydrates and relatively more fats ad cholesterol, is likely a protective measure against Alzheimer's disease.[citation needed]

Additionally, folic acid has also been found to improve the memory of older people. There is some evidence that deficiency in folic acid may increase the risk of dementia, especially Alzheimer's disease and vascular dementia, but there is debate about whether it lowers risk of cognitive impairment in the older population.[59][60] Folic acid supplementation is shown to lower blood homocysteine levels, while folic acid deficiency can lead to a condition of high levels of homocysteine (Hcy) in the bloodstream called hyperhomocysteinemia (HHcy). HHcy is related to several vascular diseases such as coronary artery disease, peripheral vascular disease, and stroke. Recently, HHcy was found to play a role in the development of Alzheimer's disease. In an experiment that gave one group of mice a folic acid deficient diet and the other group a diet treated with placebo, the folic acid deficient group developed higher blood Hcy levels as well as more beta amyloid (Aβ) peptides, the building blocks of Beta Amyloid plaques which are deposits found in the brains of those with Alzheimer's disease.[61]


Dementia is a common form of age related cognitive decline. Dementia interferes with normal functioning operations, as well as a significant amount of memory loss. 25–29 million people over the world suffer from dementia.[citation needed] Alzheimer's disease is considered as the most common cause of dementia in people age 65 and older, estimated at 15–20% in this age group. The incidence and prevalence of Alzheimer's disease tends to increase exponentially with age, leading experts to suggest that the reported 5 million persons in the US (2010) would quadruple by year 2050, unless effective treatment is developed.[62] One kind of Dementia is Vascular dementia, which has risk factor for strokes that are related to nutrition such has diabetes and obesity. Increased blood pressure can raise the risk for dementia. There have been several amino acid studies done on dementia. There is a significant less amount of tryptophan and methionine in people who have dementia. Another amino acid, homocysteine plays a role in the physiology of people with dementia. Antioxidants play a role in neutralizing free radicals, which put you at a higher risk for cancer as well as dementia.[63]

Alzheimer's dementia[edit]

The Alzheimer's Association estimates that 1 in 10 people over age 65 and nearly half of people over 85 have Alzheimer's disease. There is no clear identifying impairment pattern. It is identified by the presence of amyloid plaques and neurofibrallary tangles in the hippocampus. Some symptoms are forgetting, trouble with words and names, delusions and hallucinations. Moderate or mild malnutrition can cause an increased risk for Alzheimer's. About 4 million Americans a year are classified with Alzheimer's.

See also[edit]


  1. ^ a b c Gómez-Pinilla, Fernando (2008). "Brain foods: The effects of nutrients on brain function". Nature Reviews Neuroscience. 9 (7): 568–78. doi:10.1038/nrn2421. PMC 2805706Freely accessible. PMID 18568016. 
  2. ^ a b c d Bourre, JM (2006). "Effects of nutrients (in food) on the structure and function of the nervous system: Update on dietary requirements for brain. Part 1: Micronutrients". The journal of nutrition, health & aging. 10 (5): 377–85. PMID 17066209. 
  3. ^ Vitamin Basics: The facts about Vitamins in Nutrition (PDF). Germany: DSM Nutritional Products. 2007. [page needed]
  4. ^ Choline (at Linus Paulin Inst)[full citation needed]
  5. ^ a b c Zeisel, Steven H; Da Costa, Kerry-Ann (2009). "Choline: An essential nutrient for public health". Nutrition Reviews. 67 (11): 615–23. doi:10.1111/j.1753-4887.2009.00246.x. PMC 2782876Freely accessible. PMID 19906248. 
  6. ^ "Dietary Reference Intakes". Institute of Medicine. 
  7. ^ Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline (PDF). Washington, DC: National Academy Press. 1998. ISBN 0-309-06554-2. [page needed]
  8. ^ a b Thompson, J (2005). "Vitamins, minerals and supplements: Part two". Community practitioner. 78 (10): 366–8. PMID 16245676. 
  9. ^ a b c Ogershok, Paul R.; Rahman, Aamer; Nestor, Scott; Brick, James (2002). "Wernicke Encephalopathy in Nonalcoholic Patients". American Journal of the Medical Sciences. 323 (2): 107–11. doi:10.1097/00000441-200202000-00010. PMID 11863078. 
  10. ^ a b c d e Bond, Nigel W.; Homewood, Judi (1991). "Wernicke's encephalopathy and Korsakoff's psychosis: To fortify or not to fortify?". Neurotoxicology and Teratology. 13 (4): 353–5. doi:10.1016/0892-0362(91)90083-9. PMID 1921914. 
  11. ^ a b c Cooper, Jack R.; Pincus, Jonathan H. (1979). "The role of thiamine in nervous tissue". Neurochemical Research. 4 (2): 223–39. doi:10.1007/BF00964146. PMID 37452. 
  12. ^ a b c Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline (PDF). Washington, DC: National Academy Press. 1998. ISBN 0-309-06554-2. [page needed]
  13. ^ a b c d e f Singleton., C.K.; Martin, P.R. (2001). "Molecular Mechanisms of Thiamine Utilization". Current Molecular Medicine. 1 (2): 197–207. doi:10.2174/1566524013363870. PMID 11899071. 
  14. ^ Hoyumpa, Anastacio M. (1983). "Alcohol and Thiamine Metabolism". Alcoholism: Clinical and Experimental Research. 7: 11–14. doi:10.1111/j.1530-0277.1983.tb05403.x. 
  15. ^ a b c Harper, C (1979). "Wernicke's encephalopathy: A more common disease than realised. A neuropathological study of 51 cases". Journal of Neurology, Neurosurgery & Psychiatry. 42 (3): 226–31. doi:10.1136/jnnp.42.3.226. PMC 490724Freely accessible. PMID 438830. 
  16. ^ a b Harper, C G; Giles, M; Finlay-Jones, R (1986). "Clinical signs in the Wernicke-Korsakoff complex: A retrospective analysis of 131 cases diagnosed at necropsy". Journal of Neurology, Neurosurgery & Psychiatry. 49 (4): 341–5. doi:10.1136/jnnp.49.4.341. PMC 1028756Freely accessible. PMID 3701343. 
  17. ^ Vitamin Basics: The facts about Vitamins in Nutrition (PDF). Germany: DSM Nutritional Products Ltd. 2007. [page needed]
  18. ^ a b c d e f Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vita1min B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline (PDF). Washington, DC: National Academy Press. 1998. ISBN 0-309-06554-2. [page needed]
  19. ^ Yehuda, Shlomo; Rabinovitz, Sharon; Mostofsky, David I. (1999). "Essential fatty acids are mediators of brain biochemistry and cognitive functions". Journal of Neuroscience Research. 56 (6): 565–70. doi:10.1002/(SICI)1097-4547(19990615)56:6<565::AID-JNR2>3.0.CO;2-H. PMID 10374811. 
  20. ^ a b c d e f Hegyi, Juraj; Schwartz, Robert A.; Hegyi, Vladimir (2004). "Pellagra: Dermatitis, dementia, and diarrhea". International Journal of Dermatology. 43 (1): 1–5. doi:10.1111/j.1365-4632.2004.01959.x. PMID 14693013. 
  21. ^ a b Flicker, Leon; Ames, David (2005). "Metabolic and endocrinological causes of dementia". International Psychogeriatrics. 17: S79–92. doi:10.1017/S1041610205001961. PMID 16240485. 
  22. ^ Zimmerman, HM (1939). "The Pathology of the Nervous System in Vitamin Deficiencies". The Yale Journal of Biology and Medicine. 12 (1): 23–28.7. PMC 2602501Freely accessible. PMID 21433862. 
  23. ^ Rainer, M.; Kraxberger, E.; Haushofer, M.; Mucke, H. A. M.; Jellinger, K. A. (2000). "No evidence for cognitive improvement from oral nicotinamide adenine dinucleotide (NADH) in dementia". Journal of Neural Transmission. 107 (12): 1475–81. doi:10.1007/s007020070011. PMID 11459000. 
  24. ^ Morris, M C (2004). "Dietary niacin and the risk of incident Alzheimer's disease and of cognitive decline". Journal of Neurology, Neurosurgery & Psychiatry. 75 (8): 1093–1099. doi:10.1136/jnnp.2003.025858. 
  25. ^ a b c d e f g h i j Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline (PDF). Washington, DC: National Academy Press. 1998. ISBN 0-309-06554-2. [page needed]
  26. ^ a b c Hauck, MR (1991). "Cognitive abilities of preschool children: Implications for nurses working with young children". Journal of pediatric nursing. 6 (4): 230–5. PMID 1865312. 
  27. ^ a b c Moyers, S; Bailey, LB (2001). "Fetal malformations and folate metabolism: Review of recent evidence". Nutrition Reviews. 59 (7): 215–24. doi:10.1111/j.1753-4887.2001.tb07013.x. PMID 11475447. 
  28. ^ a b Homocysteine Lowering Trialists' Collaboration (2005). "Dose-dependent effects of folic acid on blood concentrations of homocysteine: A meta-analysis of the randomized trials". The American Journal of Clinical Nutrition. 82 (4): 806–12. PMID 16210710. 
  29. ^ a b Malouf, R; Grimley Evans, J; Areosa Sastre, A; Malouf, Reem (2003). "Folic acid with or without vitamin B12 for cognition and dementia". The Cochrane Database of Systematic Reviews. doi:10.1002/14651858.CD004514. 
  30. ^ a b c Bottiglieri, T (1996). "Folate, vitamin B12, and neuropsychiatric disorders". Nutrition Reviews. 54 (12): 382–90. doi:10.1111/j.1753-4887.1996.tb03851.x. PMID 9155210. 
  31. ^ a b Botto, Lorenzo D.; Moore, Cynthia A.; Khoury, Muin J.; Erickson, J. David (1999). "Neural-Tube Defects". New England Journal of Medicine. 341 (20): 1509–19. doi:10.1056/NEJM199911113412006. PMID 10559453. 
  32. ^ Quadri, P; Fragiacomo, C; Pezzati, R; Zanda, E; Forloni, G; Tettamanti, M; Lucca, U (2004). "Homocysteine, folate, and vitamin B-12 in mild cognitive impairment, Alzheimer disease, and vascular dementia". The American Journal of Clinical Nutrition. 80 (1): 114–22. PMID 15213037. 
  33. ^ Shorvon, S D; Carney, M W; Chanarin, I; Reynolds, E H (1980). "The neuropsychiatry of megaloblastic anaemia". BMJ. 281 (6247): 1036–8. doi:10.1136/bmj.281.6247.1036. PMC 1714413Freely accessible. PMID 6253016. 
  34. ^ Bryan, J; Calvaresi, E; Hughes, D (2002). "Short-term folate, vitamin B-12 or vitamin B-6 supplementation slightly affects memory performance but not mood in women of various ages". The Journal of Nutrition. 132 (6): 1345–56. PMID 12042457. 
  35. ^ Wahlin, Åke; Hill, Robert D.; Winblad, Bengt; Bäckman, Lars (1996). "Effects of serum vitamin B-sub-1-sub-2 and folate status on episodic memory performance in very old age: A population-based study". Psychology and Aging. 11 (3): 487–96. doi:10.1037/0882-7974.11.3.487. PMID 8893317. 
  36. ^ Durga, Jane; Van Boxtel, Martin PJ; Schouten, Evert G; Kok, Frans J; Jolles, Jelle; Katan, Martijn B; Verhoef, Petra (2007). "Effect of 3-year folic acid supplementation on cognitive function in older adults in the FACIT trial: A randomised, double blind, controlled trial". The Lancet. 369 (9557): 208–216. doi:10.1016/S0140-6736(07)60109-3. 
  37. ^ Fioravanti, M; Ferrario, E; Massaia, M; Cappa, G; Rivolta, G; Grossi, E; Buckley, AE (1998). "Low folate levels in the cognitive decline of elderly patients and the efficacy of folate as a treatment for improving memory deficits". Archives of gerontology and geriatrics. 26 (1): 1–13. doi:10.1016/s0167-4943(97)00028-9. PMID 18653121. 
  38. ^ Subar, AF; Block, G; James, LD (1989). "Folate intake and food sources in the US population". The American Journal of Clinical Nutrition. 50 (3): 508–16. PMID 2773830. 
  39. ^ a b c Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline (PDF). Washington, DC: National Academy Press. 1998. ISBN 0-309-06554-2. [page needed]
  40. ^ a b c Vitamin Basics: The facts about Vitamins in Nutrition (PDF). DSM Nutritional Products. 2007. [page needed]
  41. ^ a b c d e Baik, H.W.; Russell, R.M. (1999). "Vitamin B12Deficiency in the Elderly". Annual Review of Nutrition. 19: 357–77. doi:10.1146/annurev.nutr.19.1.357. PMID 10448529. 
  42. ^ Schenk, BE; Kuipers, EJ; Klinkenberg-Knol, EC; Bloemena, EC; Sandell, M; Nelis, GF; Snel, P; Festen, HP; Meuwissen, SG (1999). "Atrophic gastritis during long-term omeprazole therapy affects serum vitamin B12 levels". Alimentary Pharmacology and Therapeutics. 13 (10): 1343–6. doi:10.1046/j.1365-2036.1999.00616.x. PMID 10540050. 
  43. ^ a b c d e Hvas, AM; Nexo, E (2006). "Diagnosis and treatment of vitamin B12 deficiency--an update". Haematologica. 91 (11): 1506–12. PMID 17043022. 
  44. ^ "Neurological Manifestations of Vitamin B-12 Deficiency". The Internet Journal of Nutrition and Wellness. 2. 2005. doi:10.5580/5a9. 
  45. ^ a b c d e f Epstein, Franklin H.; Toh, Ban-Hock; Van Driel, Ian R.; Gleeson, Paul A. (1997). "Pernicious Anemia". New England Journal of Medicine. 337 (20): 1441–8. doi:10.1056/NEJM199711133372007. PMID 9358143. 
  46. ^ a b c Stabler, Sally P.; Allen, Robert H. (2004). "Vitamin B12 Deficiency As a Worldwide Problem". Annual Review of Nutrition. 24: 299–326. doi:10.1146/annurev.nutr.24.012003.132440. PMID 15189123. 
  47. ^ a b Holmes, J. M. (1956). "Cerebral Manifestations of Vitamin-B12 Deficiency". BMJ. 2 (5006): 1394–8. doi:10.1136/bmj.2.5006.1394. PMC 2035923Freely accessible. PMID 13374343. 
  48. ^ Sanders, T. A. B.; Ellis, F. R.; Dickerson, J. W. T. (2007). "Haematological studies on vegans". British Journal of Nutrition. 40 (1): 9–15. doi:10.1079/BJN19780089. PMID 667007. 
  49. ^ a b c d Edem, D.O. (2009). "Vitamin A: A Review". Asian Journal of Clinical Nutrition. 1: 65–82. doi:10.3923/ajcn.2009.65.82. 
  50. ^ a b Li, T.-Y.; Huang, H.-M.; Mao, C.-T.; Liu, Y.; Qu, P.; Yang, L. (2008). "Marginal Vitamin a Deficiency in Pregnancy Can Induce Memory Deficit in Adult Offspring". Pediatrics. 121: S152. doi:10.1542/peds.2007-2022NNNNNN. 
  51. ^ Li, T.-Y.; Mao, C.-T.; Huang, H.-M.; Liu, Y.-X.; Qu, P.; Yang, L. (2008). "Effects of Marginal Vitamin a Deficiency on Long-Term Potentiation in Young Rats". Pediatrics. 121: S153. doi:10.1542/peds.2007-2022OOOOOO. 
  52. ^ a b Etchamendy, Nicole; Enderlin, Valérie; Marighetto, Aline; Pallet, Véronique; Higueret, Paul; Jaffard, Robert (2003). "Vitamin a deficiency and relational memory deficit in adult mice: Relationships with changes in brain retinoid signalling". Behavioural Brain Research. 145 (1–2): 37–49. doi:10.1016/S0166-4328(03)00099-8. PMID 14529804. 
  53. ^ a b Cocco, S; Diaz, G; Stancampiano, R; Diana, A; Carta, M; Curreli, R; Sarais, L; Fadda, F (2002). "Vitamin a deficiency produces spatial learning and memory impairment in rats". Neuroscience. 115 (2): 475–82. doi:10.1016/S0306-4522(02)00423-2. PMID 12421614. 
  54. ^ a b Hernández-Pinto, A.M.; Puebla-Jiménez, L.; Arilla-Ferreiro, E. (2006). "A vitamin A-free diet results in impairment of the rat hippocampal somatostatinergic system". Neuroscience. 141 (2): 851–61. doi:10.1016/j.neuroscience.2006.04.034. PMID 16757122. 
  55. ^ a b Kheirvari, Sorayya; Uezu, Kayoko; Sakai, Tohru; Nakamori, Masayo; Alizadeh, Mohammad; Sarukura, Nobuko; Yamamoto, Shigeru (2006). "Increased Nerve Growth Factor by Zinc Supplementation with Concurrent Vitamin a Deficiency Does Not Improve Memory Performance in Mice". Journal of Nutritional Science and Vitaminology. 52 (6): 421–7. doi:10.3177/jnsv.52.421. PMID 17330505. 
  56. ^ Vakhapova, Veronika; Cohen, Tzafra; Richter, Yael; Herzog, Yael; Korczyn, Amos D. (2010). "Phosphatidylserine Containing ω–3 Fatty Acids May Improve Memory Abilities in Non-Demented Elderly with Memory Complaints: A Double-Blind Placebo-Controlled Trial". Dementia and Geriatric Cognitive Disorders. 29 (5): 467–74. doi:10.1159/000310330. PMID 20523044. 
  57. ^ Jicha, GA; Markesbery, WR (Apr 7, 2010). "Omega-3 fatty acids: potential role in the management of early Alzheimer's disease.". Clinical interventions in aging. 5: 45–61. doi:10.2147/cia.s5231. PMC 2854051Freely accessible. PMID 20396634. 
  58. ^ Miranda S, Opazo C, Larrondo LF, Muñoz FJ, Ruiz F, Leighton F, Inestrosa NC (2000). "The role of oxidative stress in the toxicity induced by amyloid ß-peptide in Alzheimer's disease". Progress in Neurobiology. 62 (6): 633–648. doi:10.1016/S0301-0082(00)00015-0. PMID 10880853. 
  59. ^ Berry, RJ; Carter, HK; Yang, Q (July 2007). "Cognitive impairment in older Americans in the age of folic acid fortification.". The American Journal of Clinical Nutrition. 86 (1): 265–7; author reply 267–9. PMID 17616791. 
  60. ^ Reynolds, EH (Jun 22, 2002). "Folic acid, ageing, depression, and dementia.". BMJ (Clinical research ed.). 324 (7352): 1512–5. doi:10.1136/bmj.324.7352.1512. PMC 1123448Freely accessible. PMID 12077044. 
  61. ^ Zhuo, JM; Praticò, D (March 2010). "Acceleration of brain amyloidosis in an Alzheimer's disease mouse model by a folate, vitamin B6 and B12-deficient diet.". Experimental Gerontology. 45 (3): 195–201. doi:10.1016/j.exger.2009.12.005. PMC 2826592Freely accessible. PMID 20005283. 
  62. ^ Jicha, GA; Carr, SA (2010). "Conceptual evolution in Alzheimer's disease: implications for understanding the clinical phenotype of progressive neurodegenerative disease". Journal of Alzheimer's disease : JAD. 19 (1): 253–72. doi:10.3233/JAD-2010-1237. PMC 2881218Freely accessible. PMID 20061643. 
  63. ^ González-Gross, M.; Marcos, Ascensión; Pietrzik, Klaus (2007). "Nutrition and cognitive impairment in the elderly". British Journal of Nutrition. 86 (3): 313–21. doi:10.1079/BJN2001388. PMID 11570983.