Nutrition and cognition

Choline is an essential nutrient and its primary function within the human body is the synthesis of cellular membranes,[3] 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 deficiencies may be related to some liver and neurological disorders.[4] Because of its role in cellular synthesis, choline is an important nutrient during the prenatal and early postnatal development of offspring as it contributes to brain development.[3] Choline intakes from food for men, women and children may be below the Adequate Intake levels.[4] Women, especially when pregnant or lactating, the elderly, and infants, are at risk for choline deficiency.[4][5] Beef liver, wheat germ, and egg yolks are common foods providing choline.[3]

Lutien and Zeaxanthin are carotenoids that contain very strong antioxidants. Most of the research thus far has focused on the effect that these cartenoids have on vision and increased processing speeds of the eye. In recent years, scientists have shifted their focus to their contribution to brain development and cognition due to newly found bio-accumulation of lutien and zeaxanthin on the brain. These nutrients can be found mostly in dark, leafy greens. Some other foods include eggs, broccoli, zucchini, corn, and brussel sprouts. These foods should be raw or steamed in order to get the most nutrients out of them.[6]

Salmon is very high in omega 3 acids and DHA. There are other lean "white" fish meats, like albacore white tuna, that are a good source of protein but because they are more lean they are not high in fats. Salmon salad sandwiches, instead of tuna salad, will provide both protein and omega 3 fatty acids.[8]

Aside from many other nutrients contained in flax seeds, just one tablespoon of flax seeds contains 1,597 mg of omega 3 fatty acids.

Many dark, rich colored berries are shown to improve memory.[9]

Peanut butter is a very good source of vitamin E which is an antioxidant. It also contains thiamin that helps support the brain and nervous systems. Nuts are also a very good source of protein for providing energy and increased concentration.[7]

Whole grains provide a lot of glucose and fiber. The fiber from the grains helps to regulate the release of glucose into the body. Glucose sugars are used by your body for energy. Higher levels of energy are shown to improve concentration levels of the brain. Lean beef is an excellent source of iron which is also shown to provide energy levels and increase concentration.[7] a

These types of foods are rich with antioxidants needed to cleanse the blood stream and help to keep brain cells strong.[7]

Dairy foods provide the body with Vitamins B and D. Vitamin B is essential for brain tissue growth and also provides the body with enzymes.[7]

Leafy greens such as collard greens, spinach, cabbage, romaine lettuce, and kale are a good source of folate and very rich in vitamins.[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.[11] Thiamine is found throughout mammalian nervous tissue, including the brain and spinal cord. Metabolism and coenzyme function of the vitamin suggest a distinctive function for thiamine within the nervous system.[12] 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.[13]

Lack of thiamin causes the disease known as beriberi.[14] There are two forms of beriberi: "wet", and "dry". Dry beriberi is also known as cerebral beriberi and characterized by peripheral neuropathy.[12] Thiamine deficiency has been reported in up to 80% of people who are alcoholic due to inadequate nutritional intake, reduced absorption, and impaired utilization of thiamine.[15][16] Clinical signs of B₁ deficiency include mental changes such as apathy, decrease in short-term memory, confusion, and irritability;[14] also increased rates of depression, dementia, falls, and fractures in old age.[16]

The lingering symptoms of neuropathy associated with cerebral beriberi are known as Korsakoff's syndrome, or the chronic phase of Wernicke-Korsakoff's.[17] Wernicke encephalopathy is characterized by ocular abnormalities, ataxia of gait, a global state of confusion, and neuropathy.[16] The state of confusion associated with Wernicke's may consist of apathy, inattention, spatial disorientation, inability to concentrate, and mental sluggishness or restlessness.[18] Clinical diagnosis of Wernicke's disease cannot be made without evidence of ocular disturbance, yet these criteria may be too rigid.[19] Korsakoff's syndrome likely represents a variation in the clinical manifestation of Wernicke encephalophathy, as they both share similar pathological origin.[19] It is often characterized by confabulation, disorientation, and profound amnesia.[17] 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.[16][17] 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.[18][13] Improvements in brain functioning of chronic alcoholics may occur with abstinence-related treatment, involving the discontinuation of alcohol consumption and improved nutrition.[16]

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. Niacin is involved in the synthesis of fatty acids and cholesterol, known mediators of brain biochemistry, and in effect, of cognitive function.[20] Pellagra is a niacin deficiency disease. Pellagra is classically characterized by four 4 "D's": diarrhea, dermatitis, dementia, and death. 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. 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.[21]

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 people 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.[22] Though treatment with niacin does little to alter the effects of Alzheimer's dementia, niacin intake from foods is inversely associated with the disease.[23]

Folate and vitamin B₁₂ play a vital role in the synthesis of S-adenosylmethionine, which is of key importance in the maintenance and repair of all cells, including neurons.[24] 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] 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.[26] The relationship between folate and B₁₂ is so interdependent that deficiency in either vitamin can result in megaloblastic anemia, characterized by organic mental change.[27]

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,[26] 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.[28]

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.[27][29] Neurological effects are not often associated with folate-related megaloblastic anemia, although demyelinating disorders may eventually present.[27] In one study, mood disturbances were recorded for the majority of people with megaloblastic anemia in the absence of B₁₂ deficiency.[25] In addition, folate concentrations within blood plasma have been found to be lower in people 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.[30]

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.[31] 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,[32] 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.[33]

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.[34] 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.[24]

Also known as cobalamin, B₁₂ is important for the maintenance of neurological function and psychiatric health.[35] B₁₂ deficiency, also known as hypocobalaminemia, often results from complications involving absorption into the body.[36] 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,[37] and may be expressed behaviorally 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. 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 behavior, visual and auditory hallucinations, dysphasia, violent maniacal behavior 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.[37]

Mild to moderate cases of pernicious anemia may show poor concentration. In severe cases of pernicious anemia, individuals may present with various cognitive problems such as dementia, and memory loss. It is not always easy to determine whether B₁₂ deficiency is present, especially within older adults.[36] People may present with violent behavior 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 behavior in Alzheimer's and other dementias as well.

People who are deficient in B₁₂ despite normal absorption functionality may be treated through oral administration of at least 6 µg/day of the vitamin in pill form. People 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 person's level of deficiency as well as their level of cognitive functioning.[36] Treatment for those with severe deficiency involves 1000 µg of B₁₂ administered intramuscularly daily for one week, weekly for one month, then monthly for the rest of the person's life. The progression of neurological manifestations of cobalamin deficiency is generally gradual. As a result, early diagnosis is important or else irreversible damage may occur.[35] People who become demented usually show little to no cognitive improvement with the administration of B₁₂. 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, peoplewould still be at risk for neurological deficits associated with B₁₂ deficiency-related anemia, which are not associated with anemia related to folate deficiency.[38]