Nutrition and cognition

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. Human bodily processes, including the brain, all require both macronutrients, as well as micronutrients. 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. Human bodily processes, including the brain, all require both macronutrients, as well as micronutrients. 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. Choline is an essential nutrient and its primary function within the human body is the synthesis of cellular membranes, 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. 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. 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. Women, especially pregnant or lactating women, older people, and infants, are especially at risk for choline deficiency. 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. 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. It is possible to identify broad cognitive effects of certain B vitamins, as they are involved in many significant metabolic processes within the brain. This vitamin is important for the facilitation of glucose use, thus ensuring the production of energy for the brain, and normal functioning of the nervous system, muscles and heart. 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. 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. Lack of thiamin causes the disease known as beriberi. There are two forms of beriberi: 'wet', and 'dry'. Dry beriberi is also known as cerebral beriberi and characterized by peripheral neuropathy. Thiamine deficiency has been reported in up to 80% of alcoholic patients due to inadequate nutritional intake, reduced absorption, and impaired utilization of thiamine. Clinical signs of B1 deficiency include mental changes such as apathy, decrease in short-term memory, confusion, and irritability; also increased rates of depression, dementia, falls, and fractures in old age. The lingering symptoms of neuropathy associated with cerebral beriberi are known as Korsakoff's syndrome, or the chronic phase of Wernicke-Korsakoff's. Wernicke encephalopathy is characterized by ocular abnormalities, ataxia of gait, a global state of confusion, and neuropathy. The state of confusion associated with Wernicke's may consist of apathy, inattention, spatial disorientation, inability to concentrate, and mental sluggishness or restlessness. Clinical diagnosis of Wernicke's disease cannot be made without evidence of ocular disturbance, yet these criteria may be too rigid. Korsakoff's syndrome likely represents a variation in the clinical manifestation of Wernicke encephalophathy, as they both share similar pathological origin. It is often characterized by confabulation, disorientation, and profound amnesia. 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. 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. Improvements in brain functioning of chronic alcoholics may occur with abstinence-related treatment, involving the discontinuation of alcohol consumption and improved nutrition. 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. 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. 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. Though treatment with niacin does little to alter the effects of Alzheimer's dementia, niacin intake from foods is inversely associated with the disease.