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. 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. b12 is produced in the digestive tracts of all animals, including humans. thus, animal-origin food is the only natural food source of vitamin b12 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. deficiencies 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. b12 deficiency, also known as hypocobalaminemia, often results from complications involving absorption into the body. b12 deficiency is often associated with pernicious anemia, as it is the most common cause. 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. 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. those affected by 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. 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. 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. 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. symptoms 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, 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. 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. all of these symptoms may present with or without additional mood changes. 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. it is not always easy to determine whether b12 deficiency is present, especially within older adults. 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. tests must be run on individuals presenting with such signs to confirm or negate cobalamin deficiency within the blood. treatment 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 have 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. 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 patient's 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. the progression of neurological manifestations of cobalamin deficiency is generally gradual. as a result, early diagnosis is important or else irreversible damage may occur. patients who become demented usually show little to no cognitive improvement with the administration of b12. 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. prevention in addition to meeting intake requirements through food consumption, supplementation of diet with vitamin b12 is seen as a viable preventive measure for deficiency. it has been recommended for the elderly to supplement 50 mcg a day in order to prevent deficit from occurring. 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. 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. 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. vitamin d vitamin d is an essential regulator of the vitamin d receptor that controls gene transcription during development. the vitamin d receptor is strongly expressed in the substantia nigra. accordingly, vitamin d deficiency can disrupt neurogenesis leading to altered dopamine signaling and increased exploratory behavior in rats. this is considered a rodent model of the schizophrenia phenotype and vitamin d deficiency has been proposed as an explanation for the increased incidence of schizophrenia among children that were conceived during winter months. a finnish study found that vitamin d supplement use is associated with reduced risk of schizophrenia. vitamin d deficiency may also have downstream effects on neurosteriod synthesis. vitamin d supplementation appears to increase both free and total testosterone levels in healthy men, with serum vitamin d levels between 70-80 nmol/l having been shown to maximize testosterone production in overweight men. 5a-androstanediol, a metabolite of testosterone, is a potent positive allosteric modulator of the gabaa receptor. the synthesis of 5a-androstanediol is generally correlated with that of testosterone production. lipids fat fatty acids are necessary for the synthesis of cell membranes neurotransmitters and other signaling molecules. while excessive fat intake can be harmful, deficiency of essential fatty acids can disrupt neurodevelopment and synaptic plasticity. saturated fat consuming large amounts of saturated fat can negatively affect the brain. eating foods with saturated fats elevates the level of cholesterol and triglycerides in the body. studies have shown that high levels of triglycerides strongly link with mood problems such as depression, hostility and aggression. this may occur because high triglyceride levels decrease the amount of oxygen that blood can carry to the brain. the american heart association recommends that people consume no more than 16g of saturated fat daily. common sources of saturated fat are meat and dairy products. essential fatty acids there are two kinds of essential fatty acids that people must consume (omega-3 and omega-6). many academics recommend a balanced amount of omega-3s and omega-6s. however, some estimate that americans consume twenty times more omega-6s than omega-3s. there is a theory that an imbalance of essential fatty acids may lead to mental disorders such as depression, hyperactivity and schizophrenia, but it still lacking evidences. an omega-3 deficient diet increases omega-6 levels in the brain disrupting endocannabinoid signaling in the prefrontal cortex and nucleus accumbens contributing to anxiety and depression-like behaviors in mice. sources of omega-3 include flax seeds, chia seeds, walnuts, sea vegetables, green leafy vegetables, and cold water fish. sources of omega-6 include walnuts, hazelnuts; sunflower, safflower, corn, and sesame oils. cholesterol while cholesterol is essential for membranes and steroid hormones, excess cholesterol affects blood flow impairing cognitive function in vascular dementia. carbohydrates studies have shown that learning and memory improve after consuming carbohydrates. there are two kinds of carbohydrates people consume: simple and complex. simple carbohydrates are often found in processed foods and release sugar into the bloodstream quickly after consumption. complex carbohydrates are digested more slowly and therefore cause sugar to be released into the bloodstream more slowly. good sources of complex carbohydrates are whole-grain breads, pasta, brown rice, oatmeal, and potatoes. it is recommended that people consume more complex carbohydrates because consuming complex carbohydrates will cause the level of sugar in the bloodstream to be more stable, which will cause less stress hormones to be released. consuming simple carbohydrates may cause the levels of sugar in the bloodstream to rise and fall, which can cause mood swings. low carbohydrate ketogenic diets the ketone body beta-hydroxybutyrate is a fuel source for the brain during times of fasting when blood glucose levels fall. although the mechanism is not understood, it is well established that eating a diet low in carbohydrates can be therapeutic for children with epilepsy. this is likely a result of ketone bodies providing an alternative fuel source to glucose for neuronal function. furthermore, a ketogenic diet can be beneficial for dementia patients. medium-chain triglycerides can stimulate ketone synthesis and coconut oil is a rich source of medium chain triglycerides that several anecdotal reports suggest can improve cognitive function in alzheimer's type dementia patients. protein when protein is consumed, it is broken down into amino acids. these amino acids are used to produce many things like neurotransmitters, enzymes, hormones, and chromosomes. proteins known as complete proteins contain all eight of the essential amino acids. meat, cheese, eggs, and yogurt are all examples of complete proteins. incomplete proteins contain only some of the eight essential amino acids and it is recommended that people consume a combination of these proteins. examples of incomplete proteins include nuts, seeds, legumes, and grains. when animals are fed a diet deficient in essential amino acids, uncharged trnas accumulate in the anterior piriform cortex signaling diet rejection . the body normally interconverts amino acids to maintain homeostasis, but muscle protein can be catabolized to release amino acids during conditions of amino acid