nutritional neuroscience nutritional neuroscience nutritional neuroscience is the scientific discipline that studies the effects various components of the diet such as minerals, vitamins, protein, carbohydrates, fats, dietary supplements, synthetic hormones, and food additives have on neurochemistry, neurobiology, behavior, and cognition. poor diet in early childhood affects the number of neurons in parts of the brain. recent research on nutritional mechanisms and their effect on the brain show they are involved in almost every facet of neurological functioning including alterations in neurogenesis, neurotrophic factors, neural pathways and neuroplasticity, throughout the life cycle. relatively speaking, the brain consumes an immense amount of energy in comparison to the rest of the body. the human brain is approximately 2% of the human body mass and uses 20–25% of the total energy expenditure. therefore, mechanisms involved in the transfer of energy from foods to neurons are likely to be fundamental to the control of brain function. insufficient intake of selected vitamins, or certain metabolic disorders, 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 neurotransmission, synaptic plasticity, and cell survival. minerals deficiency or excess of essential minerals (e.g. iron, zinc, copper, and magnesium) can disrupt brain development and neurophysiology to affect behavior. furthermore, minerals have been implicated in the pathophysiology of neurodegenerative diseases including alzheimer's dementia. iron iron is essential for several critical metabolic enzymes and a deficiency of this mineral can disrupt brain development. for, example chronic marginal iron affects dopamine metabolism and myelin fatty acid composition and behavior in mice. in rats a marginal iron deficiency that does not cause anemia disrupted axon growth in the auditory nerve affecting auditory brainstem latency without major changes in myelination. in rhesus macaques, prenatal iron deficiency disrupts emotional behavior and polymorphisms that reduce the expression of monoamine oxidase interact with gestational iron deficiency to exacerbate the response to a stressful situation leading to increased aggressiveness. inexpensive and effective iron supplementation is an available preventive strategy recommended by the world health organization. however, iron supplementation can exacerbate malaria infection. therefore, individuals receiving iron supplementation in malaria-endemic areas must be carefully monitored. zinc zinc is essential for the structure and function of thousands of proteins critical for the function of every cell. zinc can also serve as a neurotransmitter in the brain, thus a deficiency of this mineral can clearly disrupt development as well as neurophysiology. for example, zinc deficiency during early development impairs neurogenesis leading to memory impairments. however, zinc deficiency later in life can disrupt appetite and cause depression like behavior. however, it is important to consider copper intake relative to zinc supplementation because excess zinc can disrupt copper absorption. deficiency conservative estimates suggest that 25% of the world's population is at risk of zinc deficiency. hypozincemia is usually a nutritional deficiency, but can also be associated with malabsorption, diarrhea, acrodermatitis enteropathica, chronic liver disease, chronic renal disease, sickle cell disease, diabetes, malignancy, pyroluria, and other chronic illnesses. it can also occur after bariatric surgery, heavy metal exposure and tartrazine. zinc deficiency is typically the result of inadequate dietary intake of zinc, disease states that promote zinc losses, or physiological states that require increased zinc. populations that consume primarily plant based diets that are low in bioavailable zinc often have zinc deficiencies. diseases or conditions that involve intestinal malabsorption promote zinc losses. fecal losses of zinc caused by diarrhea are one contributing factor, often common in developing countries. changes in intestinal tract absorbability and permeability due, in part, to viral, protozoal, and bacteria pathogens may also encourage fecal losses of zinc. physiological states that require increased zinc include periods of growth in infants and children as well as in mothers during pregnancy. anorexia main article: anorexia (symptom) zinc deficiency may cause a decrease in appetite which can degenerate into anorexia or anorexia nervosa. appetite disorders, in turn, cause malnutrition and, notably, inadequate zinc intake. anorexia itself is a cause of zinc deficiency, thus leading to a vicious cycle: the worsening of anorexia worsens the zinc deficiency. a 1994 randomized, double-blind, placebo-controlled trial showed that zinc (14 mg per day) doubled the rate of body mass increase in the treatment of anorexia nervosa. cognitive and motor function impairment cognitive and motor function may also be impaired in zinc deficient children. zinc deficiency can interfere with many organ systems especially when it occurs during a time of rapid growth and development when nutritional needs are high, such as during infancy. in animal studies, rats who were deprived of zinc during early fetal development exhibited increased emotionality, poor memory, and abnormal response to stress which interfered with performance in learning situations. zinc deprivation in monkeys showed that zinc deficient animals were emotionally less mature, and also had cognitive deficits indicated by their difficulty in retaining previously learned problems and in learning new problems. human observational studies show weaker results. low maternal zinc status has been associated with less attention during the neonatal period and worse motor functioning. in some studies, supplementation has been associated with motor development in very low birth weight infants and more vigorous and functional activity in infants and toddlers. plasma zinc level has been associated with many psychological disorders. however, the nature of this relationship remains unclear in most instances. an increasing amount of evidence suggests that zinc deficiency could play a causal role in the etiology of depression. indeed, zinc supplementation has been reported to improve measures of depression in randomized double blind placebo controlled trials. deficiency the neurodegenerative syndrome of copper deficiency has been recognized for some time in ruminant animals, in which it is commonly known as "swayback". the disease involves a nutritional deficiency in the trace element copper. copper is ubiquitous and daily requirement is low making acquired copper deficiency very rare. copper deficiency can manifest in parallel with vitamin b12 and other nutritional deficiencies. the most common cause of copper deficiency is a remote gastrointestinal surgery, such as gastric bypass surgery, due to malabsorption of copper, or zinc toxicity. on the other hand, menkes disease is a genetic disorder of copper deficiency involving a wide variety of symptoms that is often fatal. neurological presentation copper deficiency can cause a wide variety of neurological problems including, myelopathy, peripheral neuropathy, and optic neuropathy. myelopathy affected individuals typically present difficulty walking (gait difficulty) caused by sensory ataxia (irregular muscle coordination) due to dorsal column dysfunction or degeneration of the spinal cord (myelopathy). patients with ataxic gait have problems balancing and display an unstable wide walk. they often feel tremors in their torso, causing side way jerks and lunges. in brain mri, there is often an increased t2 signalling at the posterior columns of the spinal cord in patients with myelopathy caused by copper deficiency. t2 signalling is often an indicator of some kind of neurodegeneration. there are some changes in the spinal cord mri involving the thoracic cord, the cervical cord or sometimes both. copper deficiency myelopathy is often compared to subacute combined degeneration (scd). subacute combined degeneration is also a degeneration of the spinal cord, but instead vitamin b12 deficiency is the cause of the spinal degeneration. scd also has the same high t2 signalling intensities in the posterior column as copper deficient patient in mri imaging. peripheral neuropathy another common symptom of copper deficiency is peripheral neuropathy, which is numbness or tingling that can start in the extremities and can sometimes progress radially inward towards the torso. in an advances in clinical neuroscience & rehabilitation (acnr) published case report, a 69-year-old patient had progressively worsened neurological symptoms. these symptoms included diminished upper limb reflexes with abnormal lower limb reflexes, sensation to light touch and pin prick was diminished above the waist, vibration sensation was lost in the sternum, and markedly reduced proprioception or sensation about the self's orientation. many people with the neurological effects of copper deficiency complain about very similar or identical symptoms as the patient. this numbness and tingling poses danger for the elderly because it increases their risk of falling and injuring themselves. peripheral neuropathy can become very disabling leaving some patients dependent on wheel chairs or walking canes for mobility if there is lack of correct diagnosis. rarely can copper deficiency cause major disabling symptoms. the deficiency will have to be present for an extensive amount of time until such disabling conditions manifest. optic neuropathy some patients with copper deficiency have shown signs of vision and color loss. the vision is usually lost in the peripheral views of the eye. the bilateral vision loss is usually very gradual. an optical coherence tomography (oct) shows some nerve fiber layer loss in most patients, suggesting the vision loss and color vision loss was secondary to optic neuropathy or neurodegeneration. toxicity copper toxicity can occur from excessive supplement use, eating acid foods cooked in uncoated copper cookware, exposure to excess copper in drinking water, or as the result of an inherited metabolic disorder in the case of wilson's disease. a significant portion of the toxicity of copper comes from its ability to accept and donate single electrons as it changes oxidation state. this catalyzes the production of very reactive radical ions, such as hydroxyl radical in a manner similar to fenton chemistry. this catalytic activity of copper is used by the enzymes with which it is associated, thus is only toxic when unsequestered and unmediated. this increase in unmediated reactive radicals is generally termed oxidative stress, and is an active area of research in a variety of diseases where copper may play an important but more subtle role than in acute toxicity. some of the effects of aging may be associated with excess copper. in addition, studies have found that people with mental illnesses, such as schizophrenia, had heightened levels of copper in their systems. however, it is unknown at this stage whether the copper contributes to the mental illness, whether the body attempts to store more copper in response to the illness, or whether the high levels of copper are the result of the mental illness. alzheimer's disease elevated free copper levels exist in alzheimer's disease. copper and zinc are known to bind to amyloid beta proteins in alzheimer's disease. this bound form is thought to mediate the production of reactive oxygen species in the brain. a preliminary clinical trial suggests that zinc supplementation may be able to decrease copper levels and slow degeneration in alzheimer's disease. manganese manganese is a component of some enzymes and stimulates the development and activity of other enzymes. manganese superoxide dismutase (mnsod) is the principal antioxidant in mitochondria. several enzymes activated by manganese contribute to the metabolism of carbohydrates, amino acids, and cholesterol. deficiency of manganese causes skeletal deformation in animals and inhibits the production of collagen in wound healing. on the other hand, manganese toxicity is associated with neurological complications. toxicity manganese poisoning is a toxic condition resulting from chronic exposure to manganese and first identified in 1837 by james couper. presentation chronic exposure to excessive mn levels can lead to a variety of psychiatric and motor disturbances, termed manganism. generally, exposure to ambient mn air concentrations in excess of 5 mg mn/m3 can lead to mn-induced symptoms. in initial stages of manganism, neurological symptoms consist of reduced response speed, irritability, mood changes, and compulsive behaviors. upon protracted exposure symptoms are more prominent and resemble those of idiopathic parkinson's disease, as which it is often misdiagnosed, although there are particular differences in both the symptoms (nature of tremors, for example), response to drugs such as levodopa, and affected portion of the basal ganglia. symptoms are also similar to lou gehrig's disease and multiple sclerosis. causes manganism has become an active issue in workplace safety as it has been the subject of numerous product liability lawsuits against manufacturers of arc welding supplies. in these lawsuits, welders have accused the manufacturers of failing to provide adequate warning that their products could cause welding fumes to contain dangerously high manganese concentrations that could lead welders to develop manganism. companies employing welders are also being sued, for what colloquially is known as "welders' disease". however, studies fail to show any link between employment as a welder and manganism (or other neurological problems). manganism is also documented in reports of illicit methcathinone manufacturing. this is due to manganese being