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19 Cards in this Set

  • Front
  • Back
why nutrition and brain?
1. no other organ system in the body has a greater minute-to-minute dependence on its nutrient supply than the CNS. CNS requires a constant supply of glucose
2. adequate brain function and maintenance depend on almost all the essential nutrients.
role of vitamin B in brain
deficiency of or congenital defects in the enzymes involved in the one-carbon pathways is associated with severe impairment of brain function.
folate deficiency causes what neurologic and behavioral dysfunction?
b12 deficiency causes what neurologic and behavioral dysfunction?
subacute combined degeneration (weakness,
abnormal sensations),
peripheral neuropathy,
b6 deficiency causes what neurologic and behavioral dysfunction?
peripheral neuropathy, seizures
cystathionine-gamma-synthase defect causes what neurologic and behavioral dysfunction?
mental retardation, psychiatric distrubances, seizures
MTHFR deficiency defect causes what neurologic and behavioral dysfunction?
subacute combined degneration, dementia, psychiatric disturbances, seizures
methyl-b12 defect causes what neurologic and behavioral dysfunction?
hypotonia (decreased muscle tone), seizures
Why are subclinical vitamin deficiencies of these important?
severe deficiencies and congenital defects are rare, milder subclinical vitamin deficiencies are not uncommon.
Interest is increasing in learning the extent to which these mild, reversible deficiencies contribute to some decline in cognitive function in the later years of life
why b status would decline with age
One of themost striking age-related changes in gastric histology and function is the increasing prevalence of ATROPHIC GASTRITIS WITH HYPOCHLORHYDRIA or achlorhydria. Prevalence ranges from 20-50%
the physiologic consequences of atrophic gastritis
1)changes in gastric emptying and 2)decreased secretion of intrinsic factor==> the stomach appears to have a large reserve capacity for IF secretion; only in the most severe cases of gastric atrophy does IF secretion become a rate-limiting factor for b12 absorption
3)gastric atrophy limits bioavailability of vitamin b12 because of impaired acid secretion and reduced digestion by pepsin.
4) another potential effect of atrophic gastritis is bacterial overgrowth in the stomach and proximal small bowel, which in turn can reduce b12 availability because some types of bacteria take up b12 for their own use
5)increased alkalinity (increased pH) in the stomach and proximal small intestine. This increase limits folic acid absorption; the optimum pH for active folate uptake is 6.3 (with gastritis: 7.1)
prevalence of inadequate b vitamin status
~30 for folate, 20-25% for b12, ~20% b6
types of epidemiologic data to date:
1. associations between b vitamin status, homocysteine and those with no dementia
2. supplementation with vitamins improve cognition (especially of short duration)
the part of the metabolism that is most crucial to the brain
methionine synthesis: a considerable proportion of methionine is activated by ATP to form SAM, which serves primarily as a universal methyl donor in a variety of reactions. In the brain, SAM-dependent methylations are extensive and the products of these reactions include neurotransmitters (catecholamines and indoleamines), phospholipids, and myelin. One hypothesis proposes that the loss of neurocognitive function in the elderly is ude in part to impaired methylation reactions in brain tissue. Because SAM is formed from metylation reactions involving folate, b12 and homocystein, the hypothesis states that the observed association between loss of cognitive function is due to lower production of SAM. Studies that have shown the efficacy of SAM as an antidepressant have provided some support for this hypothesis.
how SAH interferes with SAM
SAM is converted to SAH,after transfer of methyl group, which is subsequently hydrolyzed to homocysteine and adenosine. This hydrolysis is a reversible reaction that favors SAH synthesis. Thus, in the state of folate or vitamin b-12 deficiency, inability to methylate homocysteine leads to SAH accumulation. SAH is a potent inhibitor of the various SAM-dependent methylations. Hence the impaired methylations resulting from lower rates of SAM synthesis are augmented by the intracellular accumulation of SAH
which vitamin seems particularly associated with dementia?
AD subjects usually have low serum vitamin concentrations, particularly vitamin b12.
methionine hypothesis again
b12, folate (one or either) deficiency may lead to reduced synthesis of methionine and SAM, which in turn could restrict the availability of the methyl groups that are essential for the metabolism of myelin, neurotransmitters such as aceylcholine, and membrane phospholipids. This putative hypomethylation could disturb some aspects of brain metabolism, which may be responsible for the develpment of cognitive impairment.
homocysteine hypothesis
deficiencies of folate, b12, b6 are associated with increased plasma hcy concentrations==> increased risk of vascular, cardiac, and cerebral pathologies. Excess hcy==> deleterious effect on the blood vessel walls. This effect could explain why elderly subjects with long-term vitamin deficiencies develop minior neurologic disorders caused by small cerebrovascular lesions.
folate and mood
1) SAM's role as a cofactor in methylation reactions in catecholamine synthesis and metabolism. Catecholamines are known to be important in maintaining mood, and exogenous SAM is reputed to elevate mood.
2) folate has also been linked to the maintenance of adequate brain concentrations of tetrahydrobiopterin, a cofactor in the synthesis of serotonin and catecholamines. These transmitters, are important in maintaining normal affective state (mood)