2. Pharmacy
Regulating body levels of zinc tends to occur on the intestinal absorption by the organization and the level of fecal excretion [35] [36] In cases of intestinal absorption of zinc deficiency can be near 100%. [35] This has been repeated in humans where the absorption of zinc deficiency in the cases and dims smugly. [37] [38] [39]
One animal study has suggested at least that the liberalization happens with the intestinal absorption of zinc during aging, food and adequate intake can in turn be sufficient metabolism due to poor absorption. [40]
Zinc absorption tends to be regulated, with increased intake of oral bioavailability associated with less, and about 5 mg absorbed in postmenopausal women, regardless of quantity or nutritional supplements. [41]
2.2. Transportation serum
In healthy men supplemented with zinc, fasting plasma concentrations may increase within five days of zinc supplementation regardless of the status of reference. [42] The 10 mg and 20 mg of zinc (syrup) which is equivalent in their ability to increase zinc levels in plasma were normalized after two weeks of zinc supplementation. [42]
2.3. Nervous distribution
Zinc, and trace mineral, is present in the cerebral cortex, pineal, and the hippocampus, which acts as a nervous rate atypical. [43] [44] [45] in the hippocampus, including vesicles fiber Moses and zinc can 220-300μM concentrations of up to about 8% of the total zinc in the brain [46] (free zinc concentrations are more modest in 1-20μM [ 47] [48]) and is sensitive for long periods (but not severe zinc deficiency), [49], whereas in the pineal gland can regulate the body's response to the hormone leptin. [50]
Like most neuromodulators, zinc is released from the clamp on the action potential. [51]
Zinc is a neurological rate of self which is present in high concentrations in the hippocampus and the pineal gland, and is released in the clamp potential actions
Cell can take up zinc through ion channels, such as calcium channel AMPK / kainate (in nerve cells) [52] where then move up by the mitochondria in the cell. [52] [53]
3. Neuroscience
3.1. Glutaminergic nervous
It has been found to possess a zinc ion inhibitory actions of NMDA receptors moderating force within 100-1,000μM without affecting the basic currents while activity was 10 .mu.m and a weak IC 50 and placed near the 100μM. [54] The effects of that appeared on the NMDA receptor agonists to be similar to magnesium. [54]
Zinc may also activate the release of potassium sodium channels in nerve cells and reduce the clamp. [55]
It seems that zinc ions antiglutaminergic to be able to limit the release of glutamate signal, through glutaminergic receptor modulators. Concentration to do this is rather high, however, and this may not be appropriate physiologically to zinc
3.2. Nervous hormone serotonin
In the corpus callosum (commissure between the cerebral hemispheres, and it seems that the function of a change in depression [56] [57] and can hinder the absorption of serotonin by fluoxetine antidepressants and imipramine [58]), elemental zinc zinc sulfate may improve absorption in the relevant concentration From 1 MICROM to 45%. [59] It is noted that the increase in absorption also cingulate cortex (58%) and raphe nucleus (65%), and the concentrations of zinc between 10-100nM ineffective, and to prevent the effects of antidepressants in this function was denied with one or zinc. [59]
Zinc seems to be involved in the increased absorption of serotonin in selected areas of the brain, due to what is required for this effect may be related to the concentration of physiologically. It seems that some antidepressants may reduce the absorption of serotonin in these areas in the brain if zinc concentrations too low
3.3. Neurogenesis
Neurotrophic factor (BDNF) derivative of the brain is a protein found in both the blood and the brain (serum levels and is believed to be a reflection of the concentration of the brain [60]) that are involved in the organization of neural plasticity cell growth; and participate [61] BDNF signal in both depression and function memory. It is known [62] Zinc to be involved with BDNF where zinc deficiency appears to reduce the ability to activate BDNF of receptors [63] themselves and zinc may constitute a complex with BDNF protein, [64] although I think it is mainly through the activation of some enzymes metalloproteinase ( MMP-2 and MMP-9) has been observed with oral zinc in mice [65] that zinc helps to stick to an inactive form of the BDNF (pro-BDNF) in the 'mature' or BDNF activity. [66]
High zinc levels in the diet in mice was observed (30 ppm up to 60 pages per diet minute supplemented through the water) to reduce the actions of BDNF in the brain and impairs memory, which is observed to be associated with zinc deficiency in the hippocampus. [67] Zinc injection directly increase BDNF, [67] and why oral intake of high led to a decline in the hippocampus of zinc is unknown.
It is believed that the anti-depressant effects of zinc to be mediated by an increase in BDNF has been observed in human serum depressed given 30 mg of zinc in the course of 12 weeks compared to placebo. [68] In this study, it was observed that the foundation of BDNF in the blood, 15.37 +/- 8.28ng / ml, and increased 42%, to 21.84 +/- 6.87ng / ml although no change in the placebo and this happened 41% increase in zinc in the blood serum. [68]
This increase in BDNF can not happen in any other place than when given 25mg as assistant for the same length of time of the people already in the treatment of depression SSRI Although zinc improve the symptoms of depression. [69]
Zinc has been found to increase serum levels of BDNF, with the amount of the increase is linked to a large extent with an increase in zinc in the blood
Despite its importance in the brain, can be high concentrations of zinc are excitotoxic material [70] This is sometimes seen in brain lesion that is released amount in excess zinc from the clamp and mediates cell death [70] [71] and stroke. [72] This is why zinc chelators and treatment in cases of stroke rehabilitation. [73]
Although that may not reflect the supplements (zinc unless ingested high doses abnormally), zinc may be a mediator of cell death when ischemia or hypoxia occur
3.5. Addiction and Obsession
It is known OCD at least be associated with abnormalities glutaminergic, excessive glutamate in particular, and the level of synaptic indicates that [74] [75] that is associated positively correlated with the severity of symptoms. [76] As previously that the involvement of glutamate antagonists in the treatment of obsessive-compulsive disorder [77] and zinc has the ability to be anti-glutaminergic, has been investigating the potential benefits.
Adding zinc (220 mg twice daily) treatment with fluoxetine (20 mg) for OCD can reduce the symptoms of obsessive-compulsive disorder and assessed by the rating scale Y-BOCS, although the benefits were served in eight weeks, but not 4-6 . [78]
3.6. Appetite and food intake
It is known that zinc deficiency to be the cause of anorexia (lack of appetite, are not the same as anorexia nervosa), are usually the first symptoms of zinc deficiency [79], followed by symptoms of depression and anhedonia soon. [80]
It is well known aspects of zinc deficiency to reduce appetite, and these are usually the first symptoms of zinc deficiency
In mice supplemented orally Zinc (19mcg / kg) seems to stimulate food intake did this effect seen with other cations dual parity. [81] Zinc injection look ineffective, [81] even in mice that are deficient. [82]
Zinc seems to oral to stimulate the vagus nerve (vagotomy cancellation effects [81]), and then increase the translator flexible of the two nerve stimulation of appetite and orexin neuropeptide Y factors (opponents also canceled from these receptors [81]). Zinc is known to activate the receptor GPR39 (one ghrelin) receptors [83] Since ghrelin is known to stimulate these two neurological fators through the vagus nerve [84] [85] It is believed that this future is the molecular target of zinc.
Zinc seems to positively influence appetite in mice that are not deficient in zinc, and this may be related to the activation of the receptor (GPR39) that are involved in signal ghrelin
3.7. Attention and focus
In children with ADHD, 30 mg of zinc per day initial period of 13 weeks (the last five weeks that with the D- amphetamine) was able to reduce the amount of D- steroids were required by 37% emotional and lower repel 21% (ATS placebo) to 11 %. However, zinc supplementation does not inherently benefit the symptoms of ADHD. [86]
While zinc 30 mg of zinc element seems to be a little bit effective as an addition to the d-doping treatment does not appear to have significant therapeutic benefits inhernetly
It seems depressed patients have reduced circulating concentrations of zinc in serum [87] which further reduced in people resist treatment on non-resistance (treatment being imipramine) treatment [88] and the size of the deficit zinc correlated with the severity of depression. [89] [90] In general, people with depression generally be less than the zinc concentration in the blood serum seems worse than the symptoms of depression is less zinc concentration tends to be.
At least in mice, and depression [91] and behavioral symptoms (increased susceptibility to stress [92]) that there is two weeks of deprivation of zinc and zinc supplemetnation normalization. Interestingly, denial of zinc cause mice to be resistant to treatment fluoxetine (SSRI). [91]
In patients with primary treatment zinc depression die (25 mg zinc element) with his antidepressant medication (SSRI) noted that the supplements had a supporting role by reducing the symptoms of depression more than 12 weeks, compared with SSRIs that side side with placebo. [69] a single depression alone 30mg of zinc element in the weight / obesity increase also appears to reduce the symptoms of depression (BDI evaluated by II) for a period of 12 weeks, compared with placebo. [68]
Serum concentrations of zinc and zinc negatively associated with the case of the risk of depression, and people who are depressed zinc case more negative associated with the severity of depression. Zinc supplementation in 25 mg (elementary) or higher initial evidence to work in humans, either as adjunctive therapy with SSRIs or nature
Zinc has been reported is not competitive inhibition of glycogen synthase kinase -3 β (GSK-3) with IC50 of 15 .mu.m. [93] as GSK3 is the molecular target for mood disorder [94] and mood disorder is associated with some changes in the metabolism of zinc is believed [95] supplements that have a potential role in their treatment. [17]
Zinc is an inhibitor of glycogen synthase kinase self -3 β, which is involved in mood disorder and depression. It is believed that this is the molecular target of zinc and its interactions with the mood and depression
In healthy young women given 7 mg of zinc in the form of vitamins (vitamins given the same placebo), it has been reduced symptoms of depression and aggressive modestly but close to a large extent in the placebo. [96] This modest benefit to mood failed perosns occur in healthy older people (70-87yrs) given 15-30mg of zinc, as assessed by POMS. [97]
In people given imipramine but resistant to treatment, supplementation of 25 mg of zinc a racist for twelve weeks can reduce the symptoms of the relative depression and placebo to levels recorded with individuals who are not resistant According to assess the BDI, HAM-D, and CGI. [98]
Zinc seems to be especially effective in cases of treatment-resistant depression and other drugs, but seem to have no effect on depression inhernetly respond to treatment. At the same antidepressant of zinc supplementation in people without depression effects fairly modest at best deal
3.9. Memory and learning
It is well known that zinc is significantly concentrated in the hippocampus [43] [46] and zinc deficiency is associated with each of the mood disorder, as well as the formation of a poor memory. [99] while the food zinc deficiency than to cause a similar drop in the hippocampus of zinc (attenuated with zinc supplements [99]), is known to eat through the high-mouth in mice (60ppm additional drinking water) also noted the irony to limit the concentration Zinc in the hippocampus [67] that do not resemble with moderate gains in mice (10 ppm). [100]
The negative effects of low concentrations of zinc in the hippocampus seems related to spatial memory, it is known [99] and spatial memory to be associated with derived from brain neurotrophic factor (BDNF) signaling; [101] Therefore, the injection caused the zinc in the rat brain increase in BDNF signals and protein content [67] and results in reducing the shortage of BDNF signals but high protein indicates dose dependent TrkB sensitivity [63] receptors.
Zinc deficiency is associated with the formation of memory impairment and indicates lower growth factor BDNF, and improve the state of zinc is associated with improvement in all accounts. A high amount associated with abnormally of zinc also with twice the memory, and surprisingly associated with low rather than excess of zinc in the brain
In general, studies on how to (10 ppm) zinc was associated with the effects of the formation of spatial memories, low dose of zinc in drinking water with interest, [65] [102], [100] and any changes importance. [67] major negative elevations (60ppm) has been observed that the imposition of a reduction in spatial learning is associated with low [67], although one study found at least double the memory at 10 pages per minute with an increase in brain concentrations of zinc. [100] This has the negative effect of zinc and zinc hippocampal BDNF on spatial memory was observed in a study of mice that significantly decreased by participating in the management of copper (about 2.5% of the dose of zinc). [103]
If there is evidence and found superior to the standard dietary intake of zinc is beneficial or detrimental to the formation of spatial memory, although at least one study has shown that low doses of copper exert a protective effect against zinc (in the study in which zinc has a negative impact)
In people who have suffered under severe stroke and was zinc optimal (6.6 mg or less) dietary intake, supplementation of 10 mg of zinc was associated with greater improvement than placebo in cognition as assessed by size NIH stroke after 30 days. [104]
In people who suffer from stroke and have malnutrition, and improve cognitive after stroke appear to accelerate relative to placebo
List of Essential Vitamin or Mineral Supplements on National Health Advisor
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