tag:blogger.com,1999:blog-3045634714760830992.post24217872320988767..comments2023-06-05T11:51:38.383-04:00Comments on Evolutionary Psychiatry: Zinc, Depression, and EverythingAnonymoushttp://www.blogger.com/profile/04429177284200775781noreply@blogger.comBlogger11125tag:blogger.com,1999:blog-3045634714760830992.post-83082670343903266012014-06-04T18:15:26.464-04:002014-06-04T18:15:26.464-04:00Hi Emily and Interpolations,
I only came across t...Hi Emily and Interpolations,<br /><br />I only came across this post now, but recently, my colleagues and I conducted a meta-analysis to estimate the magnitude of zinc deficiency in depression (Biol Psychiatry. 2013 Dec 15;74(12):872-8).<br /><br />We found that on average, those with depression had blood concentrations that were about 1.85 micromol/L lower than controls. For reference, this is about a quarter of the span of the reference range suggested by Merck (10.1-16.8 micromol/L).<br /><br />Best regards,<br /><br />Walter SwardfagerWalterhttps://www.blogger.com/profile/07045277073702992533noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-82671546598880706442013-08-02T12:48:15.574-04:002013-08-02T12:48:15.574-04:00Zinc also inhibits GSK3, quite potently too, it mi...Zinc also inhibits GSK3, quite potently too, it might have a role in its effects. <br />fusion809https://www.blogger.com/profile/14316408440182908236noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-66663670275606767372013-03-15T10:06:58.670-04:002013-03-15T10:06:58.670-04:00These just out studies suggest the mechanism of zi...These just out studies suggest the mechanism of zinc helping relieve depression is it elevates the GPR39 receptor. Increasing this receptor's activity lowers inflammation as described at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3163234/ <br /><br /><br />Behav Brain Res. 2013 Feb 1;238:30-5. doi: 10.1016/j.bbr.2012.10.020. Epub 2012 Oct 23.<br />The role of the GPR39 receptor in zinc deficient-animal model of depression.<br />Młyniec K, Budziszewska B, Reczyński W, Sowa-Kućma M, Nowak G.<br />Source<br />Department of Biochemical Toxicology, Jagiellonian University Medical College, Medyczna 9, PL 30-0688 Kraków, Poland. katarzyna.mlyniec@uj.edu.pl<br />Abstract<br />During the last decade it has been shown that zinc may activate neural transmissions via the GPR39 Zn(2+)-sensing receptor, which can be involved in the regulation of neuronal plasticity. According to the neurotrophic hypothesis of depression, decreased brain derived neurotrophic factor (BDNF) levels in depressed patients play a key role in the pathogenesis of this disorder. BDNF, similarly as zinc, is known to be involved in the process of neuron survival and the regulation of neuronal plasticity. The aim of the present study was to determine whether the administration of a 6-week diet deficient in zinc would cause depressive-like behaviour and if such behavioural alterations would correlate with changes in the expression of the BDNF protein and GPR39 receptor. In the first part of the present study the animal behaviour after a 6-week zinc-deficient diet, in the forced swim test (FST) was investigated. In the second part expression of the GPR39 and BDNF protein level in the frontal cortex was measured using the Western Blot method. Administration of a zinc-deficient diet for 6 weeks increased immobility time in the FST by 24%, so exerted depression-like behaviour. A biochemical study showed a significant reduction in GPR39 (by 53%) and BDNF (by 49%) protein expression in the frontal cortex in mice receiving the zinc deficient diet for 6 weeks. Our study provides evidence that the GPR39 Zn(2+)-sensing receptor may be responsible for lowering the BDNF protein level and in consequence may be involved in the pathogenesis of depression.<br />Copyright © 2012 Elsevier B.V. All rights reserved.<br />PMID: 23089648<br /><br /><br />Neurochem Int. 2013 Mar 5. pii: S0197-0186(13)00069-7. doi: 10.1016/j.neuint.2013.02.024. [Epub ahead of print]<br />GPR39 up-regulation after selective antidepressants.<br />Młyniec K, Nowak G.<br />Source<br />Department of Biochemical Toxicology, Jagiellonian University Medical College, Medyczna 9, PL 30-688 Kraków, Poland; Institute of Pharmacology, Polish Academy of Sciences and Center of Excellence in Neuropsychopharmacology, Smętna 12, PL 31-343 Kraków, Poland. Electronic address: katarzyna.mlyniec@uj.edu.pl.<br />Abstract<br />Recent studies indicated that zinc activates neural transmission via the GPR39 Zn2+-sensing receptor. Preclinical and clinical studies demonstrated the antidepressant properties of zinc. To investigate whether the GPR39 receptor is involved in the mechanism of antidepressant action, we measured the expression of the GPR39 receptor (Western Blot) in the frontal cortex of mice treated intraperitoneally with imipramine (30 mg/kg), escitalopram (4 mg/kg), reboxetine (10 mg/kg) or bupropion (15 mg/kg) for 14 days. The present study shows the up-regulation of the GPR39 receptor protein level after escitalopram (by 290%), reboxetine (by 816%) and bupropion (by 272%), but not imipramine treatment. This is the first report to indicate the involvement of the GPR39 Zn2+-sensing receptor in the antidepressant effect of selective monoamine reuptake inhibitors.<br />Copyright © 2013. Published by Elsevier Ltd.<br />PMID: 23474197Nerissahttps://www.blogger.com/profile/08188786959596205027noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-1867784239129314242013-03-05T21:14:48.560-05:002013-03-05T21:14:48.560-05:00There are people who encountered problems in terms...There are people who encountered problems in terms of their sex life and I heard that people are looking for more information on <a href="http://www.explicitnutrition.com/blogs/articles/6547829-how-to-boost-testosterone-through-lifestyle-adjustments" rel="nofollow">how to boost testosterone</a>.teresa bowenhttps://www.blogger.com/profile/07534290439844564640noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-25101965597860875152012-02-04T11:34:17.342-05:002012-02-04T11:34:17.342-05:00Wow! This is extremely interesting to me. We came...Wow! This is extremely interesting to me. We came across the zinc connection quite by accident. In a nutshell: My 16 yo ds had always been a bit ADHD; at 13 yo felt "out of focus"; visited neurologist who put him on Concerta which put him into full blown psychosis. Took him to psychiatrist who did blood work and found extremely low ceruloplasmin and copper imbalance. DS was tested to exhaustion for Wilson's Disease which was eliminated. During that time he was placed on a massive amount of zinc (150 mg/day) as well as Symbyax. Symbyax did not help until zinc added. He was taken off Symbyax and did great with just the zinc until doctor tried to reduce zinc dosage. He went back into depression, albeit,not as severe. Doctor increased zinc dosage back up and we are trying to avoid Symbyax. Recent blood work also showed a significant methyltetrahydrafolate deficiency, so he was also put on 5-methyltetrathydrofolate 4000 mg daily. We are awaiting results of celiac disease testing. This is only specific discussion I have seen of questions into depression, zinc, and inflammation connection. Wow!HSMomhttps://www.blogger.com/profile/18050531164713631972noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-251903358191797332011-02-04T16:21:20.759-05:002011-02-04T16:21:20.759-05:00I wonder to what extent wheat consumption and indu...I wonder to what extent wheat consumption and industrial seed oils are responsible for the inflammatory assault in the first place.Stephen Boulethttps://www.blogger.com/profile/04170061924588693181noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-68079841618989829912010-12-28T20:40:19.878-05:002010-12-28T20:40:19.878-05:00It seems trendy to implicate chronic inflammation ...It seems trendy to implicate chronic inflammation to every / all diseases at the present – kind of like how low serotonin was once implicated in all psychiatric manifestations. Consider how inflammation has been implicated in the demyelination in MS. New work by Moses Rodriguez, suggests that the inflammatory process can also serve to kick-start remyelination (certain omega-6s are involved in the proliferation of oligodendrocyte cells?). Is chronic inflammation really the cause of depression, or rather simply a response to a deeper seated set of imbalances? How is it possible for sleep deprivation, for instance, to result in prompt clinical remission in 65%+ of depressed patients? (sleep deprivation throws the immune system for a loop, elevates synaptic glutamate levels and would probably have no acute effects on zinc status)? The neurotrophic explanation of antidepressant action is also very limited too. In the flinders animal model of depression (in which hippocampal neurogenesis is elevated) nortriptyline or citalopram produces behavioral effects in parallel with an overall decrease in hippocampal neurogenesis. IMHO depression is much simpler than that. Its about bad brain circuitry turned on and good circuitry not functioning too well. All the SSRIs can do is throw brain chemistry for a loop and hope that when the dust settles, more productive brain pathways are somehow functioning. The intracellular bipolar treatments and/or gabaergics (sometimes tried when ADs fail) just indiscriminately slows activity in all brain regions (in the process hopefully taming some of the painful negative circuitry. Things like DBS are the only cure IMHO, just zap the one area that’s causing you problems. As far as every day depression…calm down, eat better, stop overworking, pet your dog, get some exercise (but that’s not a different condition entirely).Unknownhttps://www.blogger.com/profile/11490612495450404860noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-66987217906188214992010-09-24T19:16:53.009-04:002010-09-24T19:16:53.009-04:00If low zinc levels are due to sequestration in the...If low zinc levels are due to sequestration in the liver and/or a cell-mediated immune response, it seems as though supplementation might be useless at best or possibly even harmful. Still... hmmmmmm.<br /><br />Donnasome random femalehttps://www.blogger.com/profile/06993643929678996000noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-15984854159431381902010-07-26T19:55:52.255-04:002010-07-26T19:55:52.255-04:00From Maes "Hypozincemia in Depression" J...From Maes "Hypozincemia in Depression" Journal of Affective Disorders 31:135-40 (1994)-<br /><br />80 subjects - 32 controls, 16 minor depression, 14 major depression, 18 melancholia (anyone with zinc absorption issues such as being on thiazides, inflammatory bowel disease, or alchoholism were excluded) - <br /><br />Zinc level in controls: 2.02 +/- 0.2 mg/l<br />Major depression with melancholia: 1.78 +/- 0.22<br />Major depression without melancholia: 1.77 +/- 0.25<br />minor depression: 1.89 +/- 0.34<br /><br />From Nowak, "Serum Trace Elements in Animal Models and Human Depression. Part 1. Zinc" Hum Psychopharmacol Clin Exp 14: 83-6 (1999)<br /><br />19 subjects with major depression, 16 controls, serum zinc level varied linearly with the hamilton D depression ratings (higher the rating, the more depressed, and the lower the serum zinc) Controls had a level of 1.51 +/- 0.15, depressed group 1.22 +/- 0.12 - depressed zinc was 12% lower than control group.<br /><br />From Maes et al "Lower serum zinc in major depression is a sensitive marker of treatment resistance and of the immune inflammatory response in that illness." Biological Psychiatry 1997 42:349-58<br /><br /> (as a side note - this paper reinforces that clinical depression is characterized by two inflammatory responses, increased IL-6 leading to sequestration of zinc by metallothionein in the liver, and decreased zinc by some sort of cell-mediated immunity response)<br /><br />15 controls, 31 depressed inpatients. All inpatients had a 10 day washout period (no one who had been on fluoxetine, which has a 6 week washout, was allowed in the study). Zinc was drawn in the morning on day 10. Then a 5 week treatment period with antidepressants (that's about 6X longer than most admissions to any inpatient unit I ever worked on!) - the antidepressants used were trazodone alone (100mg), trazodone (100mg) + fluoxetine (20mg), and trazodone (100mg) + pindolol (7.5mg) - around 6 patients in each group.<br /><br />Controls zinc level = 115 mcg/dl<br />MD zinc level = 95<br />Treatment resistant MD (did not respond to medication) zinc level = 91<br />Treatment responsive MD = 103<br /><br />Not that useful clinically as trazodone isn't exactly the antidepressant du jour. Fluoxetine is prozac.Anonymoushttps://www.blogger.com/profile/04429177284200775781noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-46860819875401770742010-07-26T08:10:19.595-04:002010-07-26T08:10:19.595-04:00Hi Interpolations. The article I got that informa...Hi Interpolations. The article I got that information from was a review article and did not have that level of detail. However, I'm interested in those answers too, so I'm going to chase down the references over the next couple days. <br /><br />I can tell you right now that in a rat study, tricyclic (imipramine), SSRI (citalopram), and electroshock therapy increased zinc levels in the hippocampus by 10%, 20%, and 30% respectively.Anonymoushttps://www.blogger.com/profile/04429177284200775781noreply@blogger.comtag:blogger.com,1999:blog-3045634714760830992.post-13463502710496540832010-07-25T22:02:55.198-04:002010-07-25T22:02:55.198-04:00"(1) Depressed patients in studies have a low..."(1) Depressed patients in studies have a lower serum zinc level than normal controls.<br /><br />What's the actual differential? And what's considered a normal range?<br /><br />"(4) Treatment with antidepressants normalizes zinc levels..."<br /><br />What kind of anti-depressants? And were these compared to placebos?<br /><br />Best,<br />KevinAnonymousnoreply@blogger.com