809 replies to this topic

[Nealio]

Thanks for the info ScienceGuy. I had done pub-med searches on it before, but I don't have the background to interpret all the conflicting info!
Looks like I will need to replace niacinamide with something else.

Also : do you think you can produce a similar thread for depression in the future ?

[hippocampus]

... and for OCD too .

I've tried theanine, magnesium (although now I'm buying malate, so I'll report back), piracetam (although in low doses - I can't buy it in my country, so this is not a long-term option), rhodiola (needs cycling). Others aren't available in my country, so they are not an option (maybe from time to time, when I get a chance to order something from iherb - but it's kind of a lottery to get some pharmaceuticals over the border). I also don't have strong anxiety, mostly just OCD and situational anxiety, so I help myself with kava (I limit use to once a week max.), turmeric and omega-3 also help me (and of course meditation, psychotherapy and other lifestyle changes). I'm also buying lithium (I'm not worried about antinootropic effects but if it would be to bad I'll quit it). I'll also buy bacopa in few months probably.

Have you tried inositol for your OCD?

http://www.sciencedi...278584601002445
http://www.europeann...0409-4/abstract
http://www.springerl...7115101k3677p4/

I don't remember the dosage but it was very high. You can probably find it by a simple search.

I've just order it this week from iherb, so I'll report in a month or so

[Ampa-omega]

at high gram doses inositol is known to effect 5ht2a

http://biopsychiatry...ositol-5ht2.htm
/ Is it understood how inositol works to effect ocd?
i think ginseng also effects 5ht2a as well

just want to mention that

Edited by Ampa-omega, 25 February 2012 - 10:22 PM.

[ScienceGuy]

do you think you can produce a similar thread for depression in the future ?

I've added it to my TO DO LIST

However please be a little patient with me since I have a work project that is taking up most of my time at the moment. I will get onto it shortly

[ScienceGuy]

... and for OCD too .

Please kindly note that OBSESSIVE-COMPULSIVE DISORDER (OCD) is in fact an ANXIETY DISORDER and hence falls within the confines of this thread; since, in relation to this thread "ANXIETY" is defined as ALL types of ANXIETY DISORDERS

Edited by ScienceGuy, 26 February 2012 - 11:01 AM.

[ScienceGuy]

Have you tried inositol for your OCD?

Thanks for suggesting this Brainfogged! Nice one!

INOSITOL (MYO-INOSITOL)

Firstly, it is important to note that there are in fact many different forms of INOSITOL and that MYO-INOSITOL specifically is the form that possesses possible ANXIOLYTIC and ANTIDEPRESSANT physiological therapeutic effects.

MYO-INOSITOL’s primary mechanism of action specifically with regards to its ANXIOLYTIC effects appears to be that of UPREGULATION of the SEROTONIN RECEPTORS; possibly through functioning as a PRECURSOR to the PHOSPHATIDYLINOSITOL CYCLE, which is the second messenger system for several neurotransmitters including several subtypes of SEROTONIN RECEPTORS.

MYO-INOSITOL does not appear to affect actual MONOAMINE levels, which would include SEROTONIN and GABA.

The scientific evidence supporting MYO-INOSITOL’s ANXIOLYTIC efficacy is somewhat inconclusive, in that there exists some conflicting evidence supporting its ANXIOLYTIC effects; this is further compounded by mixed anecdotal user feedback reports, in that some individuals report that they find it to be an effective ANXIOLYTIC, whereas others report no ANXIOLYTIC effect whatsoever.

Furthermore, there is substantiated evidence that MYO-INOSITOL’s ANXIOLYTIC efficacy is somewhat dependent on firstly what is the SCALE of the ANXIETY, in that MYO-INOSITOL appears to be significantly less effective in treating ACUTE ANXIETY than it is in treating CHRONIC ANXIETY; and secondly on what is the TYPE of the ANXIETY DISORDER, in that for example it appears that MYO-INOSITOL may be somewhat effective in treating OBSESSIVE-COMPULSIVE DISORDER (OCD) and PANIC DISORDER, but less effective in treating STRESS RELATED ANXIETY, such as POST TRAUMATIC STRESS DISORDER (PTSD).

SAFETY & SIDE EFFECTS:

MYO-INOSITOL is SAFE and NON-TOXIC; no changes have been found in studies of hematology, kidney, or liver function.

However, it should be noted that SIDE EFFECTS include: INCREASED ANXIETY, INSOMNIA, and GASTROINTESTINAL UPSET, including (but not limited to) DIARRHEA, NAUSEA, FLATULENCE, and STOMACH UPSET.

Some of these SIDE EFFECTS can occur upon commencement of usage, but then subsequently dissipate within two weeks consistent usage. For example, INOSITOL may for some (but not all) people initially induce ANXIOGENIC effects; however, in such instances the ANXIOGENIC effects typically vanish entirely within two weeks usage, and are subsequently replaced with ANXIOLYTIC effects. It is therefore recommended if trying out INOSITOL for treating ANXIETY to take it consistently for a period of at least 3-4 weeks in order to properly evaluate its therapeutic effects.

CONTRAINDICATIONS:

MYO-INOSITOL has been demonstrated to EXACERABATE pre-existing symptoms of ATTENTION DEFICIT DISORDER WITH HYPERACTIVITY (ADDH), and hence should not be used by ADDH sufferers.

MYO-INOSITOL should be avoided by pregnant women, since high dose MYO-INOSITOL may induce uterine contractions.

Therefore, taking into consideration all of the above information, I have added INOSITOL to the ‘POSSIBLY SAFE & EFFECTIVE TO TAKE’ LIST for treating ANXIETY

See the following:

Behav Brain Res. 2001 Jan 8;118(1):77-83.

The antidepressant activity of inositol [Myo-Inositol] in the forced swim test involves 5-HT(2) receptors.

Einat H, Clenet F, Shaldubina A, Belmaker RH, Bourin M.

Source
Beer Sheva Mental Health Center, Faculty of Health Sciences, Ben Gurion University of the Negev, P.O. Box 4600, Beer Sheva, Israel.

Abstract
The effect of Inositol [Myo-Inositol] as an antidepressant was previously demonstrated in both animal models of depression-like behavior and in clinical trials. Unlike most antidepressant drugs, Inositol [Myo-Inositol] does not have a clear target in the synapse and was not demonstrated to alter monoamine levels in the brain. The present study attempted to draw a psychopharmacological profile of Inositol [Myo-Inositol]'s behavioral effects by exploring the interactions between the drug and specific receptor agonists and antagonists in the forced swim test. Rats received Inositol [Myo-Inositol] treatment (or control) in combination with the serotonergic metabolism inhibitor PCPA or with the noradrenergic neurotoxin DSP-4. Results indicated that PCPA but not DSP-4 abolished the ability of Inositol [Myo-Inositol] to cause a reduction in immobility time in the forced swim test. In mice, the specific 5-HT(2A)/5-HT(2C) antagonist ritanserin, but not the 5-HT(1A)/5-HT(1B)/beta adrenergic antagonist pindolol, abolished Inositol [Myo-Inositol]'s effect in the forced swim test. The 5-HT(2A)/5-HT(2C) agonist DOI and the 5-HT(1A) agonist 8-OH-DPAT did not have any significant effects on Inositol [Myo-Inositol]'s activity. The present data indicates that the antidepressant effect of Inositol [Myo-Inositol] may involve 5-HT(2) receptors. It is thus possible that the effects of reuptake antidepressant drugs and the effects of Inositol [Myo-Inositol] may have a common final pathway.

PMID: 11163636
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Brain Res. 1993 Dec 24;631(2):349-51.

Myo-inositol reduces serotonin (5-HT2) receptor induced homologous and heterologous desensitization.

Rahman S, Neuman RS.

Source
Faculty of Medicine, Memorial University, St. John's, Nfld, Canada.

Abstract
The effect of myo-inositol was examined on 5-HT2 receptor mediated facilitation of NMDA depolarization of rat neocortical neurons in vitro. Myo-inositol (1-10 mM) potentiated the 5-HT facilitation, the potentiation increasing linearly with log 5-HT concentration. Myo-inositol also eliminated 5-HT induced heterologous desensitization of muscarinic and alpha 1-adrenergic receptor mediated facilitation. Our findings suggest that 5-HT induced homologous and heterologous desensitization results in part from depleting phosphoinositide substrate.

PMID: 8131066
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Metab Brain Dis. 2004 Jun;19(1-2):51-70.

Effects of myo-inositol versus fluoxetine and imipramine pretreatments on serotonin 5HT2A and muscarinic acetylcholine receptors in human neuroblastoma cells.

Brink CB, Viljoen SL, de Kock SE, Stein DJ, Harvey BH.

Source
Division of Pharmacology, Potchefstroom Campus of the North-West University, Potchefstroom, South Africa.

Abstract
myo-Inositol (mI) is a key metabolic precursor to the phospoinositide (PI) metabolic pathway as a key component of central G-protein coupled receptor signaling systems, including several subtypes of adrenergic, cholinergic, serotonergic and metabotropic glutamatergic receptors. High dose mI [Myo-Inositol] has also been shown to be clinically effective in the treatment of obsessive-compulsive disorder, as well as panic and depression, although its mechanism of action remains elusive. The current study aimed to investigate the possible modulatory role of mI [Myo-Inositol] versus fluoxetine or imipramine pretreatments on serotonin-2A receptor (5HT2A-R) and muscarinic acetylcholine receptor (mAChR) function and binding in in vitro systems. After pretreating human neuroblastoma cells with different concentrations of mI [Myo-Inositol], fluoxetine, or imipramine, receptor function was measured by second messenger [3H]-IPx accumulation and [35S]-GTPgammaS binding to G alpha(q) protein. Total [3H]-mI [Myo-Inositol] uptake into cells was measured, as well as specific receptor binding to determine receptor binding after the pretreatments. Results suggest that mI [Myo-Inositol] reduces 5HT2A-R function at the receptor-G protein level. While fluoxetine also reduced 5HT2A-R function, but to a lesser degree, imipramine increased 5HT2A-R function, which may explain why mI [Myo-Inositol] seems to be effective exclusively in selective serotonin reuptake inhibitor-sensitive disorders. In addition mI [Myo-Inositol], and at high concentrations fluoxetine and imipramine, also reduces mAChR function. Furthermore the results suggest that the attenuating effect of mI [Myo-Inositol] on mAChRs is partially dependent on the PI metabolic pathway. The data provide novel information on understanding the mechanism of action of mI [Myo-Inositol] in depression and related anxiety disorders and added to the evidence suggesting a role for the cholinergic system in the pathophysiology of depression.

PMID: 15214506

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Eur Neuropsychopharmacol. 1997 May;7(2):147-55.

Controlled trials of inositol [Myo-Inositol] in psychiatry.

Levine J.

Source
Ministry of Health Mental Health Center, Faculty of Health Sciences, Ben Gurion University of the Negev, Beersheva, Israel.

Abstract
Inositol [Myo-Inositol] is a simple polyol precursor in a second messenger system important in the brain. Cerebrospinal fluid Inositol [Myo-Inositol] has been reported as decreased in depression. A double-blind controlled trial of 12 g daily of Inositol [Myo-Inositol] in 28 depressed patients for four weeks was performed. Significant overall benefit for Inositol [Myo-Inositol] compared to placebo was found at week 4 on the Hamilton Depression Scale. No changes were noted in hematology, kidney or liver function. Since many antidepressants are effective in panic disorder, twenty-one patients with panic disorder with or without agoraphobia completed a double-blind, placebo-controlled, four week, random-assignment crossover treatment trial of Inositol [Myo-Inositol] 12 g per day. Frequency and severity of panic attacks and severity of agoraphobia declined significantly with Inositol [Myo-Inositol] compared to placebo. Side-effects were minimal. Since serotonin re-uptake inhibitors benefit obsessive compulsive disorder (OCD) and Inositol [Myo-Inositol] is reported to reverse desensitization of serotonin receptors, thirteen patients with OCD completed a double-blind controlled crossover trial of 18 g Inositol [Myo-Inositol] or placebo for six weeks each. Inositol [Myo-Inositol] significantly reduced scores of OCD symptoms compared with placebo. A controlled double-blind crossover trial of 12 g daily of Inositol [Myo-Inositol] for a month in twelve anergic schizophrenic patients, did not show any beneficial effects. A double-blind controlled crossover trial of 6 g of Inositol [Myo-Inositol] daily vs. glucose for one month each was carried out in eleven Alzheimer patients, with on clearly significant therapeutic effects. Antidepressant drugs have been reported to improve attention deficit disorder (ADDH) with hyperactivity symptomatology. We studied oral Inositol [Myo-Inositol] in children with ADDH [Attention Deficit Disorder with Hyperactivity] in a double-blind, crossover, placebo-controlled manner. Eleven children, mean age 8.9 +/- 3.6 years were enrolled in an eight week trial of Inositol [Myo-Inositol] or placebo at a dose of 200 mg/kg body weight. Results show a trend for aggravation of the syndrome with myo-inositol as compared to placebo. Recent studies suggest that serotonin re-uptake inhibitors are helpful in at least some symptoms of autism. However a controlled double-blind crossover trial of Inositol [Myo-Inositol] 200 mg/kg per day showed no benefit in nine children with autism. Cholinergic agonists have been reported to ameliorate electroconvulsive therapy (ECT)-induced memory impairment. Inositol [Myo-Inositol] metabolism is involved in the second messenger system for several muscarinic cholinergic receptors. Inositol [Myo-Inositol] 6 g daily was given in a crossover-double-blind manner for five days before the fifth or sixth ECT to a series of twelve patients, without effect. These results suggest that Inositol [Myo-Inositol] has therapeutic effects in the spectrum of illness responsive to serotonin selective re-uptake inhibitors, including depression, panic and OCD, and is not beneficial in schizophrenia, Alzheimer's, ADDH [Attention Deficit Disorder with Hyperactivity], autism or ECT-induced cognitive impairment.

PMID: 9169302
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Am J Psychiatry. 1996 Sep;153(9):1219-21.

Inositol [Myo-Inositol] treatment of obsessive-compulsive disorder.

Fux M, Levine J, Aviv A, Belmaker RH.

Source
Ministry of Health Mental Health Center, Faculty of Health Sciences, Ben Gurion University of the Negev, Beersheva, Israel.

Abstract

OBJECTIVE:
Earlier studies reported that inositol [Myo-Inositol], a simple polyol second messenger precursor, was effective in controlled trials for patients with depression and panic. In this study its effectiveness in obsessive-compulsive disorder was investigated.

METHOD:
Thirteen patients with obsessive-compulsive disorder completed a double-blind, controlled crossover trial of 18 g/day of inositol [Myo-Inositol] or placebo for 6 weeks each.

RESULTS:
The subjects had significantly lower scores on the Yale-Brown Obsessive Compulsive Scale when taking inositol [Myo-Inositol] than when taking placebo.

CONCLUSIONS:
The authors conclude that inositol [Myo-Inositol] is effective in depression, panic, and obsessive-compulsive disorder, a spectrum of disorders responsive to selective serotonin reuptake inhibitors.

PMID: 8780431
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Am J Psychiatry. 1995 Jul;152(7):1084-6.

Double-blind, placebo-controlled, crossover trial of Inositol [Myo-Inositol] treatment for panic disorder.

Benjamin J, Levine J, Fux M, Aviv A, Levy D, Belmaker RH.
Source

Soroka Medical Center, Kupat Holim Sick Fund of the Histadrut, Beersheba, Israel.
Abstract

OBJECTIVE:

Because they found in an earlier study that Inositol [Myo-Inositol], an important intracellular second-messenger precursor, was effective against depression in open and double-blind trials, the authors studied its effectiveness against panic disorder.
METHOD:

Twenty-one patients with panic disorder with or without agoraphobia completed a double-blind, placebo-controlled, 4-week, random-assignment crossover treatment trial of 12 g/day of Inositol [Myo-Inositol].
RESULTS:

The frequency and severity of panic attacks and the severity of agoraphobia declined significantly more after Inositol [Myo-Inositol] than after placebo administration. Side effects were minimal.
CONCLUSIONS:

The authors conclude that Inositol [Myo-Inositol]'s efficacy, the absence of significant side effects, and the fact that Inositol [Myo-Inositol] is a natural component of the human diet make it a potentially attractive therapeutic for panic disorder.
PMID: 7793450
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J Clin Psychopharmacol. 2001 Jun;21(3):335-9.

Double-blind, controlled, crossover trial of inositol [Myo-Inositol] versus fluvoxamine for the treatment of panic disorder.

Palatnik A, Frolov K, Fux M, Benjamin J.

Source
Ministry of Health Mental Health Center, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer-Sheba, Israel.

Abstract
Only 70% of patients respond to current treatments for panic disorder, and many discontinue drugs because of side effects. myo-Inositol, a natural isomer of glucose and a precursor for the second-messenger phosphatidyl-inositol system, has previously been found superior to placebo in the treatment of depression, panic disorder, and obsessive-compulsive disorder (OCD), but a direct comparison with an established drug has never been performed. A double-blind, controlled, random-order crossover study was undertaken to compare the effect of inositol [Myo-Inositol] with that of fluvoxamine in panic disorder. Twenty patients completed 1 month of inositol [Myo-Inositol] up to 18 g/day and 1 month of fluvoxamine up to 150 mg/day. Improvements on Hamilton Rating Scale for Anxiety scores, agoraphobia scores, and Clinical Global Impressions Scale scores were similar for both treatments. In the first month, inositol [Myo-Inositol] reduced the number of panic attacks per week (mean and SD) by 4.0 (2) compared with a reduction of 2.4 (2) with fluvoxamine (p = 0.049). Nausea and tiredness were more common with fluvoxamine (p = 0.02 and p = 0.01, respectively). Because inositol [Myo-Inositol] is a natural compound with few known side effects, it is attractive to patients who are ambivalent about taking psychiatric medication. Continuing reports of inositol's [Myo-Inositol’s] efficacy in the treatment of depression, panic disorder, and OCD should stimulate replication studies.

PMID: 11386498
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Anxiety. 1996;2(1):51-2.

Inositol [Myo-Inositol] treatment of post-traumatic stress disorder.

Kaplan Z, Amir M, Swartz M, Levine J.

Source
Beer-Sheva Mental Health Center, Ben-Gurion University of the Negev, Israel.

Extract from Full Text

INTRODUCTION
Inositol [Myo-Inositol] is a second messenger system precursor that can affect the function of several neurotransmitters including serotonin (Rahman and Newman, 1993). Inositol [Myo-Inositol] has been shown in controlled double-blind studies to ameliorate symptoms of depression (Levine et al., 1995) and panic disorder (Benjamin et al., 1995). Several antidepressants and antipanic medications were reported to have some effect on post-traumatic stress disorder (PTSD; Katz et al., 1995). We therefore carried out a study of Inositol [Myo-Inositol] in PTSD.

RESULTS
Table 1 shows the means and standard deviations for the overall score and the two subscales of the IES for Inositol [Myo-Inositol] and placebo. No significant difference was found between Inositol [Myo-Inositol] and placebo for the improvement score (difference between baseline and four weeks) mean and S.D. for the overall IES score (3.76 *6.42 for Inositol [Myo-Inositol] and -.38 f 8.46 for placebo), for the avoidance subscale (.15 c 3.81 for Inositol [Myo-Inositol] and -.77 –c 5.95 for placebo) or for the intrusion subscale (3.62 * 3.75 for Inositol [Myo-Inositol] and .38 c 5.72 for placebo).

Among the eight patients at the Abarbanel clinic we did not find any significant differences between the improvement score for Inositol [Myo-Inositol] and placebo on the Hamilton Depression Scale (mean and S.D. = 2.5 f 1.9 for Inositol [Myo-Inositol] and 3.1 -c 3.1 for placebo, p > 0.05) or for the Hamilton Anxiety Scale (mean and S.D. = 5.3 * 3.5 for Inositol [Myo-Inositol] and 4.4 f 5.0 for placebo, p 1 0.05).

For the five patients at the Beer-Sheva clinic we found a significant difference on the depression subscale of the SCL-90 (mean and S.D. = 3.4 6.03 for Inositol [Myo-Inositol] and -5.6 2 2.70 for placebo, p = 0.04, one-tailed), but no difference on the anxiety subscale (mean and S.D. =.80 2 2.28 for Inositol [Myo-Inositol] and .40 8.62 for placebo, p > 0.05). All the analyses were done by paired t-tests.

DISCUSSION
This preliminary double-blind crossover study showed no effect of Inositol [Myo-Inositol] on PTSD core symptoms of intrusion and avoidance. However, depression was lowered in the Beer-Sheva subsample of five patients as a resultof the Inositol [Myo-Inositol] treatment. The results from the present study are in line with several other studies that did not find any effect of pharmacological treatment on intrusion and avoidance in PTSD (Katz et al., 1995)…

PMID: 9160600
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World J Biol Psychiatry. 2002 Jul;3(3):147-9.

Myo-inositol has no beneficial effect on premenstrual dysphoric disorder.

Nemets B, Talesnick B, Belmaker RH, Levine J.

Source
Department of Psychiatry, Faculty of Health Sciences, Ben Gurion University of the Negev, Israel.

Abstract
Inositol [Myo-Inositol], a simple isomer of glucose, which serves as a precursor in the phosphatidyl-inositol (PI) second messenger cycle, was shown to be effective in double-blind, placebo-controlled studies of depression, panic and obsessive compulsive disorders as well as in bulimia. The following study was designed to investigate whether inositol [Myo-Inositol] has beneficial effects in another disorder shown to be responsive to SSRIs: premenstrual dysphoric disorder (PMDD). Eleven female patients with PMDD diagnosed according to DSM-IV participated in a cross-over, double-blind, placebo-controlled trial. The active drug was myo-inositol, 12 g daily, whereas placebo was d-glucose administered at the same dose. Each drug was given during the luteal phase only (14 days prior to menses). For each patient treatment alternated between these two drugs for six menstrual cycles. No beneficial effect was demonstrated for inositol [Myo-Inositol] over placebo.

PMID: 12478879

The ABOVE study indicates that MYO-INOSITOL is INEFFECTIVE in treating PREMENSTRUAL DYSPHORIC DISORDER (PMDD); whereas the BELOW study indicates that MYO-INOSITOL is EFFECTIVE in treating PREMENSTRUAL DYSPHORIC DISORDER (PMDD); hence, there currently is conflicting evidence regards MYO-INOSITOL’s efficacy in treating PMDD.

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Hum Psychopharmacol. 2011 Oct;26(7):526-30. doi: 10.1002/hup.1241.

Myo-inositol in the treatment of premenstrual dysphoric disorder.

Gianfranco C, Vittorio U, Silvia B, Francesco D.

Source
AGUNCO Obstetrics and Gynecology Centre, via G. Cassiani, Rome, Italy. gianfranco.carlomagno@gmail.com

Abstract

OBJECTIVE:
Premenstrual dysphoric disorder (PMDD) is a mood disorder disrupting social and/or occupational life of affected women. Premenstrual dysphoric disorder etiology is unknown, although a pivotal role is played by the serotoninergic system. Indeed, one of the most effective treatments is selective serotonin reuptake inhibitors. Several studies have proposed a selective serotonin reuptake inhibitor-like role for myo-inositol, likely due to the fact that myo-inositol is the second messenger of serotonin. In the present study, we aimed to investigate the effect of myo-inositol in the treatment of PMDD.

METHODS:
We used a two-phase clinical trial approach (phase I: placebo washout; phase II: comparisons between treatment and placebo) and treated PMMD patients with two different myo-inositol formulations: powder or soft gel capsules. We decided to test these two formulations because according to the manufacturer, 0.6 g of myo-inositol in soft gel capsule has a pharmacokinetic equivalent to 2 g of myo-inositol in powder.

RESULTS:
Our results showed a significant improvement of three different scales: a reduction in the Daily Symptoms Records scale and an improvement of the Hamilton Depression Rating and Clinical Global Impression-Severity of Illness scales. Results were similar for both formulations.

CONCLUSIONS:
In the present study, by using a new pharmaceutical formulation, we were able to clearly prove the efficacy of myo-inositol in PMDD [premenstrual dysphoric disorder].

PMID: 22031267

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J Neural Transm. 2000;107(2):241-53.

The anxiolytic effect of chronic inositol [Myo-Inositol] depends on the baseline level of anxiety.

Kofman O, Einat H, Cohen H, Tenne H, Shoshana C.

Source
Department of Behavioral Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Abstract
Inositol [Myo-Inositol], a precursor for membrane phosphoinositides involved in signal transduction, has been found to be clinically effective in a number of psychiatric disorders and to reverse behavioural effects of lithium. To gain insight into the mechanism of action of inositol [Myo-Inositol], it is critical to establish its efficacy in animal models. Following the initial report by Cohen et al. (1997b) that inositol [Myo-Inositol] was anxiolytic in the elevated plus maze model of anxiety, the effect of chronic intraperitoneal and chronic dietary inositol [Myo-Inositol] administration in rats was tested in four experiments. There was a significant increase in closed arm and total arm entries following chronic injection of inositol [Myo-Inositol], but no effect of inositol [Myo-Inositol] when it was given chronically in rat chow. Because the first 2 experiments suggested that the mode of drug administration affected the control levels of anxiety (open arm entries and time in open arms) in control groups, the effect of chronic dietary inositol [Myo-Inositol] was tested in rats that were exposed to a mild and a more severe form of stress. Chronic saline injections elevated anxiety in the plus maze, which was only marginally affected by chronic dietary inositol [Myo-Inositol]. Following 3 weeks administration of 5% dietary inositol [Myo-Inositol] rats were pre-exposed to a cat. There was a clear increase in number of entries into open arms, suggesting an anxiolytic effect of inositol [Myo-Inositol].

PMID: 10847563
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J Affect Disord. 2001 Jan;62(1-2):113-21.

The effects of inositol [Myo-Inositol] treatment in animal models of psychiatric disorders.

Einat H, Belmaker RH.

Source
Ministry of Health Mental Health Center, Faculty of Health Sciences, Ben Gurion University of the Negev, Beersheva, Israel.

Abstract
Clinical trials indicate that inositol [Myo-Inositol] may be effective in the treatment of patients with depression, panic disorder and obsessive compulsive disorder (OCD), but not in the treatment of patients with schizophrenia, Alzheimer's disease, ADHD or autism. This spectrum of clinical action parallels that of serotonin selective reuptake inhibitors (SSRIs), but inositol [Myo-Inositol] is a precursor in the phosphatidylinositol cycle, a second messenger system distal to the receptor for 5HT-2. To study its mechanism of therapeutic action there is a need to test inositol's [Myo-Inositol’s] activity in animal models of psychopathology. In rats, chronic inositol [Myo-Inositol] was demonstrated to increase activity levels, reduce immobility time in the forced swim test and in the reserpine-induced hypoactivity models of depression, and reduce anxiety-like behaviors in the elevated plus-maze. The reduction in anxiety-like behaviors appears to be related to baseline levels of activity. Inositol [Myo-Inositol] treatment was not observed to have any effect on amphetamine-induced hyperactivity, apomorphine-induced stereotypy, or on the performance of memory tasks by monkeys. Clinical controlled trials of inositol [Myo-Inositol] in patients with depression, panic disorder, and OCD were small, and positive psychoactive effects in animals clearly strengthen the case for further clinical trials and potential for general therapeutic use in humans.

PMID: 11172878
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Am J Psychiatry. 1995 May;152(5):792-4.

Double-blind, controlled trial of inositol [Myo-Inositol] treatment of depression.

Levine J, Barak Y, Gonzalves M, Szor H, Elizur A, Kofman O, Belmaker RH.

Source
Yehuda Abarbanel Mental Health Center, Bat Yam, Israel.

Abstract

OBJECTIVE:
CSF levels of inositol [Myo-Inositol] have been reported to be lower than normal in depressed subjects. The authors administered inositol [Myo-Inositol] to depressed patients in a double-blind, controlled trial.

METHOD:
Under double-blind conditions, 12 g/day of inositol [Myo-Inositol] (N = 13) or placebo (N = 15) was administered to depressed patients for 4 weeks.

RESULTS:
The overall improvement in scores on the Hamilton Depression Rating Scale was significantly greater for inositol [Myo-Inositol] than for placebo at week 4. No changes were noted in hematology or in kidney or liver function.

CONCLUSIONS:
This may be the first use of the precursor strategy for a second messenger rather than a neurotransmitter in treating depression. Although inositol [Myo-Inositol] had a significant antidepressant effect in this study, replication is crucial.

PMID: 7726322
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Behav Brain Res. 2001 Jan 8;118(1):77-83.

The antidepressant activity of inositol [Myo-Inositol] in the forced swim test involves 5-HT(2) receptors.

Einat H, Clenet F, Shaldubina A, Belmaker RH, Bourin M.

Source
Beer Sheva Mental Health Center, Faculty of Health Sciences, Ben Gurion University of the Negev, P.O. Box 4600, Beer Sheva, Israel.

Abstract
The effect of inositol [Myo-Inositol] as an antidepressant was previously demonstrated in both animal models of depression-like behavior and in clinical trials. Unlike most antidepressant drugs, inositol [Myo-Inositol] does not have a clear target in the synapse and was not demonstrated to alter monoamine levels in the brain. The present study attempted to draw a psychopharmacological profile of inositol's behavioral effects by exploring the interactions between the drug and specific receptor agonists and antagonists in the forced swim test. Rats received inositol treatment (or control) in combination with the serotonergic metabolism inhibitor PCPA or with the noradrenergic neurotoxin DSP-4. Results indicated that PCPA but not DSP-4 abolished the ability of inositol to cause a reduction in immobility time in the forced swim test. In mice, the specific 5-HT(2A)/5-HT(2C) antagonist ritanserin, but not the 5-HT(1A)/5-HT(1B)/beta adrenergic antagonist pindolol, abolished inositol's effect in the forced swim test. The 5-HT(2A)/5-HT(2C) agonist DOI and the 5-HT(1A) agonist 8-OH-DPAT did not have any significant effects on inositol's [Myo-Inositol’s] activity. The present data indicates that the antidepressant effect of inositol [Myo-Inositol] may involve 5-HT(2) receptors. It is thus possible that the effects of reuptake antidepressant drugs and the effects of inositol [Myo-Inositol] may have a common final pathway.

PMID: 11163636
-----------------------------------------------------------------------------------------------------------------------------------------------------------

Int Clin Psychopharmacol. 1999 Nov;14(6):353-6.

Inositol [Myo-Inositol] augmentation of serotonin reuptake inhibitors in treatment-refractory obsessive-compulsive disorder: an open trial.

Seedat S, Stein DJ.
Source

Department of Psychiatry, University of Stellenbosch, Tygerberg, South Africa.
Erratum in

• Int Clin Psychopharmacol 2000 Jul;15(4):244.

Abstract

Inositol [Myo-Inositol], an isomer of glucose and precursor in the phosphatidylinositol cycle, may be effective in a number of psychiatric disorders, including obsessive-compulsive disorder (OCD). There is little data, however, on inositol [Myo-Inositol] as an augmenting agent of serotonin reuptake inhibitors (SRIs) in treatment-refractory patients. Ten OCD patients who had failed to respond to current and previous trials of serotonin reuptake inhibitors participated in open-label trial of inositol [Myo-Inositol] (18 gm/day) [corrected] augmentation for 6 weeks. Symptoms were rated at 2-weekly intervals using the Yale-Brown Obsessive-Compulsive Scale, the Montgomery-Asberg Depression Rating Scale, and the Clinical Global Impressions (CGI) Scale. The majority of patients (n = 7) did not respond to treatment with inositol [Myo-Inositol] augmentation on the CGI improvement item. However, a small number of patients (n = 3) did report a clinically significant response on the CGI improvement item. OCD patients who fail to respond to a number of trials of SRIs may be a particularly treatment-refractory group of subjects. Unfortunately, inositol [Myo-Inositol] augmentation of a SRI did not lead to significant improvement in the majority of such cases. Nevertheless, further research on the mechanism of inositol [Myo-Inositol] efficacy in some patients with anxiety and mood disorders is warranted.

PMID: 10565802

Edited by ScienceGuy, 26 February 2012 - 04:50 PM.

[user1]

Benzos sometimes have their place for more continuous use. Personally, I'm staying away from them. However, it's one of the few medications that people with a drug induced visual perception disorder which I have (HPPD) respond to. Some people have it so bad (there can be many co-existing problems other than visuals) that they would be completely non-functional without them. I'm not entirely sure how they work to alleviate the visuals, but they do. It seems somehow related to epilepsy. They work on the (sometimes very serious) non-visual symptoms too.

Anyway, enough of that, what are your thoughts on uridine? (And co-factors: http://www.longecity...ne-uridine-dha/) After 5 days, I can feel a slight lift in mood and energy. Best results are seen closer to two weeks of supplementation. I don't have anxiety as such, but I'm pretty pissed that my visuals are messed up!

Edited by user1, 27 February 2012 - 12:44 AM.

[Ark]

What's your guys thoughts on Schizandra Berry & Shank Pushpi?

[Ark]

What about... Atarax?

HYDROXYZINE (Brand name: Atarax) is classified as a HIGH RISK MEDICATION and as such cannot be categorised as SAFE; consequently, it has a high incidence of SIDE EFFECTS and physicians are cautioned against prescribing it to the elderly, or pregant women (due to potential for causing harm to the unborn baby), or children;

Furthermore, HYDROXYZINE can in fact CAUSE or EXACERBATE ANXIETY

For these reasons, HYDROXYZINE is not on the positive list

Also, for someone who was using low doses of GABA agonists who wanted to start tapering down even more and/or wanted to avoid/lessen tolerance would cycling between GABA-A agonists and GABA-B agonsits be of any benefit?

I recommend against prolonged usage of all GABA RECEPTOR AGONISTS for the medium to long-term

Any thoughts on Berberis aristata?

[Ampa-omega]

science guy quick question,

firstly, I really do appreciate this entire thread its a godsend to me really, i am highly thankfull for the work put into it, although it probably was more fun for you perhaps. i hope there isn't too much for you to handle.

secondly,
my question is, i understand most of the reccomendations in this thread are targeted toward just anxiety but are any suggested for insomnia, and in regards to things that specifically to induce sleep is there anything that you recommend? and, is ambien a sleepaid that you would suggest? i understand most of these recommendations may not specifically induce sleep but are to work for anxiety. yes, i would like to have natural alternatives if possible..

Edited by Ampa-omega, 27 February 2012 - 06:29 AM.

[ScienceGuy]

my question is, i understand most of the reccomendations in this thread are targeted toward just anxiety but are any suggested for insomnia, and in regards to things that specifically to induce sleep is there anything that you recommend?

yes, i would like to have natural alternatives if possible...

1) MAGNESIUM MALATE, 4-6grams taken PER ORALLY all at once 30-40 minutes before bedtime; and ideally IN ADDITION to this, MAGNESIUM SULFATE adminstered TRANSDERMALLY via adding 1-2 cups EPSOM SALTS to a HOT bath within which you soak for at least 12 minutes

2) RELORA

3) BACOPA

4) THEANINE

I recommend immediately doing the MAGNESIUM (if you are not willing or able to do the TRANSDERMAL administration method, then at the very least do the PER ORAL 4-6g MAGNESIUM MALATE), and then try ADDING to the MAGNESIUM each of the others individually to ascertain how you personally respond to them, starting with the RELORA

is ambien a sleepaid that you would suggest?

In short, NO

ZOLPIDEM (brand name: AMBIEN) is a drug with NONBENZODIAZEPINE (a.k.a. BENZODIAZEPINE-LIKE DRUGS) classification, and as such it
possesses similar pharmacological effects to the BENZODIAZEPINES, in spite of having a dissimilar organic chemical structure. ADDICTION and TOLERANCE will occur will prolonged use, followed by WITHDRAWAL and REBOUND symptoms upon its cessation.

Personally, I strongly recommend against its usage for treating INSOMNIA when application is to be any longer than the EXTREMELY SHORT-TERM

Edited by ScienceGuy, 27 February 2012 - 12:43 PM.

[Ampa-omega]

thanks, i already am actively looking into all of your previously mentioned suggestions.
i could have no anti anxiety at all (not to say i dont sometimes) but for some reason i have a hard time inducing sleep, once im up i tend to stay up until i knock out.. which is why ambien a hypnotic and muscle relaxant looked so ideal.
so i just wanted to seek some stronger alternatives just in case the potency of the already recommended stuff is not working.and is that much magnesium a good thing to take every day?
i read magnesium needs to be in balance with other minerals
http://www.health-sc...umchloride.html

Edited by Ampa-omega, 27 February 2012 - 06:37 PM.

[ScienceGuy]

...is that much magnesium a good thing to take every day?

In short, YES

For a variety of reasons at least 1000mg elemental MAGNESIUM is recommended daily; and note that circa 75% of the US population are currently DEFICIENT in MAGNESIUM

Edited by ScienceGuy, 27 February 2012 - 06:45 PM.

[Ampa-omega]

...is that much magnesium a good thing to take every day?

In short, YES

For a variety of reasons at least 1000mg elemental MAGNESIUM is recommended daily; and note that circa 75% of the US population are currently DEFICIENT in MAGNESIUM

yup i heard that, i just hope this is a sustainable solution, will do . oh, does the concentration of magnesium deplete fast or does it tend to build up? thanks for all your help, your a very valuable member to me.

edit: just want to say i will be checking out all your recommendations, but if i still have a problem with sleep ill report back.

Edited by Ampa-omega, 27 February 2012 - 06:57 PM.

[Steve_86]

It's a shame that Beta-Alanine + Taurine give pretty good benefits in weight training. I will try dropping them to see if my anxiety improves.

[ScienceGuy]

It's a shame that Beta-Alanine + Taurine give pretty good benefits in weight training. I will try dropping them to see if my anxiety improves.

Why not simply take a long break from them to let your GABA RECEPTORS recover, then after this perhaps CYCLE them both ON and OFF

[ScienceGuy]

...is that much magnesium a good thing to take every day?

In short, YES

For a variety of reasons at least 1000mg elemental MAGNESIUM is recommended daily; and note that circa 75% of the US population are currently DEFICIENT in MAGNESIUM

yup i heard that, i just hope this is a sustainable solution, will do . oh, does the concentration of magnesium deplete fast or does it tend to build up? thanks for all your help, your a very valuable member to me.

edit: just want to say i will be checking out all your recommendations, but if i still have a problem with sleep ill report back.

If you are worried about accumulation over time (which is unlikely as your body will tend to naturally excrete the excess) then simply undergo a BLOOD TEST for MAGNESIUM LEVELS circa every 3-6 months; if your test results show you to be slightly high in MAGNESIUM (which in itself isn't reason to panic) then you can simply adjust your dosage accordingly.

Please do feedback how you get on; and I am always happy to help out

[Ampa-omega]

...is that much magnesium a good thing to take every day?

In short, YES

For a variety of reasons at least 1000mg elemental MAGNESIUM is recommended daily; and note that circa 75% of the US population are currently DEFICIENT in MAGNESIUM

yup i heard that, i just hope this is a sustainable solution, will do . oh, does the concentration of magnesium deplete fast or does it tend to build up? thanks for all your help, your a very valuable member to me.

edit: just want to say i will be checking out all your recommendations, but if i still have a problem with sleep ill report back.

If you are worried about accumulation over time (which is unlikely as your body will tend to naturally excrete the excess) then simply undergo a BLOOD TEST for MAGNESIUM LEVELS circa every 3-6 months; if your test results show you to be slightly high in MAGNESIUM (which in itself isn't reason to panic) then you can simply adjust your dosage accordingly.

Please do feedback how you get on; and I am always happy to help out

so far so good ive been taking 2 grams of magnesium malate per night which i feel is a mentally comfortable dose for me, and added some epsom salts, i definitely feel more calm and relaxed and less mentally anxious, only issue is that i could still stay awake with this magnesium, it assist in relaxing me, it doesn't induce sleep or anything. but its working so far. i also have melatonin, and l-theanine which i use occasionally.

Edited by Ampa-omega, 28 February 2012 - 06:20 PM.

[ScienceGuy]

For a variety of reasons at least 1000mg elemental MAGNESIUM is recommended daily; and note that circa 75% of the US population are currently DEFICIENT in MAGNESIUM

yup i heard that, i just hope this is a sustainable solution, will do . oh, does the concentration of magnesium deplete fast or does it tend to build up? thanks for all your help, your a very valuable member to me.

edit: just want to say i will be checking out all your recommendations, but if i still have a problem with sleep ill report back.

If you are worried about accumulation over time (which is unlikely as your body will tend to naturally excrete the excess) then simply undergo a BLOOD TEST for MAGNESIUM LEVELS circa every 3-6 months; if your test results show you to be slightly high in MAGNESIUM (which in itself isn't reason to panic) then you can simply adjust your dosage accordingly.

Please do feedback how you get on; and I am always happy to help out

so far so good ive been taking 2 grams of magnesium malate per night which i feel is a mentally comfortable dose for me, and added some epsom salts, i definitely feel more calm and relaxed and less mentally anxious, only issue is that i could still stay awake with this magnesium, it assist in relaxing me, it doesn't induce sleep or anything. but its working so far. i also have melatonin, and l-theanine which i use occasionally.

MAGNESIUM isn't going to knock you out akin to a brick between the eyes, like say for example BENZODIAZEPINES do when you first start taking them; but what it WILL do is IMPROVE both SLEEP ONSET and SLEEP QUALITY; i.e you will fall asleep more quickly when you get into bed, and you will sleep better once you fall asleep

Furthermore, unlike BENZODIAZEPINES and Z-DRUGS, you can administer MAGNESIUM every day, indefinitely (i.e. the LONG-TERM) without any possible manifestation of TOLERANCE developing, nor any other DEPENDANCE ISSUES (e.g. WITHDRAWAL and/or REBOUND symptoms upon its cessation)

It is worth noting that in addition to MAGNESIUM's direct ANXIOLYTIC effect via NMDA RECEPTOR ANTAGONIST mechanism of action, it will also INDIRECTLY improve ANXIETY through IMPROVING SLEEP QUALITY

See the following for example:

Am J Physiol Regul Integr Comp Physiol. 2000 Dec;279(6):R2173-8.

Blood and brain magnesium in inbred mice and their correlation with sleep quality.

Chollet D, Franken P, Raffin Y, Malafosse A, Widmer J, Tafti M.

Source
Biochemistry and Neurophysiology Unit, Department of Psychiatry, University of Geneva, 1225 Geneva, Switzerland.

Abstract
A strong genetic component in the regulation of blood magnesium (Mg) levels has been demonstrated. The regulation and distribution of brain Mg levels, however, have never been assessed. Herein we report on the genetic variation of peripheral and central Mg levels in six inbred strains of mice. In addition, the possible involvement of Mg in sleep regulation was assessed by establishing correlations between Mg and sleep parameters obtained before and after a 6-h sleep deprivation. Although genotype strongly determined blood Mg levels, it did not affect brain Mg, suggesting that central and peripheral Mg are regulated differently. Central Mg displayed a highly structure-specific distribution with frontal cortex having the highest and brain stem the lowest values. Whereas for the amount and distribution of baseline sleep only marginal correlations with Mg were found, Mg contents in four of nine brain structures were highly positively correlated with the length of slow-wave sleep episodes during recovery. This relationship suggests that higher levels of Mg in specific brain sites promote sleep quality as part of a recovery process.

PMID: 11080083
-------------------------------------------------------------------------------------------------------------------------------------------
Alcohol Clin Exp Res. 2004 Nov;28(11):1702-9.

Magnesium treatment of primary alcohol-dependent patients during subacute withdrawal: an open pilot study with polysomnography.

Hornyak M, Haas P, Veit J, Gann H, Riemann D.
Source

Department of Psychiatry and Psychotherapy, University Hospital of Freiburg, Hauptstrasse 5, D-79104 Freiburg, Germany. magdolna_hornyak@psyallg.ukl.uni-freiburg.de
Abstract

BACKGROUND:
Sleep electroencephalogram alterations and insomnia complaints persist after alcohol withdrawal in dependent patients and are considered strong predictors of relapse. Although disturbances of magnesium household due to alcohol consumption are well known, the relationship of magnesium metabolism and sleep disturbances has not been investigated in this patient group. We conducted an open pilot study to evaluate the effects of magnesium treatment on the sleep of primary alcohol-dependent patients during subacute withdrawal.

METHODS:
Patients were treated with 30 mmol magnesium daily over 4 weeks. Eleven of the 14 included patients were evaluated. Patients were free of any kind of psychotropic medication or other substances known to influence sleep. Polysomnographic recordings with monitoring of periodic leg movements in sleep (PLMS) were performed for two consecutive nights 2 weeks after acute withdrawal (baseline) and 4 weeks later at the end of the treatment period. After the baseline polysomnography, patients were investigated by the magnesium loading test to verify magnesium depletion.

RESULTS:
We found a significant decrease of sleep onset latency from 40.6 to 21.7 min (p = 0.03) and a significant improvement of subjective sleep quality, as assessed by the Pittsburgh Sleep Quality Index, from 8.1 to 5.8 (p = 0.05) during magnesium treatment. Changes in PLMS indices revealed two subgroups of patients: one with an increase of PLMS from 30.7 to 39.4 per hour of sleep (n = 4) and the other one with a decrease of PLMS from 8.9 to 2.1 per hour of sleep (p = 0.04). Patients with PLMS decreases seemed to have a more favorable prognosis: total sleep time, gamma-glutamyltransferase, carbohydrate-deficient transferrin, and Beck Depression Inventory scores improved significantly during treatment in this group. The magnesium loading test revealed a magnesium deficiency in only one patient, five patients showed normal retention values, and the remaining five patients had an increased magnesium excretion, indicating a possible continued renal magnesium loss during abstinence.

CONCLUSIONS:
The results of this study should be interpreted with caution, because no control group with placebo was investigated. Both subjective and, partly, objective parameters of sleep improved during the 4-week study period. Further research is needed to clarify the relationship of magnesium metabolism and sleep alterations.

PMID: 15547457

Edited by ScienceGuy, 28 February 2012 - 07:50 PM.

[Ampa-omega]

i will correct what i said, it does improve sleep onset, so in that sense it means it induces sleep quicker, but not all at once i meant, its more like a relaxant to transition yourself to sleep.

Edited by Ampa-omega, 28 February 2012 - 08:32 PM.

[ScienceGuy]

i will correct what i said, it does improve sleep onset, so in that sense it means it induces sleep quicker, but not all at once i meant, its more like a relaxant to transition yourself to sleep.

Agreed. You won't find yourself staggering around feeling DRUNK or STONED; it's more like a NATURAL FEELING of RELAXATION

[ScienceGuy]

Prolonged usage of BENZODIAZEPINES and Z-DRUGS for the medium to long-term is ill advised due to inducing DOWN-REGULATION of the GABA RECEPTORS though GABA RECEPTOR AGONISM mechanism of action, causing TOLERANCE as well as WITHDRAWAL and REBOUND symptoms upon their cessation, as well as ADDICTION.

However, recent research now indicates that ANY usage of BENZODIAZEPINES and Z-DRUGS, even SHORT-TERM or INFREQUENT USAGE is ill advised, due to usage being associated with INCREASED MORTALITY (REDUCED LIFESPAN).

See THIS thread for details: BENZODIAZEPINE & Z-DRUG use associated with INCREASED MORTALITY

[Raptor87]

I recently bought a magnesium/calcium supplement.

This is what I get from 3 pills;
Calcium (as calcium citrate/malate) 500 mg 50%
Magnesium (as magnesium citrate/malate) 250 mg 63%

The bottle says that I should take up to 6 pills a day but I can barely take 2 at the same time. So I have been taking 2 a day divided on two different meals. When I take two on the same time or if I go above 2 pills a day, well it give´s me the runs.

I know that if Mg isn´t absorbed properly it causes GI problems. What I am wondering is, why isn´t the Mg absorbed on such low dosages?

[ScienceGuy]

I recently bought a magnesium/calcium supplement.

This is what I get from 3 pills;
Calcium (as calcium citrate/malate) 500 mg 50%
Magnesium (as magnesium citrate/malate) 250 mg 63%

The bottle says that I should take up to 6 pills a day but I can barely take 2 at the same time. So I have been taking 2 a day divided on two different meals. When I take two on the same time or if I go above 2 pills a day, well it give´s me the runs.

I know that if Mg isn´t absorbed properly it causes GI problems. What I am wondering is, why isn´t the Mg absorbed on such low dosages?

The problem is specifically the MAGNESIUM CITRATE, which functions as a strong LAXATIVE when taken PER ORALLY

Furthermore, you should be aware that unless the product specifically states the pecentage inclusion levels for each of the respective MAGNESIUM FORMS, then in almost all cases you will find that the ratio is akin to 90% or more the CHEAPEST FORM, which in this case would be the MAGNESIUM CITRATE, and 10% or less of the MORE EXPENSIVE FORM, which in this case would be the MAGNESIUM MALATE. Manufacturers do this to minimize their manufacturing costs. I.e. your product, unless it speficies otherwise, is almost certainly 90% MAGNESIUM CITRATE and only 10% MAGNESIUM MALATE

Please note that MAGNESIUM MALATE has only a weak LAXATIVE effect when taken PER ORALLY

The MAGNESIUM form that I recommend for PER ORAL administration is specifically MAGNESIUM MALATE; this is for a variety of reasons, including: MAGNESIUM MALATE is highly absorbed when taken PER ORALLY; has a much weaker LAXATIVE effect than other forms, such as MAGNESIUM CITRATE; and because it also supplies MALATE which supports ENERGY PRODUCTION via optimization of KREBS CYCLE FUNCTION. Please note that the average diet already contains too much CITRATE as compared to the other KREBS CYCLE INTERMEDIATES, and hence supplementing with CITRATE forms of MINERALS can potentially further imbalance KREBS CYCLE FUNCTION; whereas MALATE enhances it to the extent that it is a clinically effective treating for CHRONIC FATIGUE SYNDROME (CFS).

Therefore, you might like to cease taking any product that contains MAGNESIUM CITRATE and switch to taking solely MAGNESIUM MALATE for PER ORAL administration

Administration TRANSDERMALLY via 1-2 cups EPSOM SALTS dissolved into a hot bath within which you soak for at least 12 minutes is also recommended.

Edited by ScienceGuy, 29 February 2012 - 05:14 PM.

[Deckah]

...is that much magnesium a good thing to take every day?

In short, YES

For a variety of reasons at least 1000mg elemental MAGNESIUM is recommended daily; and note that circa 75% of the US population are currently DEFICIENT in MAGNESIUM

Do you have any studies or a link to support 1g usage? I currently get around(stopped taurate) 300mg malate/300mg glycinate daily and if 1g seems to be the case/new norm, then I might have to throw some citrate in. I split the dosage forms(mal/gly) at different intervals. Does this start to burden the system after throwing in multiple forms of mag? Reason I mentioned adding citrate, is that it's cheaper and isn't a lax @ smaller dosages from what Ive used(past)/heard.

[Nealio]

ScienceGuy, any experience with the South American herb Mulungu ?
I've heard it's used for stress and anxiety in Brazil, with a subjective effect similar to Kava.

[nito]

is anyone still taking afobazol and could report on it's proposed benefits?

[Nootr]

Scienceguy, do you know that people with low blood pressure may have brachycardia from taking additional magnesium and this can be even lethal? That means that magnesium is not a safe way to treat anxiety since it can cause death.

[Nootr]

I obtain magnesium acetate from magnesium sulfate. I dissolve two full teaspoons of baking soda in two glasses of boling water and stur untill the bubbles disappear. Then i dissolve two full teaspoons of magnesium sulfate in a glass of hot water. Then I slowly pour the liquied with magnesium sulfate into the boilding water with dissolved baking soda and stur for 2-3 minutes and i get a milk-like liquid. Then I pour the obtained liquid into a one-litre bottle and add a water to the top. I let the liquid stay for an hour till the residue appears on the bottom and liquid becomes transparent. Then i remove the liquid and add water to the remaining residue again to the top of the bottle. After that I again remove all water and pore one glass of hot water in the bottle and after that I start to add 6% apple vinegar to the bottle sturring at the same time. When the liquid becomes transparent and the gases stop to form it is the moment when Magnesium Acetate is ready. The obtained liquid is about the size of a glass and this is considered to be the dose for three days. So each day you drink one third of the obtained liquid. This is quite cheaper than buying magnesuim supplements and more healthy coz you also get benefits from all the vitamins of the apple vinegar.

Edited by Dan Brown, 01 March 2012 - 06:32 PM.

[hooter]

Scienceguy, do you know that people with low blood pressure may have brachycardia from taking additional magnesium and this can be even lethal? That means that magnesium is not a safe way to treat anxiety since it can cause death.

I like this, it's good advice. Taking huge amounts of magnesium is completely BS for anxiety. You'll mess up your blood levels. Spend your money on something useful.

Edited by hooter, 01 March 2012 - 07:10 PM.