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    Nutritional & Herbal Supplements for Anxiety! 
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    Nutr J. 2010 Oct 7;9:42.
    Nutritional and herbal supplements for anxiety and anxiety-related disorders: systematic review.
    Lakhan SE, Vieira KF.

    Abstract
    BACKGROUND: Over the past several decades, complementary and alternative medications have increasingly become a part of everyday treatment. With the rising cost of prescription medications and their production of unwanted side effects, patients are exploring herbal and other natural remedies for the management and treatment of psychological conditions. Psychological disorders are one of the most frequent conditions seen by clinicians, and often require a long-term regimen of prescription medications. Approximately 6.8 million Americans suffer from generalized anxiety disorder. Many also suffer from the spectrum of behavioural and physical side effects that often accompany its treatment. It is not surprising that there is universal interest in finding effective natural anxiolytic (anti-anxiety) treatments with a lower risk of adverse effects or withdrawal.

    METHODS: An electronic and manual search was performed through MEDLINE/PubMed and EBSCO. Articles were not discriminated by date of publication. Available clinical studies published in English that used human participants and examined the anxiolytic potential of dietary and herbal supplements were included. Data were extracted and compiled into tables that included the study design, sample population, intervention, control, length of treatment, outcomes, direction of evidence, and reported adverse events.

    RESULTS: A total of 24 studies that investigated five different CAM monotherapies and eight different combination treatments and involved 2619 participants met the inclusion criteria and were analyzed. There were 21 randomized controlled trials and three open-label, uncontrolled observational studies. Most studies involved patients who had been diagnosed with either an anxiety disorder or depression (n = 1786). However, eight studies used healthy volunteers (n = 877) who had normal levels of anxiety, were undergoing surgery, tested at the upper limit of the normal range of a trait anxiety scale, had adverse premenstrual symptoms or were peri-menopausal, reported anxiety and insomnia, or had one month or more of elevated generalized anxiety. Heterogeneity and the small number of studies for each supplement or combination therapy prevented a formal meta-analysis. Of the randomized controlled trials reviewed, 71% (15 out of 21) showed a positive direction of evidence. Any reported side effects were mild to moderate.

    CONCLUSIONS: Based on the available evidence, it appears that nutritional and herbal supplementation is an effective method for treating anxiety and anxiety-related conditions without the risk of serious side effects. There is the possibility that any positive effects seen could be due to a placebo effect, which may have a significant psychological impact on participants with mental disorders. However, based on this systematic review, strong evidence exists for the use of herbal supplements containing extracts of passionflower or kava and combinations of L-lysine and L-arginine as treatments for anxiety symptoms and disorders. Magnesium-containing supplements and other herbal combinations may hold promise, but more research is needed before these products can be recommended to patients. St. John's wort monotherapy has insufficient evidence for use as an effective anxiolytic treatment.

    PMID: 20929532
    The full text is available at pubmed.

    I found this to be a very easy article for a quick summary of kava kava, passionflower, L-lysine, magnesium, and St.Johns effectiveness for treating anxiety. I wanted to create this thread as a place for people to look for information on different herbs and nutritional supplements for treating anxiety. I'm interested in personal experiences, additional research, or anything else that helps our understanding of safer alternatives for treatment. I'm also happy to answer questions but I am not an expert.

    I found this article while doing research on l-lysine and magnesium. I starting taking supplements about a week ago with the goal of reducing my Xanax use. I take l-lysine two-three times a day (1g each time) on an empty stomach and I take the magnesium (with calcium & Vitamin D) once a day with dinner. With minimal withdrawal symptoms and several positive benefits I've reduced my Xanax use by 33% (down from 1.5mg to 1mg). The first night I made the reduction I got less/worse sleep than normal. I also felt anxious the next day, although not nearly as badly as I usually feel (the absence of a headache was worth it alone). The second night was considerable better and I actually got much BETTER sleep than I did while on a higher dose of Xanax. In addition, I feel more high on Xanax when I do take it (that .5 or even .25 can go a long way). I plan to continue to take the l-lysine and magnesium and work toward reducing my dose down to .5mg once a day. I wanted to post this to help spread both my success story as well as the information.

    I will continue to post personal progress & relevant journal abstracts to help fellow members of BL in their quest for HR.

    NOTE: I did notice that it took several days for the nutrients to build up and gain effectiveness. If you plan to attempt this, you may want to give it a few days on the supplements before attempting to reduce your dose.

    Biomed Res. 2007 Apr;22):85-90.
    Oral treatment with L-lysine and L-arginine reduces anxiety and basal cortisol levels in healthy humans.
    Smriga M, Ando T, Akutsu M, Furukawa Y, Miwa K, Morinaga Y.

    Abstract
    Dietary supplementation with an essential amino acid L-lysine has been shown to reduce chronic anxiety in humans with low dietary intake of L-lysine. A combination of L-lysine and L-arginine has been documented to normalize hormonal stress responses in humans with high trait anxiety. The present study was carried out in one hundred eight healthy Japanese adults. The aim of study was to find out whether a week-long oral treatment with L-lysine (2.64 g per day) and L-arginine (2.64 g per day) reduces trait and stress-induced state anxiety and basal levels of stress hormones. We confirmed that, without regard to gender, the amino acid treatment significantly reduced both trait anxiety and state anxiety induced by cognitive stress battery. In addition, we found that the treatment with L-lysine and L-arginine decreased the basal levels of salivary cortisol and chromogranin-A (a salivary marker of the sympatho-adrenal system) in male subjects. These results of this double-blind, placebo controlled and randomized study confirm the previous findings in humans and animals and point to a combination of L-lysine and L-arginine as a potentially useful dietary intervention in otherwise healthy humans with high subjective levels of mental stress and anxiety.

    PMID: 17510493
    This is one of the articles looked in in the review from the first post. It is also perhaps the most interesting study concerning the effect of l-lysine on human health.

    Lysine fortification reduces anxiety and lessens stress in family members in economically weak communities in Northwest Syria.
    Smriga M, Ghosh S, Mouneimne Y, Pellett PL, Scrimshaw NS.
    Proc Natl Acad Sci U S A. 2004 Jun 1;101(22):8285-8. Epub 2004 May 24.

    Abstract
    Lysine is a limiting amino acid in diets based on wheat as the staple. In experimental animals, prolonged dietary lysine inadequacy increases stress-induced anxiety. If observed in humans, such a result would have a strong implication for the relationship between nutrition and communal quality of life and mental health. As part of a 3-month randomized double-blind study, we tested whether lysine fortification of wheat reduces anxiety and stress response in family members in poor Syrian communities consuming wheat as a staple food. In the lysine-fortified group, the plasma cortisol response to the blood drawing as a cause of stress was reduced in females, as was sympathetic arousal in males as measured by skin conductance. Lysine fortification also significantly reduced chronic anxiety as measured by the trait anxiety inventory in males. These results suggest that some stress responses in economically weak populations consuming cereal-based diets can be improved with lysine fortification.

    PMID: 15159538
    This article looks at the health benefits of l-lysine in a population with lysine deficiencies.

    J Nutr. 2002 Dec;132(12):3744-6.
    Dietary L-lysine deficiency increases stress-induced anxiety and fecal excretion in rats.
    Smriga M, Kameishi M, Uneyama H, Torii K.

    Abstract
    Little is known about the psychobehavioral consequences of a dietary deficiency of the amino acid, L-lysine. This report demonstrates that a 4-d long L-lysine deficiency in rats interfered with the normal circadian release of the neurotransmitter serotonin, but not dopamine, measured by in vivo microdialysis in the central nucleus of the amygdala. L-Lysine deficiency was induced by feeding rats a L-lysine-deficient diet. Controls were pair-fed a L-lysine-sufficient diet. Footshock stress-induced anxiety, measured in an elevated plus-maze paradigm, and wrap-restraint stress-stimulated fecal excretion were significantly greater in the L-lysine-deficient rats than in the controls. We conclude that a severe deficiency of dietary L-lysine enhances serotonin release in the amygdala, with subsequent changes in psychobehavioral responses to stress.

    PMID:12468617
    Nutr Neurosci. 2003 Oct;6(5):283-9.
    A diet fortified with L-lysine and L-arginine reduces plasma cortisol and blocks anxiogenic response to transportation in pigs.
    Srinongkote S, Smriga M, Nakagawa K, Toride Y.

    Abstract
    We studied the effects of diet fortified with L-lysine HCl (Lys) and L-arginine (Arg) on stress (transportation) responses in male finishing pigs (Landrace x LargeWhite x Duroc). Pigs (n = 16) were randomly divided into two equally sized groups so that the average starting body weight in the groups was identical. For 1 week immediately preceding the transportation, the first group of pigs received a control diet while the second group received a Lys and Arg fortified diet. Plasma aminogram, cortisol and body weight were evaluated. Behavior of pigs was measured with the help of a video camera, recorded for 2 h at the same time, as on the day, before a day and immediately after transportation. The study revealed main stimulatory effects of transportation and main inhibitory effect of Lys and Arg on plasma cortisol (P < 0.05) without transportation x treatment interactions. Pigs fed with Lys and Arg diet tend to have higher body weight at the end of the experiment, when compared to their normally fed counterparts, but the difference did not reach a significant level (P < 0.21). Lys and Arg diet significantly inhibited stress-induced increase in locomotion (P < 0.05), without affecting feeding pattern. Transportation stress decreased plasma Lys and Arg. This decrease was reversed in the fortified group, and what is more the plasma Lys and Arg levels were significantly higher than in controls (P < 0.05). Lys and Arg enhanced plasma urea production (P < 0.05), without regards to stress. The behavioral results indicate a reduction in stress-induced anxiety in pigs fed with Lys and Arg fortified diet, that parallels similar observations in research with rats and broilers. The mechanism probably involves a decreased plasma cortisol, and/or normalized plasma Lys, Arg levels.

    PMID: 14609314
    Prog Clin Biol Res. 1985;192:477-84.
    On the brain endocoid for benzodiazepine recognition sites.
    Guidotti A, Ferrero P, Costa E.

    Abstract
    Human and rat brain contain a neuropeptide with 105 amino acid residues which inhibits the binding of 3H-diazepam and other specific benzodiazepine recognition site ligands to crude brain synaptic membranes. DBI injected intracerebroventricularly in thirsty rats which are subjected to a conflict test (Corda et al., 1983), lowers the threshold for behavioral suppression by punishment. In this test DBI acts like an anxiogenic endocoid for the benzodiazepine recognition sites. The large abundance of lysine and arginine residues in the DBI molecule suggest that this polypeptide functions as a precursor of a putative endocoid which regulates anxiety levels. This endocoid acts as an agonist for the benzodiazepine recognition site. Because of the anxiogenic properties of this endocoid, it is proposed that anxiolytic benzodiazepine should be classified as an antagonist and beta-carboline as an agonist at the receptor level.

    PMID: 3001768
    Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):11043-8.
    Inter- and intraspecies polymorphisms in the cholecystokinin-B/gastrin receptor alter drug efficacy.
    Kopin AS, McBride EW, Gordon MC, Quinn SM, Beinborn M.

    Abstract
    The brain cholecystokinin-B/gastrin receptor (CCK-BR) is a major target for drug development because of its postulated role in modulating anxiety, memory, and the perception of pain. Drug discovery efforts have resulted in the identification of small synthetic molecules that can selectively activate this receptor subtype. These drugs include the peptide-derived compound PD135,158 as well as the nonpeptide benzodiazepine-based ligand, L-740,093 (S enantiomer). We now report that the maximal level of receptor-mediated second messenger signaling that can be achieved by these compounds (drug efficacy) markedly differs among species homologs of the CCK-BR. Further analysis reveals that the observed differences in drug efficacy are in large part explained by single or double aliphatic amino acid substitutions between respective species homologs. This interspecies variability in ligand efficacy introduces the possibility of species differences in receptor-mediated function, an important consideration when selecting animal models for preclinical drug testing. The finding that even single amino acid substitutions can significantly affect drug efficacy prompted us to examine ligand-induced signaling by a known naturally occurring human CCK-BR variant (glutamic acid replaced by lysine in position 288; 288E --> K). When examined using the 288E --> K receptor, the efficacies of both PD135,158 and L-740, 093 (S) were markedly increased compared with values obtained with the wild-type human protein. These observations suggest that functional variability resulting from human receptor polymorphisms may contribute to interindividual differences in drug effects.

    PMID: 9380756
    J Rheumatol Suppl. 1989 Nov;19:158-63.
    Serum amino acids in fibrositis/fibromyalgia syndrome.
    Russell IJ, Michalek JE, Vipraio GA, Fletcher EM, Wall K.

    Abstract
    Free plasma tryptophan levels in patients with fibrositis syndrome were measured by Moldofsky and Warsh with the view that the pathogenesis of fibrositis syndrome might involve a functional deficiency of serotonin. The hypothesis was supported by the finding of an inverse relationship between tryptophan concentration and the severity of musculoskeletal pain. Our study examined the total serum amino acid pool in fibrositis syndrome. Twenty patients with primary fibrositis syndrome and matched normal controls were evaluated clinically. After denaturation of macromolecules, serum amino acids were quantitated by automated analysis. Patients with fibrositis syndrome exhibited significantly lower levels of total serum tryptophan (p = 0.002), as well as 6 other amino acids: alanine (p less than 0.0005), histidine (p = 0.001), lysine (p = 0.02), proline (p = 0.039), serine (p = 0.028 ), and threonine (p = 0.013). These findings support the serotonin deficiency hypothesis for fibrositis syndrome pathogenesis but also imply a more generalized defect in amino acid homeostasis among affected individuals.

    PMID: 2607510
    Last edited by Gyrospeck; 30-08-2012 at 01:14. Reason: merged five posts together
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    #2
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    Use the edit function. Double, triple and quadruple posting is not permitted here. I'm going to merge all five of your posts into one.

    What sort of discussion were you trying to generate here? I think this may be more appropriate for ADD.

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    #3
    I apologize for the misunderstanding. I was trying to hold the first several posts so that I could edit additional article abstracts in later.

    I am attempting to generate a discussion around alternative options for anxiety treatment besides benzos, opiates, gabapentin, alcohol etc. I am currently very interested in L-Lysine due to personal success. I wanted to post all of the article abstracts here related to l-lysine and then build from there. I left it open for other nutritional and herbal supplements because I am interested in anything that will help. This may be more appropriate for the ADD; please feel free to move it where it belongs.

    Neurochem Res. 1995 Aug;20(:931-7.
    L-lysine is a barbiturate-like anticonvulsant and modulator of the benzodiazepine receptor.
    Chang YF, Gao XM.

    Abstract
    Our earlier observations showed that L-lysine enhanced the activity of diazepam against seizures induced by pentylenetetrazol (PTZ), and increased the affinity of benzodiazepine receptor binding in a manner additive to that caused by gamma-aminobutyric acid (GABA). The present paper provides additional evidence to show that L-lysine has central nervous system depressant-like characteristics. L-lysine enhanced [3H]flunitrazepam (FTZ) binding in brain membranes was dose-dependent and stimulated by chloride, bromide and iodide, but not fluoride. Enhancement of [3H]FTZ binding by L-lysine at a fixed concentration was increased by GABA but inhibited by pentobarbital between 10(-7) to 10(-3)M. While GABA enhancement of [3H]FTZ binding was inhibited by the GABA mimetics imidazole acetic acid and tetrahydroisoxazol pyridinol, the enhancement by pentobarbital and L-lysine of [3H]FTZ binding was dose-dependently increased by these two GABA mimetics. The above results suggest that L-lysine and pentobarbital acted at the same site of the GABA/benzodiazepine receptor complex which was different from the GABA binding site. The benzodiazepine receptor antagonist imidazodiazepine Ro15-1788 blocked the antiseizure activity of diazepam against PTZ. Similar to pentobarbital, the anti-PTZ effect of L-lysine was not blocked by Ro15-1788. Picrotoxinin and the GABA, receptor antagonist bicuculline partially inhibited L-lysine's enhancement of [3H]FTZ binding with the IC50s of 2 microM and 0.1 microM, respectively. The convulsant benzodiazepine Ro5-3663 dose-dependently inhibited the enhancement of [3H]FTZ binding by L-lysine. This article shows the basic amino acid L-lysine to have a central nervous system depressant characteristics with an anti-PTZ seizure activity and an enhancement of [3H]FTZ binding similar to that of barbiturates but different from GABA.

    PMID: 8587651
    Last edited by Gyrospeck; 01-09-2012 at 21:54.
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    #4
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    No worries man, and it's been moved to ADD.

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    #5
    IME, you can take every OTC herbal anxiolytic available and it still won't compare to a micro benzo dose, or a couple beers.
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    #6
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    Quote Originally Posted by Tussmann View Post
    IME, you can take every OTC herbal anxiolytic available and it still won't compare to a micro benzo dose, or a couple beers.
    Yep! But its to be expected i spose. Just herbs xanax aint a herb oh well stick to the xanax
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    #7
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    Good thread

    I take kpins (never start take them daily if you plan too)! and weed (best not to start with) for anxiety. Dexedrine helps me to reduce hyper focus (untill it wears off) that also helps me. I used to take cymbalta for anxiety/depression but I have the feeling it interferes with my speed.

    Some supplements are really solid tho. Magnesium (and other micro nutrients) helps me and I have tried many other successful semi-drug supplements and herbs that I found helpful, my memory is shot ( i need some good quality brand ginkgo biloba again (cannabis users get this) (important). If I knew about this stuff earlier i would never touch the kpin. I have only read succesful posts about l-lysine that i want it to try it again. I'm always looking for quick fixes :/ l-theanine goes well with kpin.
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    #8
    Last night I successfully reduced my Xanax dose down to .5mg with ZERO withdrawal symptoms. In fact, I slept for 9 hours last night.

    For the last week, I have been keeping detailed information on my Xanax use. That information is below. Before doing this experiment, my daily dose was about 3mg/day (this would range from 2mg up to 4mg). WITHOUT using any supplements, I successfully reduced my daily dose down to 1.5mg, but was experiencing withdrawal (such as bad sleep, irritability, headaches). A little over a week ago, I began taking lysine and magnesium supplements and continued to reduce my dose. It took about 3 days of using the supplements to feel the effects, but I have noticed that my withdrawal symptoms are nearly 100% non-existent. I plan to stay at .5mg-1mg/day as my standard and only increase my dose for special occasions.

    Spoiler for Detailed Xanax Use:

    8/24:
    1:30 p.m., .5mg, XR
    6:00 p.m., .5mg, IR
    12:30 a.m., .5mg, IR

    8/25:
    12:20 p.m., .5, XR
    8:00 p.m., .25, IR

    8/26: This was a friends birthday, so we drank and I did a little extra
    9:40 a.m., .5, XR
    6:00 p.m., .25mg, IR
    8:00 p.m., .5mg, IR
    10:30 p.m., .25mg, IR

    8/27:
    1:00 p.m., .5, XR
    10:00 p.m., .5mg, IR

    8/28:
    12:15 p.m., .5mg, XR
    10:20 p.m., .5mg, IR

    8/29:
    12:20 p.m., .5mg, XR
    10:30 p.m., .25mg, IR

    8/30: I ended up doing lots of oxy (for me that's 20mg or so) and Kratom (4g) this day with a friend. Also played as a guest in a shitty science fiction movie. Fun day!
    3:00 p.m., .5mg, XR
    4:20 p.m., .25mg, IR
    2:10 a.m., .5mg, IR
    3:00 a.m., .25mg, IR

    8/31:
    7:10 p.m., .5, IR

    9/1: My wife got a new job and my friend got accepted into his master's program. We celebrated with alcohol
    2:00 p.m. .5, XR
    11:50 p.m. .5 IR

    9/2:
    9:00 p.m. .5 IR
    12:30 a.m. .5 IR

    9/3:
    8:30 p.m. .75 IR

    9/4: Ended up drinking two margaritas this night.
    10:30 p.m. .5 IR

    9/5:
    8:20 p.m. .25 IR
    10:50 p.m. .5 IR

    9/6:
    5:45 p.m. .5 IR
    7:45 p.m. .5 IR

    9/7: Helped a friend move and was sore as hell. Excuse for 10mg oxy and 2 shots
    6:30 p.m. .5 Klonopin

    9/8: Still very sore and had 4g Kratom, 10mg Hydro, and 1.5 shots
    7:30 p.m. .5 IR

    9/9:
    1:30 p.m. .5 XR

    9/10:
    5:40 p.m. .5 IR

    9/11:
    12:45 p.m. .5 Klonopin
    6:00 p.m. .5 IR


    Magnesium:

    Aust J Prim Health. 2012;12):172-6.
    Nutrition status of primary care patients with depression and anxiety.
    Forsyth AK, Williams PG, Deane FP.

    Abstract
    The objective of this study was to evaluate the nutrition status of people referred to a nutrition and physical activity program for the management of mental health in general practice. Patients currently being treated for depression and/or anxiety were referred by their GPs to a lifestyle intervention program. The nutrition status was assessed during a comprehensive assessment at the commencement of the program. The lifestyle intervention program, including all assessments, was offered at multiple sites including GP clinics in the Illawarra, and in clinic rooms at the University of Wollongong. Thirty-two men and seventy-seven women completed the assessment. Patients were referred with depression (52% ), anxiety (19% ) or both (28% ). Eighty percent of participants were overweight or obese. All participants completed an assessment that included a diet history, anthropometric measurements and the completion of several questionnaires including the Depression, Anxiety and Stress Scale (DASS). Nutrition status was assessed using mean nutrient intakes and Australian modified Healthy Eating Index scores evaluated against the National Nutrition Survey intakes and DASS scores. Participants met the estimated average requirements for all nutrients except folate (17% ), magnesium (78% ) and calcium (57% ). Intakes were similar to those reported in the National Nutrition Survey. Only magnesium intakes were significantly related to depression (r=-0.26). Australian modified Healthy Eating Index scores were significantly negatively correlated with DASS scores (P<0.01). The associations presented here support the existing body of literature. Nutrition recommendations for patients with depression and anxiety should be based on the Australian Guide to Healthy Eating with particular attention to fruit, vegetables and wholegrains.

    PMID: 22551840
    J Neurosci. 2011 Oct 19;31(42):14871-81.
    Effects of elevation of brain magnesium on fear conditioning, fear extinction, and synaptic plasticity in the infralimbic prefrontal cortex and lateral amygdala.
    Abumaria N, Yin B, Zhang L, Li XY, Chen T, Descalzi G, Zhao L, Ahn M, Luo L, Ran C, Zhuo M, Liu G.

    Abstract
    Anxiety disorders, such as phobias and posttraumatic stress disorder, are among the most common mental disorders. Cognitive therapy helps in treating these disorders; however, many cases relapse or resist the therapy, which justifies the search for cognitive enhancers that might augment the efficacy of cognitive therapy. Studies suggest that enhancement of plasticity in certain brain regions such as the prefrontal cortex (PFC) and/or hippocampus might enhance the efficacy of cognitive therapy. We found that elevation of brain magnesium, by a novel magnesium compound [magnesium-l-threonate (MgT)], enhances synaptic plasticity in the hippocampus and learning and memory in rats. Here, we show that MgT treatment enhances retention of the extinction of fear memory, without enhancing, impairing, or erasing the original fear memory. We then explored the molecular basis of the effects of MgT treatment on fear memory and extinction. In intact animals, elevation of brain magnesium increased NMDA receptors (NMDARs) signaling, BDNF expression, density of presynaptic puncta, and synaptic plasticity in the PFC but, interestingly, not in the basolateral amygdala. In vitro, elevation of extracellular magnesium concentration increased synaptic NMDAR current and plasticity in the infralimbic PFC, but not in the lateral amygdala, suggesting a difference in their sensitivity to elevation of brain magnesium. The current study suggests that elevation of brain magnesium might be a novel approach for enhancing synaptic plasticity in a regional-specific manner leading to enhancing the efficacy of extinction without enhancing or impairing fear memory formation.

    PMID: 22016520
    Neuropharmacology. 2012 Jan;62(1):304-12. Epub 2011 Aug 4.
    Magnesium deficiency induces anxiety and HPA axis dysregulation: modulation by therapeutic drug treatment.
    Sartori SB, Whittle N, Hetzenauer A, Singewald N.

    Abstract
    Preclinical and some clinical studies suggest a relationship between perturbation in magnesium (Mg(2+)) homeostasis and pathological anxiety, although the underlying mechanisms remain largely unknown. Since there is evidence that Mg(2+) modulates the hypothalamic-pituitary adrenal (HPA) axis, we tested whether enhanced anxiety-like behaviour can be reliably elicited by dietary Mg(2+) deficiency and whether Mg(2+) deficiency is associated with altered HPA axis function. Compared with controls, Mg(2+) deficient mice did indeed display enhanced anxiety-related behaviour in a battery of established anxiety tests. The enhanced anxiety-related behaviour of Mg(2+) deficient mice was sensitive to chronic desipramine treatment in the hyponeophagia test and to acute diazepam treatment in the open arm exposure test. Mg(2+) deficiency caused an increase in the transcription of the corticotropin releasing hormone in the paraventricular hypothalamic nucleus (PVN), and elevated ACTH plasma levels, pointing to an enhanced set-point of the HPA axis. Chronic treatment with desipramine reversed the identified abnormalities of the stress axis. Functional mapping of neuronal activity using c-Fos revealed hyper-excitability in the PVN of anxious Mg(2+) deficient mice and its normalisation through diazepam treatment. Overall, the present findings demonstrate the robustness and validity of the Mg(2+) deficiency model as a mouse model of enhanced anxiety, showing sensitivity to treatment with anxiolytics and antidepressants. It is further suggested that dysregulations in the HPA axis may contribute to the hyper-emotionality in response to dietary induced hypomagnesaemia. This article is part of a Special Issue entitled 'Anxiety and Depression'.

    PMID: 21835188
    Last edited by Gyrospeck; 12-09-2012 at 02:58.
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    #9
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    Xanax is a great "as needed" benzo, fast acting, short duration.
    Perfect for panic attacks.
    Klonopin is typically used once to twice a day for anxiety.
    Long acting, builds up in system, its what an ssri wishes it could do.
    taken at the right dose, tolerance is not that big an issue.
    abuse for fun just a few times and tolerance goes up the mountain.
    They are life savers if you really need them and take right,
    As far as symptoms....make sure to check your BP (the silent killer)
    thats a reason to be on benzos at low dose, sometimes your endocrine system just puts out a little too much cortisol and that increase in BP is not good.
    congrats! I find most people who really do have anxiety with panic, tend to not abuse. I cant stress enough to keep a blood pressure journal.
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    #10
    How does magnesium help & to what extent ?
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    #12
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    Cannabis is great. At first it gave me intense anxiety but later I could control those thoughts into positive thoughts Best not to smoke at daytime tho . It makes me slightly depressed.
    Indica looks great but I can never find it.

    Kava kava is great too, but you need a good brand.

    Take magnesium, if you want to have a intelligent mind. Around ~400 mg and plenty of fish oil. DO NOT BUY magnesium OXIDE. Other forms are ok.

    I'm really interested now in L-lysine with Arginine. They should be taken together. http://www.ncbi.nlm.nih.gov/pubmed/17510493
    Last edited by retard; 05-09-2012 at 17:43.
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    #13
    How long does Valerian root last?
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    #14
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    I would hazard a guess at 3-5 hours but it would be very dependent on personal physiology & the dose of valerian root
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    #15
    Bluelighter
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    my personal experience with Ashwhaganda/ Withania Somniferum makes me believe it has a profound effect on anxiety among others. I have high hopes for Brahmi/ Bacopa Monnieri and Tulsi/ Ocimum Basilicum all three are Ayurvedic herbs which are used for over thousands years.
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    #16
    I once ate about 10 500mg valerian tablets and had the most amazing tingling over my body for about 15 minutes. Then it passed and I realized those tablets smell terrible and that smell was going to linger with me for some time.
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    #17
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    Apparently valerian is a cat attractant - if you had any cats nearby I bet they would find you irresistable.
    Guidelines for OD ||| OD Standards ||| OD Directory Read Me First! ||| NPD Rules
    Please read the links above or PM me if I lock your post. R.I.P. F28
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    #18
    Bluelighter Ho-Chi-Minh's Avatar
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    Be careful as herbs can be very addictive just as benzodiazepines are. I've gotten harsh withdrawal from Valerian and Kava, though they were relied on a lot and I have had prior addiction to GABAergics.
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    #19
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    Quote Originally Posted by Ho-Chi-Minh View Post
    Be careful as herbs can be very addictive just as benzodiazepines are. I've gotten harsh withdrawal from Valerian and Kava, though they were relied on a lot and I have had prior addiction to GABAergics.
    can't be worse from getting off 4 mg kpin. but yeah it makes sense. if you take enough stuff that inhibits gaba its just as addicting. actually i'm addicted to my herbal teas. at least not a bad addiction.
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    #20
    Bluelighter Ho-Chi-Minh's Avatar
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    Oh definitely. Benzodiazepines and Kava/Valerian overlap when it comes to dependency/addiction severity but its rare to find the latter as severe as the former. Its just so much easier and in some ways more accessible to pop those little pills on a doctor's order than shove mass amounts of crap into your mouth every few hours.
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    #21
    Umm... it's hard to find ANY cases of valerian dependency. It's tough enough to find kava dependency. Finding it as severe as you get with benzos? I don't buy it. Show even ONE case study.

    Those drugs have limited GABAergic effects, are almost entirely limited to sodium channels.
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    #22
    Bluelighter Ho-Chi-Minh's Avatar
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    I am such a case. Eight days of 50 grams/day.
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    #23
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    Valerian did fuck all for me except give me a sloppy, chocolate coloured, inconsistent, overpowerring smelly shit the next day. Cross that off the list.
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    #24
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    So what's the go with this l-lysine? How much did the op take or have others taken to produce an anxiolytic effect & do you build tolerance. Any info on l-arginine as well much appreciated
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    #25
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    I wanted to create this thread as a place for people to look for information on different herbs and nutritional supplements for treating anxiety.
    I hear Lithium can work wonders for some people suffering from anxiety.

    Being a one year sufferer of MDMA/BZP induced anxiety I have just ordered some Lithium so will report back how it works out.

    I was warned you have to be quite careful with Lithium and start on low doses and work up.

    Apparently it tricks certain glands in some way and can sometimes help restore a better body balance. The exact science behind it i dont fully understand but I hear some very glowing reports.
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