Withdrawal Disorders Resulting from Chronic Use of SSRIs, Benzodiazapines and Other Pharmacological Agents

Paul Reller, L.Ac.

Benzo withdrawal and withdrawal syndromes from SSRIs and SSNRIs have become a widespread problem in our population. The marketing of these anti-anxiety and anti-depressant medications resulted in an apparent belief that the standard differential diagnosis and application of specific treatments to correct the causes of anxiety and depression could now be ignored by prescribing a class of drugs that would alter neurotransmitter metabolism and relieve symptoms, regardless of the underlying cause. Consequently, a large number of patients were prescxribed medications that were of limited or short term benefit, and the patients decided that the adverse effects outweighed the benefits. They also realized that their actual medical problem had not been corrected and that very significant problems of additive anxiety and depression now resulted from the discontinuation of these drugs. In essence, the manufacturers of these drugs had once again succeeded, as they did in the past with the drug Valium, a 'classic' benzodiazepine derivative, in creating drugs of addiction.

Benzodiazepines are a class of drugs that include lorazepam (Ativan), clonazepam (Paxam), flurazapam (Dalmane), alprazolam (Xanax), nitrazepam (Insoma). SSRIs and SSNRIs are a class of selective serotonin and norepinephrine reuptake inhibitors that include fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft) and citalopram (Celexa), as well as duloxetine (Cymbalta), venlafaxine (Effexor), and others.

In order to resolve the problems with withdrawal syndrome from benzodiazepines and selective serotonin and norepinephrine reuptake inhibitors, the patient needs to confront a number of issues. The first issue is to gain an understandinng of the mechanisms of these drugs and how they create a chemical dependancy. The second issue is how to alleviate the symptoms of the withdrawal by means of safe and benign treatment methods that achieve some of the same metabolic goals of the drugs themselves, while following a protocol of controlled and tapered withdrawal. Lastly, the patient must achieve a more sound diagnosis and understanding of the cause of their anxiety and depression so that these underlying causes may be resolved. Complementary Medicine must play a significant role in this process.

The reasons behind discontinuation of these drugs include not only the obvious side effects of chronic use and the failure in many cases to achieve the medical goals, especially as the patient's body adapts to the drugs and the effect is decreased over time, but also the new body of research findings into the complexity of harm potentially caused by chronic use of these medications. This subject has been the focus of many medical doctors and researchers around the world as the clinical reports of health problems associated with the drugs' use have reached alarming levels, and reports concerning the alarming symptoms of withdrawal of the drugs poses extreme challenges to the medical system.

History and science of withdrawal physiology and pharmakodynamics of selective seretonin reuptake inhibitors and benzodiazepines

Benzodiazepines, as well as barbituates, potentiate gamma-aminobutyric acid (GABA) receptors thought to be located near GABA receptors in the brain. GABA is the chief known inhibitory neurotransmitter in our central nervous system, which is made up of the brain, brainstem and spinal cord. GABA is active at 20-40% of all neuronal synapses, and is active in many other functions in the brain beside neuroinhibition. GABA is an excitatory neurotransmitter as well, and is also directly responsible for regulation of muscle tone.

GABA works by binding to neuroreceptors and opening ion, or charged molecule, channels to trigger neural firing, or by releasing G-proteins to affect the ion channels. The inhibitory or excitatory action of GABA depends on a number of factors, especially the magnitude of the ionic current, or levels of potassium and chloride in or outside of the cells, and whether the neurological cell is receiving a signal or giving off a signal. In a child, GABA predominantly plays an excitatory role, whereas in the adult, the predominant role in the brain is inhibitory. This is important as we examine the prescription of benzodiazepines to children. It is also important as we look at the development of glutamate metabolism in the adult brain and its role in regulating our mood and mood swings.

GABA plays a significant role in other important aspects of our neurological health other than regulation of mood and inhibition of anxiety. GABA regulates the health and growth of our central nervous system, controlling the proliferation of new neural progenitor cells, neural stem cells, differentiation and migration of neurites, or connecting axons and dendrites, and the formation of synapses. Benzodiazepines are thought to work by potentiating the chloride ion channels and stimulating mainly inhibitory actions, rather than the potassium ion channels.

Benzodiazepines have negative consequences for a number of reasons. Studies show that benzodiazepines produce significant immediate decreases in circulating plasma GABA levels in anxiety disorder patients, but increased cerebral spinal fluid levels in neurologically ill patients undergoing a spinal tap. This was an indication to researchers that benzodiazepines have varied effects on various types of patients, and could explain why some patients are affected to a greater extent by benzo withdrawal syndrome. Benzodiazepine effects in the central nervous system have been shown to be greater in patients that do not suffer from the deficiency of the glutamate decarboxylase enzyme that is perhaps a genetic trait, and prescription of benzodiazepines to a patient without a true panic disorder problem could result in a greater rebound effect when the patient tries to stop taking the drug.

In the study of pharmacology in medical schools, benzodiazepines present some of the greatest warnings concerning side effects. Extra-pyramidal side effect symptoms of are particular concern. The extrapyramidal system in the brain is a neural network that includes much of the brainstem, the pons and medulla, as well as key areas of the cerebellum, the basal ganglia, cerebral cortex, vestibular nuclei and substantium nigrum, all of which act together to control our movement and muscle control. Extrapyramidal symptoms include movement disorders, such as facial twitch, tremor, restless leg movements, and muscle spasms, as well as psychological disorder, and were first noticed when drugs that reduced dopamine in the brain were used widely, such as tricyclic antidepressants. Parkinsons-like syndromes may also be induced by drugs with extrapyramidal side effects. What is confusing is that benzodiazepines are actually prescribed to treat some types of extrapyramidal side effects.

Other common side effects of benzodiazepines include dryness of the mouth and membranes, and constipation, as well as increased mouth and bronchial secretions and diarrhea, implying problems with autonomic regulation in the body. Loss of libido and erectile dysfunction, visual changes, nagging nausea, and problems with urination also imply a negative effect on the autonomic nervous system. Psychological effects include a false sense of well-being, unusual tiredness, anxiety and confusion, irritability, as well as memory problems and mental depression, which were reported with some frequency. In a small percentage of patients, abnormal thoughts, confusion, delusion and a loss of a sense of reality were reported, as well as paresthesias and tremors. Clinically, these symptoms were often reported by the patients that sought to stop taking the drugs but found that the withdrawal syndrome, which includes acutely rising blood pressure and a sense of profound panic and autonomic disorder, prevented them from stopping the drug regimen.

Modern research and revelations about the mechanisms of depression and anxiety

The World Health Organization (WHO) now estimates that depression is one of, or perhaps the most prevalent health problems in the world today. In 2003, the WHO estimated that 1% of European GDP, or gross domestic product, was spent on treatment of depression and anxiety, and this number is rising. Clinical depression was estimated as affecting over 120 million people globally.

A number of theories concerning the mechanisms of depression have emerged from scientific study. One is that the there is a reduced nerve cell volume in parts of the brain, especially the prefrontal cortex and hippocampus, that harms the ability to control mood and regulate GABA production. A 2007 fMRI study of monozygotic, or identical, twins, with high risk of for anxiety and depression did not show a distinct pattern of reduced nerve volume in the temporal lobe and posterior hippocampus, which suggests that this reduced nerve volume seen in studies is probably specific to an environmental, rather than genetic cause. Accumulating data in scientific study has shown that herbal medicine is effective both as a neuroprotective agent and as a means of promoting neurite growth, and combined in a holistic protocol to decrease the environmental causes of neuronal degeneration, may present a better alternative to GABA inhibition or inhibition of serotonin and norepinephrine reuptake in the cure of anxiety or depression, especially if herbal and nutrient medicine could in part play a significant role in providing increased bioavailability of GABA, serotonin and norepinephrine.

Bipolar disorder is a syndrome of difficulty in control of mood swing resulting in long periods of hyperactive mood suddenly turning to depression. Many researchers believe that bipolar disorder is also a GABAergic dysfunction, and that increasing DNA demethylation results in a positive change in regulation of GABA production.

Physical causes of depression include subclinical hyperparathyroidism with elevated blood calcium and parathyroid hormone, sometime stimulated by a period of calcium deficiency, Vitamin D3 deficiency, magnesium deficiency, or other metabolic and nutritional deiciencies. All of these underlying causes must be considered in the holistic therapeutic protocol.

How herbal formulas and nutritional supplements may have a positive effect on GABA metabolism and help control anxiety disorder safely, enhanced by acupuncture and healthy routines, such as yoga

In the adult, GABA is synthesized from glutamate, or glutamic acid, using cofactors derived from pyroxidine, or Vitamin B6, and an enzyme derived from the glutamic acid metabolism, which is affected by the amino acid L-glutamine. L-glutamine readily crosses the blood brain barrier in circulation and is converted to glutamic acid and increases bioavailability of GABA. A formula of nutrient supplements potentially has a beneficial effect on increasing GABA bioavailability, whose need increases with periods of poorly controlled anxiety. L-glutamine, Vitamin B6 (P5P is the bioactive form), inositol (inositol hexacotinate is the bioactive form), choline (phosphatidylcholine is the most useful form), and nicotinic acid, or niacin (niacinamide has none of the alarming flushing effects), has this effect on many patients. Since GABA primarily has an effect to control sudden mood swings, the patient with poor control of anxiety, or sudden episodes, will benefit from this course more than the patient with constant anxiety, or an anxious depression. GABA itself is a nutrient supplement, but many patients do not experience a positive effect from taking this supplement in pill form. While the precursor formula above aids bioavailability, GABA supplement in excess dosage may cause increased anxiety, as well as mild shortness of breath and tingling in the extremities. Foods that contain GABA may be of benefit, and include oranges and mandarin oranges, as well as pumpkin seed and shitake mushroom. Herbs that contain GABA include dang gui, ginseng, valerian, bitter melon, and the food herb tarragon.

In addition to herbs and supplements, researchers at the Boston Universtiy School of Medicine found that the practice of yoga elevates brain GABA levels, reducing anxiety and depression (see the article in information resources below). As always, a comprehensive and holistic treatment protocol will insure the best outcome. Acupuncture is well known as a treatment to relieve anxiety and depression as well, and should be included in the protocol. Various studies have measured the effects of specific acupuncture stimulations on GABA metabolism. A 2010 study at Daegu Haany University in South Korea (cited below as well) found that acupuncture stimulation at a single point (HT7) significantly modulated GABA neuron excitability in the ventral tegmental area of the brain and decreased harmful effects of alcohol withdrawal by normalizing GABA effects and dopamine release. As with many such studies, acupuncture has been proven to exert modulating homeostatic effects, rather than the allopathic alterations achieved by drug use. In other words, acupuncture stimulation works to normalize the healthy balancing that the body is always programmed to achieve, which we call homeostasis.

Certain herbs have been studied and found to have proven benzodiazepine effects, without side effects. These include magnolia and California poppy. Other herbs are well known to have positive effects on GABA receptors, acting as GABA analogues or GABA production stimulators. These include Kava-kava (kavalactones), valerian, and skullcap (baicalin from scutellaria lateriflora). Diazepam is a benzodiazepine derivative and MAO inhibitor found in wheat sprouts and potatoes, and was synthetically derived to form Valium. The basis for many of these drugs originated in herbal and nutrient medicine, and many patients are going back to the more natural forms of the chemicals to avoid side effects.

There are herbs with known anxiolytic effects such as MAO inhibition, a focus of another type of antidepressant and anti-anxiety drug. Magnolia stem, or hou po, in Chinese medicine, not only has benzodiazepine activity, but also contains honokiol, which has an MAO inhibition. St. John's Wort, or Hypericum perforatum, has the active ingredient hypericin, which acts as an MAO inhibitor and is anxiolytic. Apigenin is also an herbal chemical with this effect and is found in Passiflora incarnata, Gingko biloba, yarrow, scullcap, qing hao (artemesia), bohe (field mint), gegen (kudzu), Huang qin (Scutellaria baicalensis), chamomile, echinacea, saw palmetto, and milk thistle, as well as foods such as alfalfa sprouts, cilantro, tea (camellia), rosemary, and thyme. Of course, concentrations of these active chemicals in these common foods and herbs are relatively small, but professional herbal extracts contain a sufficient dosage to exert the right effect. Each patient may need a somewhat different dosage to have the best effect, though, and a Licensed Acupuncturist and herbalist will often start at the lowest effective dosage and gradually increase the dosage for the individual when the appropriate effect is achieved. Self-medication and purchase of products from the health food store may be problematic.

Passiflora incarnata, or passionflower, contains not only apigenin, but other active chemicals that exert MAO inhibition and positive CNS effects, and has been well studied in Europe. Passiflora contains harmaline, harmalol, harmane, and harmine, all MAO inhbitors that are also shownt to modulate dopamine metabolism, and scopoletin, an anticholinergic, CNS effector, MAO inhibitor, and muscle relaxant. In addition, passiflora contains some potent antioxidants, such as quercetin, luteolin, kaempferol, and anti-inflammatory ingredients as well. The wide array of chemicals in passiflora exert a balanced effect, and this herb is now well studies and approved by the Commission E in Germany for insomnia and anxiety disorders.

As of 2010, there still has not been a large number of sufficiently funded studies of herbal chemicals to treat anxiety in human clinical trials yet. Still, as this meta-analysis from the Universidade Fereral do Parana in Brazil shows, there have been sound studies demonstrating the effectiveness of Passiflora incarnata, Valeriana officianalis, Gingko biloba, and Matricaria recutita. Click here to see the study link: http://www.ncbi.nlm.nih.gov/pubmed/21308265. In Germany, the official government Commission E (founded in 1985) approved Passiflora for the treatment of insomnia, and in 2011, the NIH MedlinePlus database lists the effectiveness ratings for Passiflora (as determined by the Natural Medicines Comprehensive Database) as proven as effective as some prescription medications for anxiety, as effective in combination with clonidine to relieve symptoms of narcotic drug withdrawal, and effective in relieving symptoms of adjustment disorder with anxious mood when used in combination with other herbs, such as Valerian, crataegus, and ballota. Passiflora was in fact given FDA approval as an over-the-counter sleep aid and sedative in the U.S. in 1977, but was taken off the market in 1978 when pharmaceutical companies objected that its safety and effectiveness had not been sufficiently proven in rigorous human clinical trials. Of course, 31 years is not an unreasonable time period to conduct such studies, I guess, especially when talking about a flower extract that has been used safely for centuries.

The most well known nutrient substance with anxiolytic, or antianxiety, effects is L-tryptophan, and essential amino acid found in all meats and many vegetables and grains. Tryptophan may also act as a precursor to serotonin, if serotonin is deficient and there is demand. Like many herbs and supplements, the body responds to these chemicals in a modulatory manner that is different from the responses to synthetic chemicals. Because of this, the synthetic drugs are more powerful even when they are not needed by the metabolism, but also are able to produce more unwanted effects. Tryptophan was one of the most popular nutrient supplements in world history until and indicidence of manufacturing contamination prompted the cautionary banning of its sale in the United States in 1996. The CDC investigation immediately proved that the problems from the supplement product were tied to a rare bacteria contaminating a batch of L-Tryptophan, but pharmaceutical lobbying insured that the FDA did not lift the ban on this nutrient supplement for over ten years in order to decrease the competition and insure greater use of pharmaceutical anti-anxiety and anti-depressant drugs. During this time, the amino acid precursor, 5-HTP, or hydroxy-tryptophan-precursor, became popular, and this supplement is often a key ingredient in the treatment protocol of withdrawal syndrome from SSRIs, along with Sam-E, a type of methionine that aids the action of 5HTP, aids neurotransmitter transformation and bioavailability, and aid liver and glutamate metabolism. Tryptophan is found in many foods and herbs, including spinach, asparagus, potato, corn, oats, amaranth, fenugreek, sesame seed, thyme, lotus seed, Gingko biloba seed, sunflower oil, evening primrose oil, and watercress.

5HTP, an extract from Griffonia seed, is a bioidentical chemical to the tryptophan precursor found in the human body. 5-Hydroxytryptophan is a naturally occurring amino acid that the body utilizes as a precursor to both trypthophan and melatonin. Tryptophan is a bioactive amino acid that may be utilized in the body as a precursor to serotonin, melatonin, niacin, N-acetlytransferase, 5-hydroxyindole-O-methyltransferase, and Auxin. In addition, there are many 5HT receptors in the cells of the body as well, with 5HTP potentially exerting direct effects. This all adds up to the ability of 5HTP to be utilized to create an improved bioavailability for a number of important neurotransmitters and enzymes that regulate neurotransmitters. 5HTP may have immediate effects, with many patients noticing sound sleep and less anxiety related insomnia with a short course of 5HTP. On the other hand, studies show that the best effects of 5HTP therapy come after prolonged use, with about 2 months of taking a mild dose improving mood and sleep quality considerably. Since 5HTP is a precursor chemical, allowing better bioavailability of neurotransmitter production in the brain, studies have also found that this herbal and food chemical works well in tandom with other related herbs and nutrients. The formula that combines a low dosage of 5HTP with active Vitamin B6 (P5P), melatonin, and St. Johns Wort extract, provides the brain with a combination of effectors that allow for increased chance of homeostatic balance. This product is available from Vitamin Research, and called Positrol.

Widespread warnings that 5HTP could potentially cause a condition termed “serotonin syndrome” when combined with SSRI medication or MAO inhibitors have been disseminated. The key words here are potentially and theoretically as searches reveal no actual cases of serotonin syndrome induced by concurrant 5HTP usage, despite the widespread use of 5HTP by patients with concurrant use of SSRI medication. These warnings are based on one small laboratory study where a high dose of 5HTP was combined with an MAO inhbitor in laboratory animals, and induced an apparent serotonin crisis, or excess accumulation of serotonin. Most of the theoretical potentiality of this herbal chemical causing serotonin syndrome was derived from studies of pharmaceutical interactions causing this syndrome, which are well documented, but rarely warned against. The concurrent prescription of MAO inhibitors with SSRI medications or other serotonergic meds carries interaction warnings common to all prescribing manuals, yet is often ignored by MDs. The occurrence of serotonin syndrome is relatively rare. The dosage of 5HTP by a professional herbalist is small in almost all circumstances. Tryptophan itself is found in all meats and a wide variety of foods, and obviously, tryptophan, the serotonin precursor, is eaten by all patients taking SSRI medications. Still, the level of caution in the herbal profession almost always precludes the prescription of 5HTP concurrantly with SSRI medication. 5HTP is useful, though, in the withdrawal syndrome of SSRI medication, as a precipitous drop in serotonin bioavailability occurs with SSRI withdrawal, and is thought to be responsible for the alarming symptoms that may occur. The text Encyclopedia of Dietary Supplements by the reknowned Paul M. Coates, states that “To our knowledge, there are no published cases of serotonin syndrome linked to 5HTP consumption.” This was published in 2005. Dr. Coates was appointed the Director of the Office of Dieatary Supplements (ODS) at the NIH in 1999, and prior to this was on the faculty of the University of Pennsylvania School of Medicine.

Some nutritional supplements have some effect on GABA but are highly regulated in the body and so mainly affect the GABA system when they are deficient, not when the patient takes in an abundance of the supplement. One of these nutrients is manganese, which has a GABA stimulating effect in its natural form in the body, and is a cofactor for many enzymatic activities, as well as a necessary part of the mitochondria, or oxygen metabolizers, in our central nervous system cells. Manganese is an important constituent of the powerful antioxidant super oxide dismutase (SOD), and the type of SOD with manganese is an important part of our brain cells, protecting the cell from the oxidant superoxide, which is toxic to the cell. Deficiency of manganese-SOD may be a key component to neurodegeneration. While manganese is an essential trace nutrient to all forms of life, certain isotopes and compounds of manganese are toxic, especially those that are generated by smelters and coal fired power plants, which form organic manganese compounds that permeate our air, and are ingested in the water and food that are exposed. These toxic manganese compounds are very small and light, and difficult to break down, even entering our air via the water that we shower with. This type of toxic manganese compound is neurotoxic and has been linked to cognitive disorders and Parkinson-like neurodegenerative disease, like the compounds of mercury and lead from the coal-fired power plants and smelters. The nutrient manganese is a much different molecule, and is not toxic, but, like all charged minerals in the body, is highly regulated, and taking the supplement will aid defiencies but will probably not stimulate a GABA mechanism if one is not deficient in manganese. It would be best to insure that manganese is obtained from the diet, but mild dosage in supplementation may be warranted for some patients. Do not expect a noticeable effect on regulation of mood like one observes for the anxiolytic herbs, but nervertheless, manganese may be an important aid to patients with neurodegenerative disease, thyroid deficiency, and other deficiencies related to mood disorders.

Calcium and magnesium are also nutrients that are highly regulated in the body but do have some anxiolytic or calming effects, especially if the patient is deficient in these minerals, or if there is a hypothyroid or hyperparathyroid disorder, or a hormonal deficiency of estrogens. Unfortunately, the subject of calcium supplementation is not simple, like we are led to believe. Calcium may be the most regulated molecule in the body, and is found in almost every cell. Specific hormonal systems have been evolved in the body mainly to regulate calcium metabolism in all aspects of absorption in the digestive track, utilization and transportation, storage in the bone, and resorption from the bone as needed. There are many types of calcium supplement, and each type is a molecule of calcium combined with another substance, which is the prime determinant of where it goes and how it is utilized in the body. Magnesium absorption and utilization may be partially controlled or affected by levels of calcium in the diet, local calcium concentrations in cells and tissues, and perhaps even by calcium regulating hormones. Different types of magnesium will be carried to different tissues as well, producing different effects. To learn more about calcium metabolism, go to the article on this website entitled Calcium Supplementation. Calcium aspartate may help the patient to calm muscle spasticity, and calcium AEP is a molecule often found to be deficient in syndromes related to hypothalamic dysfunction or hypofunction. These are two examples of calcium supplements that may be used to normalize symptoms in a protocol to treat withdrawal syndromes.

The history of negative advertising and propaganda directed toward anxiolytic herbs that were competing with benzodiazepines and SSRIs in the 1990s is a subject that has not elicited enough scrutiny. A campaign to discredit the growing popularity of St. Johns Wort, Kava kava, and the amino acid L-tryptophan, proved extremely easy for the pharmaceutical companies with the aid of standard medicine. These benign herbs and a common essential amino acid were successfully vilified and their use curbed dramatically, despite a long history of use of the herbs with almost no actual clinical ill effects, and the fact that L-tryptophan was an amino acid consumed daily throughout history by almost every human. Many articles were published citing the potential for harm from these herbs and this amino acid, all based on theoretical research that was too complicated for the average patient to understand, and having no basis in actual clinical cases of proven harm to a single patient. Nevertheless, this campaign succeeded in generating FDA warnings and the end of prescription of these herbs and this amino acid, despite no actual restriction on use in herbalism. These products were removed from the market esentially, and became difficult to obtain for a number of years. In the meantime, the many thousands of patients that were successfully relying on these herbs and this amino acid to calm anxiety disorders probably joined the lucrative market for benzodiazepines and SSRI medications.

Information Resources

1. A comprehensive report from 2006 on SSRI and benzodiazapine withdrawal syndrome: http://www.benzo.org.uk/ssri.htm
2. A study of the effects of benzodiazepines on plasma GABA in anxious patients: http://resources.metapress.com/pdf-preview.axd?code=f73x435p413218pq&size=larger
3. A study of benzodiazepine responses indicates that panic disorder patients have a much different response to benzodiazepines than normal patients. The study found that levels of GABA were peristently low even with chronic benzodiazepine use in these patients, and that a deficient glutamate metabolism was perhaps the key to panic or anxiety disorders: http://ajp.psychiatryonline.org/cgi/content/full/161/12/2186
4. A 2007 study by the Boston University School of Medicine and Maclean Hospital showed surprising results demonstrating that the practice of yoga could result in healthy levels of GABA: http://www.anxietyinsights.info/yoga_elevates_brain_gaba_levels_reduces_anxiety_and_depress.htm
5. A 2007 study of neural cell volume reductions associated with anxiety and depressive disorder that appears to confirm an environmental cause, suggesting that a holistic change of environmental factors, including diet, lifestyle, phytochemical therapy, behavioral and congnitive changes is appropriate to therapeutic protocol: http://www.anxietyinsights.info/abstract_reduced_temporal_lobe_volume_in_anxiety_depressio.htm/a>
6. A 2007 review of research data in China shows that herbal medicine shows much potential to reverse neurodegneration as well as promote neuronal survival, addressing the issue of loss of nerve cells in the hippocampus and prefrontal cortex that has been linked to anxiety and depression: http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17691984
7. A 2010 study of the GABA modulating effects at the Daegu Haany University in South Korea in 2010 followed up on similar study in 2006 (Zhao et al) and found that acupuncture stimulation at a single point (HT7) effectively modulated GABA neuron excitability and dopamine release: http://www.ncbi.nlm.nih.gov/pubmed/20860620

The information on this website is not intended to be used as a specific medical advice or cure. Please consult with the practitioner or an appropriate physician, such as a licensed acupuncturist, naturopath, or medical doctor, to discuss the proper application of the information contained on this website.