A personal choice and a choice for every one to take at their own free will, personally I have always steered to a herbal alternative, reason being I believe the chemo theraphy made my mum's later years worse than they would have been in the long run, in some way I lost respect for the medical profession and their methods in such situations and started looking at alternatives with myself in regards to the medical study, when you have experienced a negative or traumatic experience in early life for some reason it is easy to slip back there.
The doctor's answer would be anti depressants, a refined form of st jons wart that will tell your mind what to do, that is what causes wars and in my mind causes a war in peoples minds hence the side effects, if you listen to the doctors and pharmaceuticals there is no alternative, after alot of time meeting various people living in different countries I now know there is.
5HTP
5-Hydroxytryptophan
From Wikipedia, the free encyclopedia
Not to be confused with serotonin (5-hydroxytryptamine, 5-HT).
| 5-Hydroxytryptophan | |
|---|---|
| Identifiers | |
| CAS number | 4350-09-8 |
| PubChem | 144 |
| ChemSpider | 388413 |
| UNII | C1LJO185Q9 |
| KEGG | D07339 |
| MeSH | 5-Hydroxytryptophan |
| ChEBI | CHEBI:17780 |
| ChEMBL | CHEMBL350221 |
| ATC code | N06 |
| Jmol-3D images | Image 1 |
| Properties | |
| Molecular formula | C11H12N2O3 |
| Molar mass | 220.22 g mol−1 |
| Density | 1.484 g/mL |
| Melting point | 298 to 300 °C (568 to 572 °F; 571 to 573 K) |
| Boiling point | 520.6 °C (969.1 °F; 793.8 K) |
| Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa) | |
| | |
| Infobox references | |
5-Hydroxytryptophan (5-HTP), also known as oxitriptan (INN), is a naturally occurring amino acid and chemical precursor as well as a metabolic intermediate in the biosynthesis of theneurotransmitters serotonin and melatonin from tryptophan.
5-HTP is sold over the counter in the United Kingdom, the United States and Canada as a dietary supplement for use as an antidepressant, appetite suppressant, and sleep aid, and is also marketed in many European countries for the indication of major depression under trade names like Cincofarm, Levothym, Levotonine, Oxyfan, Telesol, Tript-OH, and Triptum.[1][2] Severaldouble-blind placebo-controlled clinical trials have demonstrated the effectiveness of 5-HTP in the treatment of depression,[1] though a lack of high quality studies has been noted.[3] More and larger studies are needed to determine if 5-HTP is truly effective in treating depression,[4] but funding for such studies is lacking due to its non-patentable status.[5]
Contents
[hide]Metabolism[edit]
5-HTP is decarboxylated to serotonin (5-hydroxytryptamine or 5-HT) by the enzyme aromatic-L-amino-acid decarboxylase with the help of vitamin B6.[6] This reaction occurs both in nervous tissue and in the liver.[7] 5-HTP crosses the blood–brain barrier,[8] while 5-HT does not. Excess 5-HTP, especially when administered with vitamin B6, is thought to be metabolized and excreted.[9][10]
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Pharmacology[edit]
The psychoactive action of 5-HTP is derived from its increase in production of serotonin in central nervous system tissue.[11]
Research shows that co-administration with carbidopa greatly increases plasma 5-HTP levels.[12] However, several studies have reported that 5-HTP is effective even without a peripheral decarboxylase inhibitor (e.g. carbidopa).[13] Other studies have indicated the risk of a scleroderma-like condition resulting from the combination of 5-HTP and carbidopa.[14]
Dietary sources[edit]
Though 5-HTP is found in food only in insignificant quantities, it is a chemical involved intermediately in the metabolism of tryptophan, an amino acid found in milk, meat, potatoes, pumpkin, and various greens.[15] See also the Dietary sources section of the article on L-tryptophan.
Therapeutic use[edit]
5-HTP is sold over-the-counter in the United States, the United Kingdom, and Canada as a dietary supplement for use as an antidepressant,appetite suppressant, and sleep aid. 5-HTP in supplement form is typically sold in 50 mg or 100 mg gelatin or vegetarian capsules, however in the United Kingdom 5-HTP became available in transdermal patch form in early 2014.[16] It is usually sourced from the seeds of Griffonia simplicifolia.
In 2001 a Cochrane Review of the effect of 5-HTP and tryptophan on depression was published. The authors included only studies of a high rigor and included both 5-HTP and tryptophan in their review because of the limited data on either. Of 108 studies of 5-HTP and tryptophan on depression published between 1966 and 2000, only two met the authors' quality standards for inclusion, totaling 64 study participants. The substances were more effective than placebo in the two studies included but the authors state that, "the evidence was of insufficient quality to be conclusive," and note, "because alternative antidepressants exist which have been proven to be effective and safe, the clinical usefulness of 5-HTP and tryptophan is limited at present."[3]
5-HTP is often taken by people coming down from MDMA to relieve post-MDMA dysphoria. The basis for doing this is that 5-HTP is a necessary precursor for the brain to produce more serotonin, and MDMA use depletes a person's natural serotonin levels, thus taking 5-HTP after consuming MDMA is speculated as helping improve serotonin production. While the practice is common, the theory is physiologically reasonable, and anecdotal evidence is widespread,[17] no scientifically verifiable evidence can currently be found to confirm whether the practice actually works. No conclusive evidence suggests coadministration of 5-HTP and serotonin releasing agents such as MDMA carry increased risk of serotonin syndrome, and anecdotal evidence suggests coadministration may decrease some of the neurotoxic metabolites produced as degradation products of MDMA (see Alpha-Methyldopamine)
Possible risks or side effects[edit]
Because 5-HTP has not been thoroughly studied in a clinical setting, possible side effects and interactions with other drugs are not well known. However, it is noteworthy that no published reports of serious side effects (from non-contaminated 5-HTP) exist, despite that 5-HTP is freely available as a nutraceutical.[18][19][20] This could indicate that serious side effects are relatively rare with 5-HTP, at least in moderate doses[quantify]. On the other hand, acute moderate gastrointestinal effects, such as diarrhea and vomiting, are common upon administration of 5-HTP, probably due to rapid formation of serotonin in the upper intestinal tract.[18][21][22]
Oral 5-HTP results in an increase in urinary 5-HIAA, a serotonin metabolite, indicating that 5-HTP is peripherally metabolized to serotonin, which is then metabolized. This might cause a false positive test in tests looking for carcinoid syndrome.[23]
Known drug interactions:
- When combined with antidepressants of the MAOI or SSRI class, high dose 5-HTP can cause acute serotonin syndrome in rats.[24][25]
In humans 5-HTP has never been clinically associated with serotonin syndrome. Due to the rate-limiting nature of the decarboxylase enzyme which converts 5-HTP into serotonin, the risk of serotonin syndrome with monoamine oxidase inhibitors is thought to be quite low unless both MAOIs and 5-HTP are taken in large quantities.
- When combined with carbidopa (as a treatment for symptoms of Parkinson's disease), 5-HTP causes nausea and vomiting; however this can be alleviated via administration of granisetron.[26] As mentioned above under pharmacology, cases of scleroderma-like illness have been reported in patients using carbidopa and 5-HTP.[27]
It has been suggested by the pharmaceutical industry that 5-HTP may cause eosinophilia-myalgia syndrome (EMS), a serious condition which results in extreme muscle tenderness, myalgia, and blood abnormalities. However, there is evidence to show that EMS was caused by a contaminant in early 5-HTP supplements, before the introduction of the current Good Manufacturing Practices by the United States FDA in 2007. Many countries now employ similar regulation.[28]
See also[edit]
References[edit]
- ^ a b Turner EH, Blackwell AD (2005). "5-Hydroxytryptophan plus SSRIs for interferon-induced depression: synergistic mechanisms for normalizing synaptic serotonin". Medical Hypotheses 65 (1): 138–44. doi:10.1016/j.mehy.2005.01.026. PMID 15893130.
- ^ Swiss Pharmaceutical Society (2000). Index Nominum 2000: International Drug Directory (Book with CD-ROM). Boca Raton: Medpharm Scientific Publishers. ISBN 3-88763-075-0.
- ^ a b Shaw K, Turner J, Del Mar C (2002). Shaw, Kelly A, ed. "Tryptophan and 5-hydroxytryptophan for depression". Cochrane Database of Systematic Reviews (Online) (1): CD003198.doi:10.1002/14651858.CD003198. PMID 11869656.
- ^ 5-Hydroxytryptophan (5-HTP) University of Maryland Medical Center. 2011. Accessed: 9 January 2012.
- ^ Baker, Dean, Financing Drug Research: What are the Issues?. 2008 Industry Studies Conference Paper. Available at SSRN:http://ssrn.com/abstract=1134983 orhttp://dx.doi.org/10.2139/ssrn.1134983
- ^ Rahman MK, Nagatsu T, Sakurai T, Hori S, Abe M, Matsuda M (1982). "Effect of pyridoxal phosphate deficiency on aromatic L-amino acid decarboxylase activity with L-DOPA and L-5-hydroxytryptophan as substrates in rats". Jpn. J. Pharmacol. 32 (5): 803–11.doi:10.1254/jjp.32.803. PMID 6983619.
- ^ Bouchard, S; Bousquet, C; Roberge, AG (1981). "Characteristics of dihydroxyphenylalanine/5-hydroxytryptophan decarboxylase activity in brain and liver of cat". Journal of Neurochemistry 37 (3): 781–7.doi:10.1111/j.1471-4159.1982.tb12555.x. PMID 6974228.
- ^ Gomes P, Soares-da-Silva P. (1999). "L-DOPA transport properties in an immortalised cell line of rat capillary cerebral endothelial cells, RBE 4". Brain Res. 829 (1–2): 143–150. doi:10.1016/S0006-8993(99)01387-6. PMID 18445233.
- ^ Bouchard S, Roberge AG (1979). "Biochemical properties and kinetic parameters of dihydroxyphenylalanine--5-hydroxytryptophan decarboxylase in brain, liver, and adrenals of cat". Can. J. Biochem.57 (7): 1014–8. doi:10.1139/o79-126. PMID 39668.
- ^ Amamoto T, Sarai K (1976). "On the tryptophan-serotonin metabolism in manic-depressive disorders. Changes in plasma 5-HT and 5-HIAA levels and urinary 5-HIAA excretion following oral loading of L-5HTP in patients with depression". Hiroshima J. Med. Sci. 25 (2–3): 135–40. PMID 1088369.
- ^ "5-HTP: Uses, Side Effects, Interactions and Warnings - WebMD". Archived from the original on 16 November 2009. Retrieved 2009-10-05.
- ^ Magnussen I, Jensen TS, Rand JH, Van Woert MH (1981). "Plasma accumulation of metabolism of orally administered single dose L-5-hydroxytryptophan in man". Acta pharmacologica et toxicologica 49(3): 184–9. doi:10.1111/j.1600-0773.1981.tb00890.x.PMID 6175178.
- ^ Birdsall TC (1998). "5-Hydroxytryptophan: a clinically-effective serotonin precursor". Alternative medicine review : a journal of clinical therapeutic 3 (4): 271–80. PMID 9727088.
- ^ Sternberg EM, Van Woert MH, Young SN, et al. (1980). "Development of a scleroderma-like illness during therapy with L-5-hydroxytryptophan and carbidopa". N. Engl. J. Med. 303 (14): 782–7.doi:10.1056/NEJM198010023031403. PMID 6997735.
- ^ "5-Hydroxytryptophan". University of Maryland Medical Center.Archived from the original on 6 January 2010. Retrieved 2010-01-21.
- ^ ""Revolutionary" 5-HTP transdermal patch launches in United Kingdom". 5htppatch.co.uk. Retrieved 2014-06-18.
- ^ "Ecstasy and Depression". DanceSafe.Org. Retrieved 2014-01-09.
- ^ a b Turner EH, Loftis JM, Blackwell AD. Serotonin a la carte: supplementation with the serotonin precursor 5-hydroxytryptophan. Pharmacol Ther. 2006 Mar;109(3):325-38. Epub 2005 Jul 14. Review. PubMed PMID 16023217.
- ^ Byerley WF, Judd LL, Reimherr FW, Grosser BI. 5-Hydroxytryptophan: a review of its antidepressant efficiency and adverse effects. J Clin Psychopharmacol. 1987 Jun;7(3):127-37. Review. PubMed PMID 3298325.
- ^ van Hiele LJ. l-5-Hydroxytryptophan in depression: the first substitution therapy in psychiatry? The treatment of 99 out-patients with 'therapy-resistant' depressions. Neuropsychobiology. 1980;6(4):230-40. PubMed PMID 6967194.
- ^ Gijsman HJ, van Gerven JM, de Kam ML, Schoemaker RC, Pieters MS, Weemaes M, de Rijk R, van der Post J, Cohen AF. Placebo-controlled comparison of three dose-regimens of 5-hydroxytryptophan challenge test in healthy volunteers. J Clin Psychopharmacol. 2002 Apr;22(2):183-9. PubMed PMID 11910264.
- ^ 1: Lowe SL, Yeo KP, Teng L, Soon DK, Pan A, Wise SD, Peck RW. L-5-Hydroxytryptophan augments the neuroendocrine response to a SSRI. Psychoneuroendocrinology. 2006 May;31(4):473-84. Epub 2005 Dec 27. PubMed PMID 16378695.
- ^ Joy T, Walsh G, Tokmakejian S, Van Uum SH (January 2008)."Increase of urinary 5-hydroxyindoleacetic acid excretion but not serum chromogranin A following over-the-counter 5-hydroxytryptophan intake". Can. J. Gastroenterol. 22 (1): 49–53. PMC 2659120.PMID 18209781.
- ^ Ma Z, Zhang G, Jenney C, Krishnamoorthy S, Tao R. (July 2008). "Characterization of serotonin-toxicity syndrome (toxidrome) elicited by 5-hydroxy-l-tryptophan in clorgyline-pretreated rats". Eur J Pharmacol.588 (2–3): 198–206. doi:10.1016/j.ejphar.2008.04.004.PMID 18499101.
- ^ Izumi T, Iwamoto N, Kitaichi Y, Kato A, Inoue T, Koyama T. (2006). "Effects of co-administration of a selective serotonin reuptake inhibitor and monoamine oxidase inhibitors on 5-HT-related behavior in rats".Eur J Pharmacol. 532 (3): 258–264.doi:10.1016/j.ejphar.2005.12.075. PMID 16488409.
- ^ Jacobs G, Kamerling I, de Kam M, et al. (Nov 2008). "Enhanced tolerability of the 5-hydroxytryptophane challenge test combined with granisetron". J Psychopharmacol. (Oxford) 24 (1): 65–72.doi:10.1177/0269881108094299. PMID 18719048.
- ^ "Carbidopa/Levodopa". Truestarhealth.com. Retrieved 2014-01-09.
- ^ Michelson, D; Page, SW, Casey, R, Trucksess, MW, Love, LA, Milstien, S, Wilson, C, Massaquoi, SG, Crofford, LJ, Hallett, M (December 1994). "An eosinophilia-myalgia syndrome related disorder associated with exposure to L-5-hydroxytryptophan". The Journal of rheumatology 21 (12): 2261–5. PMID 7699627.
Further reading[edit]
- den Boer JA, Westenberg HG (1990). "Behavioral, neuroendocrine, and biochemical effects of 5-hydroxytryptophan administration in panic disorder". Psychiatry Research 31 (3): 267–78. doi:10.1016/0165-1781(90)90096-N. PMID 2139731.
- Angst J, Woggon B, Schoepf J (1977). "The treatment of depression with L-5-hydroxytryptophan versus imipramine. Results of two open and one double-blind study". Archiv für Psychiatrie und Nervenkrankheiten 224 (2): 175–86. PMID 336002.
- article at Psychology Today
- Turner EH, Loftis JM, Blackwell AD (2006). "Serotonin a la carte: supplementation with the serotonin precursor 5-hydroxytryptophan".Pharmacol. Ther. 109 (3): 325–38. doi:10.1016/j.pharmthera.2005.06.004. PMID 16023217.
- 5-Hydroxytryptophan (5-HTP) Supplement Information at University of Maryland Medical Center
- 5- HTP- Myth Or Miracle? at Vanderbilt University · Nashville, Tennessee
- Ron Sturtz (2009). "what is the difference between L-Tryptophan and 5-HTP?". Neuropsychopharmacology: 1
Depression
What is Depression?
Depression is characterized by feelings of low self-esteem, pessimism, and despair. Clinical depression is more than feeling depressed. The official definition of clinical depression is based on the following eight primary criteria:
- Poor appetite accompanied by weight loss, or increased appetite accompanied by weight gain
- Insomnia or excessive sleep habits (hypersomnia)
- Physical hyperactivity or inactivity
- Loss of interest or pleasure in usual activities, or decrease in sexual drive
- Loss of energy; feelings of fatigue
- Feelings of worthlessness, self-reproach, or inappropriate guilt
- Diminished ability to think or concentrate
- Recurrent thoughts of death or suicide
The presence of five of these eight symptoms definitely indicates clinical depression; an individual with four is probably depressed. The symptoms must be present for at least one month to be called clinical depression.
What causes Depression?
Depression can be the result of psychological as well as physiological factors. The most significant psychological theory is the “learned helplessness” model, which theorizes that depression is the result of habitual feelings of pessimism and hopelessness. The chief physiological theory is the “monoamine hypothesis,” which stresses imbalances of monoamine neurotransmitters such as serotonin, epinephrine, and norepinephrine. Serotonin deficiency is the most common biochemical cause
It is important to rule out the simple organic factors that are known to contribute to the depression such as nutrient deficiency, drugs (prescription, illicit, alcohol, caffeine, nicotine, etc.), hypoglycemia, and hypothyroidism.
What dietary factors are important in Depression?
A deficiency of any single nutrient can alter brain function and lead to depression, anxiety, and other mental disorders, especially deficiencies of vitamin B12, folic acid, other B vitamins, and omega-3 fatty acids. Alcohol utilizes many of these nutrients in its metabolism and drinking alcohol regularly replaces calories one would otherwise get from food. In this case, nutrients are just not adequately consumed, and those that are consumed are often needed to rid the body of the alcohol. In the case of hypothyroidism, inadequate iodine intake can be a cause.
Since the brain requires a constant supply of blood sugar to function properly, hypoglycemia must be avoided. Symptoms of hypoglycemia can range from mild to severe and include depression, anxiety, irritability, and other psychological disturbances; fatigue; headache; blurred vision; excessive sweating; mental confusion; incoherent speech; bizarre behavior; and convulsions. Several studies have shown hypoglycemia to be very common in depressed individuals. Simply eliminating refined carbohydrates and caffeine (which can aggravate hypoglycemia) from the diet is sometimes all that is needed for effective therapy in patients whose depression results from reactive hypoglycemia.
Food allergy is also a significant factor in some people suffering from depression. Eliminating offending foods can bring about tremendous relief (see Food Allergy for more information).
What nutritional supplements should I take for Depression?
Foundation Supplements. There are three products from Natural Factors that I think are critical in supporting good health:
- MultiStart (age and gender specific multiple vitamin and mineral formulas). Follow label instructions.
- Enriching Greens – a great tasting “greens drink” containing highly concentrated “greens” like chlorella, spirulina, wheat grass juice, barley grass juice, etc., and herbal extracts. Take one serving (one tablespoon) in 8 ounces of water daily.
- RxOmega-3 Factors – A true pharmaceutical grade fish oil supplement. Take two capsules daily.
5-Hydroxytryptophan (5-HTP) is extracted from the seed of an African plant (Griffonia simplicifolia) and is the direct precursor to serotonin. In addition to increasing serotonin levels, 5-HTP causes an increase in levels of endorphin and other neurotransmitters that are often decreased in cases of depression. Numerous double-blind studies have shown that 5-HTP has equal effectiveness compared to drugs like Prozac, Paxil, and Zoloft (the selective serotonin reuptake inhibitors, SSRIs) and tricyclic antidepressant drugs like imipramine and desipramine in terms of effectiveness, and that it offers several advantages: it is less expensive, better tolerated, and associated with fewer and much milder side effects. The typical recommendation is 50 to 100 mg three times daily (best taken before meals, preferably use an “enteric-coated” product to prevent gastroinstestinal upset). 5-HTP should not be used in combination with antidepressant drugs unless under the supervision of a physician. It can be used in combination with St. John’s wort extract.
St. John’s wort extract (Hypericum perforatum) is now a well-known natural antidepressant. Over 30 double-blind studies involving over 2,000 patients with mild to moderate depression have shown St. John’s wort extract to be very effective. However, while St. John’s wort extract appears to be as or possibly even more effective than conventional antidepressant drugs in mild to moderate depression, it does not appear to be as effective as conventional drugs in severe depression. The main advantage ofusing St. John’s wort extract as opposed to antidepressant drugs was found to be not so much a difference in therapeutic outcome, but rather a significant advantage in termsof side effects, cost, and patient satisfaction. The dosage for St. John’s wort extract (0.3% hypericin content) is 900 to 1800 mg daily. In severe cases, St. Johns wort extract can be used in combination with 5-HTP.
People taking prescription drugs need to check with their doctor or pharmacist before taking St. John’s wort extract as it appears to induce enzymes in the liver and gut that detoxify certain drugs. Drugs that are metabolized by these enzymes include cyclosporine; digoxin; indinavir; oral contraceptives; theophylline; tricyclic antidepressants, such as amitriptyline; and anticoagulants, such as warfarin (Coumadin®). Do not use St. John’s wort if you are taking any of these drugs without consulting a physician first.
St. John’s wort extract may also potentiate prescription antidepressant and anti-anxiety drugs. There is one case report of simultaneous use of St. John’s wort and paroxetine (Paxil®) producing nausea, fatigue, lethargy, and weakness. Do not use St. John’s wort if you are taking a prescription antidepressant or anti-anxiety drug without consulting a physician first.
DHEA levels typically drop as people age. People over 40 patients with depression and low DHEA levels respond quite well to DHEA supplementation. The dosage recommendation for men 45+ is 15 to 25 mg daily; for women 45+ the dosage is 5 to 15 mg daily.
Comment:
If you are currently on a prescription anti-depressant drug, you will need to work with a physician to get off the drug. Stopping the drug on your own can be dangerous, you absolutely must have proper medical supervision. I have used St. John’s wort and 5-HTP successfully without incident in patients taking Prozac, Zoloft, Paxil, Effexor, and various other antidepressant drugs. The real concern that physicians have when mixing antidepressant drugs with St. John’s wort or 5-HTP is producing what is referred to as the “serotonin syndrome” – characterized by confusion, fever, shivering, sweating, diarrhea, and muscle spasms. Although this syndrome has never been produced when St. John’s wort extract or 5-HTP have been given alone, it is theoretically possible that combining St. John’s wort or 5-HTP with standard antidepressant drugs could produce this syndrome. If symptoms of serotonin syndrome appear, elimination of one of the therapies is indicated.
How do I know if the recommendations are working?
Feelings of depression are mostly subjective. Anti-depressants, whether natural or synthetic, generally take 2-6 weeks to demonstrate an effect. One of the first improvements noted by many is in sleep quality.
Testimonial:
[quote]Dear Dr. Murray,
Despite the many different antidepressants I’d been prescribed over the past several years (gaining 70 pounds in the process … ugh) the ONLY thing I could take that would give me any sense of feeling “normal” was Vicodin. Thankfully, I found your book on 5-HTP. I took my first 100mg dose one morning, and WITHIN TWO HOURS I felt better than I had in ages!!! It was/is the most amazing thing, Dr. Murray! It has been five weeks since I started taking 5-HTP, and not only do I have more HOPE than I’ve had in years, but I also have felt absolutely no inclination to take Vicodin since I started taking 5-HTP. I no longer need Ambien or Valium to sleep, nor do I need to sleep 14 hours at a time on weekends. Instead, I sleep 7 – 8 hours per night and wake up refreshed and ready to start the day. It truly is like a miracle to me. I cannot thank you enough for touching my life in the way that you have, and I hope this email finds its way to you so you will know how very grateful I am to you.
Best regards, Nancy[/quote]
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