sam-e

[Hessel]

Nogen som ved hvad sam-e er for noget stads? Og hvor det evt. kan koebes hvis det virker og ikke er skadeligt eller ulovligt?

[-Anders-]

Sam-e står står for S-adenosylmethionine, så kan du eventuelt finde mere info ved at søge på det.

så vidt jeg ved så bruger atleter det primært for at forhindre/afhjælpe led-problemer. Det tyder dog på at det også har en række andre positive effekter på bla. hjertekarsystemet og hjernen.

Edited July 26, 2003 by -Anders-

[Hessel]

Tak Anders! Ind til videre har jeg kun kunnet finde "reklame information"! Nogen som har nogle referencer? Nogen som ved hvor det kan koebes i EU?

[-Anders-]

her er hvad jeg lige umiddelbart kunne finde:

Influence of oral S-adenosylmethionine on plasma 5-methyltetrahydrofolate, S-adenosylhomocysteine, homocysteine and methionine in healthy humans.

Loehrer FM, Schwab R, Angst CP, Haefeli WE, Fowler B.

University Children's Hospital Basel, Metabolic Unit, Switzerland.

Elevated plasma homocysteine concentration is an independent risk factor for vascular disease in humans. In addition to nutritional and genetic factors, an interruption of the coordinate regulatory function of S-adenosylmethionine has been proposed to be involved in the occurrence of hyperhomocysteinemia. The effect of oral S-adenosylmethionine on homocysteine metabolism in humans is unknown. We investigated the effect of oral S-adenosylmethionine (400 mg) on plasma levels of 5-methyltetrahydrofolate, which is the active form of folate in the remethylation of homocysteine to methionine, S-adenosylhomocysteine, the demethylated product of S-adenosylmethionine, homocysteine and methionine over 24 hr in 14 healthy subjects. After oral administration, S-adenosylmethionine increased from 38.0 +/- 13.4 to 361.8 +/- 66.4 nmol/liter (mean +/- S.E., P < .001) and returned to base-line values with a half-life of 1.7 +/- 0.3 hr. Both S-adenosylhomocysteine and 5-methyltetrahydrofolate showed a significant transient increase (from 29.9 +/- 3.7 to 51.7 +/- 7.1 nmol/liter, and from 25.1 +/- 2.5 to 36.2 +/- 3.5 nmol/liter, respectively, P < .001), although homocysteine and methionine did not change over the time of measurement. These changes were not found in subjects without previous S-adenosylmethionine administration. The observed metabolic changes suggest that S-adenosylmethionine, at least in concentrations obtained in this study, does not inhibit 5,10-methylenetetrahydrofolate reductase, the 5-methyltetrahydrofolate forming enzyme. Rather they indicate a positive effect on 5-methyltetrahydrofolate, a key cofactor in homocysteine metabolism, which should be considered in homocysteine lowering strategies for the prevention of vascular disease.

og her:

J Rheumatol. 1994 May;21(5):905-11.  Related Articles, Links 

A randomized, double blind, placebo controlled trial of intravenous loading with S-adenosylmethionine (SAM) followed by oral SAM therapy in patients with knee osteoarthritis.

Bradley JD, Flusser D, Katz BP, Schumacher HR Jr, Brandt KD, Chambers MA, Zonay LJ.

Specialized Center of Research in Osteoarthritis, Indiana University School of Medicine, Indianapolis 46202.

OBJECTIVE. We evaluated the effectiveness and rapidity of onset of S-adenosylmethionine (SAM), administered as daily intravenous boluses of 400 mg for 5 days, followed by oral tablets, 200 mg thrice daily for 23 days, versus a matching placebo regimen, in the treatment of 81 patients with symptomatic knee osteoarthritis (OA). METHODS. The study was bicentric, randomized, double blinded, and placebo controlled. Patients underwent a 7-day washout of arthritis medications prior to initiation of this study treatment. Major outcome measures were the Stanford Health Assessment Questionnaire disability and pain scales, and supplemental visual analog scales for rest and walking pain. RESULTS. At one site, patients had milder OA, the baseline characteristics of the treatment groups were well matched, and the SAM treated group showed significantly greater reduction in overall pain and rest pain (p < 0.05) than the placebo treated group. At the other site, the patients had more severe OA, randomization yielded markedly different treatment groups, and the response to treatment did not differ between groups. Onset of SAM effect was seen as early as 14 days after the start of treatment. CONCLUSION. SAM may be an effective treatment for some patients with symptomatic knee OA, and merits further study. Intravenous loading before oral maintenance therapy may be advantageous.

Publication Types:

Clinical Trial

Randomized Controlled Trial

så vidt jeg kan forstå, så virker SAME ved at holde dit homocystein niveau på et acceptabelt niveau.

Grunden til det bliver brugt mod ledproblemer må være fordi at et forøget homocystein niveau er observeret hos folk med ledbetændelse...

[-Anders-]

Am J Med. 1987 Nov 20;83(5A):72-7.  Related Articles, Links 

Double-blind controlled clinical trial of oral S-adenosylmethionine versus piroxicam in knee osteoarthritis.

Maccagno A, Di Giorgio EE, Caston OL, Sagasta CL.

Department of Rheumatology, Hospital Frances, Buenos Aires, Argentina.

A double-blind, randomized, 84-day controlled clinical trial was carried out to compare orally administered S-adenosylmethionine (SAMe) (1,200 mg per day) with oral piroxicam therapy (20 mg per day) in the management of unilateral knee osteoarthritis. The ability of each drug to maintain the results achieved at the end of the treatment period was also evaluated during a 56-day follow-up period. Forty-five patients completed the study, 22 in the SAMe group and 23 in the piroxicam group. Both SAMe and piroxicam proved effective in inducing a significant improvement in the total pain score after 28 days of treatment. With regard to the other clinical parameters (i.e., morning stiffness, the distance walked before the onset of pain, active and passive motility), improvement started from about Day 56 in both groups. No significant difference was found between the two treatments in terms of efficacy and tolerability. Patients treated with SAMe maintained clinical improvement achieved at the end of treatment longer than did patients receiving piroxicam.

Publication Types:

Clinical Trial

Randomized Controlled Trial

PMID: 3318443 [PubMed - indexed for MEDLINE]

Der er en hel del flere studier, så det virker som om det er godt backet up... om det så er lovligt herhjemme er en anden sag. Med den tåbelige lovgivning vi har på kosttilskudsområdet her i Danmark, skulle det ikke undre mig om det er ulovligt. Jeg mener Jørgen Storm bruger SAME, så han ved nok hvordan man får fingrene i det, men mon ikke han svarer på din post ovre på Getbig.

PS.

Du må gerne vende tilbage med info hvis du finder ud af noget.... Det virker som et godt underbygget tilskud, og hvis det ikke er for dyrt så kunne det da godt være man skulle tilføje SAME til sit arsenal :jeep:

Edited July 26, 2003 by -Anders-

[DSB Harry]

Interessant - godt arbejde Anders ;)

[/Niels]

Supplement

SAM-e

 

  Description

S-adenosylmethionine (SAM-e) is a form of the sulfur-containing amino acid, methionine, combined with adenosine (part of the energy compound ATP). Like methionine, SAM-e is involved in numerous metabolic processes in the body which require sulfur – such as the methylation reactions. The body typically manufactures all the SAM-e that it requires (from methionine consumed in protein foods), but a defect in methylation or a deficiency in any of the cofactors required for SAM-e production (methionine, choline, B vitamins) is theorized to reduce the body's ability to produce SAM-e.

 

  Claims

Relieves depression / Elevates mood

Reduces arthritis pain

Maintains antioxidant status (via glutathione)

  Theory

It has been hypothesized that a defect in the body's methylation process is central to the biochemical basis of certain neuropsychiatric disorders. For example, folic acid, which is involved in methylation reactions in the body, has been linked to depression when consumed at deficient levels (probably due to a lowering of brain serotonin levels). There is a high incidence of folate deficiency in depression, and there are indications in the literature that some depressed patients who are folate deficient respond to folate supplementation. Folate deficiency is also known to lower levels of S-adenosylmethionine (SAM-e), while supplemental levels are an effective antidepressant that raise brain serotonin levels. It is suggested that low levels of serotonin in some depressed patients may be a secondary consequence of low levels of SAM-e.

 

  Scientific Support

Tissue levels of SAM-e have been found to be low in the elderly and in patients suffering from depression. SAM-e has performed as well as conventional antidepressant drugs in studies of depression, where it has been demonstrated that SAM-e can alter mood states. The mechanism for the effectiveness of SAM-e is unclear, but is likely to be related to increasing levels of brain neurotransmitters such as serotonin and dopamine.

 

  Safety

SAM-e has been shown to be effective in elevating mood and treating depression – without some of the more commonly reported side effects found with prescription antidepressants (impotence, nervousness, trouble sleeping and headaches)

High dietary intake of methionine, however, is associated with the potential for significant adverse side effects. High levels of methionine can lead to high levels of a particular metabolite, homocysteine, which has been associated with an increased risk for cardiovascular disease. In the presence of inadequate levels of B-complex vitamins (folic acid and vitamins B6 and B12), homocysteine levels may become increased and may damage the inner lining of blood vessels leading to cardiovascular complications.

 

  Value

SAM-e has the distinct advantage of being a naturally occurring compound in the body, which suggests that dietary supplementation with SAM-e is simply providing an additional dietary source of this nutrient. Other antidepressant compounds that are available as dietary supplements, such as St. John's wort, could be viewed by some as more of a pharmacological approach to relieving depression because they are not found in the body. This is more a matter of semantics, however, as both compounds have been shown to be effective in elevating mood and relieving mild depression.

 

  Dosage

It is important to note that dietary supplements of methionine do not appear to elevate SAM-e levels or have the same effect on mood states found with SAM-e. Doses of 200-600 mg per day may be effective in elevating mood and treating mild depression.

 

  References

1. Baldessarini RJ. Biological transmethylation involving S-adenosylmethionine: development of assay methods and implications for neuropsychiatry. Int Rev Neurobiol. 1975;18:41-67.

2. Baldessarini RJ. Neuropharmacology of S-adenosyl-L-methionine. Am J Med. 1987 Nov 20;83(5A):95-103. 3. Bottiglieri T, Godfrey P, Flynn T, Carney MW, Toone BK, Reynolds EH. Cerebrospinal fluid S-adenosylmethionine in depression and dementia: effects of treatment with parenteral and oral S-adenosylmethionine. J Neurol Neurosurg Psychiatry. 1990 Dec;53(12):1096-8.

4. Bottiglieri T, Hyland K, Reynolds EH. The clinical potential of ademetionine (S-adenosylmethionine) in neurological disorders. Drugs. 1994 Aug;48(2):137-52.

5. Bottiglieri T, Hyland K. S-adenosylmethionine levels in psychiatric and neurological disorders: a review. Acta Neurol Scand Suppl. 1994;154:19-26.

6. Bressa GM. S-adenosyl-l-methionine (SAMe) as antidepressant: meta-analysis of clinical studies. Acta Neurol Scand Suppl. 1994;154:7-14.

7. Cantoni GL, Mudd SH, Andreoli V. Affective disorders and S-adenosylmethionine: a new hypothesis. Trends Neurosci. 1989 Sep;12(9):319-24.

8. Carney MW, Edeh J, Bottiglieri T, Reynolds EM, Toone BK. Affective illness and S-adenosyl methionine: a preliminary report. Clin Neuropharmacol. 1986;9(4):379-85.

9. Carney MW, Toone BK, Reynolds EH. S-adenosylmethionine and affective disorder. Am J Med. 1987 Nov 20;83(5A):104-6.

10. Carney MW. Neuropharmacology of S-adenosyl methionine. Clin Neuropharmacol. 1986;9(3):235-43.

11. Del Vecchio M, Amati A, Vacca L, Zizolfi S. Monitoring S-adenosyl-methionine blood levels and antidepressant effect. Acta Neurol (Napoli). 1980 Dec;2(6):488-95.

12. Fava M, Rosenbaum JF, MacLaughlin R, Falk WE, Pollack MH, Cohen LS, Jones L, Pill L. Neuroendocrine effects of S-adenosyl-L-methionine, a novel putative antidepressant. J Psychiatr Res. 1990;24(2):177-84.

13. Goodnick PJ, Sandoval R. Psychotropic treatment of chronic fatigue syndrome and related disorders. J Clin Psychiatry. 1993 Jan;54(1):13-20.

14. Masturzo P, Gianrossi R, Carolei A, Barreca T, Murialdo G. Effect of S-adenosyl-methionine (SAMe) on some endocrine parameters in normal adult subjects. Minerva Med. 1976 Sep 19;67(43):2801-4.

15. Morrison LD, Becker L, Kish SJ. S-adenosylmethionine decarboxylase in human brain. Regional distribution and influence of aging. Brain Res Dev Brain Res. 1993 Jun 8;73(2):237-41.

16. Morrison LD, Bergeron C, Kish SJ. Brain S-adenosylmethionine decarboxylase activity is increased in Alzheimer's disease. Neurosci Lett. 1993 May 14;154(1-2):141-4.

17. Morrison LD, Sherwin AL, Carmant L, Kish SJ. Activity of S-adenosylmethionine decarboxylase, a key regulatory enzyme in polyamine biosynthesis, is increased in epileptogenic human cortex. Arch Neurol. 1994 Jun;51(6):581-4.

18. Morrison LD, Smith DD, Kish SJ. Brain S-adenosylmethionine levels are severely decreased in Alzheimer's disease. J Neurochem. 1996 Sep;67(3):1328-31.

19. Newman PE. Alzheimer's disease revisited. Med Hypotheses. 2000 May;54(5):774-6.

20. Otero Losada ME, Rubio MC. The importance of methylation reactions in the biochemistry of catecholaminergic and serotoninergic neurons. Medicina (B Aires). 1991;51(3):267-72.

21. Passeri M, Ceccato S. Significance of transmethylation and S-adenosylmethionine (SAM) in the management of Parkinson's disease with L-dopa. Minerva Med. 1972 Apr 21;63(30):1722-59.

22. Piccinin GL, Gerardi AU, Piccirilli M, Araco M. The neurochemical bases of the use of SAM in psychiatry. Clin Ter. 1980 Jul 15;94(1):113-6.

23. Reynolds EH, Carney MW, Toone BK. Methylation and mood. Lancet. 1984 Jul 28;2(8396):196-8.

24. Reynolds EH, Stramentinoli G. Folic acid, S-adenosylmethionine and affective disorder. Psychol Med. 1983 Nov;13(4):705-10.

25. Rosenbaum JF, Fava M, Falk WE, Pollack MH, Cohen LS, Cohen BM, Zubenko GS. The antidepressant potential of oral S-adenosyl-l-methionine. Acta Psychiatr Scand. 1990 May;81(5):432-6.

26. Salmaggi P, Bressa GM, Nicchia G, Coniglio M, La Greca P, Le Grazie C. Double-blind, placebo-controlled study of S-adenosyl-L-methionine in depressed postmenopausal women. Psychother Psychosom. 1993;59(1):34-40.

27. Tramoni AV, Azorin JM. Therapeutic indications of S-adenosyl methionine in neuropsychiatry. Encephale. 1988 May-Jun;14(3):113-8.

28. Trolin CG, Lofberg C, Trolin G, Oreland L. Brain ATP:L-methionine S-adenosyltransferase (MAT), S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH): regional distribution and age-related changes. Eur Neuropsychopharmacol. 1994 Dec;4(4):469-77. 

[tungpres]

Og det kan tilføjes, at de på the Colgan Institute anbefaler minimum 400 mg SAMe dagligt til atleter med ledproblemer. De anbefaler i øvrigt at kombinere med Glucosamin sulfat, Chondroitin sulfat, essentielle fedtsyrer samt folinsyre og vitamin B12.

Michael Colgan plejer i hvert fald at have en ide om hvad han snakker om.