| Dietary sources | |
| SAMe (S-adenosylmethionine) is the metabolically active form of the amino acid L-methionine. SAMe is contained only to a small extent in foods. | |
| Physiological effects | |
| Membrane function |
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| Liver |
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| Nervous system and hormones |
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| Nutrient requirements | |||
| Increased demand | Diseases such as burn-out syndrome, depression, fibromyalgia, joint diseases Liver diseases | ||
| Physiological significance of SAMe |
| S-adenosyl-methionine (SAMe) is the physiologically active form of L-methionine. This sulfur-containing compound occurs naturally in all organisms and is produced by the transfer of an adenosyl group from ATP to methionine. The highly reactive SAM is the most important methyl group donor in the human body and thus plays a central role in countless anabolic metabolic processes. SAMe is indispensable for cell detoxification, the formation of neurotransmitters and hormones, phospholipid synthesis and cartilage formation (1). A shortage of SAMe leads to hypomethylation of proteins of the central nervous system. The availability of SAMe depends on the enzyme activity of SAMe synthase. A decrease in the GSH/GSSG ratio reduces SAMe synthase activity and lowers the pool of transferable methyl groups (2).
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| SAMe as a therapeutic treatment for depression |
| SAMe is involved in the synthesis of important factors of brain metabolism such as neurotransmitters and phospholipids. Patients with depressions can benefit from SAMe supplementation by increases in serotonin, dopamine and phosphatidyl levels and a decrease of prolactin levels (2). In clinical studies, the daily administration of 4 x 400 mg SAMe led to a significant improvement in depressive symptoms, memory function and general well-being (3). The antidepressant and mood-lifting effects were comparable to the effects of tricyclic antidepressants in some studies (2). SAMe also appears to improve cognitive parameters associated with memory in patients with major depressive disorder (4). A pilot study of Parkinson's disease patients with depression showed that oral application of SAMe (800-3600 mg/d) over a period of 10 weeks led to a significant improvement in depressive symptoms on the Hamilton scale (5). According to the authors of the study, SAMe could be an effective therapeutic for these patients. SAMe is also suitable for reducing the dose of antidepressants such as imipramine and clomiparamine. Patients with moderate to severe depression who were additionally treated with 200 mg SAMe during the first 2 weeks of imipramine therapy (150 mg/d) showed an improvement in depressive symptoms earlier than those who received imipramine with placebo (1). |
| Pain-relieving effects in osteoarthritis |
| Chondroprotective substances are used in orthopedic practice today because of their good acceptance and high success rates (6). Numerous studies document an analgesic and antiphlogistic effect of SAMe in osteoarthritis with a pain-relieving effect comparable to that of an NSAID (7). In a double-blind study in patients with hip and knee arthrosis, 1200 mg/d SAMe had analgesic effects similar to ibuprofen (8). A randomized double-blind crossover study with 200 mg celecoxib vs. 1200 mg/d SAMe also showed comparable pain relief (9). |
| Hepatoprotective in liver diseases |
| The body's methionine metabolism primarily occurs in the liver through the formation of SAMe by methionine adenosyl transferase (10). In people with liver disease, there is often a reduced activity of the enzyme, which is why in these cases the oral administration of methionine does not lead to a significant increase in the SAMe plasma concentration. Studies suggest a hepatoprotective role of SAMe in hepatotoxic drugs such as FOLFOX (11) or ethanol-induced hepatotoxicity (14), for example, and an increase in liver damage when SAMe (12) is depleted (13). |
| Parameter | Parameter | Reference value | Description |
| SAMe | Blood (serum) | <12,0 U/l |
<12,0 U/l: Low risk of aggressive joint destruction 12 - 15 U/l: Increase risk of aggressive joint destruction > 15,0 U/l: High risk of aggressive joint destruction |
| Impact on | Symptoms |
| Oxidative Stress | Reduced antioxidative capacity Increased susceptibility to free-radical-associated diseases |
| Nervous system | Hypomethylation of central nervous system proteins |
| Homocysteine metabolism | Disorders in vitamin B12- and folic acid metabolism |
| Effect | Indication | Dosage |
| Physiological effects at a low intake |
Complementary therapy for low moods depression and burn-out Syndrome | 600 – 1600 mg/d Initial: 600 mg/d |
| For pain relief in degenerative and/or inflammatory joint diseases such as osteoarthritis or osteochondritis | 400 – 1200 mg/d | |
| For alcohol-related damage to liver | 800 – 1200 mg/d | |
| For therapeutic support of fibromyalgia | 400 – 1200 mg/d |
| General mode of administration | |
| When |
SAMe should be taken half an hour before a meal. Hint:
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| Side effects | |
| Depending on the dose, occasional gastrointestinal complaints (bloating, nausea, diarrhea, stomach acidosis), headache, dry mouth, and insomnia may occur. | |
| Contraindications | |
| In high doses SAMe can affect the effectiveness of L-dopa. Biogena SAMe 200 should therefore only be used under close control in Parkinson's patients. | |
| Durg interactions | |
| Anti Prkinson´s medication (L-Dopa) |
In high doses S-adenosyl-methionine can impair the effectiveness of L-dopa. |
| Nutrient interactions | |
| Vitamins | High niacin doses reduce SAMe levels in the liver and increase plasma homocysteine. |
| References |
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1) Gröber, U. Mikronährstoffe: Metabolic Tuning –Prävention –Therapie, 3. Auflage. Stuttgart: WVG Wissenschaftliche Verlagsgesellschaft Stuttgart, 2011. Stargrove, M. B. et al. Herb, Nutrient and Drug Interactions: Clinical Implications and Therapeutic Strategies, 1. Auflage. St. Louis, Missouri: Elsevier Health Sciences, 2008. |
