Search 
 
 
ANTI-AGING DRUGS AND SUPPLEMENTS
 
 5.1 DRUGS THAT ARE HIGHLY RECOMMENDED (for inclusion in your supplementation anti-aging program) 
   
 
  SAM  
   
Blood viscosity and red cell morphology in subjects suffering from cirrhosis before and after treatment with S-adenosyl-L-methionine (SAM).
S-adenosyl-L-methionine (SAM) in adults with ADHD, RS: preliminary results from an open trial.
The effect of S-adenosyl-L-methionine (SAM) on membrane permeability in the perfused rat liver.
Efficacy of the dietary supplement S-adenosyl-L-methionine.
Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence.
S-adenosyl-L-methionine: its role in the treatment of liver disorders.
Efficacy and tolerability of oral and intramuscular S-adenosyl-L-methionine 1,4-butanedisulfonate (SAMe) in the treatment of major depression: comparison with imipramine in 2 multicenter studies.
Chemoprevention of hepatocarcinogenesis: S-adenosyl-L-methionine.
S-Adenosyl-L-methionine and mitochondrial reduced glutathione depletion in alcoholic liver disease.
Double-blind, placebo-controlled cross-over study of intravenous S-adenosyl-L-methionine in patients with fibromyalgia.
S-adenosyl-l-methionine (SAMe) as antidepressant: meta-analysis of clinical studies.
S-adenosyl-L-methionine (SAMe) and its use in hepatology.
The antidepressant potential of oral S-adenosyl-l-methionine.
Effects of oral S-adenosyl-L-methionine on hepatic glutathione in patients with liver disease.
S-adenosyl-L-methionine in the treatment of Alzheimer's disease.
S-adenosylmethionine and depression.
 


INTRODUCTION


SAM is short for S-adenosyl-L-methionine. It is a hormone produced in the human body, but it is made in small doses and its level can be increased through supplementation. It is essential in reactions involving nucleic acid as well as to the fluidity and function of cell membrane. It prevents depletion of glutathione, one of the body's strongest antioxidants, which reduces the activity of free radicals and protects cells from oxidative damage. The usual dosage is 200-400 milligrams per day.


Below you find a list of scientific abstracts on SAM.

   
   
Clin Hemorheol Microcirc. 2000;22(3):215-21
Blood viscosity and red cell morphology in subjects suffering from cirrhosis before and after treatment with S-adenosyl-L-methionine (SAM).
Turchetti V, Bellini MA, Leoncini F, Petri F, Trabalzini L, Guerrini M, Forconi S.
Istituto di Medicina Interna e Geriatria, Universita degli Studi di Siena, Italy.

Alterations of fluidity of the hepatocytic membrane and of the transport related systems are the basis of the cholesteatic syndrome and favour the tissue accumulation of cytotoxic metabolites. S-Adenosyl-L-Methionine (SAM) is a natural molecule which acts as a giver of methylic groups and as an enzymatic activator in several enzymatic actions of transmethylase and of transulphuration and plays a key role in biochemical processes of hepatic cell. The aim of our study was to evaluate the effects of SAM on the restoration of the membrane fluidity and on the hepatic function in general. In studying the fluidity of the cell membrane we evaluated some hemorheological parameters (total blood viscosity and red cell morphology). Fluidity of the red cell membrane is one of the most important elements of red cell rheology. We studied 15 patients (Group A) suffering from micro- and macro-nodular cirrhosis verified through hepatic biopsy, with alcoholic or post-viral causes. We evaluated the values of: blood viscosity (with a cone-plate rheometer by Carri-med), haematocrit, plasma fibrinogen and the erythrocytic morphology at the optical microscope with the Zipursky-Forconi method before and after 7 days of therapy with SAM i.v.. Data were compared with those of a similar group (Group B) treated with traditional therapy only (hyposodic and hypoprotein diet supplemented with multivitamin preparations, vitamin K in particular, if necessary, and potassium sparing diuretics). We also measured biliary salts, alkaline phosphatase, transaminase and gamma-GT. In the first group we observed a statistically significant reduction of blood viscosity, haematocrit didn't change significantly; biliary salts reduced in a statistically significant way. Evaluation of red cell morphology showed in all cases a pathological percentage (>15%) of echinocytes and knizocytes which reduced to a mean of 5% after SAM therapy. We observed no further modifications of the other hemorheological parameters. Results demonstrate that SAM has a positive action on the fluidity of the membrane, as indicated by the improvement of haemorheological parameters and by the significant decrease of biliary salts, indicating the presence of cholesteasis.

   
   
Psychopharmacol Bull. 1990;26(2):249-53
S-adenosyl-L-methionine (SAM) in adults with ADHD, RS: preliminary results from an open trial.
Shekim WO, Antun F, Hanna GL, McCracken JT, Hess EB.
Neuropsychiatric Institute, University of California, Los Angeles 90024-6967.

The psychostimulants d-amphetamine and methylphenidate are thought to be the most effective treatment in children, adolescents, and adults with attention deficit-hyperactivity disorder (ADHD) because they potentiate both dopamine (DA) and norepinephrine (NE) at the synaptic cleft. These medications are not free from side effects and controversy. Newer effective and safe treatments are needed. S-Adenosyl-L-methionine (SAM), the active form of methionine, acts as a methyl donor and is involved in many metabolic pathways. It has beta adrenergic and DA receptor agonist activity. We have been using oral SAM in a sample of well-diagnosed adults with ADHD, residual state (RS) in a 4-week open trial to establish SAM effectiveness and safety and in a 9-week, double-blind, placebo-controlled crossover trial. Preliminary data from the open trial reveal that 75 percent (6 out of 8 male) patients improve on it. The 2 who did not improve had not improved on methylphenidate trial. Improvement ranged from moderate to marked, with minimal and transient side effects that did not interfere with functioning.

   
   
Boll Soc Ital Biol Sper. 1979 Oct 30;55(20):2037-43
The effect of S-adenosyl-L-methionine (SAM) on membrane permeability in the perfused rat liver.
Francavilla A, Polimeno L, Brandi M, Sciscioli A, Albano O, Del Salvatore B, Stramentinoli G.

S-adenosilmethionine is present in most human tissues and is an important factor for transmethylation, transulphuration and aminopropylation reactions. The compound improves the biological, morphological and histochemical aspects of rat liver following CCl4 intossication. At the same time has been successfully used during chronic liver disease in man. With the aim to better clarify the action mechanism of SAMe some aspects concerning its effects on cell permeability in rat liver, by using the perfusion technique, have been investigated. In particular the capacity of this compound to prevent the enzymatic loss (GPT and GOT) during liver perfusion has been studied. 30 perfusions without SAMe, as control, and 6 by infusing 2 mg of compound during the perfusion time have been accomplished. Varing the perfusion time from 0 to 120 min it has been observed that at any time the presence of the SAMe reduced by about 50% the loss of GOT. Similarly the activity of GPT ranging from 2 to 6 mU/ml indicate that no appreciable enzyme output occurs in presence of SAMe.

   
   
Ann Pharmacother. 2001 Nov;35(11):1414-25
Efficacy of the dietary supplement S-adenosyl-L-methionine.
Fetrow CW, Avila JR.

Pharmacy Services, University of Pittsburgh Medical Center, Passavant Hospital, PA 15237-5842, USA.

OBJECTiVE: To review existing published clinical evidence surrounding the dietary supplement SAMe (S-adenosyl-L-methionine). DATA SOURCES: The majority of information was obtained from primary published literature identified through MEDLINE search (1966-February 2001). Information was also obtained through secondary and tertiary sources when available. STUDY SELECTION AND DATA EXTRACTION: All articles identified from data sources were evaluated and all relevant information included in this review. DATA SYNTHESIS: The majority of clinical trial evidence surrounds the application of SAMe for various depressive disorders, osteoarthrits, and fibromyalgia. Sample sizes of these trials and the dose employed have varied considerably. Several reviews and at least two meta-analyses have examined the available evidence surrounding SAMe in the therapy of depression for trials completed prior to 1994 and concluded that SAMe was superior to placebo in treating depressive disorders and approximately as effective as standard tricyclic antidepressants. Much of this information exists in the form of isolated case reports or solitary clinical trials. SAMe appears to be well tolerated, with the majority of adverse effects presenting as mild to moderate gastrointestinal complaints. However, it is apparent that this agent is not without risk of more significant psychiatric and cardiovascular adverse events. Information documenting drug or food interactions with SAMe is very limited. CONCLUSIONS: Consumers should be instructed to avoid unmonitored consumption of this dietary supplement until sufficient discussion has taken place with their primary healthcare provider. Although there exists significant potential for therapeutic application of SAMe, its uncertain risk profile precludes definitive recommendation at this time. Healthcare providers and consumers should likely temper their enthusiasm for this dietary supplement until sufficient information becomes available.

   
   
Am J Clin Nutr. 2002 Nov;76(5):1158S-61S
Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence.
Mischoulon D, Fava M.
Harvard Medical School, Depression Clinical and Research Program, Massachusetts General Hospital, Boston 02114, USA.

Major depression remains difficult to treat, despite the wide array of registered antidepressants available. In recent years there has been a surge in the popularity of natural or alternative medications. Despite this growing popularity, there is limited evidence for the effectiveness of many of these natural treatments. S-adenosyl-L-methionine (SAMe) is one of the better studied of the natural remedies. SAMe is a methyl donor and is involved in the synthesis of various neurotransmitters in the brain. Derived from the amino acid L-methionine through a metabolic pathway called the one-carbon cycle, SAMe has been postulated to have antidepressant properties. A small number of clinical trials with parenteral or oral SAMe have shown that, at doses of 200-1600 mg/d, SAMe is superior to placebo and is as effective as tricyclic antidepressants in alleviating depression, although some individuals may require higher doses. SAMe may have a faster onset of action than do conventional antidepressants and may potentiate the effect of tricyclic antidepressants. SAMe may also protect against the deleterious effects of Alzheimer disease. SAMe is well tolerated and relatively free of adverse effects, although some cases of mania have been reported in bipolar patients. Overall, SAMe appears to be safe and effective in the treatment of depression, but more research is needed to determine optimal doses. Head-to-head comparisons with newer antidepressants should help to clarify SAMe's place in the psychopharmacologic armamentarium.

   
   
Am J Clin Nutr. 2002 Nov;76(5):1183S-7S
S-adenosyl-L-methionine: its role in the treatment of liver disorders.
Lieber CS.
Mount Sinai School of Medicine, Alcohol Research Center, Section of Liver Disease and Nutrition, Bronx Veterans Affairs Medical Center, NY 10468, USA.

S-Adenosyl-L-methionine (SAMe) exerts many key functions in the liver, including serving as a precursor for cysteine, 1 of 3 amino acids of glutathione--the major physiologic defense mechanism against oxidative stress. SAMe is particularly important in opposing the toxicity of free oxygen radicals generated by various pathogens, including alcohol, which cause oxidative stress largely by the induction of cytochrome P4502E1 (CYP2E1) and by its metabolite acetaldehyde. SAMe also acts as the main methylating agent in the liver. The precursor of SAMe is methionine, one of the essential amino acids, which is activated by SAMe-synthetase (EC 2.5.1.6). Unfortunately, the activity of this enzyme is significantly decreased as a consequence of liver disease. Because of decreased utilization, methionine accumulates and, simultaneously, there is a decrease in SAMe that acquires the status of an essential nutrient and therefore must be provided exogenously as a supernutrient to compensate for its deficiency. Administration of this innocuous supernutrient results in many beneficial effects in various tissues, mainly in the liver, and especially in the mitochondria. This was shown in alcohol-fed baboons and in other experimental models of liver injury and in clinical trials, some of which are reviewed in other articles in this issue.

   
   
Am J Clin Nutr. 2002 Nov;76(5):1172S-6S
Efficacy and tolerability of oral and intramuscular S-adenosyl-L-methionine 1,4-butanedisulfonate (SAMe) in the treatment of major depression: comparison with imipramine in 2 multicenter studies.
Delle Chiaie R, Pancheri P, Scapicchio P.
III Clinica Psichiatrica La Sapienza University, Rome, Italy.

BACKGROUND: S-Adenosyl-L-methionine (SAMe), a natural compound, is the most important methyl donor in the central nervous system. In several clinical trials, SAMe showed antidepressant activity. OBJECTIVE: Two multicenter studies were conducted in patients with a diagnosis of major depressive episode [baseline score on the 21-item Hamilton Depression Rating Scale (HAM-D) >or=18] to confirm the efficacy and safety of SAMe in the treatment of major depression. In the first study (MC3), 1600 mg SAMe/d was given orally; whereas, in the second study (MC4), 400 mg SAMe/d was given intramuscularly. In both studies, the effects of SAMe were compared with those of 150 mg imipramine/d given orally in a double-blind design. DESIGN: In MC3, 143 patients received oral SAMe and 138 patients received imipramine for 6 wk. In MC4, 147 patients received SAMe intramuscularly and 148 patients received imipramine for 4 wk. In both studies the 2 main efficacy measures were the final HAM-D score and the percentage of responders to Clinical Global Impression at the endpoint. Secondary efficacy measures were the endpoint Montgomery-Asberg Depression Rating Scale scores and the percentage of responders, responders being those patients showing a decrease in HAM-D score of >or=50% from baseline. RESULTS: In both studies, the results of SAMe and imipramine treatment did not differ significantly for any efficacy measure. However, significantly fewer adverse events were observed in the patients treated with SAMe. CONCLUSIONS: The antidepressive efficacy of 1600 mg SAMe/d orally and 400 mg SAMe/d intramuscularly is comparable with that of 150 mg imipramine/d orally, but SAMe is significantly better tolerated.

   
   
Alcohol. 2002 Jul;27(3):193-8
Chemoprevention of hepatocarcinogenesis: S-adenosyl-L-methionine.
Pascale RM, Simile MM, De Miglio MR, Feo F.
Department of Biomedical Sciences, Division of Experimental Pathology and Oncology, University of Sassari, Italy.

Accumulation of genetic changes characterizes the progression of cells, initiated by carcinogens, to full malignancy. Various epigenetic mechanisms, such as high polyamine synthesis, aberrant DNA methylation, and production of reactive oxygen species, may favor this process by stimulating growth and inducing DNA damage. We observed a decrease in S-adenosyl-L-methionine (SAM) content in the liver, associated with DNA hypomethylation in rat liver, during the development of preneoplastic foci, and in neoplastic nodules and hepatocellular carcinomas, induced in diethylnitrosamine-initiated rats by "resistant hepatocyte" (RH) protocol. Reconstitution of the methyl donor level in the liver by SAM administration inhibits growth and induces phenotypic reversion and apoptosis of preneoplastic cells. A 6-month SAM treatment results in a sharp and persistent decrease in development of neoplastic nodules, suggesting a long duration of SAM chemopreventive effect. Various observations support the suggestion of a role of DNA methylation in chemoprevention by SAM: (1) Exogenous SAM reconstitutes the SAM pool in preneoplastic and neoplastic liver lesions. (2) DNA methylation is positively correlated with SAM:S-adenosylhomocysteine (SAH) ratio in these lesions. (3) 5-Azacytidine, a DNA methyltransferase inhibitor, inhibits chemoprevention by SAM. (4) c-Ha-ras, c-Ki-ras, and c-myc are hypomethylated and overexpressed in preneoplastic liver. Their expression is inversely correlated with SAM:SAH ratio in SAM-treated rats. (5) S-Adenosyl-L-methionine treatment results in overall DNA methylation and partial methylation of these genes. Other possible mechanisms of SAM treatment include inhibition of polyamine synthesis, linked to partial transformation of SAM into 5'-methylthioadenosine (MTA), and antioxidant and antifibrogenic activities of both SAM and MTA.

   
   
Alcohol. 2002 Jul;27(3):179-83
S-Adenosyl-L-methionine and mitochondrial reduced glutathione depletion in alcoholic liver disease.
Fernandez-Checa JC, Colell A, Garcia-Ruiz C.
Liver Unit, Hospital Clinic I Provincial, 08036 Barcelona, Spain.

The pathogenesis of alcohol-induced liver disease is not well understood, and many factors have been described to contribute to the progressive loss of liver functions, including the overgeneration of reactive oxygen species. Mitochondria are specific targets of the toxic effects of ethanol, reflected in the loss of phosphorylative oxidation and defective ATP generation, which underlie one of the hallmarks of the hepatic alterations induced by chronic alcohol intake. Mitochondrial reduced glutathione (GSH), whose primary function is to maintain a competitive functional organelle, becomes depleted by alcohol intake. Furthermore, GSH depletion in hepatocyte mitochondria has been revealed as an important mechanism in the sensitization of liver to alcohol-induced injury. This depletion of the mitochondrial GSH level is determined by an impaired transport of GSH from the cytosol into the mitochondrial matrix owing to a partial inactivation of mitochondrial GSH carrier. The loss of function of this specific mitochondrial transporter is due to the alterations in the physicochemical properties of the inner mitochondrial membrane caused by alcohol. Because of the primary defect in the transport of cytosolic GSH into mitochondria, GSH precursors are inefficient in replenishing the levels of mitochondrial GSH despite significant increase in cytosolic GSH. Supplementation of S-adenosyl-L-methionine (SAM) to rats fed alcohol chronically has been shown to replete the mitochondrial GSH levels because of normalization of the microviscosity of the mitochondrial inner membrane. Because of the instrumental role of GSH in mitochondria in hepatocyte survival against inflammatory cytokines, its repletion by SAM feeding may underlie the potential therapeutic use of this hepatoprotective agent in the treatment of alcohol-induced liver injury.

   
   
Scand J Rheumatol. 1997;26(3):206-11
Double-blind, placebo-controlled cross-over study of intravenous S-adenosyl-L-methionine in patients with fibromyalgia.
Volkmann H, Norregaard J, Jacobsen S, Danneskiold-Samsoe B, Knoke G, Nehrdich D.
Department of Rheumatology, Frederiksberg Hospital, Copenhagen, Denmark.

The objective of this study was to test the efficacy of intravenously administered S-adenosyl-L-methionine (SAMe) in patients with fibromyalgia (FM). Thirty-four out-patients with fibromyalgia symptoms received SAMe 600 mg i.v. or placebo daily for 10 days in a cross-over trial. There was no significant difference in improvement in the primary outcome: tender point change between the two treatment groups. There was a tendency towards statistical significance in favour of SAMe on subjective perception of pain at rest (p = 0.08), pain on movement (p = 0.11), and overall well-being (p = 0.17) and slight improvement only on fatigue, quality of sleep, morning stiffness, and on the Fibromyalgia Impact Questionnaire for pain. No effect could be observed on isokinetic muscle strength, Zerrsen self-assessment questionnaire, and the face scale. No effect of SAMe in patients with FM was found in this short term study.

   
   
Acta Neurol Scand Suppl. 1994;154:7-14
S-adenosyl-l-methionine (SAMe) as antidepressant: meta-analysis of clinical studies.
Bressa GM.
Department of Psychiatry, University Cattolica Sacro Cuore School of Medicine, Rome, Italy.

INTRODUCTION--S-adenosyl-l-methionine (SAMe) is a naturally-occurring substance which is a major source of methyl groups in the brain. MATERIAL AND METHODS--We conducted a meta-analysis of the studies on SAMe to assess the efficacy of this compound in the treatment of depression compared with placebo and standard tricyclic antidepressants. RESULTS--Our meta-analysis showed a greater response rate with SAMe when compared with placebo, with a global effect size ranging from 17% to 38% depending on the definition of response, and an antidepressant effect comparable with that of standard tricyclic antidepressants. CONCLUSION--The efficacy of SAMe in treating depressive syndromes and disorders is superior with that of placebo and comparable to that of standard tricyclic antidepressants. Since SAMe is a naturally occurring compound with relatively few side-effects, it is a potentially important treatment for depression.

   
   
Minerva Gastroenterol Dietol. 1992 Jul-Sep;38(3):145-51
S-adenosyl-L-methionine (SAMe) and its use in hepatology.
Frezza M, Terpin MM, Peri A.
Servizio di Gastroenterologia ed Endoscopia Digestiva, Ospedale di Cattinara, Trieste.

S-adenosyl-L-methionine (SAMe), a molecule naturally present in several body tissues and fluids, is produced, by SAMe synthetase, from ATP and methionine. SAMe has a fundamental role, as methyl group donor, in transmethylation reactions in which the synthesis of membrane phospholipids (especially phosphatidylcholine) is mandatory for the maintenance of membrane fluidity. Another metabolic pathway involving SAMe, transsulphuration, is initiated with the release of -CH3 from the molecule and the formation of S-Adenosyl-homocysteine and then homocysteine and cysteine, a precursor of glutathione the main cellular antioxidant, responsible of detoxification of various compounds and xenobiotics. At last SAMe is implicated in aminopropylation process for the polyamine synthesis. The development of stable double salt of p-toluene sulphonic acid and sulphuric acid of SAMe enables the clinical use of the drug, as a therapeutical agent, for the treatment of a number of liver dysfunctions. In various animal and human models, including controlled trials, it has been demonstrated that SAMe can ameliorate some biochemical parameters and pruritus in cholestasis induced by a range of compounds (i.e. oEstrogens, lithocolate, etc) and in intrahepatic cholestasis superimposed to chronic liver disease. Concerning alcohol toxicity, SAMe prevents, in ethanol fed baboons, depletion of glutathione levels, normalizes the mitochondrial enzymes and improves the histological hepatic lesions. In human healthy volunteers it has been recently demonstrated that SAMe, after ethanol ingestion, significantly lowers plasma concentration of ethanol and acetaldehyde as well. Finally, SAMe has been proposed, instead of N-acetylcysteine, as precursor of glutathione, in patients who present late after ingestion of an overdose of paracetamol.

   
   
Acta Psychiatr Scand. 1990 May;81(5):432-6
The antidepressant potential of oral S-adenosyl-l-methionine.
Rosenbaum JF, Fava M, Falk WE, Pollack MH, Cohen LS, Cohen BM, Zubenko GS.
Clinical Psychopharmacology Unit, Massachusetts General Hospital, Boston 02114.

S-adenosyl-l-methionine (SAMe), a naturally occurring brain metabolite, has previously been found to be effective and tolerated well in parenteral form as a treatment of major depression. To explore the antidepressant potential of oral SAMe, we conducted an open trial in 20 outpatients with major depression, including those with (n = 9) and without (n = 11) prior history of antidepressant nonresponse. The group as a whole significantly improved with oral SAMe: 7 of 11 non-treatment-resistant and 2 of 9 treatment-resistant patients experienced full antidepressant response. Side effects were mild and transient.

   
   
Scand J Gastroenterol. 1989 May;24(4):407-15
Effects of oral S-adenosyl-L-methionine on hepatic glutathione in patients with liver disease.
Vendemiale G, Altomare E, Trizio T, Le Grazie C, Di Padova C, Salerno MT, Carrieri V, Albano O.
Institute of Medical Clinic I, University of Bari, Italy.

S-Adenosyl-L-methionine (SAMe) is a physiologic precursor of thiols and sulfurated compounds, which are known to be decreased in patients with liver disease. The effect of its administration on the hepatic glutathione content of liver patients was investigated. Four groups of subjects were selected: a) 9 patients with alcoholic liver disease treated with SAMe (1.2 g/day orally for 6 months); b) 7 patients with non-alcoholic liver disease treated as above; c) 8 placebo-treated patients with alcoholic liver disease; and d) 15 normal subjects as a control group. Total and oxidized glutathione were assayed by high-performance liquid chromatography of liver biopsy specimens before and after the treatment period. In all patients pre-treatment hepatic glutathione was significantly decreased as compared with controls. SAMe therapy resulted in a significant increase of hepatic glutathione levels both in patients with alcoholic and in those with non-alcoholic liver diseases as compared with placebo-treated patients. SAMe may therefore exert an important role in reversing hepatic glutathione depletion in patients with liver disease.

   
   
J Clin Psychopharmacol. 1988 Feb;8(1):43-7
S-adenosyl-L-methionine in the treatment of Alzheimer's disease.
Cohen BM, Satlin A, Zubenko GS.
Laboratory for Psychiatric Research, McLean Hospital, Belmont, MA 02178.

Patients with Alzheimer's disease (AD) have an apparent abnormality possibly representing an increase in the average fluidity of their cell membranes. Changes in membrane fluidity of similar magnitude to those observed in AD have been noted to lead to marked alterations in cell function. Therefore, the changes in fluidity observed in AD may be related to the symptoms of that disorder, representing either an underlying cause of dysfunction or cellular attempts to compensate for dysfunction in AD. To test these possibilities, we administered S-adenosyl-L-methionine (SAMe), an agent shown to increase membrane fluidity in animals, to patients with AD. Treatment with SAMe led to marked increases in membrane fluidity. However, it produced neither improvement nor worsening of symptoms. The results imply that while SAMe may be useful for other conditions associated with altered membrane fluidity (such as normal aging), changing membrane fluidity per se is not likely to lead to marked changes in symptoms in AD.


   
   
Aust Fam Physician. 2002 Apr;31(4):339-43
S-adenosylmethionine and depression.
Nguyen M, Gregan A.

BACKGROUND: Depression is one on the most common psychological problems encountered in medical practice. Conventional antidepressants, although effective, have many side effects and there is a need for effective medications with fewer side effects. OBJECTIVE: To present all the available clinical evidence on the supplement, S-adenosylmethionine (SAMe) in the treatment of depressive symptoms as well as its safety. DISCUSSION: Recent clinical studies have revealed that SAMe, a naturally occurring molecule, is safe and effective in the treatment of mild and moderate depression. Although further research is required to clarify SAMe's role as a potential first line treatment for depression, physicians should be aware of the safety and efficacy of SAMe in order to advise patients on its appropriate use as complementary or as an alternative to traditional therapy for depression.

home
top
   
FASTING / LOW CALORIE PROGRAMS
on the Adriatic Coast
The Anti-Aging Fasting Program consists of a 7-28 days program (including 3 - 14 fasting days). 7-28-day low-calorie diet program is also available .
More information
    The anti-aging story (summary)
Introduction. Statistical review. Your personal aging curve
  Aging and Anti-aging. Why do we age?
    2.1  Aging forces (forces that cause aging
     
Internal (free radicals, glycosylation, chelation etc.) 
External (Unhealthy diet, lifestyle, wrong habits, environmental pollution, stress, poverty-change "poverty zones", or take it easy. etc.) 
    2.2 Anti-aging forces
     
Internal (apoptosis, boosting your immune system, DNA repair, longevity genes) 
External (wellness, changing your environment; achieving comfortable social atmosphere in your life, regular intake of anti-aging drugs, use of replacement organs, high-tech medicine, exercise)
    2.3 Aging versus anti-aging: how to tip the balance in your favour!
 
    3.1 Caloric restriction and fasting extend lifespan and decrease all-cause mortality (Evidence)
      Human studies
Monkey studies
Mouse and rat studies
Other animal studies
    3.2 Fasting and caloric restriction prevent and cure diseases (Evidence)
        Obesity
Diabetes
Hypertension and Stroke
Skin disorders
Mental disorders
Neurogical disorders
Asthmatic bronchitis, Bronchial asthma
Bones (osteoporosis) and fasting
Arteriosclerosis and Heart Disease
Cancer and caloric restriction
Cancer and fasting - a matter of controversy
Eye diseases
Chronic fatigue syndrome
Sleeping disorders
Allergies
Rheumatoid arthritis
Gastrointestinal diseases
Infertility
Presbyacusis
    3.3 Fasting and caloric restriction produce various
      biological effects. Effects on:
        Energy metabolism
Lipids metabolism
Protein metabolism and protein quality
Neuroendocrine and hormonal system
Immune system
Physiological functions
Reproductive function
Radio-sensitivity
Apoptosis
Cognitive and behavioral functions
Biomarkers of aging
    3.4 Mechanisms: how does calorie restriction retard aging and boost health?
        Diminishing of aging forces
  Lowering of the rate of gene damage
  Reduction of free-radical production
  Reduction of metabolic rate (i.e. rate of aging)
  Lowering of body temperature
  Lowering of protein glycation
Increase of anti-aging forces
  Enhancement of gene reparation
  Enhancement of free radical neutralisation
  Enhancement of protein turnover (protein regeneration)
  Enhancement of immune response
  Activation of mono-oxygenase systems
  Enhance elimination of damaged cells
  Optimisation of neuroendocrine functions
    3.5 Practical implementation: your anti-aging dieting
        Fasting period.
Re-feeding period.
Safety of fasting and low-calorie dieting. Precautions.
      3.6 What can help you make the transition to the low-calorie life style?
        Social, psychological and religious support - crucial factors for a successful transition.
Drugs to ease the transition to caloric restriction and to overcome food cravings (use of adaptogenic herbs)
Food composition
Finding the right physician
    3.7Fasting centers and fasting programs.
  Food to eat. Dishes and menus.
    What to eat on non-fasting days. Dishes and menus. Healthy nutrition. Relation between foodstuffs and diseases. Functional foods. Glycemic index. Diet plan: practical summary. "Dr. Atkins", "Hollywood" and other fad diets versus medical science
     

Vegetables
Fruits
Bread, cereals, pasta, fiber
Glycemic index
Fish
Meat and poultry
Sugar and sweet
Legumes
Fats and oils
Dairy and eggs
Mushrooms
Nuts and seeds
Alcohol
Coffee
Water
Food composition

  Anti-aging drugs and supplements
    5.1 Drugs that are highly recommended
      (for inclusion in your supplementation anti-aging program)
        Vitamin E
Vitamin C
Co-enzyme Q10
Lipoic acid
Folic acid
Selenium
Flavonoids, carotenes
DHEA
Vitamin B
Carnitin
SAM
Vinpocetine (Cavinton)
Deprenyl (Eldepryl)
    5.2 Drugs with controversial or unproven anti-aging effect, or awaiting other evaluation (side-effects)
        Phyto-medicines, Herbs
HGH
Gerovital
Melatonin
      5.3 Drugs for treatment and prevention of specific diseases of aging. High-tech modern pharmacology.
        Alzheimer's disease and Dementia
Arthritis
Cancer
Depression
Diabetes
Hyperlipidemia
Hypertension
Immune decline
Infections, bacterial
Infections, fungal
Memory loss
Menopause
Muscle weakness
Osteoporosis
Parkinson's disease
Prostate hyperplasia
Sexual disorders
Stroke risk
Weight gaining
    5.4 The place of anti-aging drugs in the whole
      program - a realistic evaluation
 
    6.1 Early diagnosis of disease - key factor to successful treatment.
      Alzheimer's disease and Dementia
Arthritis
Cancer
Depression
Diabetes
Cataracts and Glaucoma
Genetic disorders
Heart attacks
Hyperlipidemia
Hypertension
Immune decline
Infectious diseases
Memory loss
Muscle weakness
Osteoporosis
Parkinson's disease
Prostate hyperplasia
Stroke risk
Weight gaining
    6.2 Biomarkers of aging and specific diseases
    6.3 Stem cell therapy and therapeutic cloning
    6.4 Gene manipulation
    6.5 Prosthetic body-parts, artificial organs
        Blood
Bones, limbs, joints etc.
Brain
Heart & heart devices
Kidney
Liver
Lung
Pancreas
Spleen
    6.6 Obesity reduction by ultrasonic treatment
  Physical activity and aging. Experimental and clinical data.
        Aerobic exercises
Stretching
Weight-lifting - body-building
Professional sport: negative aspects
 
  Conclusion: the whole anti-aging program
    9.1 Modifying your personal aging curve
      Average life span increment. Expert evaluation.
     
Periodic fasting and caloric restriction can add 40 - 50 years to your lifespan
Regular intake of anti-aging drugs can add 20-30 years to your lifespan
Good nutrition (well balanced, healthy food, individually tailord diet) can add 15-25 years to your lifespan
High-tech bio-medicine service can add 15-25 years to your lifespan
Quality of life (prosperity, relaxation, regular vocations) can add 15-25 years to your lifespan
Regular exercise and moderate physical activity can add 10-20 years to your lifespan
These approaches taken together can add 60-80 years to your lifespan, if you start young (say at age 20). But even if you only start later (say at 45-50), you can still gain 30-40 years


Click image
to view
    9.2 The whole anti-aging life style - brief summary 
    References eXTReMe Tracker
        The whole anti-aging program: overview
         
       

       
     
Home Contact Us ANTI-AGING GUIDE 2003