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ANTI-AGING DRUGS AND SUPPLEMENTS
 
 5.1 DRUGS THAT ARE HIGHLY RECOMMENDED (for inclusion in your supplementation anti-aging program) 
   
 
  VINPOCETINE  
   
Effect of vinpocetine on red blood cell deformability in stroke patients.
Vinpocetine treatment in acute ischaemic stroke: a pilot single-blind randomized clinical trial.
Possible Memory-Enhancing Properties of Vinpocetine.
Psychopharmacological effects of vinpocetine in normal healthy volunteers.
A double-blind placebo controlled evaluation of the safety and efficacy of vinpocetine in the treatment of patients with chronic vascular senile cerebral dysfunction.
Impact of sustained Deprenyl (selegiline) in levodopa-treated Parkinson's disease: a randomized placebo-controlled extension of the Deprenyl and tocopherol antioxidative therapy of parkinsonism trial.
In vitro antioxidant properties of pentoxifylline, piracetam, and vinpocetine.
Synaptosomal response to oxidative stress: effect of vinpocetine.
The nootropic drug vinpocetine inhibits veratridine-induced [Ca2+]i increase in rat hippocampal CA1 pyramidal cells.
Effect of ethyl apovincaminate on the cerebral circulation. Studies in patients with obliterative cerebral arterial disease.
Effect of Vinpocetine on Cerebral Blood Flow in Patients with Cerebrovascular Disorders.
On the Possible Role of Central Monoaminergic Systems in the Central Nervous System Actions of Vinpocetine.
Effect of vinpocetine on oxygen release of hemoglobin and erythrocyte organic polyphosphate concentrations in patients with vascular dementia of the Binswanger type.
Effects of aspirin, dipyridamole, nifedipine and cavinton which act on platelet aggregation induced by different aggregating agents alone and in combination.
 
 
   
   
Arzneimittelforschung 1992 Apr;42(4):425-7
Effect of vinpocetine on red blood cell deformability in stroke patients
Hayakawa M
Department of Geriatrics, Nagoya University School of Medicine, Japan

Reduction in red blood cell deformability is a contributory factor in stroke disease, and it has been postulated that red blood cell rigidification may be improved by drug treatment. In this paper the effect of vinpocetine (CAS 42971-09-5) on the deformability of red blood cells from patients with chronic ischemic cerebrovascular disease has been examined. During the administration of vinpocetine for 3 months a significant improvement in red blood cell deformability was observed without adverse effect.

   
   
Eur J Neurol 2001 Jan;8(1):81-5
Vinpocetine treatment in acute ischaemic stroke: a pilot single-blind randomized clinical trial
Feigin VL, Doronin BM, Popova TF, Gribatcheva EV, Tchervov DV
Department of Epidemiology and Preventive Medicine, Institute of Internal Medicine, Siberian Branch of the Russian Academy of Medical Science, Novosibirsk, Russia


The aim of the study was to assess the safety and feasibility of a clinical trial on the effect of vinpocetine, a synthetic ethyl ester of apovincamine, in acute ischaemic stroke. Thirty consecutive patients with computed tomography verified diagnosis of acute ischaemic stroke, who could receive drug treatment within 72 h of stroke onset, were enrolled. The patients were randomly allocated to receive either low-molecular weight dextran alone or in combination with vinpocetine. Poor outcome was defined as being dead or having a Barthel index of < 70 or a Rankin score of 3--5. Intention-to-treat analysis was applied. One-tenth of all hospitalized patients with acute ischaemic stroke were eligible for the trial. Thirty eligible patients were treated with either low-molecular weight dextran alone (mean age 57.9 +/- 11.6 years, n = 15) or in combination with vinpocetine (mean age 60.8 +/- 6.6 years, n = 15). The two treatment groups were comparable with respect to major prognostic variables. A relative risk (RR) reduction of poor outcome at 3 months follow-up was 30% (RR = 0.7; 95% confidence interval [CI] 0.1--3.4), as defined by the modified Barthel Index, and 60% as defined by the modified Ranking score (RR = 0.4, 95% CI: 0.1--1.7). The National Institute of Health (NIH--NINDS) Stroke Scale score was marginally significantly better in the vinpocetine treated group at 3 months of follow-up (P = 0.05, ANOVA). No significant adverse effects were seen. This pilot study shows that a full-scale randomized double-blind, placebo-controlled trial of vinpocetine treatment in acute ischaemic stroke is feasible and warranted.

   
   
Drug Develop Res 1988; 14: 191-3
Possible Memory-Enhancing Properties of Vinpocetine
Donna M. Coleston and Ian Hindrnarch
Human Psychopharmacology Research Unit, Department of Psychology, University of Leeds, Leeds, England

Critical flicker fusion threshold, choice reaction time, total reaction time, and Sternberg-type mernory tasks of digits/words were measured in twelve volunteers after having received vinpocetine or placebo for two days. A significant improvement was recorded in the short-terrn memory test following 40 mg of the drug when cornpared to placebo.

   
   

Eur J Clin Pharmacol 1985;28(5):567-71
Psychopharmacological effects of vinpocetine in normal healthy volunteers
Subhan Z, Hindmarch I

Twelve healthy female volunteers received pre-treatments with vinpocetine 10, 20, 40 mg and placebo (t.d.s.) for two days according to a randomised, double-blind crossover design. On the third day of treatment and 1 h following morning dosage, subjects completed a battery of psychological tests including Critical Flicker Fusion (CFF), Choice Reaction Time (CRT), Subjective Ratings of Drug Effects (LARS) and a Sternberg Memory Scanning Test. No statistically significant changes from placebo were observed on CFF, CRT or subjective ratings of drug effects. However, memory as assessed using the Sternberg technique was found to be significantly improved following treatment with vinpocetine 40 mg when compared to placebo and results suggested a localised effect of the drug on the serial comparison stage of the reaction process.

   
   
J Am Geriatr Soc 1987 May;35(5):425-30
A double-blind placebo controlled evaluation of the safety and efficacy of vinpocetine in the treatment of patients with chronic vascular senile cerebral dysfunction
Balestreri R, Fontana L, Astengo F
University of Rochester Medical Center, Rochester, NY 14620, USA

Deprenyl (selegiline) delays the need for levodopa therapy in patients with early Parkinson's disease, but the long-term benefits of this treatment remain unclear. During 1987 to 1988, 800 patients with early Parkinson's disease were randomized in the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism trial to receive Deprenyl, tocopherol, combined treatments, or a placebo and were then placed on active Deprenyl (10mg/day). A second, independent randomization was carried out in early 1993 for 368 subjects who by that time had required levodopa and who had consented to continuing the Deprenyl treatment (D subjects) or changing to a matching placebo (P subjects) under double-blind conditions. The first development of wearing off, dyskinesias, or on-off motor fluctuations was the prespecified primary outcome measure. During the average 2-year follow-up, there were no differences between the treatment groups with respect to the primary outcome measure (hazard ratio, 0.87; 95% confidence interval, 0.63, 1.19; p = 0.38), withdrawal from the study, death, or adverse events. Although 34% of D subjects developed dyskinesias and only 19% of P subjects did (p = 0.006), only 16% of D subjects developed freezing of gait but 29% of P subjects did (p = 0.0003). Decline in motor performance was less in D subjects than P subjects. levodopa-treated Parkinson's disease patients who had been treated with Deprenyl for up to 7 years, compared with patients who were changed to a placebo after about 5 years, experienced slower motor decline and were more likely to develop dyskinesias but less likely to develop freezing of gait.

   
   
Ann Neurol 2002 May;51(5):604-12
Impact of sustained Deprenyl (selegiline) in levodopa-treated Parkinson's disease: a randomized placebo-controlled extension of the Deprenyl and tocopherol antioxidative therapy of parkinsonism trial
Shoulson I, Oakes D, Fahn S, Lang A, Langston JW, LeWitt P, Olanow CW, Penney JB, Tanner C, Kieburtz K, Rudolph A;
Parkinson Study Group

In a double-blind clinical trial, vinpocetine, a synthetic ethyl ester of apovincamine, was shown to effect significant improvement in elderly patients with chronic cerebral dysfunction. Forty-two patients received 10 mg vinpocetine three times a day (tid) for 30 days, then 5 mg tid for 60 days. Matching placebo tablets were given to another 42 patients for the 90 day trial period. Patients on vinpocetine scored consistently better in all evaluations of the effectiveness of treatment including measurements on the Clinical Global Impression (CGI) scale, the Sandoz Clinical Assessment-Geriatric (SCAG) scale, and the Mini-Mental Status Questionnaire (MMSQ). There were no serious side effects related to the treatment drug.

   
   
Clin Neuropharmacol 2002 Jan-Feb;25(1):37-42
In vitro antioxidant properties of pentoxifylline, piracetam, and vinpocetine
Horvath B, Marton Z, Halmosi R, Alexy T, Szapary L, Vekasi J, Biro Z, Habon T, Kesmarky G, Toth K
First Department of Medicine Division of Cardiology, Department of Neurology, and the Department of Ophthalmology, University of Pecs' School of Medicine, Pecs, Hungary

Oxygen-free radicals play an important role in several physiologic and pathophysiologic processes. In pathologic circumstances, they can modify and damage biologic systems. Because oxygen-free radicals are involved in a wide range of diseases (cerebrovascular, cardiovascular, etc.), scavenging these radicals should be considered as an important therapeutic approach. In our in vitro study, we investigated the antioxidant capacity of three drugs: pentoxiphylline (Sigma Aldrich, St. Louis, MO, USA) piracetam (Sigma Aldrich), and vinpocetine (Richter Gedeon RT, Budapest, Hungary). Phenazine methosulphate was applied to generate free radicals, increasing red blood cell rigidity. Filtration technique and potassium leaking were used to detect the cellular damage and the scavenging effect of the examined drugs. According to our results, at human therapeutic serum concentration, only vinpocetine (Richter Gedeon RT) had significant (p < 0.01) scavenging activity with a protective effect that increased further at higher concentrations. Pentoxiphylline (Sigma Aldrich) and piracetam (Sigma Aldrich) did not have significant antioxidant capacity at therapeutic concentrations, but increasing their concentrations (pentoxiphylline at 100-times, and piracetam at 10-times higher concentrations) led to a significant (p < 0.01) scavenger effect. Our findings suggest that this pronounced antioxidant effect of vinpocetine and even the milder scavenging capacity of pentoxiphylline and piracetam may be of value in the treatment of patients with cerebrovascular disorders, but merits further investigations.

   
   
Free Radic Res 2000 Jan;32(1):57-66
Synaptosomal response to oxidative stress: effect of vinpocetine
Santos MS, Duarte AI, Moreira PI, Oliveira CR
Department of Zoology and Faculty of Medicine, Center for Neurosciences of Coimbra, University of Coimbra, Portugal

It has been suggested that reactive oxygen species (ROS) play a role in the neuronal damage occurring in ischemic injury and neurodegenerative disorders and that their neutralization by antioxidant drugs may delay or minimize neurodegeneration. In the present study we examine whether vinpocetine can act as an antioxidant and prevent the formation of ROS and lipid peroxidation in rat brain synaptosomes. After ascorbate/Fe2+ treatment a significant increase in oxygen consumption (about 5-fold) and thiobarbituric acid reactive substances (TBARS) formation (about 7-fold) occurred as compared to control conditions. Vinpocetine inhibited the ascorbate/Fe2+ stimulated consumption of oxygen and TBARS accumulation, an indicator of lipid peroxidation, in a concentration-dependent manner. The ROS formation was also prevented by vinpocetine. Oxidative stress increased significantly the fluorescence of the probes 2',7'-dichlorodihydrofluorescein (DCFH2-DA) (about 6-fold) and dihydrorhodamine (DHR) 123 (about 10-fold), which is indicative of intrasynaptosomal ROS generation. Vinpocetine at 100 microM concentration decreased the fluorescence of DCFH2-DA and DHR 123 by about 50% and 83%, respectively. We conclude that the antioxidant effect of vinpocetine might contribute to the protective role exerted by the drug in reducing neuronal damage in pathological situations.

   
   
Neurochem Res 2001 Sep;26(8-9):1095-100
The nootropic drug vinpocetine inhibits veratridine-induced [Ca2+]i increase in rat hippocampal CA1 pyramidal cells
Zelles T, Franklin L, Koncz I, Lendvai B, Zsilla G
Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest

The alkaloid derivative vinpocetine (14-ethoxycarbonyl-(3alpha,16alpha-ethyl)-14,15-eburnamine; Cavinton) has a well known beneficial effect on brain function in hypoxic and ischemic conditions. While it increases CNS blood flow and improves cellular metabolism, relatively little is known about vinpocetine's underlying molecular mechanisms on the single cell level. Since apoptotic and necrotic cell damage is always preceded by an increase in [Ca2+]i, this study investigated the effect of vinpocetine on [Ca2+]i increases in acute brain slices. Sodium influx is an early event in the biochemical cascade that takes place during ischemia. The alkaloid veratridine can activate this Na+ influx, causing depolarization and increasing [Ca2+]i in the cells. Therefore, it can be used to simulate an ischemic attack in brain cells. Using a cooled CCD camera-based ratio imaging system and cell loading with fura 2/AM, the effect of vinpocetine on [Ca2+]i changes in single pyramidal neurons in the vulnerable CA1 region of rat hippocampal slices was investigated. Preperfusion and continuous administration of vinpocetine (10 microM) significantly inhibited the elevation in [Ca2+]i induced by veratridine (10 microM). When the drug was administered after veratridine, it could accelerate the recovery of cellular calcium levels. Piracetam, another nootropic used in clinical practice, could attenuate the elevation of [Ca2+]i only at a high, 1 mM, concentration. We have concluded that vinpocetine, at a pharmacologically relevant concentration, can decrease pathologically high [Ca2+]i levels in individual rat hippocampal CA1 pyramidal neurons; this effect might contribute to the neuroprotective property of the drug.

   
   
Arzneimittelforschung 1976;26(10a):1945-7
Effect of ethyl apovincaminate on the cerebral circulation. Studies in patients with obliterative cerebral arterial disease
Solti F, Iskum M, Czako E

The effect of ethyl apovincaminate (RGH-4405, Cavinton) on the cerebral and systemic circulations has been studied in detail in ten cases of cerebrovascular disease. 10 mg doses of Cavinton were given as infusion within 4-6 min; circulatory tests were carried out prior to administration of the drug and 3-6 min after. The principal results showed the following: On Cavinton cerebral vascular resistance was strongly reduced, while cerebral fraction of cardiac output significantly increased. On acute effect of the drug arterial mean pressure slightly decreased but cerebral blood flow nevertheless increased in general. Total vascular resistance also decreased but this decrease was less marked than that registered in cerebral vascular resistance.

   
   
Effect of Vinpocetine on Cerebral Blood Flow in Patients with Cerebrovascular Disorders
Norihiko Tamaki, M.D. Tadaki Kusunoki, M.D. Satoshi Matsumoto, M.D.
Department of Neurosurgery. Kobe University School of Medicine. Kobe, Japan

The 133xenon inhalation method was used in an open-label clinical trial to examine changes in cerebral blood flow (CBF) after vinpocetine treatment in 13 patients with cerebrovascular disorders. In all patients, measurement of regional cerebral blood flow (RCBF) was made prior to and after treatment with vinpocetine 5 mg t.i.d. for five to seven weeks. In ten of the patients, treatment was continued for a total of 8 to 16 weeks with an additional RCBF measurement at the end of their treatment. The resulte showed a significant increase in the Initial Slope Index (ISI) values of mean total CBF, and RCBF for the involved hemisphere after six weeks of treatment with vinpocetine. The CBF for the involved lobe was significantly increased for ISI and flow rate of gray matter at six weeks and at the end of treatment. No adverse reactions were reported.

   
   
Drug Develop Res 1988; 14: 263-79
On the Possible Role of Central Monoaminergic Systems in the Central Nervous System Actions of Vinpocetine
Bela Kiss and Laszlo Szporny
Department of Biochemistry, Pharrnacological Research Centre, Chemical Works of Gedeon Richter Lld., Budapest, Hungary

The effects of vinpocetine, a recently described cerebral blood flow enhancer having antihypoxic, anti-ischemic, and cognitive-function-improving actions, on rat brain monoaminergic neurotransmission have been studied under normoxic and hypoxic conditions. Vinpocetine slightly affected the steady-state levels of monoamines and their metabolites in whole brain, but a tendency was seen to increase dopamine (DA) and its metabolites in lower brain parts and to reduce noradrenaline (NA) in "terminal" regions. MHPG-SO4 leveis were enhanced in whole brain and in almost all regions examined. There was a tendency to increase S-hydroxyindole-acetic acid (S-HIAA) in some areas. It accelerated the whole brain NA turnover dose-dependently, but lett that of DA unchanged. Enhancement of NA turnover was most noted in the lower brain areas. On the other hand, no change was found in DA accumulation, an index of heart NA turnover after inhibition of dopamine-beta-hydroxylase. The rate of probenecide- induced accumulation of cerebral MHPG-SO4 and, to a lesser extent, that of 5-HIAA was also increased. No change was seen in the pargyline-induced serotonin (5-HT) accumulation. Although vinpocetine had slight or no effects on regional levels of monoamines and their metabolites, and did not alter their in vivo biosynthesis rate under normoxic conditions, it was able partially or totally to prevent reductions in the biosynthesis rate of rnonoamines and antagonized the decrease of NA, 5-HT, and 5-HIAA (but not that of DA) induced by normobaric hypoxia. This effect was mainly confined to lower brain areas. From the results, we conclude that vinpocetine primarily aflects cell body regions (e.g., brainstem) of the rat brain.

   
   
Arzneimittelforschung 1990 Jun;40(6):640-3
Effect of vinpocetine on oxygen release of hemoglobin and erythrocyte organic polyphosphate concentrations in patients with vascular dementia of the Binswanger type
Tohgi H, Sasaki K, Chiba K, Nozaki Y
Department of Neurology, Iwate Medical University, Japan

Oxygen affinity of hemoglobin, erythrocyte 2,3-diphosphoglycerate (DPG) and adenosine triphosphate (ATP) concentrations were compared before and after oral administration of vinpocetine (TCV-3B) (15 mg/d), a primarily vasodilating agent, for three weeks in eight patients with vascular dementia of the Biswanger type which is characterized by diffuse myelin pallor and multiple lacunes in the cerebral white matter. After vinpocetine administration, oxygen affinity of hemoglobin (P50) was significantly increased (26.5 +/- 0.55 to 27.6 +/- 0.62 mmHg; mean and standard deviation, p less than 0.05), red blood cell (RBC) ATP concentrations were significantly increased (846 +/- 168 to 1,158 +/- 130 mumol/l RBC, p less than 0.05), while DPG concentrations were unaltered (4.46 +/- 0.48 to 4.59 +/- 0.57 mmol/l RBC). There was a significant positive correlation between the increase of P50 and the increase of erythrocyte ATP concentrations (r = 0.67, p less than 0.05). The effect of vinpocetine of enhancing oxygen release of hemoglobin may offer an additional benefit to its primary vasodilating action in the treatment of vascular dementia of the Binswanger type due to chronic ischemia.

   
   
Eur J Clin Pharmacol 1992;42(3):257-9
Effects of aspirin, dipyridamole, nifedipine and cavinton which act on platelet aggregation induced by different aggregating agents alone and in combination
Akopov SE, Gabrielian ES
Department of Pharmacology, Yerevan Medical Institute, Armenia

The effects of vinpocetine, a recently described cerebral blood flow enhancer having antihypoxic, anti-ischemic, and cognitive-function-improving actions, on rat brain monoaminergic neurotransmission have been studied under normoxic and hypoxic conditions. Vinpocetine slightly affected the steady-state levels of monoamines and their metabolites in whole brain, but a tendency was seen to increase dopamine (DA) and its metabolites in lower brain parts and to reduce noradrenaline (NA) in "terminal" regions. MHPG-SO4 leveis were enhanced in whole brain and in almost all regions examined. There was a tendency to increase S-hydroxyindole-acetic acid (S-HIAA) in some areas. It accelerated the whole brain NA turnover dose-dependently, but lett that of DA unchanged. Enhancement of NA turnover was most noted in the lower brain areas. On the other hand, no change was found in DA accumulation, an index of heart NA turnover after inhibition of dopamine-beta-hydroxylase. The rate of probenecide- induced accumulation of cerebral MHPG-SO4 and, to a lesser extent, that of 5-HIAA was also increased. No change was seen in the pargyline-induced serotonin (5-HT) accumulation. Although vinpocetine had slight or no effects on regional levels of monoamines and their metabolites, and did not alter their in vivo biosynthesis rate under normoxic conditions, it was able partially or totally to prevent reductions in the biosynthesis rate of rnonoamines and antagonized the decrease of NA, 5-HT, and 5-HIAA (but not that of DA) induced by normobaric hypoxia. This effect was mainly confined to lower brain areas. From the results, we conclude that vinpocetine primarily aflects cell body regions (e.g., brainstem) of the rat brain.

 
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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


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

       
     
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