5.1 DRUGS THAT ARE HIGHLY RECOMMENDED (for inclusion in your supplementation anti-aging program) 
The striatal dopamine dependency of life span in male rats. Longevity study with (-)Deprenyl.
Deprenyl increases the life span as well as activities of superoxide dismutase and catalase but not of glutathione peroxidase in selective brain regions in Fischer rats.
Longevity treatment with (-)Deprenyl in female rats: effect on copulatory activity and lifespan.
Why (-)Deprenyl prolongs survivals of experimental animals: Increase of anti-oxidant enzymes in brain and other body tissues as well as mobilization of various humoral factors may lead to systemic anti-aging effects.

Deprenyl. The pharmacology of survival for Parkinson's and probably for Alzheimer's disease

In the early 1960's Professor Joseph Knoll of Semmelweis University in Hungary developed the medication Deprenyl for use as an anti-depressant. Later the drug was found to benefit Parkinson's patients due to it's ability to regulate neurotransmitters such as dopamine. Parkinson's is thought to be caused by low-production of dopamine. Dopamine production in such patients decreases by 30% to 90% per decade, and when production has fallen to 10% of normal the patient dies within a short time. Dopamine production also decreases in healthy people, but at a slower rate of about 13% per decade in normally aging people and only 8% in slowly aging people. However, the difference in Parkinson's patients and healthy people is only a matter of rate of decline and time. A study done in 1988 by Professor Knoll showed that rats given medium does of Deprenyl live up to thirty percent longer because the drug slows this loss of dopamine. Later experiments also showed increased life-span, although not as high a percent as the 1988 experiment found.

Originally, the drug was thought to work only as an MAO-inhibitor (MAO, or monoamine oxidase, is the neurotransmitter that metabolizes used neurotransmitters). When MAO-levels rise, as they do as a person ages, levels of neurotransmitters such as dopamine, decrease. MAO-inhibitors help stabilize levels of neurotransmitters and thus slow aging. However, research from 1994 shows Deprenyl has benefits unconnected with its MAO-inhibiting action. Deprenyl also acts as an anti-oxidant and stimulates production of the body's natural anti-oxidant enzymes superoxide dismutase (SOD) and catalase (CAT). These effects also slow aging.

Professor Joseph Knoll, discover of the pharmacological activity of Deprenyl

Parkinson's disease is currently the only FDA approved use of the drug, but there is on-going research on its use to treat Alzheimer's. Anecdotal evidence indicates that Deprenyl may be effective in treating stoke, dementia, multiple scelrosis, and hypertension, and a number of other conditions. Dr. Clyde Reynolds, a specialist in metabolic cancer therapy in Washington State, discovered that cancer patients consistently have imbalances in the neurotransmitters epinephrine, norepinephrine, and serotonin and the balance must be restored if patients are to be cured. This is possibly due to Deprenyls ability to increase DHEA levels, which are important in maintaining the immune system.

Another benefit of Deprenyl is its aphrodisiac effect and its ability to increase sensitivity of touch. Research done by Professor Knoll in 1993 found increased mating frequency in rats and incidental evidence from those people taking Deprenyl concurs.

Healthy individuals looking at Deprenyl for life-extension purposes are advised moderate doses. Over the long term, proper dosage appears to be a crucial factor and research is underway to pin-point optimum dosage. Very high doses are not advised for healthy people. The following rate is currently recommended for starting dosage and should be lowered after several months of treatment:

Deprenil recomended rates
1mg twice a week
5 mg every day
1mg every other day
6mg every day
1mg every day
8mg every day
2mg every day
9mg every day
3mg every day
80 and over
10mg every day

Selected references on Deprenyl:

Mech Ageing Dev 1988 Dec;46(1-3):237-62
The striatal dopamine dependency of life span in male rats. Longevity study with (-)Deprenyl.
Knoll J.
Department of Pharmacology, Semmelweis University of Medicine, Budapest, Hungary.

Long-term experiments on male rats revealed that better performers in the mating test are better learners in the shuttle box and the more active animals live significantly longer than their less active peers. It was established by the aid of (-)Deprenyl, a highly specific chemical tool, which increases superoxide dismutase activity in the striatum, facilitates the activity of the nigrostriatal dopaminergic neurons with utmost selectivity, and protects these neurons from their age-related decay, that the efficiency of a male rat in behavioral tests, as well as the duration of its life are striatal dopamine dependent functions. As a measure of striatal function, sexual activity was tested once a week in a group of male rats (n = 132) from the 24th month of their life. Because of the age-related decay of this function none of the 2-year-old animals displayed full scale sexual activity. By dividing the group equally the rats were treated with saline (1 ml/kg, s.c.) and Deprenyl (0.25 mg/kg, s.c.), respectively, three times a week. In the saline-treated group (n = 66) the last signs of sexual activity vanished to the 33rd week of treatment. (-)Deprenyl treatment restored full scale sexual activity in 64 out of 66 rats. The longest living rat in the saline-treated group lived 164 weeks. The average lifespan of the group was 147.05 +/- 0.56 weeks. The shortest living animal in the (-)Deprenyl-treated group lived 171 weeks and the longest living rat died during the 226th week of its life. The average lifespan was 197.98 +/- 2.36 weeks, i.e. higher than the estimated maximum age of death in the rat (182 weeks). This is the first instance that by the aid of a well-aimed medication members of a species lived beyond the known lifespan maximum.

Ann N Y Acad Sci 1994 Jun 30;717:60-71 (-)
Deprenyl increases the life span as well as activities of superoxide dismutase and catalase but not of glutathione peroxidase in selective brain regions in Fischer rats.
Kitani K, Kanai S, Carrillo MC, Ivy GO.
Radioisotope Research Institute, Faculty of Medicine, University of Tokyo, Japan.

(-)Deprenyl, a MAO-B inhibitor that is also known to be effective for symptoms of Parkinson's disease, when injected subcutaneously (sc) in male Fischer-344 rats at a dose of 0.5 mg/kg per day (3 times a week) from 18 months of age, significantly increased the remaining life expectancy. The average life span after 24 months was 34% greater in treated rats than in saline-treated control animals. Furthermore, a short-term (3 wk) continuous sc infusion of Deprenyl significantly increased activities of superoxide dismutase and catalase but not of glutathione peroxidase in selective brain regions such as s. nigra, striatum, and cerebral cortex, but not in hippocampus or cerebellum, or the liver. The optimal dose for increasing these activities, however, differed greatly depending on the sex and age of animals, with a 10-fold lower value for young female than male rats. Interestingly, aging caused an increase and a decrease in the optimal dose in female and male rats, respectively. In addition, treatment for a longer term tended to reduce the optimal dosage in the same animal group. The results clearly demonstrate that Deprenyl increases antioxidant enzyme activities in selective brain regions. If this effect of Deprenyl is causally related to its life-prolonging effect, the dosage to be used for any life span study would be a critical factor, with the dosage differing widely depending on sex, age of animal, and mode and duration of drug administration.

Acta Physiol Hung 1996;84(3):277-8
Longevity treatment with (-)Deprenyl in female rats: effect on copulatory activity and lifespan.
Dallo J, Koles L.
Department of Pharmacology, Semmelweis University of Medicine, Budapest, Hungary.

Six months old ovariectomized female rats (n = 9) were treated with (-)Deprenyl in a dose of 0.25 mg/kg s.c. three times a week, and (n = 9) with physiologic saline (0.1 ml/100 g) till decay. It was found that control females (n = 9) decayed within the age of fifteen months while the members of the (-)Deprenyl treated group were all alive at that age. Moreover three (-)Deprenyl treated female rats reached 36 months of age. Sexual activity was quite absent in both groups. The data suggests that (-)Deprenyl extended the lifespan of female rats only in total absence of gonadal hormones and sexual activity.
Mech Ageing Dev 2002 Apr;123(8):1087-100
Why (-)Deprenyl prolongs survivals of experimental animals: Increase of anti-oxidant enzymes in brain and other body tissues as well as mobilization of various humoral factors may lead to systemic anti-aging effects.
Kitani K, Minami C, Isobe K, Maehara K, Kanai S, Ivy GO, Carrillo MC.
National Institute for Longevity Sciences, 36-3, Gengo, Morioka-cho, Obu-shi, 474-8522, Aichi, Japan.

(-)Deprenyl, a monoamine oxidase B (MAO B) inhibitor is known to upregulate activities of anti-oxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT) in brain dopaminergic regions. The drug is also the sole chemical which has been repeatedly shown to increase life spans of several animal species including rats, mice, hamsters and dogs. Further, the drug was recently found to enhance anti-oxidant enzyme activities not only in brain dopaminergic regions but also in extra-brain tissues such as the heart, kidneys, adrenal glands and the spleen. We and others have also observed mobilization of many humoral factors (interferone (INF)-gamma, tumor necrosis factor (TNF)-alpha, interleukine (IL)-1beta,2,6, trophic factors, etc.) and enhancement of natural killer (NK) cell functions by (-)Deprenyl administration. An apparent extension of life spans of experimental animals reported in the past may be better explained by these new observations that (-)Deprenyl upregulate SOD and CAT activities not only in the brain but also in extra-brain vital organs and involve anti-tumorigenic as well as immunomodulatory effect as well. These combined drug effects may lead to the protection of the homeostatic regulations of the neuro-immuno-endocrine axis of an organism against aging.

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)
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
Rheumatoid arthritis
Gastrointestinal diseases
    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
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

Bread, cereals, pasta, fiber
Glycemic index
Meat and poultry
Sugar and sweet
Fats and oils
Dairy and eggs
Nuts and seeds
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
Flavonoids, carotenes
Vitamin B
Vinpocetine (Cavinton)
Deprenyl (Eldepryl)
    5.2 Drugs with controversial or unproven anti-aging effect, or awaiting other evaluation (side-effects)
        Phyto-medicines, Herbs
      5.3 Drugs for treatment and prevention of specific diseases of aging. High-tech modern pharmacology.
        Alzheimer's disease and Dementia
Immune decline
Infections, bacterial
Infections, fungal
Memory loss
Muscle weakness
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
Cataracts and Glaucoma
Genetic disorders
Heart attacks
Immune decline
Infectious diseases
Memory loss
Muscle weakness
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
Bones, limbs, joints etc.
Heart & heart devices
    6.6 Obesity reduction by ultrasonic treatment
  Physical activity and aging. Experimental and clinical data.
        Aerobic exercises
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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