5.1 DRUGS THAT ARE HIGHLY RECOMMENDED (for inclusion in your supplementation anti-aging program) 
Intake of flavonoids, carotenoids, vitamins C and E, and risk of stroke in male smokers.
Intake of specific carotenoids and flavonoids and the risk of gastric cancer in Spain.
Comparative study of antioxidant properties and cytoprotective activity of flavonoids.
The antioxidant activity of phloretin: the disclosure of a new antioxidant pharmacophore in flavonoids.
Flavonoids and urate antioxidant interplay in plasma oxidative stress.
Effects of the flavonoids quercetin and apigenin on hemostasis in healthy volunteers: results from an in vitro and a dietary supplement study.
Flavonoids can replace alpha-tocopherol as an antioxidant.
Plasma carotenoids, tocopherols, and antioxidant capacity in a 12 week intervention study to reduce fat and/or energy intakes.
Lung function in relation to intake of carotenoids and other antioxidant vitamins in a population-based study.
Antioxidant and prooxidant properties of carotenoids.
Antioxidant activities of astaxanthin and related carotenoids.
The antioxidant and biological properties of the carotenoids.
Antioxidant effects of carotenoids.
Stroke. 2000 Oct;31(10):2301-6.
Intake of flavonoids, carotenoids, vitamins C and E, and risk of stroke in male smokers.
Hirvonen T, Virtamo J, Korhonen P, Albanes D, Pietinen P.
Department of Nutrition, National Public Health Institute, Helsinki, Finland.

BACKGROUND AND PURPOSE: Antioxidants may protect against atherosclerosis and thus prevent cerebrovascular disease. We studied the association between dietary antioxidants and subtypes of stroke. METHODS: The study cohort consisted of 26 593 male smokers, aged 50 to 69 years, without a history of stroke. They were participants of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study in Finland. The men completed a validated dietary questionnaire at baseline. Incident cases were identified through national registers. RESULTS: During a 6.1-year follow-up, 736 cerebral infarctions, 83 subarachnoid hemorrhages, and 95 intracerebral hemorrhages occurred. Neither dietary flavonols and flavones nor vitamin E were associated with risk for stroke. The dietary intake of beta-carotene was inversely associated with the risk for cerebral infarction (relative risk [RR] of highest versus lowest quartile 0.74, 95% CI 0.60 to 0. 91), lutein plus zeaxanthin with risk for subarachnoid hemorrhage (RR 0.47, 95% CI 0.24 to 0.93), and lycopene with risks of cerebral infarction (RR 0.74, 95% CI 0.59 to 0.92) and intracerebral hemorrhage (RR 0.45, 95% CI 0.24 to 0.86). Vitamin C intake was inversely associated with the risk for intracerebral hemorrhage (RR 0.39, 95% CI 0.21 to 0.74). After simultaneous modeling of the antioxidants, a significant association remained only between beta-carotene intake and risk for cerebral infarction (RR 0.77, 95% CI 0.61 to 0.99). CONCLUSIONS: Dietary intake of beta-carotene was inversely associated with the risk for cerebral infarction. No association was detected between other dietary antioxidants and risk for stroke.

Cancer Causes Control. 1999 Feb;10(1):71-5.
Intake of specific carotenoids and flavonoids and the risk of gastric cancer in Spain.
Garcia-Closas R, Gonzalez CA, Agudo A, Riboli E.
Research Unit of the University Hospital of Canarias, Tenerife, Spain.

OBJECTIVES: To investigate the relationship between gastric cancer and the intake of specific carotenoids (alpha-carotene, beta-carotene, lutein, and lycopene) and flavonoids (quercetin, kaempferol, myricetin, and luteolin) using new data on their concentration in foods. METHODS: Case-control study carried out in Spain that included 354 cases of gastric cancer and 354 controls, matched by age, gender, area of residence and hospital. Usual food intake was assessed using a dietary history questionnaire. RESULTS: In a multivariate model adjusted for several dietary factors, no association was found between intake of any of the studied carotenoids and the risk of gastric cancer. The adjusted OR of gastric cancer for the highest quartile of total flavonoid intake versus the lowest quartile was 0.44 (95 percent confidence interval [CI] = 0.25-0.78; P for trend = 0.003). Kaempferol intake was found to be protective (OR = 0.48; CI = 0.26-0.88; P for trend = 0.04) comparing the highest versus the lowest quartile of intake. A trend toward lower risk of stomach cancer with higher intake of quercetin was also found. CONCLUSIONS: The results of this study support the hypothesis that the well-established protective effect of fruit and vegetables against gastric cancer could, in part, be due to the presence of flavonoids.

Biochemistry (Mosc). 2003 May;68(5):514-9.
Comparative study of antioxidant properties and cytoprotective activity of flavonoids.
Potapovich AI, Kostyuk VA.
School of Biology, Belorussian State University, Minsk 220050, Belarus.

Antioxidant properties and cytoprotective activity of flavonoids (rutin, dihydroquercetin, quercetin, epigallocatechin gallate (EGCG), epicatechin gallate (ECG)) were studied. All these compounds inhibited both NADPH- and CCl4-dependent microsomal lipid peroxidation, and the catechins were the most effective antioxidants. The I(50) values calculated for these compounds by regression analysis were close to the I(50) value of the standard synthetic antioxidant ionol (2,6-di-tert-butyl-4-methylphenol). The antiradical activity of flavonoids to O2-* was studied in a model photochemical system. Rate constants of the second order reaction obtained by competitive kinetics suggested flavonoids to be more effective scavengers of oxygen anion-radicals than ascorbic acid. By competitive replacement all flavonoids studied were shown to be chelating agents capable of producing stable complexes with transition metal ions (Fe2+, Fe3+, Cu2+). The flavonoids protected macrophages from asbestos-induced damage, and the protective effect increased in the following series: rutin < dihydroquercetin < quercetin < ECG < EGCG. The cytoprotective effect of flavonoids was in strong positive correlation with their antiradical activity to O2-*.


Biochem Biophys Res Commun. 2002 Jul 5;295(1):9-13.
The antioxidant activity of phloretin: the disclosure of a new antioxidant pharmacophore in flavonoids.
Rezk BM, Haenen GR, van der Vijgh WJ, Bast A.
Department of Pharmacology and Toxicology, Faculty of Medicine, Universiteit Maastricht P.O. Box 616, 6200 MD Maastricht, The Netherlands.

Phloretin is a dihydrochalcone flavonoid that displays a potent antioxidant activity in peroxynitrite scavenging and the inhibition of lipid peroxidation. Comparison with structurally related compounds revealed that the antioxidant pharmacophore of phloretin is 2,6-dihydroxyacetophenone. The potent activity of 2,6-dihydroxyacetophenone is due to stabilisation of its radical via tautomerisation. The antioxidant pharmacophore in the dihydrochalcone phloretin, i.e., the 2,6-dihydroxyacetophenone group, is different from the antioxidant pharmacophores previously reported in flavonoids.

Mol Cell Biochem. 2001 May;221(1-2):79-87.
Flavonoids and urate antioxidant interplay in plasma oxidative stress.
Filipe P, Lanca V, Silva JN, Morliere P, Santus R, Fernandes A.
Centro de Metabolismo e Endocrinologia da Faculdade de Medicina de Lisboa, Portugal.

Flavonoids are naturally occurring plant compounds with antioxidant properties. Their consumption has been associated with the protective effects of certain diets against some of the complications of atherosclerosis. Low-density lipoprotein (LDL) oxidative modification is currently thought to be a significant event in the atherogenic process. Most of the experiments concerning the inhibition of LDL oxidation used isolated LDL. We used diluted human whole plasma to study the influence of flavonoids on lipid peroxidation (LPO) promoted by copper, and their interaction with uric acid, one of the most important plasma antioxidants. Lipid peroxidation was evaluated by the formation of thiobarbituric acid reactive substances (TBARS) and of free malondialdehyde (MDA). The comparative capability of the assayed flavonoids on copper (II) reduction was tested using the neocuproine colorimetric test. In our assay system, urate disappears and free MDA and TBARS formation increase during the incubation of plasma with copper. Most of the tested flavonoids inhibited copper-induced LPO. The inhibition of LPO by flavonoids correlated positively with their capability to reduce copper (II). The urate consumption during the incubation of plasma with copper was inhibited by myricetin, quercetin and kaempferol. The inhibition of urate degradation by flavonoids correlated positively with the inhibition of LPO. Urate inhibited the copper-induced LPO in a concentration-dependent mode. Luteolin, rutin, catechin and quercetin had an antioxidant synergy with urate. Our results show that some flavonoids could protect endogenous urate from oxidative degradation, and demonstrate an antioxidant synergy between urate and some of the flavonoids.

Am J Clin Nutr. 1998 Feb;67(2):255-62.
Effects of the flavonoids quercetin and apigenin on hemostasis in healthy volunteers: results from an in vitro and a dietary supplement study.
Janssen K, Mensink RP, Cox FJ, Harryvan JL, Hovenier R, Hollman PC, Katan MB.
Department of Human Nutrition, Agricultural University, Wageningen, The Netherlands.

Intake of dietary flavonols and flavones was inversely associated with risk for cardiovascular disease in several epidemiologic studies. This may have been due to effects on hemostasis because flavonoids have been reported to inhibit platelet aggregation in vitro. We indeed found that 2500 micromol/L of the flavonol quercetin and the flavone apigenin significantly inhibited collagen- and ADP-induced aggregation in platelet-rich plasma and washed platelets by approximately 80-97%. However, lower concentrations, such as might occur in vivo, had no effect. To test this in vivo we fed 18 healthy volunteers 220 g onions/d providing 114 mg quercetin/d, 5 g dried parsley/d providing 84 mg apigenin/d, or a placebo for 7 d each in a randomized crossover experiment with each treatment period lasting 2 wk. Onion consumption raised mean plasma quercetin concentrations to 1.5 micromol/L; plasma apigenin could not be measured. No significant effects of onions or parsley were found on platelet aggregation, thromboxane B2 production, factor VII, or other hemostatic variables. We conclude that the antiaggregatory effects of flavonoids seen in vitro are due to concentrations that cannot be attained in vivo. Effects of dietary flavonols and flavones on cardiovascular risk are possibly not mediated by hemostatic variables.

FEBS Lett. 2000 May 12;473(2):145-8.
Flavonoids can replace alpha-tocopherol as an antioxidant.
van Acker FA, Schouten O, Haenen GR, van der Vijgh WJ, Bast A.
Department of Medical Oncology, BR-232, University Hospital Vrije Universiteit, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands.

Endogenous antioxidants such as the lipid-soluble vitamin E protect the cell membranes from oxidative damage. Glutathione seems to be able to regenerate alpha-tocopherol via a so-called free radical reductase. The transient protection by reduced glutathione (GSH) against lipid peroxidation in control liver microsomes is not observed in microsomes deficient in alpha-tocopherol. Introduction of antioxidant flavonoids, such as 7-monohydroxyethylrutoside, fisetin or naringenin, into the deficient microsomes restored the GSH-dependent protection, suggesting that flavonoids can take over the role of alpha-tocopherol as a chain-breaking antioxidant in liver microsomal membranes.

Nutrition. 2003 Mar;19(3):244-9.
Plasma carotenoids, tocopherols, and antioxidant capacity in a 12 week intervention study to reduce fat and/or energy intakes.
Djuric Z, Uhley VE, Naegeli L, Lababidi S, Macha S, Heilbrun LK.
Barbara Ann Karmanos Cancer Institute, Detroit, Michigan 48201, USA.

OBJECTIVE: We examined plasma levels of carotenoids, tocopherols, and total antioxidant activity in women before and after dietary intervention to reduce fat and/or energy intakes. Dietary fat and energy may affect intake and bioavailability of carotenoids and tocopherols, and these micronutrient levels in turn can contribute to the antioxidant capacity of plasma. METHODS: Women were randomized onto one of four diets for 12 wk: non-intervention, low fat (15% of energy from fat with maintenance of energy intake), low energy (25% energy reduction with maintenance of percentage of energy from fat), and combined low fat and low energy. Fasting plasma was available for analysis from a subset (n = 41) of women enrolled in the study. RESULTS: Levels of carotenoids and tocopherols did not change significantly over 12 wk on any diet arm, despite a modest but statistically significant increase in fruit and vegetable intake in the women following the low-fat diet (from 3.3 to 5.2 servings/d excluding potatoes). Levels of Trolox-equivalent antioxidant capacity (TEAC), total cholesterol, and two major plasma antioxidants (urate and bilirubin) also did not change significantly. Of the individual micronutrients measured, lycopene and lutein/zeaxanthin correlated most strongly with TEAC values, and the correlation with lycopene was statistically significant before intervention. CONCLUSION: The decreases in dietary fat and energy intakes in this study were quite large, but this did not appear to have detrimental effects on plasma micronutrient levels, nor did it appreciably affect plasma antioxidants. Because lycopene levels were significantly associated with plasma TEAC before intervention, interventions that increase levels of lycopene might be more likely to increase the antioxidant capacity of plasma.

Am J Epidemiol. 2002 Mar 1;155(5):463-71.
Lung function in relation to intake of carotenoids and other antioxidant vitamins in a population-based study.
Schunemann HJ, McCann S, Grant BJ, Trevisan M, Muti P, Freudenheim JL.
Department of Medicine, School of Medicine and Biomedical Sciences, State University of New York, 207 Farber Hall, 3435 Main Street, Buffalo, NY 14214-3000, USA.

Accumulating evidence suggests that dietary antioxidant vitamins are positively associated with lung function. No evidence exists regarding whether dietary carotenoids other than beta-carotene are related to pulmonary function. In 1995--1998 the authors studied the association of forced expiratory volume in 1 second and forced vital capacity as the percentage of the predicted value (FEV(1)% and FVC%, respectively) after adjustment for height, age, gender, and race with the intakes of several carotenoids (alpha-carotene, beta-carotene, beta-cryptoxanthin, lutein/zeaxanthin, and lycopene) in a random sample of 1,616 men and women who were residents of western New York State, aged 35--79 years, and free from respiratory disease. They observed significant associations of lutein/zeaxanthin and vitamins C and E with FEV(1)% and FVC% using multiple linear regression after adjustment for total energy intake, smoking, and other covariates. When they analyzed all of these antioxidant vitamins simultaneously, they observed the strongest association of vitamin E with FEV(1)% and of lutein/zeaxanthin with FVC%. The differences in forced expiratory volume in 1 second and forced vital capacity associated with a decrease of 1 standard deviation of dietary vitamin E or lutein/zeaxanthin were equivalent to the influence of approximately 1--2 years of aging. Their findings support the hypothesis that carotenoids, vitamin C, and vitamin E may play a role in respiratory health and that carotenoids other than beta-carotene may be involved.

Arch Biochem Biophys. 2001 Jan 1;385(1):20-7.
Antioxidant and prooxidant properties of carotenoids.
Young AJ, Lowe GM.
School of Biological and Earth Sciences, Liverpool John Moores University, UK.

The ability of dietary carotenoids such as beta-carotene and lycopene to act as antioxidants in biological systems is dependent upon a number of factors. While the structure of carotenoids, especially the conjugated double bond system, gives rise to many of the fundamental properties of these molecules, it also affects how these molecules are incorporated into biological membranes. This, in turn, alters the way these molecules interact with reactive oxygen species, so that the in vivo behavior may be quite different from that seen in solution. The effectiveness of carotenoids as antioxidants is also dependent upon their interaction with other coantioxidants, especially vitamins E and C. Carotenoids may, however, lose their effectiveness as antioxidants at high concentrations or at high partial pressures of oxygen. It is unlikely that carotenoids actually act as prooxidants in biological systems; rather they exhibit a tendency to lose their effectiveness as antioxidants.

J Agric Food Chem. 2000 Apr;48(4):1150-4.
Antioxidant activities of astaxanthin and related carotenoids.
Naguib YM.
Phytochem Technologies, Chelmsford, MA 01824, USA.

The antioxidant activities of astaxanthin and related carotenoids have been measured by employing a newly developed fluorometric assay. This assay is based on 4,4-difluoro-3,5-bis(4-phenyl-1, 3-butadienyl)-4-bora-3a,4a-diaza-s-indacene (BODIPY 665/676) as an indicator; 2,2'-azobis-2,4-dimethylvaleronitrile (AMVN) as a peroxyl radical generator; and 6-hydroxy-2,5,7, 8-tetramethylchroman-2-carboxylic acid (Trolox) as a calibrator in an organic and liposomal media. By employing this assay, three categories of carotenoids were examined: namely, the hydrocarbon carotenoids lycopene, alpha-carotene, and beta-carotene; the hydroxy carotenoid lutein; and the alpha-hydroxy-ketocarotenoid astaxanthin. The relative peroxyl radical scavenging activities of Trolox, astaxanthin, alpha-tocopherol, lycopene, beta-carotene, lutein, and alpha-carotene in octane/butyronitrile (9:1, v/v) were determined to be 1.0, 1.0, 1.3, 0.5, 0.4, 0.3, and 0.2, respectively. In dioleoylphosphatidyl choline (DOPC) liposomal suspension in Tri-HCl buffer (pH 7.4 at 40 degrees C), the relative reactivities of astaxanthin, beta-carotene, alpha-tocopherol, and lutein were found to be 1.00, 0.9, 0.6, and 0.6, respectively. When BODIPY 665/676 was replaced by 4,4-difluoro-5-(4-phenyl-1,3-butadienyl)-4-bora-3a, 4a-diaza-s-indacene-3-undecanoic acid (BODIPY 581/591 C(11)) as an indicator, astaxanthin showed the highest antioxidant activity toward peroxyl radicals. The relative reactivities of Trolox, astaxanthin, alpha-tocopherol, alpha-carotene, lutein, beta-carotene, and lycopene were determined to be 1.0, 1.3, 0.9, 0.5, 0.4, 0.2, and 0.4, respectively.

Ann N Y Acad Sci. 1998 Nov 20;854:443-7.
The antioxidant and biological properties of the carotenoids.
Krinsky NI.
Department of Biochemistry, School of Medicine, Tufts University, Boston, Massachusetts 02111, USA.

Much effort has been expended in evaluating the relative antioxidant potency of carotenoid pigments in both in vitro and in vivo experiments. It is quite clear that in vitro, carotenoids can inhibit the propagation of radical-initiated lipid peroxidation, and thus fulfill the definition of antioxidants. When it comes to in vivo systems, it has been much more difficult to obtain solid experimental evidence that carotenoids are acting directly as biological antioxidants. In fact, under nonphysiological circumstances, carotenoids may act as prooxidants. These results can be modified by altering the oxidant stress, the cellular or subcellular system, the type of animal, and environmental conditions, such as oxygen tension. Results of this type raise the question as to whether it is still appropriate to group the carotenoids with such antioxidant vitamins as vitamin E and vitamin C. Thus, the biological properties of the carotenoids may be much more related to the products of the interaction of carotenoids with oxidant stress, that is, such breakdown products as apocarotenoids and retinoids.

Int J Vitam Nutr Res. 1998;68(6):399-403.
Antioxidant effects of carotenoids.
Bast A, Haenen GR, van den Berg R, van den Berg H.
Department of Pharmacology, Faculty of Medicine, University of Maastricht, Netherlands.

Surprisingly, neither the precise pharmacological effect nor the toxicological profile is usually established for food components. Carotenoids are no exception in this regard. Only limited insight into the pharmacology and toxicology of carotenoids exists. It is known that the antioxidant action of carotenoids is determined by 1. electron transfer reactions and the stability of the antioxidant free radical, 2. the interplay with other antioxidants and 3. the reaction with active oxygen. Numerous metabolites of carotenoids are formed upon their action as an antioxidant. Most of these metabolites have an unknown biological activity. It is concluded that a severe lack of knowledge hampers adequate suggestions for human supplementation.

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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