(clinical and experimental data)
Oxidative stress and protein glycation in patients with chronic obstructive pulmonary disease.
Enzyme activity and AGE formation in a model of AST glycoxidation by D-fructose in vitro.
The effect of caloric restriction on glycation and glycoxidation in skin collagen of nonhuman primates.
Food restriction prevents advanced glycation end product accumulation and retards kidney aging in lean rats.
Indian J Physiol Pharmacol. 2005 Jan;49(1):95-8.
Oxidative stress and protein glycation in patients with chronic obstructive pulmonary disease.
Parija M, Bobby Z, Kumar V, Saradha B.
Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry - 605 006.

Several studies have indicated the presence of increased oxidative stress as a critical feature in the pathogenesis of chronic obstructive pulmonary disease (COPD). Another biochemical complication leading to pathogenesis is protein glycation. The nexus between oxidative stress and protein glycation in various pathological conditions is being unraveled. Increased oxidative stress can lead to enhanced protein glycation by a process of auto-oxidative glycation. No information is available in the literature regarding protein glycation among COPD patients. Eleven non-diabetic COPD patients were included in the study and equal number of age and sex-matched healthy individuals were enrolled as controls. The whole-blood reduced glutathione was found to be less among the patients while lipid peroxides and fructosamine were elevated in comparison to control. The present study confirmed oxidative stress and enhanced protein glycation among the COPD patients. Antioxidant therapy may be considered as part of the treatment regimen for COPD patients.

Acta Pharm. 2005 Mar;55(1):107-14.
Enzyme activity and AGE formation in a model of AST glycoxidation by D-fructose in vitro.
Bousova I, Vukasovic D, Juretic D, Palicka V, Drsata J.
Department of Biochemical Sciences Charles University in Prague Faculty of Pharmacy, Hradec Kralove Czech Republic.

Non-enzymatic glycation as the chain reaction between reducing sugars and free amino groups of proteins has been shown to correlate with physiological ageing and severity of diabetes. The process involves oxidative steps (glycoxidation). In this paper, the effect of D-fructose as a reactive sugar on aspartate aminotransferase (AST) as a model protein was monitored by measurements of the enzyme activity and formation of fluorescent advanced glycation end products (AGEs). Change in the AST activity was considered as a measure of the overall protein damage caused by glycation, and total AGEs and pentosidine represent, at least partly, the formation of glycoxidation products. Catalytic activity of AST in an incubation mixture containing D-fructose (50 mmol L(-1)), decreased compared to control values to 42% (p < 0.05) and to 11% (p < 0.05) on the 5th and on 21st day of incubation, respectively. In the presence of fructose, total fluorescent AGEs concentration was significantly higher since 5th day of incubation (110%, p < 0.05) and the fluorescent pentosidine concentration from 15th day of incubation (117%, p < 0.05) compared to control values, respectively. Catalytic activity of AST clearly and quantitatively demonstrated functional changes in the enzyme molecule caused by structural modifications initiated by fructose, while the evaluation of AGE formation and especially that of pentosidine by fluorescence measurement was less reliable.

J Gerontol A Biol Sci Med Sci. 2003 Jun;58(6):508-16.
The effect of caloric restriction on glycation and glycoxidation in skin collagen of nonhuman primates.
Sell DR, Lane MA, Obrenovich ME, Mattison JA, Handy A, Ingram DK, Cutler RG, Roth GS, Monnier VM.
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA.

The accumulation of Maillard reaction products increases with age in long-lived proteins and can be retarded by caloric restriction. Here we determined whether caloric restriction inhibits formation of glycation and glycoxidation products in skin collagen of squirrel and rhesus monkeys between 1990-1997. Restricted monkeys (n = 11, n = 30, respectively) were maintained at 70% of caloric intake of controls (n = 25, n = 32, respectively). Glycation was assessed by furosine and glycoxidation by pentosidine and carboxymethyl-lysine. With age, the rate of furosine formation moderately but nonsignificantly (p >.05) increased in both control monkey groups. It significantly (p =.011) decreased in the caloric-restricted rhesus, but not squirrel monkeys. Caloric restriction did not significantly decrease the pentosidine or carboxymethyl-lysine rates in either species of monkeys. These results suggest that caloric restriction, when maintained long-term in nonhuman primates, tends to decrease glycation, but not glycoxidation.

J Am Soc Nephrol 2000 Aug;11(8):1488-97
Food restriction prevents advanced glycation end product accumulation and retards kidney aging in lean rats.
Teillet L, Verbeke P, Gouraud S, Bakala H, Borot-Laloi C, Heudes D, Bruneval P, Corman B.
Service de Biologie Cellulaire, Commissariat a l'Energie Atomique/Saclay, Gif-sur-Yvette, France.

ABSTRACT.: Tissue content of advanced glycation end products (AGE) increases with age and contributes to the changes in structure and function of the renal and cardiovascular systems. The effect of chronic food restriction on this AGE accumulation was investigated in lean WAG/Rij rats. A 30% food restriction performed from 10 to 30 mo in female rats reduced their mean body weight from 240 +/- 7 to 160 +/- 12 g, but did not modify their survival. AGE collagen content increased from 14.3 +/- 5.5 to 104.7 +/- 13.0 arbitrary units per microgram (AU/microg) of hydroxyproline (OHPro) in kidney between 10 and 30 mo, and from 9.7 +/- 1.2 to 310.6 +/- 34.6 AU/microg OHPro in the abdominal aorta. Food restriction reduced AGE accumulation to 21.4 +/- 3.3 and 74.6 +/- 16.5 AU/microg OHPro in kidney and aorta of 30-mo-old animals. Similar results were found for collagen prepared from isolated glomeruli (7.8 +/- 1.2, 81.2 +/- 16.1, and 10.3 +/- 4.3 AU/microg OHPro in 10-mo, 30-mo, and restricted 30-mo-old rats). Reduction of intrarenal and arterial AGE accumulation by food restriction was confirmed by immunostaining in optical microscopy. Age-related changes in arterial and kidney structures as polyuria and proteinuria were mainly prevented by food restriction. These data indicate that chronic food restriction reduces the accumulation of AGE and preserves the structure and function of the renal and cardiovascular systems in learn rats, although it did not affect survival of the animals between 10 and 30 m.

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

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