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PERIODICAL FASTING AND CALORIC RESTRICTION FOR LIFE EXTENSION, DISEASE TREATMENT AND CREATIVITY.
(clinical and experimental data)
 
 3.3 FASTING AND CALORIC RESTRICTION PRODUCE VARIOUS BIOLOGICAL EFFECTS 
   
 
  COGNITIVE AND BEHAVIORAL  
   
 
Intentional weight loss reduces mortality rate in a rodent model of dietary obesity.
Effects of dietary restriction on physical performance in mice.
Effects of weight loss and calorie restriction on carbohydrate metabolism.
Dietary restriction enhances neurotrophin _expression and neurogenesis in the hippocampus of adult mice.
Aging and caloric restriction in nonhuman primates: behavioral and in vivo brain imaging studies.
Effects of Age and Dietary Restriction on Lifespan and Oxidative Stress of SAMP8 Mice with Learning and Memory impairments.
Dietary restriction increases the number of newly generated neural cells, and induces BDNF _expression, in the dentate gyrus of rats.
Modulation of endogenous opiate production: effect of fasting.
Changes of endogenous morphine and codeine contents in the fasting rat.
Plasma beta-endorphin during fasting in man.
Effects of dietary restriction on radial-arm maze performance and flavor memory in aged rats.
Dietary restriction benefits learning and motor performance of aged mice.
 
   
   

2005

Obes Res. 2005 Apr;13(4):693-702.
Intentional weight loss reduces mortality rate in a rodent model of dietary obesity.
Vasselli JR, Weindruch R, Heymsfield SB, Pi-Sunyer FX, Boozer CN, Yi N, Wang C, Pietrobelli A, Allison DB.
Department of Biostatistics, University of Alabama, Ryals Public Health Building, Room 327, 1665 University Boulevard, Birmingham, Alabama 35294-0022.

OBJECTIVE: We used a rodent model of dietary obesity to evaluate effects of caloric restriction-induced weight loss on mortality rate. Research Measures and Procedures: In a randomized parallel-groups design, 312 outbred Sprague-Dawley rats (one-half males) were assigned at age 10 weeks to one of three diets: low fat (LF; 18.7% calories as fat) with caloric intake adjusted to maintain body weight 10% below that for ad libitum (AL)-fed rat food, high fat (HF; 45% calories as fat) fed at the same level, or HF fed AL. At age 46 weeks, the lightest one-third of the AL group was discarded to ensure a more obese group; the remaining animals were randomly assigned to one of three diets: HF-AL, HF with energy restricted to produce body weights of animals restricted on the HF diet throughout life, or LF with energy restricted to produce the body weights of animals restricted on the LF diet throughout life. Life span, body weight, and leptin levels were measured. RESULTS: Animals restricted throughout life lived the longest (p < 0.001). Life span was not different among animals that had been obese and then lost weight and animals that had been nonobese throughout life (p = 0.18). Animals that were obese and lost weight lived substantially longer than animals that remained obese throughout life (p = 0.002). Diet composition had no effect on life span (p = 0.52). DISCUSSION: Weight loss after the onset of obesity during adulthood leads to a substantial increase in longevity in rats.

   
   
J Physiol Anthropol Appl Human Sci. 2005 May;24(3):209-13.
Effects of dietary restriction on physical performance in mice.
Ishihara H, Wenying F, Kouda K, Nakamura H, Kohno H, Nishio N, Sonoda Y.
Department of Hygiene, Kansai Medical University.

Dietary restriction is known to prolong life in laboratory animals. However, little is known about the effects of dietary restriction on physical performance. To evaluate physical performance, we measured four item indices: time to climb out of obstacles, time to escape restraint by gummed tape, time hanging from a bar, and ability to resist slipping every week. The diets of ICR mice were restricted from the age of 7 weeks through 24 weeks. Body weight of the diet-restricted mice decreased during the 7th to 9th weeks of age. After the 10th week, weight gain resumed. In response to assigned tasks, the diet-restricted mice performed better in all activities: they climbed out of obstacles faster, freed themselves sooner from restraint by gummed tape, hung from a bar longer, and better resisted slipping down a slope. These results suggest that diet-restricted mice have superior physical abilities, such as those required to overcome or avoid risks to life, than do ad-libitum-fed mice.

   
   
Curr Opin Clin Nutr Metab Care. 2005 Jul;8(4):431-9..
Effects of weight loss and calorie restriction on carbohydrate metabolism.
Manco M, Mingrone G.
Department of Internal Medicine and Clinical Science, Catholic University, Rome, Italy.

PURPOSE OF REVIEW: This article provides an overview of the most recent molecular and clinical outcomes of studies that investigate the effect of weight loss and calorie restriction on carbohydrate metabolism, obtained either by dieting or bariatric surgery. It will focus on aspects of carbohydrate metabolism related to insulin action. The discussion begins by describing attempts to restrain calories by shifting the macronutrient balance from carbohydrates to a higher protein and fat content. The topics covered include insulin secretion and resistance, glucose homeostasis and allostasis, changes in the secretive patterns of adipose tissue and the entero-insular axis. RECENT FINDINGS: Any improvement in glucose homeostasis, insulin sensitivity and secretion after a low-carbohydrate high-fat diet is still unproved. However, the restriction of dietary carbohydrate seems to reduce glycogenolysis and endogenous glucose production in type 2 diabetes mellitus, thus inducing the amelioration of plasma glucose levels, ultimately resulting in a reduction in the glycated haemoglobin concentration. The increased endogenous glucose production caused by enhanced gluconeogenesis and glycogenolysis, reduced insulin sensitivity, mainly caused by acquired defects of glucose transport and phosphorylation, and the impairment of insulin secretion all together contribute to maintain a chronic status of hyperglycaemia. Weight loss and calorie restriction restore glucose homeostasis and produce changes in the secretive activities of adipose tissue and the entero-insular axis. SUMMARY: Weight loss and calorie restriction partly explain the positive changes of glucose disposal. The multistep interaction of several factors at sites of insulin action, insulin secretion, adipose tissue and the entero-insular axis needs further investigation.

   
   

2002

J Neurochem 2002 Feb;80(3):539-47.
Dietary restriction enhances neurotrophin _expression and neurogenesis in the hippocampus of adult mice.
Lee J, Seroogy KB, Mattson MP.
Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center Baltimore, Maryland 21224, USA.

The adult brain contains small populations of neural precursor cells (NPC) that can give rise to new neurons and glia, and may play important roles in learning and memory, and recovery from injury. Growth factors can influence the proliferation, differentiation and survival of NPC, and may mediate responses of NPC to injury and environmental stimuli such as enriched environments and physical activity. We now report that neurotrophin _expression and neurogenesis can be modified by a change in diet. When adult mice are maintained on a dietary restriction (DR) feeding regimen, numbers of newly generated cells in the dentate gyrus of the hippocampus are increased, apparently as the result of increased cell survival. The new cells exhibit phenotypes of neurons and astrocytes. Levels of _expression of brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) are increased by DR, while levels of _expression of high-affinity receptors for these neurotrophins (trkB and trkC) are unchanged. In addition, DR increases the ratio of full-length trkB to truncated trkB in the hippocampus. The ability of a change in diet to stimulate neurotrophin _expression and enhance neurogenesis has important implications for dietary modification of neuroplasticity and responses of the brain to injury and disease.

   
   

2001

Ann N Y Acad Sci 2001 Apr;928:316-26.
Aging and caloric restriction in nonhuman primates: behavioral and in vivo brain imaging studies.
Ingram DK, Chefer S, Matochik J, Moscrip TD, Weed J, Roth GS, London ED, Lane MA.
Laboratory of Neurosciences, Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA.

In a long-term longitudinal study of aging in rhesus monkeys, a primary objective has been to determine the effects of aging and caloric restriction (CR) on behavioral and neural parameters. Through the use of automated devices, locomotor activity can be monitored in the home cages of the monkeys. Studies completed thus far indicate a clear age-related decline in activity consistent with such observations in many other species, including humans. However, no consistent effects of CR on activity have been observed. Selected groups of monkeys have also been involved in brain imaging studies, using magnetic resonance imaging (MRI) and positron emission tomography (PET). MRI studies completed thus far reveal a clear age-related decline in the volumes of the basal ganglia, the putamen, and the caudate nucleus, with no change in total brain volume. PET analysis has revealed an age-related decline in the binding potential of dopamine D2 receptors in the same brain regions. These results are consistent with findings in humans. Although additional longitudinal analysis is needed to confirm the present results, it would appear that locomotor activity, volume of the basal ganglia, as well as dopamine D2 receptor binding potential provide reliable, noninvasive biomarkers of aging in rhesus monkeys.

   
   

2000

J Nutr Health Aging 2000;4(3):182-186.
Effects of Age and Dietary Restriction on Lifespan and Oxidative Stress of SAMP8 Mice with Learning and Memory impairments.
Choi J, Kim D
Faculty of Food Science and Biotechnology, Pukyong National University; 599-1 Daeyeon-Dong, Nam-Gu, Pusan 608-737, Korea.

This study was to evaluate the effect of dietary restriction (DR) on lifespan and oxidative stress of dementia mouse model SAMP8 with impaired learning and memory. SAMP8 female mice were fed either ad libitum (AL) or fed 60% of food intake of AL. Results showed that basal metabolic rates (BMR) were significantly lower (15 to 22%) in DR with increased median and maximum lifespans, suggesting feed and gross efficiencies were significantly lower in DR than in AL. Grading score of senescence resulted in a marked improvement about 2-fold by DR compared with AL. The amounts of lipofuscin at 12 months were significantly lowered 16% in DR than that of AL. Median and maximal lifespans significantly increased (28.5% and 16.4%, respectively) by DR, and also lowered superoxide radical about 15~45% in DR compared with AL at 4, 8 and 12 months of age. On the other hand, superoxide dismutase (SOD) activities were higher (about 15~30%) in DR than those in AL group of SAMP8 except for 4 months of age. Our results suggest that 40% calorie restricted SAMP8 can effectively suppress dementia-related abnormalities during aging.

   
   

J Mol Neurosci 2000 Oct;15(2):99-108.
Dietary restriction increases the number of newly generated neural cells, and induces BDNF _expression, in the dentate gyrus of rats.
Lee J, Duan W, Long JM, Ingram DK, Mattson MP.
Laboratory of Neurosciences, Gerontology Research Center, National Institute on Aging, Baltimore, MD 21224, USA.

The adult brain contains neural stem cells that are capable of proliferating, differentiating into neurons or glia, and then either surviving or dying. This process of neural-cell production (neurogenesis) in the dentate gyrus of the hippocampus is responsive to brain injury, and both mental and physical activity. We now report that neurogenesis in the dentate gyrus can also be modified by diet. Previous studies have shown that dietary restriction (DR) can suppress age-related deficits in learning and memory, and can increase resistance of neurons to degeneration in experimental models of neurodegenerative disorders. We found that maintenance of adult rats on a DR regimen results in a significant increase in the numbers of newly produced neural cells in the dentate gyrus of the hippocampus, as determined by stereologic analysis of cells labeled with the DNA precursor analog bromodeoxyuridine. The increase in neurogenesis in rats maintained on DR appears to result from decreased death of newly produced cells, rather than from increased cell proliferation. We further show that the _expression of brain-derived neurotrophic factor, a trophic factor recently associated with neurogenesis, is increased in hippocampal cells of rats maintained on DR. Our data are the first evidence that diet can affect the process of neurogenesis, as well as the first evidence that diet can affect neurotrophic factor production. These findings provide insight into the mechanisms whereby diet impacts on brain plasticity, aging and neurodegenerative disorders.

   
   

1995

Biochem Biophys Res Commun 1995 Feb 6;207(1):312-7.
Modulation of endogenous opiate production: effect of fasting.
Molina PE; Hashiguchi Y; Meijerink WJ; Naukam RJ; Boxer R; Abumrad NN
Department of Surgery, SUNY, School of Medicine, Stony Brook 11794-8191.

The endogenous opiate alkaloid content in tissues from fed, 24 h and 48 h fasted rats was determined. Plasma morphine and codeine concentrations did not change in response to fasting. Morphine levels in the spleen increased 3-fold after 24 h of fasting and were lower than fed rats by 48 h of fasting; no change was detected in spleen codeine levels. Brain morphine levels were elevated 5-fold after 24 h of fasting and were two-fold higher than those of fed rats after 48 h of fasting. Brain codeine levels did not change with fasting. These results indicate that opiate alkaloids are endogenously produced in rodent tissues, particularly in the spleen, liver, and adrenals. The synthesis of morphine, in the spleen and brain, is maximally stimulated after 24 h of fasting, without alterations in tissue codeine synthesis. These suggest differential regulation of the endogenous synthetic pathways of morphine and codeine in response to the stress of fasting.

   
   

1991

J Pharmacol Exp Ther 1991 May;257(2):647-50.
Changes of endogenous morphine and codeine contents in the fasting rat.
Lee CS; Spector S.
Department of Neurosciences, Roche Institute of Molecular Biology, Nutley, New Jersey.

The alteration of endogenous opiate alkaloids during fasting state was investigated in rats. The concentrations of morphine and codeine in the cortex, midbrain, pons plus medulla, cerebellum, adrenal gland and pancreas were measured using radioimmunoassay for the opiates following high pressure liquid chromatography. The morphine and codeine contents of fasting rats showed maximum elevated levels in cortex, pons plus medulla and pancreas after 2 days of fasting, but after 1 day in midbrain. The opiate content of the cerebellum showed a tendency for a continuous increase during the 4 days. Adrenal glands of fasting rats had elevated levels at days 3 and 4, although there were great fluctuations within the groups.

   
   

1990

Horm Res 1990;33(6):239-43.
Plasma beta-endorphin during fasting in man.
Komaki G; Tamai H; Sumioki H; Mori T; Kobayashi N; Mori K; Mori S; Nakagawa T.
Department of Psychosomatic Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

To identify the effects of acute starvation on endogenous opioids in man, plasma beta-endorphin (beta-EP) was measured in 17 patients before, during and after fasting (Komaki, G. et. al. 1990). Patients were assigned a posteriori into two groups: group A, comprised of 11 patients able to tolerate 5-7 days of fasting, and group B, comprised of 6 patients able to tolerate 10 days of fasting. Changes in plasma beta-EP, serum cortisol, circulating nutritional markers, and their relative levels were assessed on the 5th and 10th days of fasting, and on the 5th and 10th days of the refeeding period. Beta-EP had increased by the 5th day (group A: 4.74 +/- 0.42 to 6.91 +/- 0.65 pmol/l, p less than 0.01; group B: 3.60 +/- 0.48 to 5.14 +/- 0.22 pmol/l, p less than 0.05, and remained at 5.05 +/- 0.65 pmol/l on the 10th day (group B: 0.05 less than p less than 0.1) during fasting. Group B had lower levels of plasma beta-EP on the 5th day of fasting than group A (p less than 0.05). However, serum cortisol levels changed similarly in both groups. Plasma beta-EP showed no significant correlation with either the percentage of body weight lost or the body mass index (kg/m2) over this study period. These findings indicate that plasma beta-EP is elevated in the early phase of fasting, while not directly being associated with body weight changes. Plasma beta-EP is lower and less activated in subjects who are able to tolerate fasting for longer periods.

   
   

1989

Neurobiol Aging 1989 Jan-Feb;10(1):27-30.
Effects of dietary restriction on radial-arm maze performance and flavor memory in aged rats.
Bond NW, Everitt AV, Walton J.
School of Behavioural Sciences, Macquarie University, Sydney, NSW, Australia.

Two groups of aged rats, a dietary restricted group fed approximately 10 g per day from 6 weeks of age and a group fed ad lib throughout their life span, were compared with a young adult group on an 8-arm radial maze and a flavor memory task. The young adult displayed efficient performance on the radial-arm maze within the 15 day test period. In contrast, both aged groups exhibited significantly poorer performance in the maze in comparison with the young adult group neither aged group differed from chance at the end of the 15 days. The flavor memory task required the animals to consume a novel flavor. Their loss of neophobia, as indexed by their subsequent consumption, was then taken as an indication of the extent to which they remembered the novel flavor and its effects. The young adult group lost their neophobia more rapidly than either of the aged groups, which did not appear to differ from each other. Taken together, this pattern of results indicates that dietary restriction does not protect animals from the memory loss observed in aged animals.

   
   

1987

J Gerontol 1987 Jan;42(1):78-81.
Dietary restriction benefits learning and motor performance of aged mice.
Ingram DK, Weindruch R, Spangler EL, Freeman JR, Walford RL.

Female C3B10RF1 mice maintained on either a control (approximately 95 kcal/week) or restricted (approximately 55 kcal/week) diet since weaning were tested in a behavioral battery at 11 to 15 or 31 to 35 months of age (middle-aged vs. aged). Age-related declines observed among control groups in tests of motor coordination (rotorod) and learning (complex maze) were prevented by the restriction regime. In addition, diet restriction increased locomotor activity in a runwheel cage among mice of both ages but did not affect exploratory activity in a novel arena.

   
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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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