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PERIODICAL FASTING AND CALORIC RESTRICTION FOR LIFE EXTENSION, DISEASE TREATMENT AND CREATIVITY.
(clinical and experimental data)
 
 3.2 FASTING AND CALORIC RESTRICTION PREVENT AND CURE DISEASES (Evidence) 
   
 
  INFERTILITY  
   
 
Dietary protein restriction of pregnant rats induces and folic Acid supplementation prevents epigenetic modification of hepatic gene expression in the offspring.
Effect of dietary restriction, pregnancy, and fetal type on intestinal cellularity and vascularity in Columbia and Romanov ewes.
Womens' beliefs and practices regarding food restrictions during pregnancy and lactation: a hospital based study.
A case of obesity, diabetes and hypertension treated with very low calorie diet (VLCD) followed by successful pregnancy with intrauterine insemination (IUI).
Rejuvenating effects of 10-week underfeeding period on estrous cycles in young and old rats.
 
   
   

2005

J Nutr. 2005 Jun;135(6):1382-6.
Dietary protein restriction of pregnant rats induces and folic Acid supplementation prevents epigenetic modification of hepatic gene expression in the offspring.
Lillycrop KA, Phillips ES, Jackson AA, Hanson MA, Burdge GC.
Development and Cell Biology.

Environmental constraints during early life result in phenotypic changes that can be associated with increased disease risk in later life. This suggests persistent alteration of gene transcription. DNA methylation, which is largely established in utero, provides a causal mechanism by which unbalanced prenatal nutrition results in such altered gene expression. We investigated the effect of unbalanced maternal nutrition on the methylation status and expression of the glucocorticoid receptor (GR) and peroxisomal proliferator-activated receptor (PPAR) genes in rat offspring after weaning. Dams were fed a control protein (C; 180 g/kg protein plus 1 mg/kg folic acid), restricted protein (R; 90 g/kg casein plus 1 mg/kg folic acid), or restricted protein plus 5 mg/kg folic acid (RF) diet throughout pregnancy. Pups were killed 6 d after weaning (n = 10 per group). Gene methylation was determined by methylation-sensitive PCR and mRNA expression by semiquantitative RT-PCR. PPARalpha gene methylation was 20.6% lower (P < 0.001) and expression 10.5-fold higher in R compared with C pups. GR gene methylation was 22.8% lower (P < 0.05) and expression 200% higher (P < 0.01) in R pups than in C pups. The RF diet prevented these changes. PPARgamma methylation status and expression did not differ among the groups. Acyl-CoA oxidase expression followed that of PPARalpha. These results show that unbalanced prenatal nutrition induces persistent, gene-specific epigenetic changes that alter mRNA expression. Epigenetic regulation of gene transcription provides a strong candidate mechanism for fetal programming.

   
   
J Anim Sci. 2004 Oct;82(10):3024-33.
Effect of dietary restriction, pregnancy, and fetal type on intestinal cellularity and vascularity in Columbia and Romanov ewes.
Scheaffer AN, Caton JS, Redmer DA, Arnold DR, Reynolds LP.
Center for Nutrition and Pregnancy, Department of Animal and Range Sciences, North Dakota State University, Fargo 58105, USA.

The objectives of this study were to evaluate intestinal cellularity and vascularity in mature ewes in response to dietary restriction and pregnancy status and to quantify the response of these variables to increased nutrient demand of fetal growth. In Exp. 1, 28 mature Dorset x crossbred white-faced ewes (61.6+/-1.8 kg initial BW) were fed a pelleted, forage-based diet. Treatments were arranged in a 2 x 3 factorial, with dietary restriction (60% restriction vs. 100% maintenance for respective states of pregnancy) and pregnancy status (nonpregnant, NP; d 90 and 130) as main effects. Dietary treatments were initiated on d 50 of gestation and remained at 60 or 100% maintenance throughout the experiment. Nonpregnant ewes were fed dietary treatments for 40 d. In Exp. 2, four Romanov ewes were naturally serviced (Romanov fetus and Romanov dam; R/R); two Romanov embryos per recipient were transferred to four Columbia recipients (Romanov fetus and Columbia recipient; R/C), and three Columbia ewes were naturally serviced (Columbia fetus and Columbia dam; C/C). In Exp. 1, dietary restriction and pregnancy status interacted with regard to maternal jejunal DNA concentration (P < 0.01), with restricted ewes having a greater DNA concentration (mg/g; fresh basis) at d 130. Vascularity (percentage of total tissue area) in the jejunum was increased (P < 0.06) as a result of dietary restriction and pregnancy status. Total microvascular volume ofjejunal tissue was not altered by dietary restriction and increased (P < 0.01) at d 130 of pregnancy. In Exp. 2, R/R ewes had less (P < 0.09) DNA (g) in the jejunum compared with R/C and C/C ewes. Jejunal vascularity (%) was increased (P < 0.05) in R/R ewes compared with R/C or C/C ewes, whereas total jejunal microvascular volume remained unchanged. These data demonstrate intestinal vascular density responds to changes in diet and physiological state. In addition, pregnancy increased total jejunal microvascular volume.

   
   
J Ayub Med Coll Abbottabad. 2004 Jul-Sep;16(3):29-31.
Womens' beliefs and practices regarding food restrictions during pregnancy and lactation: a hospital based study.
Ali NS, Azam SI, Noor R.
Department of Family Medicine, Aga Khan University, Karachi, Pakistan.

BACKGROUND: Maternal diet is an important determinant of outcomes of pregnancy. Malnutrition during pregnancy and its consequences maximally affect the health and long-term outcomes of the population. Low birth weight accounts for almost 30% of all births; with maternal malnutrition as a dominant risk factor. This study aims to investigate the existing beliefs and practices regarding food restrictions during pregnancy and lactation and also to assess whether there is any relationship with education level of the respondent and their beliefs and practices. METHODS: A cross-sectional survey was conducted at Community Health Center (CHC) of The Aga Khan University Hospital, Karachi from July-September 2000. Four hundred adult female respondents, who came to the outpatient services as a patient or as an attendant, were interviewed after taking verbal consent. A self administered pre-coded and pre-tested questionnaire was filled by the respondent. RESULTS: More than three fourths of respondents were literate. Twelve percent believed in restricting some food item during pregnancy and about 25% believed the same during lactation. No statistically significant association was found between belief about food restriction during pregnancy or during lactation and education level of the respondent. CONCLUSION: Undue food restrictions during pregnancy and lactation do exist in our culture. To assess the true picture we need to conduct larger studies in the community. The information obtained from the studies will help us in addressing these issues for improvement of nutritional knowledge and dietary practices and to avoid undue food restrictions.

   
   

2000

Endocr J 2000 Dec;47(6):787-91.
A case of obesity, diabetes and hypertension treated with very low calorie diet (VLCD) followed by successful pregnancy with intrauterine insemination (IUI).
Katsuki A, Sumida Y, Ito K, Murashima S, Gabazza EC, Furuta M, Yano Y, Sugiyama T, Toyoda N, Adachi Y.
Third Department of Internal Medicine, Mie University School of Medicine, Tsu, Japan.

The patient was a 32-year-old obese woman with a history of type 2 diabetes and hypertension for 6 years. Although she was treated with antihypertensive agents and intensive insulin therapy, her hyperglycemia was difficult to control. She wanted to have a baby but pregnancy was not recommended because her diabetes was under poor control and the use of antihypertensive medication. To achieve good control of obesity, diabetes and hypertension, she was admitted to our clinical department for weight reduction using very low calorie diet (VLCD). During VLCD she had a 19.8 kg reduction in body weight and her blood glucose and blood pressure were in good control without the use of drugs. Five months later, she became pregnant after the fourth trial of intrauterine insemination (IUI) and gave birth to a female baby under insulin therapy. This is the first report that showed the usefulness of VLCD for prepregnant control of glucose metabolism and blood pressure in an obese hypertensive patient with type 2 diabetes mellitus.

   
   

1987

Neurobiol Aging 1987 May-Jun;8(3):225-32.
Rejuvenating effects of 10-week underfeeding period on estrous cycles in young and old rats.
Quigley K; Goya R; Meites J.

The effects of providing 50% of normal feed intake for 10 weeks followed by 16 weeks of ad lib feeding on estrous cycles and mammary tumor incidence were studied in female rats initially 4 months and 15-16 months old. Initially all young rats exhibited regular or irregular estrous cycles and only about 41% of the older rats cycled regularly or irregularly; the remainder of the older rats did not cycle. During underfeeding, both the young and older rats lost body weight and ceased to cycle. After refeeding 100% of both young and old rats resumed cycling, the young rats for a much longer period than the old rats, and more of both groups continued to cycle than their ad lib-fed controls. Upon refeeding, the young and old rats reached the body weights of the ad lib-fed controls in about 3 weeks. Mammary tumors were initially present only in old rats and regressed during underfeeding; they rapidly reached control size upon refeeding. Plasma PRL levels declined during underfeeding but rebounded to higher than control values upon refeeding in both young and old rats. In young but not in old rats, plasma LH levels fell during underfeeding but returned to control values upon refeeding. These results demonstrate that a relatively short period of underfeeding, followed by refeeding, can delay the decline in reproductive cycles in young rats and reinitiate estrous cycles in older rats. These effects appear to be mediated via the neuroendocrine system.

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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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