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Egg consumption and coronary heart disease: an epidemiologic overview.
Dietary cholesterol--the role of eggs in the prudent diet.
The impact of egg limitations on coronary heart disease risk: do the numbers add up?
Eggs, serum cholesterol, and coronary heart disease.

J Am Coll Nutr 2000 Oct;19(5 Suppl):549S-555S
Egg consumption and coronary heart disease: an epidemiologic overview.
Kritchevsky SB, Kritchevsky D.
Department of Preventive Medicine, University of Tennessee Health Sciences Center, Memphis 38105, USA.

Serum cholesterol has been established as a modifiable risk factor for coronary heart disease. Experimental feeding studies show that saturated fat and cholesterol increase serum cholesterol levels; thus, dietary recommendations for lowering the risk of heart disease proscribe the intake of both substances. Recommendations have also included limits on the intake of eggs because of their high cholesterol content. In free-living populations, diet reflects a pattern of associated choices. Increases in one food may lead to changes in the consumption of other foods that may modulate disease risk. Epidemiologic data are helpful in assessing the importance of foods and nutrients in the context in which they are actually consumed. We review epidemiologic data relating dietary cholesterol and eggs to coronary disease risk. Cholesterol intake was associated with a modest increase in the risk of coronary events. The true magnitude of the association is difficult to estimate because most studies fail to account for potential confounding by other features of the diet. When a full-range of confounding factors was considered, the association between cholesterol intake and heart disease risk was small (6% increase in risk for 200mg/1,000kcal/day difference in cholesterol intake). Several studies have examined egg intake and its relationship with coronary outcomes. All but one failed to consider the role of other potentially confounding dietary factors. When dietary confounders were considered, no association was seen between egg consumption at levels up to 1 + egg per day and the risk of coronary heart disease in non-diabetic men and women.

S Afr Med J 1995 Apr;85(4):253-6
Dietary cholesterol--the role of eggs in the prudent diet.
Vorster HH, Beynen AC, Berger GM, Venter CS.
Department of Nutrition, Potchefstroom University, N.-W.

The recommendation that not more than 300 mg cholesterol be consumed daily to prevent high serum cholesterol levels and coronary heart disease is often used to justify a restriction of egg intake to three or four per week. One egg contains about 200 mg of cholesterol, but eggs are also excellent and relatively inexpensive sources of essential amino acids and certain vitamins. In this paper, the place of eggs in a prudent, cholesterol-lowering diet as a substitute for other animal products, is scrutinised. The extra cholesterol, where considered as the only variable, will increase serum cholesterol levels, but the effect is relatively small. The exclusion of eggs from the diet should be weighed against deprivation of essential nutrients especially in vulnerable groups. While restriction of egg intake in westernised populations seems justifiable, the upper limit of three or four per week may not always be applicable, depending on the overall diet and lipid profile of the individual.

J Am Coll Nutr 2000 Oct;19(5 Suppl):540S-548S
The impact of egg limitations on coronary heart disease risk: do the numbers add up?
McNamara DJ.
Egg Nutrition Center, Washington, DC 20036, USA.

For over 25 years eggs have been the icon for the fat, cholesterol and caloric excesses in the American diet, and the message to limit eggs to lower heart disease risk has been widely circulated. The "dietary cholesterol equals blood cholesterol" view is a standard of dietary recommendations, yet few consider whether the evidence justifies such restrictions. Over 50 years of cholesterol-feeding studies show that dietary cholesterol does have a small effect on plasma cholesterol concentrations. The 167 cholesterol feeding studies in over 3,500 subjects in the literature indicate that a 100 mg change in dietary cholesterol changes plasma total cholesterol by 2.2 mg/dL. Today we recognize that dietary effects on plasma cholesterol must be viewed from effects on the atherogenic LDL cholesterol as well as anti-atherogenic HDL cholesterol since the ratio of LDL:HDL cholesterol is a major determinant of heart disease risk. Cholesterol feeding studies demonstrate that dietary cholesterol increases both LDL and HDL cholesterol with little change in the LDL:HDL ratio. Addition of 100 mg cholesterol per day to the diet increases total cholesterol with a 1.9 mg/dL increase in LDL cholesterol and a 0.4 mg/dL increase in HDL cholesterol. On average, the LDL:HDL ratio change per 100 mg/day change in dietary cholesterol is from 2.60 to 2.61, which would be predicted to have little effect on heart disease risk. These data help explain the epidemiological studies showing that dietary cholesterol is not related to coronary heart disease incidence or mortality across or within populations.

Am J Clin Nutr 1982 Oct;36(4):617-25
Eggs, serum cholesterol, and coronary heart disease.
Dawber TR, Nickerson RJ, Brand FN, Pool J.

Beans were pearled to evaluate the feasibility of increasing antioxidant activity and phenolic antioxidants. Phenolics were concentrated mostly in the hull fraction at about 56 mg of catechin equivalents per gram of sample. The methanolic extracts of the pearled bean samples were screened for antioxidant potential using the beta-carotene-linoleate and the 1,1-diphenyl-2-picrylhydrazyl (DPPH) in vitro model systems. The pearled material, also referred to as milled samples, exhibited antioxidant activity that correlated with phenolic content and inhibited DPPH significantly in a dose-dependent manner. Phenolics and antioxidant activities were also examined in chromatographic fractions of methanolic extracts of manually obtained hulls that represented a model used previously to ascertain antimutagenic activity. Fractions extracted with ethyl acetate/acetone and acetone displayed antioxidant activity, which implies potent free radical scavenging activity with antimutagenic activity.

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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