Fasting / Calorie Restriction Diet for Weight Loss & Cleanse

Fasting / Calorie Restriction Diet for Weight Loss & Cleanse

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Fasting and Calorie Restriction - Page 3
Reprinted by permission from Bill Faloon of The Life Extension Foundation

Calorie Restriction Benefits Diabetics
Rats on a CRON diet showed a 15% reduction in blood glucose, which could also mean less non-enzymatic glycosylation. This glycosylation contributes to aging, perhaps cancer, and the complications arising from diabetes.  Reduction of blood levels of glycated hemoglobin has been observed in human studies when hyperglycemia was treated with a CRON diet. Glycation of collagen in the kidney could be a factor in diabetic kidney failure and glycation of capillary membranes could contribute to age-related insulin resistance (Best 1995).  Rhesus monkeys (fed ad libitum, 6-8 hours per day [energy intake without increasing hunger or decreasing satiety while having rapid and marked effects on metabolic risk variables]) had higher basal glucose, basal insulin, insulin responses to glucose, and decreased insulin sensitivity.  Conversely, monkeys fed a dietary-restricted diet (30% less than controls) showed decreases in glucose/insulin parameters, and increased insulin sensitivity.  Insulin changes were significantly related to changes in obesity measured by weight and abdominal circumference (Kemnitz et al. 1994).

A lean body may be more significant in determining life span in mice than a calorie-restricted diet (Bluher et al. 2003).  The mice ate whatever they wanted and stayed slim because their fat tissue had been altered and could not respond to insulin.

Insulin is the primary hormone that transports sugar into the cells and facilitates storage of fat in adipose cells.  Altered mice ate 55% more food per their body weight than normal mice, yet they had 70% less body fat at three months of age.  Essentially, these mice were protected against obesity.  These mice increased mean life span (134 days or 18%), median and maximum life spans.  A reduction of fat mass (even without caloric restriction) was associated with increased longevity, possibly through effects mediated by insulin.  These findings raise the possibility that a new drug for obesity and diabetes mellitus Type-2 (DM-2) might act by blocking insulin receptors in fat tissue.  The drug would need to target fat tissue only because a loss of insulin sensitivity throughout the body would mimic DM-2 (Bluher et al. 2003; Mercola 2003b).  The dangers of hyperinsulinemia (high blood insulin) are well-established (many degenerative diseases develop secondary to an excess of insulin).

How the Immune System Responds to Calorie Restriction
Moderate caloric restriction in humans has a beneficial effect on cell-mediated immunity (Santos et al. 2003).  Cell-mediated immune reactions are triggered by bacterial, fungal, and viral pathogens, malignant cells, foreign proteins or tissues.  Allergic dermatitis is a cell-mediated immune response.  Tumor necrosis factor-alpha (TNF-a) and interleukin-6 (IL-6) are generally increased in the serum of aged humans and mice.  The abnormal regulation of these cytokines is common in immune dysfunction.  Old mice subjected to long-term calorie restriction had serum levels of TNF-a and IL-6 comparable to young mice (Spaulding et al. 1997; Kim et al. 2002).  Production of TNF-a can activate nuclear factor-kappa-B (NF-kB), a transcription factor.  Once activated, NF-kB becomes a potent stimulus to cytokine production.  Excesses of IL-6 (a pro-inflammatory cytokine) have been demonstrated in irregularities in immune function, heart disease, arthritis, and cancer.

Calorie Restriction and Malignancies
Tumors transplanted into underfed mice did not grow as well as those transplanted into mice fed ad libitum.  Caloric restriction affects the growth of spontaneous tumors.  Researchers have shown that caloric restriction is beneficial despite the source of calories.  Energy restriction enhances DNA repair, moderates oxidative damage to DNA, and reduces the expression of oncogenes (cancer-causing genes).  Reduced caloric intake influences insulin metabolism and may link overconsumption (elevated release of insulin) with the establishment and proliferation of tumors (Moreschi 1909; Kritchevsky 1995, 2001).  There was a delay in the onset of spontaneous hepatomas (malignant liver tumors) and a reduction in their frequency following calorie-restriction.  The incidence of hepatoma in calorie-restricted mice was reduced (Yoshida et al. 1999).

Even moderate dietary restriction is an effective antiangiogenic (anti-cancer) therapy against recurrent brain cancers.  Dietary restriction shifted the tumor vascular environment from pro-angiogenic (favoring a well-developed vascular system to nurture the growing tumor) to an anti-angiogenic state through multiple effects on tumor cells and tumor-associated host cells (Mukherjee et al. 2002).

Calorie restriction favors apoptosis (programmed cell death) of damaged cells.  Damaged cells either undergo repair or trigger apotosis.  Chaperones are stress proteins that enable polypeptides to assume their proper shape (quaternary structure) and participate in mechanisms of apoptosis by secretion of proteins that inhibit apoptosis.  High levels of chaperone occur with aging and prevents the useful induction of apotosis.  Calorie restriction lowers chaperone levels, favoring apotosis of damaged and pre-cancerous cells.  A balance must exist in the need to maintain sufficient cell numbers for a particular tissue function and the need to eliminate damaged, potentially toxic cells.  Non-dividing cells, such as neurons, cannot be replaced.  Calorie restriction induces chaperone expression in neuronal cells and may delay the onset of neurologic disorders of aging, including Alzheimer's disease, Parkinson's disease and stroke.  Rapidly dividing cells, such as liver cells, has shown that calorie restriction reduces chaperones, encouraging the death of aged and pre-cancerous cells (Wickner et al. 1999;Spindler, 2001a; Suh et al. 2002; Ken t, 2003).

Although the anti-cancer effects of calorie restriction are well-established, Spindler (BioMarker Pharmaceuticals) does not recommend calorie restriction for individuals with cancer.  There is no question that calorie-restriction improves health, but it is impractical to try to improve the health of very sick people by under-feeding them.

The Effects of Calorie Restriction on p53, IGF- 1, and Leptin
Heterozygous p53-deficient mice are prone to spontaneous neoplasms, most commonly sarcoma and lymphoma.  The median time to death is 18 months.  Juvenile mice (eating 60% of an ad libitum diet) delayed tumor development by mechanisms dependent of insulin-like growth factor-1 (IGF-1).  Calorie restriction or a fast limited to one-day per week suppressed carcinogenesis, even when this restriction started late in life, in mice prone to develop tumors because of this deficient p53 gene (Poetschke et al. 2000; Berrigan et al. 2002).  Plasma IGF-1 levels in calorie-restricted mice were reduced by 20% after 4 weeks treatment.  Leptin levels were reduced by 71% (Berrigan et al. 2002).

The following technical comments explain how caloric restriction (acting upon p53, IGF-1, and leptin) might influence life span.

p-53 (The Guardian of the Genome)
p-53 prevents replication of damaged DNA in normal cells and promotes apoptosis of cells with abnormal DNA.  Faulty p53 molecules allow cells with damaged DNA to survive and to replicate.  A lack of p53 regulation promotes the continued growth of spontaneous emergent mutant cells, precursors to cancer (Greenblatt et al. 1994; Oliff et al. 1996).

Most natural systems function best when in balance, neither showing hyper nor hypo-responsiveness to any natural stimulus.  High activity of the tumor-suppressing p53 genes lowers cancer rates, but causes premature aging.  This finding suggests that aging might relate to the body's innate vigilance against cancer.  Mutant mice with over-active p53 genes were more resistant to cancer than normal mice, but had a 20% shorter life span.  Instead of cancer, these animals showed bone thinning, organ breakdown, vulnerability to physical stress, sagging skin, and balding.  Hyperactivity of the p53 gene may prematurely compromise the body's reserve of stem cells.  This might prevent undifferentiated stem cells from replenishing necessary tissues and lead to premature tissue degeneration (Ferbeyre et al. 2002; 2003).

Insulin-like Growth Factor-1 (IGF-1)
A reduction in caloric intake dramatically slowed cancer progression in rodents, suggesting a prophylactic and a therapeutic advantage (Dunn et al. 1997).  Part of the mechanism may relate to the fact that dietary restriction lowers IGF-1, a growth factor involved in cell proliferation, apoptosis, and tumorigenesis, by about 24.  Mice dosed with a carcinogen, while consuming 20% fewer calories, developed fewer tumors.  A cancer shows uncontrolled development and malignant properties when stimulated by IGF-1.  Calorie restriction reduces this multi-faceted growth factor.  As IGF-1 levels are reduced, the stage and virulence of existing cancerous tumors are also reduced.  When IGF-1 levels are restored, the protective effect of caloric restriction disappears and the cancer advances.  Rates of apoptosis were ten times higher among calorie-restricted mice compared to ad libitum-fed or calorie-restricted mice undergoing IGF-1 restoration.  Administration of IGF-1 to dietary-restricted mice increased cell proliferation six-fold.  IGF-1 may modulate pivotal stages in cancer development in general (Dunn et al. 1997; Hansen 2002).

Measuring of a woman's leptin levels could be an indicator of risk of developing breast cancer.  A woman's production of leptin might reveal her history of fat consumption (Anson et al. 2003).  Leptin levels may offer prognostic data beyond the measurement of body mass index and fat consumption (ANI 2003).  Hyperleptinemia (or excess leptin in blood) increases proliferation of breast cancer cell through acceleration of the progression of the cell cycle (Okumura et al. 2002).  Leptin influences cellular differentiation and progression of prostate cancer.  Leptin has a role in the development of prostate cancer mediated by testosterone and other factors related to obesity (Saglam et al. 2003).

Hyperleptinemia is linked with cardiovascular disease.  Moderate increases in the level of leptin enhance the relative risk of a cardiovascular event by 25%.  Leptin is a novel, independent risk factor for coronary heart disease (Wallace et al. 2001).  Levels of leptin are increased in obesity.  This hormone may play a role in the development of insulin resistance and non-insulin dependent diabetes mellitus (Haque et al. 2003).

Calorie Restriction and the Heart
If people reduce their current caloric intake from 20-40%, even starting in middle age, they may prevent or delay the development of heart disease.  Animals whose food intake was reduced by one-third showed less heart disease.  The hearts of mice on a low-calorie diet showed 20% fewer age-related genetic changes and had less DNA damage (Parker, 2002).  Recall the persuasive cardiovascular results obtained from the Biosphere II experiment:  In the first 6 months body weight dropped 15%, blood sugar 20%, blood cholesterol 38%, and systolic/diastolic blood pressure dropped 30%/27% on a calorie-restricted diet (Walford , 1994; Best, 1995).  A 30% reduction in caloric intake in 30 rhesus monkeys led to a 25-point elevation in HDL-2B and a 20-point decrease in triglycerides.  Increases in HDL-2B and decreases in triglycerides of this magnitude in humans would be a great health benefit, especially for those at risk for stroke or heart disease (Verdery et al. 1997; Lane et al. 1999).  Multiple studies have shown increased insulin sensitivity (four-fold) and decreased levels of insulin on calorie-restricted diets (Spindler 2001b), suggesting that hyperinsulinemia may be a risk factor associated with heart disease.

Convincing Summation
Calorie restriction has been shown to increase longevity in organisms ranging from yeast to mammals (Bluher et al. 2003).  These remarkable effects that result from restricting food intake 50% to 70% of normal may occur through three mechanisms: (1) reduction in oxidative damage; (2) modulation of glycemia and insulinemia; and (3) hormesis (a beneficial biological action from a small dose of an agent generally toxic at higher doses.  Extension of life span by dietary restriction (small doses of food) is an example of hormesis (Masoro 1998, 2000).

At least a 30% reduction in calories is necessary to realize significant health advantages.  Such austerity requires a psychological profile that only 1 person in 1000 possesses.  Thus, the best objective may not be to develop another diet that people will not follow, but rather to develop a medicine that mimics the beneficial effects of calorie restriction (Taubes, 2000). An agent that mimics the function of a compound called PPAR-delta seems to provide similar benefits to calorie restriction (at least in monkeys).

Middle-aged, insulin-resistant, male monkeys (with imbalances in blood lipids) were administered an agent that mimics PPAR.  PPAR-delta activates genes that regulate fat transport and insulin sensitivity.  After four weeks of treatment with this PPAR imitator, monkeys showed higher HDL cholesterol levels (79%), lower triglycerides (56%), and increased insulin sensitivity.  It is unknown whether the drug mimicking PPAR-delta would lengthen life span in humans through actions on insulin sensitivity and cholesterol levels, particularly in people that are not at risk for developing diabetes or heart disease (Christensen 2001).

Many "longevity medicines" have yielded disappointing results.  For example, 2-deoxy-D-glucose (2-DG), a compound that inhibits glucose metabolism, was toxic for some animals even at low levels or when given over long periods.  The narrowness of this range of safety (low therapeutic index) precludes it from human use, although studies provide some clues that inhibition of glucose metabolism can mimic some effects of caloric restriction (Lane et al. 2002).

BioMarker Pharmaceuticals has discovered that metformin (Glucophage), a drug used to treat diabetes, can mimic many of the changes in gene expression found in calorie-restricted mice (Kent 2003).  Metformin has a unique mechanism of action compared to many antidiabetic agents; it does not increase insulin production; rather it lowers blood sugar by decreasing sugar production, absorption, while increasing insulin sensitivity.  Metformin was more effective in mimicking the genetic responses to caloric-restriction than Glucotrol (Glipizide), which stimulates the pancreas to secrete more insulin, or Rosiglitazone, which reduces resistance to insulin.  A number of studies have linked aging to poor glucose control, lack of insulin sensitivity, and hyperinsulinemia.  Metformin impacts genes involved in (drug) metabolism and detoxification, energy metabolism, protein biosynthesis and degradation, cell growth and proliferation, and in the formation of the cytoskeleton.

The cytoskeleton is an internal reinforcement of the cytoplasm of a cell.  Microtubules contained in the cytoskeleton of most cells, provide structure to the cell and a conduit for intracellular transport.  It is speculated that microtubules act as processors of electrical information.  When a cell divides, it may pass on genetic information, not just in the form of DNA, but also in the form of microtubules, integral to the mechanics of cell division.

Metformin has been shown to increase the life span of mice by 20%.  BioMarker Pharmaceuticals is conducting a life span study using metformin to see if they can replicate this study.  The results of multiple studies suggest that metformin needs to be evaluated as a longevity medicine.  (Visit to read The Multiple Benefits of Metformin, September 2001 Life Extension Magazine for dosing instructions and caveats.  For additional information about BioMarker Pharmaceuticals, contact

Interventions to Support Longevity
Until potent and practical medicines are found to enhance longevity, many useful natural options still offer significant benefits (alternatives that The Life Extension Foundation has recommended to members for decades).  The Journal of the American Medical Association (JAMA) reported that underfed animals (consuming 50% less food) live up to 50% longer, perhaps because of higher levels of dehydroepiandrosterone (DHEA), lower body temperature, and lower insulin levels (JAMA 2002).  The following sections will address the findings reported in JAMA.

The Glycemic Index and Glycemic Load
Consideration of a food's glycemic index, and its glycemic load, may be valuable in keeping blood glucose and insulin levels within healthy ranges.  The glycemic index is a numerical representation of how quickly 50 grams of the food's carbohydrate content will raise blood sugar levels, compared to 50 grams of a reference food (such as glucose or white bread).  The reference food is given an arbitrary value of 100, and the glycemic index of a food is expressed as a percentage of that value.  Many factors contribute to the glycemic index, including its fat and fiber content, and how much it has been processed.

The glycemic index does not indicate the level of carbohydrate contained in food.  While the carbohydrates in carrots have a high glycemic index, carrots contain relatively fewer carbohydrates than corn chips.  The unfavorably high glycemic index of carrots (131%) is based on the blood-sugar response to eating 50 grams of carbohydrate (or a pound and a half of carrots), which few people would consume.  The net effect of carrots on blood sugar levels is considerably less than corn chips, even though the glycemic indices are similar.

The glycemic load is calculated by taking the amount of carbohydrate in a serving of food multiplied by that food's glycemic index.  A half-cup serving of carrots (which has 8 grams of carbohydrate) has a glycemic load of about 10 (8 131% or 1.31 = 10.48).  Many advocate assessing the overall glycemic load of a diet, rather than focusing too much on any one food.  Increased risk for cardiovascular disease begins at a daily glycemic load of 161 (Faloon, 2002; Harvard Women's Health Watch, 2002).

It is obvious that living to the maximum (well beyond 100 years) is no longer just a whim, but rather a cooperative effort, one pursued by committed individuals and scientists.  It is reassuring to know that one can influence the odds of living long and living well (through mind-set, diet, and exercise), and that the scientific community is passionate about helping achieve this objective.

Fasting / Calorie Restriction Diet for Weight-Loss & Cleanse - Page 1 | Page 2 |
Glycemic Index Load Response | Glycemic Index | References

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