Diet manipulation and prevention of aging, cancer and autoimmune disease.

[LurePer]

Fant denne på et annet forum. En av mange studier som støtter kalorirestriksjonsteorien.

Curr Opin Clin Nutr Metab Care. 2005 Jul;8(4):382-7. Related Articles, Lin
Diet manipulation and prevention of aging, cancer and autoimmune disease.

Jolly CA.

Division of Nutritional Sciences, The University of Texas at Austin, Austin, Texas, USA.

PURPOSE OF REVIEW: Dietary supplementation and other dietary regimens have become increasingly popular in the US population. Information regarding how different dietary constituents interact when consumed simultaneously is needed. This review examines the recent literature on how different dietary constituents may interact physiologically when consumed in combination. Furthermore, the potential human relevance of calorie restriction and nonclassical function of vitamin E is discussed. RECENT FINDINGS: Long-term calorie restriction in monkeys has shown similar beneficial effects as has been shown in rodents. Limited calorie restriction studies in humans have shown promise in reducing the incidence of heart disease and breast cancer. The combination of calorie restriction and omega-3 fatty acids may be a more potent antiinflammatory diet than either regimen alone. The type of fiber that is most protective against colon cancer may be dependent on the type of dietary fat consumed simultaneously. Vitamin E derivatives that possess no antioxidant activity may be potent inhibitors of cancer, but not normal, cell growth. SUMMARY: Dietary modification has shown its greatest beneficial effect when started prior to or immediately after the onset of disease. Also, understanding how the subtypes or isoforms of nutrients function is important since their physiological effects may be drastically different. It is important to understand the entire dietary profile of an individual when making dietary recommendations because one nutrient, or dietary ingredient, may enhance or cancel out the beneficial effects of another dietary ingredient.

[LurePer]

Mer.

Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans.

Proc Natl Acad Sci U S A 2004 Apr 27;101(17):6659-63 (ISSN: 0027-8424)

Fontana L; Meyer TE; Klein S; Holloszy JO

Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.

Little is known regarding the long-term effects of caloric restriction (CR) on the risk for atherosclerosis. We evaluated the effect of CR on risk factors for atherosclerosis in individuals who are restricting food intake to slow aging. We studied 18 individuals who had been on CR for an average of 6 years and 18 age-matched healthy individuals on typical American diets.

We measured serum lipids and lipoproteins, fasting plasma glucose and insulin, blood pressure (BP), high-sensitivity C-reactive protein (CRP), platelet-derived growth factor AB (PDGF-AB), body composition, and carotid artery intima-media thickness (IMT).

The CR group were leaner than the comparison group (body mass index, 19.6 +/- 1.9 vs. 25.9 +/- 3.2 kg/m(2); percent body fat, 8.7 +/- 7% vs. 24 +/- 8%). Serum total cholesterol (Tchol), low-density lipoprotein cholesterol, ratio of Tchol to high-density lipoprotein cholesterol (HDL-C), triglycerides, fasting glucose, fasting insulin, CRP, PDFG-AB, and systolic and diastolic BP were all markedly lower, whereas HDL-C was higher, in the CR than in the American diet group.

Medical records indicated that the CR group had serum lipid-lipoprotein and BP levels in the usual range for individuals on typical American diets, and similar to those of the comparison group, before they began CR. Carotid artery IMT was approximately 40% less in the CR group than in the comparison group. Based on a range of risk factors, it appears that long-term CR has a powerful protective effect against atherosclerosis. This interpretation is supported by the finding of a low carotid artery IMT.

[LurePer]

Enda mer:

Mech Ageing Dev. 2005 May 28; [Epub ahead of print] Related Articles, Links

Rapid and reversible induction of the longevity, anticancer and genomic effects of caloric restriction.

Spindler SR.

Department of Biochemistry, University of California, Riverside, CA 92521, USA.

It is widely held that caloric restriction (CR) extends lifespan by preventing or reducing the age-related accumulation of irreversible molecular damage. In contrast, our results suggest that CR can act rapidly to begin life and health span extension, and that its rapid genomic effects are closely linked to its health effects. We found that CR begins to extend lifespan and reduce cancer as a cause of death within 8 weeks in older mice, apparently by reducing the rate of tumor growth. Further, 8 weeks of CR progressively reproduces nearly three quarters of the genomic effects of long-term CR (LTCR) in liver. Fewer of the genomic effects of LTCR are rapidly reproduced by the initiation of CR in the heart, but the changes produced are keys to cardiovascular health. Thus, the genomic effects of CR may be established more rapidly in mitotic than in postmitotic tissues. Most of the genomic effects of LTCR dissipate 8 weeks after switching to a control diet. Consistent with these results, others have shown that acute CR rapidly and reversibly reduces the short-term risk of death in Drosophila to that of LTCR treated flies. Further, in late adulthood, acute CR partially or completely reverses age-related alterations of liver, brain and heart proteins. CR also rapidly and reversibly mitigates biomarkers of aging in adult rhesus macaques and humans. These data argue that highly conserved mechanisms for the rapid and reversible enhancement of life- and health-span exist for mitotic and postmitotic tissues.

[LurePer]

Ser ut til at jeg må fordumme det litt for folket.

Mye tyder på at hvis du spiser lite (f.eks 1000 kcal daglig), kan du forlenge levetiden din med en god del år.

[Baahh]

Mer:

Med Hypotheses. 2004;63(2):334-9. Related Articles, Links


Chronic activation of AMP-activated kinase as a strategy for slowing aging.

McCarty MF.

NutriGuard Research, 1051 Hermes Ave., Encinitas, CA 92024, USA.

Caloric restriction down-regulates insulin secretion and systemic IGF-I activity, and there is reason to suspect that these effects are key mediators of caloric restriction's favorable impact on longevity. Alternative strategies for down-regulating these hormones are thus of great interest; chronic activation of AMP-activated kinase (ampk) - clinically achievable with the drug metformin - may have utility in this regard. In the liver, ampk slows hepatic glucose output by down-regulating expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase; in skeletal muscle, it boosts the efficiency of insulin-stimulated glucose uptake by increasing expression of GLUT-4. These effects evidently mandate a down-regulation of insulin secretion. The resulting reduction of hepatic insulin activity can be expected to suppress hepatic production of IGF-I while boosting that of IGFBP-1, thereby decreasing plasma free IGF-I. ampk can also directly stimulate IGFBP-1 synthesis in hepatocytes, and interfere with the ras/raf/erk pathway of IGF-I signaling. In non-diabetics, metformin therapy is indeed reported to reduce plasma levels of insulin and of free IGF-I; indeed, this is thought to be the mechanism whereby metformin suppresses excess androgen production in PCOS. A pro-longevity effect of the related biguanide phenformin has already been reported in tumor-prone mice, and mouse longevity studies with metformin are currently in progress. The development of ampk activators which do not share metformin's modest risk of inducing lactic acidosis - apparently reflecting an inhibition of mitochondrial complex 1 that is not intrinsic to ampk activity - might aid the practical applicability of this pro-longevity strategy.

[Baahh]

Hvordan kan egentlig dette forklares enkelt, LurePer?

Frie radikaler skader celler. Mye mat øker antall frie radikaler. Spis lite mat, mye antioksidanter - lev lenge?

[LurePer]

Dette hadde overrasket meg veldig om det kan forklares enkelt.

[UpAndComming]

Vær sulten i 80 år fremfor mett i 75.... ??

Er forøvrig enig med LurePer at grunnen nok ikke er så enkel, i så fall ville det jo vært mulig å manimulere videre til å spise mer, men med lite frie radikaler og mye antioksidanter. Og det virker jo å være bittelitt for lett liksom....

[LurePer]

Deler av grunnen er nok også lavere nivåer av insulin og blodglukose. I tillegg vil kalorirestriksjon sikkert redusere farten kroppens vev fornyes i, og dermed kanskje aldringsprosessen samtidig.