X-Message-Number: 21861 Date: Mon, 2 Jun 2003 20:17:52 -0700 (PDT) From: Doug Skrecky <> Subject: could lowering IGF-1 postpone "aging"? Med Hypotheses 2003 Jun;60(6):784-92 A low-fat, whole-food vegan diet, as well as other strategies that down-regulate IGF-I activity, may slow the human aging process. A considerable amount of evidence is consistent with the proposition that systemic IGF-I activity acts as pacesetter in the aging process. A reduction in IGF-I activity is the common characteristic of rodents whose maximal lifespan has been increased by a wide range of genetic or dietary measures,including caloric restriction. The lifespans of breeds of dogs and strains of rats tend to be inversely proportional to their mature weight and IGF-I levels. The link between IGF-I and aging appears to be evolutionarily conserved; in worms and flies, lifespan is increased by reduction-of-function mutations in signaling intermediates homologous to those which mediate insulin/IGF-I activity in mammals. The fact that an increase in IGF-I activity plays a key role in the induction of sexual maturity, is consistent with a broader role for-IGF-I in aging regulation. If down-regulation of IGF-I activity could indeed slow aging in humans, a range of practical measures for achieving this may be at hand. These include a low-fat, whole-food, vegan diet, exercise training, soluble fiber, insulin sensitizers, appetite suppressants, and agents such as flax lignans, oral estrogen, or tamoxifen that decrease hepatic synthesis of IGF-I. Many of these measures would also be expected to decrease risk for common age-related diseases. Regimens combining several of these approaches might have a sufficient impact on IGF-I activity to achieve a useful retardation of the aging process. However, in light of the fact that IGF-I promotes endothelial production of nitric oxide and may be of especial importance to cerebrovascular health, additional measures for stroke prevention-most notably salt restriction-may be advisable when attempting to down-regulate IGF-I activity as a pro-longevity strategy. Caloric restriction has been shown to increase longevity in organisms ranging from yeast to mammals. In some organisms, this has been associated with a decreased fat mass and alterations in insulin/insulin-like growth factor 1 (IGF-1) pathways. To further explore these associations with enhanced longevity, we studied mice with a fat-specific insulin receptor knockout (FIRKO). These animals have reduced fat mass and are protected against age-related obesity and its subsequent metabolic abnormalities, although their food intake is normal. Both male and female FIRKO mice were found to have an increase in mean life-span of approximately 134 days (18%), with parallel increases in median and maximum life-spans. Thus, a reduction of fat mass without caloric restriction can be associated with increased longevity in mice, possibly through effects on insulin signaling. Nutr Cancer 2002;43(2):187-92 Dietary flaxseed inhibits human breast cancer growth and metastasis and downregulates expression of insulin-like growth factor and epidermal growth factor receptor. Recent studies indicate that diets rich in phytoestrogens and n-3 fatty acid have anticancer potential. This study determined the effect of flaxseed (FS), the richest source of lignans and alpha-linolenic acid, on growth and metastasis of established human breast cancer in a nude mice model. Estrogen receptor-negative human breast cancer cells, MDA-MB-435, were injected into the mammary fat pad of mice (Ncr nu/nu) fed a basal diet (BD). At Week 8, mice were randomized into two diet groups, such that the groups had similar tumor size and body weight. One continued on the BD, while the other was changed to BD supplemented with 10% FS, until sacrifice at Week 15. A significant reduction (P < 0.05) in tumor growth rate and a 45% reduction (P = 0.08) in total incidence of metastasis were observed in the FS group. Lung metastasis incidence was 55.6% in the BD group and 22.2% in the FS group, while the lymph node metastasis incidence was 88.9% in the BD group and 33.3% in the FS group (P < 0.05). Mean tumor number (tumor load) of total and lymph node metastasis was significantly lower in the FS than in the BD group (P < 0.05). Metastatic lung tumor number was reduced by 82%, and a significantly lower tumor trend (P < 0.01) was observed in the FS group. Lung weight, which also reflects metastatic tumor load, in the FS group was reduced by 20% (P < 0.05) compared with the BD group. Immunohistochemical study showed that Ki-67 labeling index and expression of insulin-like growth factor I and epithelial growth factor receptor in the primary tumor were lower in the FS (P < 0.05) than in the BD group. In conclusion, flaxseed inhibited the established human breast cancer growth and metastasis in a nude mice model, and this effect is partly due to its downregulation of insulin-like growth factor I and epidermal growth factor receptor expression. Cancer Epidemiol Biomarkers Prev 2002 Sep;11(9):852-61 Dietary correlates of plasma insulin-like growth factor I and insulin-like growth factor binding protein 3 concentrations. Plasma levels of insulin-like growth factor I (IGF-I) have been associated with risk of several cancers. Although protein-calorie malnutrition is known to decrease IGF-I levels, few published studies have related diet to IGF-I levels in well-nourished humans. We examined the cross-sectional association of plasma IGF-I and IGF-binding protein 3 (IGFBP-3) levels with intakes of alcohol, energy, macronutrients, micronutrients, and specific foods in 1037 healthy women. Adjusted mean hormone levels across categories of dietary variables were calculated by linear regression. Results were adjusted for non-dietary factors found to be associated with IGF levels. Total energy intake was positively associated with IGF-I levels when adjusted for covariates. Adjusted mean levels of IGF-I (ng/ml) across increasing quintiles of energy intake were 181, 185, 191, 199, and 195 (P for the linear trend = 0.006). In other multivariate analyses, energy-adjusted fat and carbohydrate intake had no association with IGF-I levels. The most consistent finding was a positive association between protein intake with circulating IGF-I concentration (174, 188, 201, 192, and 196 ng/ml across quintiles of protein intake; P = 0.002), which was largely attributable to milk intake. Adjusted mean levels of IGF-I (ng/ml) across increasing quartiles of milk intake were 183, 189, 188, and 200 (P = 0.01). Higher fat intake, in particular saturated fat, was associated with lower levels of IGFBP-3. We conclude that higher energy, protein, and milk intakes were associated with higher levels of IGF-I. These associations raise the possibility that diet could affect cancer risk through influencing IGF-I level. Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=21861