Insulin controls energy metabolism and increases the activity of IGF-1 by increasing its synthesis and by decreasing binding proteins, such as IGFBP-1. Both Insulin and IGF-1 stimulated anabolic processes based on the availability of energy and basic substrates, such as amino acids. Insulin and IGF-1 promote cancer by inhibiting apoptosis and by stimulating cell proliferation (Kaaks and Lukanova, 2001; Parr, 1999). In addition, insulin and IGF-1 promote the synthesis of sex hormones and inhibit the synthesis of Sex Hormone Binding Globulin (S.H.B.G.), which regulates the bio-availability of circulating sex hormones to tissues (Kaaks and Lukanova, 2001; Cordain et al 2003). Elevated levels of insulin and IGF-1 are thus ties to increased cancer experienced in the developed world (Giovannucci et al, 2004). Bartke et al (2003) and Parr (1999) have suggested that low levels of insulin may be an effective way of increasing longevity. Their conclusions are based on calorie restricted animals which have much reduced insulin and IGF-1 concentrations compared to normally fed shorter lived animals.
McCarty (2000) suggested that simultaneous intake of animal protein and high-glycemic foods cause sharp raises in insulin that subsequently lead to Syndrome X, which is also associated with insulin resistance which leads to increased hyperinsulinmia, decreased IGFBP-1 and S.H.B.G. production and increased free serum IGF-1 (Hursting et al, 2003).
It should be noted that although protein and high-glycemic foods are often identified as drivers of insulin and IGF-1 levels, Cordain et al (2002) reported that hunter-gather diets were very high in meat intake, but low in high glycemic carbohydrates. Possible explanations for this paradox are the consumption of low-fat animals, high intake of plants and vegetables, and relatively low total calorie intake in comparison to a high-energy expenditure. In addition high levels of monounsaturated and polyunsaturated fat and a higher omega-3/omega-6 ratio, antioxidants, fiber, vitamins and phytochemicals with low salt intake was favorable for cardio vascular disease.
S.H.B.G. is an important regulator of plasma sex hormones and a sensitive marker of insulin resistance (gates et al, 1996). Low S.H.B.G. levels are tied to increased risk of type 2 diabetes, cancer, cardio vascular disease and mortality (Gates et al, 1996). Higher insulin levels reduce serum levels of S.H.B.G. (Lonning et al, 1995; Gates et al, 1996; Chen et al, 1990; Cordain et al, 2003), which as mentioned before are related to protein and high-glycemic carbs. Food types affect levels of S.H.B.G.; e.g., wheat lowers S.H.B.G. while vegetables appear to raise it. However, total food intake is negatively related to S.H.B.G. when it increases weight and B.M.I. because weight and B.M.I. are independently and negatively correlated with S.H.B.G.
The level of IGFBP-1 controls the bioavailability of IGF-1. Wolk et al (2004) found low levels of IGFBP-1 correlate with increased insulin resistance, obesity and cardio vascular disease. They also found that the only significant positive association between IGFBP-1 and diet was attained when carb intake was increased. They also reported that a study of women vegans had 20-40% higher IGFBP-1 and IGFBP-2 levels compared to women on both vegetarian and meat diets.
Another study (Giovannucci et al, 2004), found insulin secretion positively correlated with greater intakes of meat, dairy, refind carbs, saturated and trans fat and lower intakes of whole grain products and fiber. Since IGFBP-1 and insulin are inversely related, their findings indicate that reducing the consumption of animals; dairy, and sugar can increase IGFBP-1.