Visualization for Weight Loss -The Gabriel Method

Appendix: The Chemistry of the FAT Programs

the reverse may also be true. Studies have shown that insulin can activate the expression of the suppressor of the cytokine sig- naling 3 (SOCS3) gene in certain cells. 21 Activating the SOCS3 in the arcuate and paraventrical nucleus of the hypothalamus can cause leptin resistance by preventing downstream signaling. Insulin resistance leads to hyperinsulinemia, or chronically elevated insulin levels. Hyperinsulinemia could then possibly cause leptin resistance. It is interesting to note that chronically ele- vated cortisol levels, both plasma and intracellular, can cause elevated triglycerides and insulin resistance. 22 Proinflammatory Cytokines and Leptin Resistance TNF-A and IL-6 have been shown to both activate the expres- sion of the 11-BHSD-1 enzyme in certain fat cells 23 and cause insulin resistance. 24 They may also increase the expression of the SOCS3 gene in certain cells. 25 The Metabolic Profile of Obesity Nearly all obese people are leptin resistant, and they characteris- tically have elevated cortisol levels (either serum or intracellular), elevated triglycerides, insulin resistance, and hyperinsulinemia. The proinflammatory cytokines mentioned are also considered biomarkers for obesity. Starvation and cold weather are environmental stresses that favor the accumulation and preservation of fat for survival rea- sons. Chronic exposure to starvation and/or cold weather should, in theory, make the body want to be fatter and cause the internal set-point to shift. In fact, studies support this notion. For example, rats exposed to cold weather for the first two months of their life grow to be heavier than normal as adults. 26 This indi- cates that the chronic exposure to cold weather caused their internal set-point to shift. Interestingly, a study of over four thou- The Famine and Temperature Stress Response and Obesity

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