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Epidemiological studies have found strong direct associations between increasing body mass index (BMI) and risks of developing type 2 diabetes, cardiovascular disease, and several types of cancer, beginning from BMI of 20–21 kg m−2.
Accumulating evidence indicates that adipose tissue is not just an inert store of excessive energy intake, but is also an active endocrine organ that produces key hormones, called adipokines, that regulate several important biological functions (Fig. 4) (Kershaw & Flier, 2004). Excessive energy intake, particularly in sedentary people, leads to a chronic positive energy balance, resulting in weight gain, increased visceral adiposity, dysfunctional enlarged adipocytes with macrophages infiltration, lipid overflow, and deposition of ectopic fat in key organs, such as liver, heart, skeletal muscle, kidney, and pancreas (Tchernof & Després, 2013). Both hypertrophic fat cells and infiltrated inflammatory cells secrete inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor (TNF)-α, causing a local and systemic low-grade inflammation. This chronic inflammation is known to play a central role in the pathogenesis of atherosclerosis, cancer, dementia, and aging (Fontana et al., 2007a; Gregor & Hotamisligil, 2011). Inflammation and reduced production of adiponectin (an adipocyte-derived adipokine) from enlarged visceral fat cells in overweight and obese individuals are associated with insulin resistance, increased hepatic glucose production, and altered lipoprotein–lipid metabolism (i.e., hypertriglyceridemia, low HDL cholesterol, and small, dense LDL particles), contributing to the development of type 2 diabetes, nonalcoholic fatty liver disease, and CVD (Tchernof & Després, 2013; National Institutes of Health, 1998; Gregor & Hotamisligil, 2011; Turer & Scherer, 2012). Moreover, adipokine-mediated insulin resistance triggers compensatory hyperinsulinemia, which exerts powerful mitogenic procancer effects directly, and also indirectly by increasing the bioavailability of sex hormones and insulin-like growth factor (IGF)-1, and the ovarian production of androgens. Enlarged adipocytes also secrete molecules such as leptin, IGF-1, IL-6, and type VI collagen that promote cell survival and tumor growth (Calle & Kaaks, 2004; Roberts et al., 2010). Insulin resistance, hyperinsulinemia, and adipokine imbalance, in conjunction with overactivation of the renin-angiotensin-aldosterone and the sympathetic nervous systems, have also been implicated in the pathogenesis of hypertension in overweight and obese individuals (Tchernof & Després, 2013).
A 5–10% weight loss induced by a negative energy balance (i.e., calorie restriction, endurance exercise, bariatric surgery) simultaneously improves multiple metabolic and hormonal factors implicated in the pathogenesis of several lethal chronic diseases, as well as in the biology of aging itself (Goldstein, 1992). Weight loss induced by a negative energy balance is associated with a reduction in visceral, hepatic, and skeletal muscle fat, decreased fat cell size, increased adiponectin and insulin sensitivity, and reduced circulating levels of insulin and leptin (Larson-Meyer et al., 2006; Uusitupa et al., 2003; Turer & Scherer, 2012). Weight loss is also associated with improved blood pressure, serum triglycerides, and HDL-cholesterol concentrations. (Dattilo & Kris-Etherton, 1992; Stevens et al., 2001). Decreases in adiposity also leads to reductions in inflammatory cytokines and prostaglandins, oxidative stress and DNA damage, and circulating estrogens due to inhibition of aromatases (Davì et al., 2002; Ziccardi et al., 2002; Hofer et al., 2008). Other hormonal adaptations associated with fat loss, improved insulin sensitivity, and reduced cancer risk include increased serum steroid hormone binding globulin and reduced levels of free estrogens and testosterone, and increased serum IGFBP-1 and reduced free IGF-1 concentrations (Longo & Fontana, 2010; Demark-Wahnefried et al., 2012).
Crider wrote:That is absolutely amazing the results were so close! I've been following your journal with anticipation. The calorie counts in the database CRON-o-meter uses are much more accurate that I expected.
So, what is the best way to successfully count calories?
There is none.
Unless we lock you up in a metabolic chamber where we carefully monitor every single issue mentioned above. Or, unless you want to carefully weigh and/or measure every morsel of food and beverage that you put in your mouth.
Since this is not practical or possible for most people, there just is no real practical way for anyone to micro manage all these details on a daily basis and to count calories accurately.
strivn2bhealthy wrote:I've concluded that the weight gain was my body still adjusting. I think I've read where others ebbed and flowed somewhat as their bodies cleansed/purged/healed. I want the weight to come off quicker, but, ultimately, I want health. It's a process. I am glad to know that I really am on the right track. My body will come around as it continues healing and correcting all the damage done through the years.
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