Chronic Meditation

Chronic inflammation has been shown to be a consistent pre-cursor to many metabolic diseases, such as obesity, fatty liver disease, atherosclerosis, insulin resistance, type II diabetes, degenerative disorders such as dementia, airway disease and some cancers.1 The relationship between diet, and more specifically refined carbohydrates, and chronic inflammation has been of high interest in the media in recent years. This interest could have a lot to do with the alarming rate that these metabolic diseases are growing. For example, The World Health Organization estimates that one billion adults worldwide are over weight, and 300 million of those are clinically obese, defined as having a body mass index equal to or greater than 30 kg m-3. (1)
There has been evidence showing a predisposition of people having symptoms of metabolic syndrome such as 1) abdominal obesity, 2) elevated TG levels 3) low HDL cholesterol levels, 4) increased blood pressure, and 5) impaired fasting glucose, to having a greater risk for developing cardiovascular disease or type II diabetes. These symptoms are not necessarily manifestations of age, but develop over a predisposed background of unhealthy eating, physical inactivity and chronic stressful situations at a young age2. More importantly, obesity has been linked because of the effect of being insulin resistant2. Although, diets high in fat were often to blame for weight gain, insulin resistance, and hyperlipidemia in humans and animals, recent research has shown the high intake of refined carbohydrates may also increase the risk of insulin resistance.2 Specifically those that are high in fructose have been shown to cause metabolic challenges resulting in weight gain, hypertension, and de nova lipogenesis.2, 3,
Since fructose bypasses the last two regulatory steps (the reactions catalyzed by hexokinase and PFK-1), two key events can occur, 1) it is metabolized faster than glucose and 2) since fructose is independent of phosphofructose kinase (PFK) regulation, overconsumption of fructose (>40g in a 2000 calorie diet), results in increases of levels of visceral adipose tissue (VAT), and increased hepatic lipid levels from de nova lipogenesis. This reaction results in increased very low density lipoproteins (VLDL) synthesis and secreation.4 The over consumption of fructose might be explained by the insufficient signaling of appetite regulating hormones, insulin, leptin, and ghrelin to work at correct times, resulting in excess body weight and insulin resistance, both which are symptoms of metabolic syndrome.1,2,3,