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Diabetes mellitus is a chronic disease, for which there is no known cure except in very specific situations. Management concentrates on keeping blood sugar levels as close to normal, without causing low blood sugar. This can usually be accomplished with a healthy diet, exercise, weight loss, and use of appropriate medications (insulin in the case of type 1 diabetes; oral medications, as well as possibly insulin, in type 2 diabetes).
Along with the increased hunger and cravings comes the metabolic slow down. This is most impacted by the hormone leptin. Less insulin exposure to the fat cell and a shrinking fat cell means the metabolic hormone leptin is reduced. Low leptin means increased hunger. Low leptin also means decreased activity of the body’s two major metabolic engines, the thyroid and the adrenal glands. So as leptin decreases, your metabolism gets the signal to stop burning energy and to start consuming it.
The progression of nephropathy in patients can be significantly slowed by controlling high blood pressure, and by aggressively treating high blood sugar levels. Angiotensin converting enzyme inhibitors (ACE inhibitors) or angiotensin receptor blockers (ARBs) used in treating high blood pressure may also benefit kidney disease in patients with diabetes.
^ Jump up to: a b c Vemuri VK, Janero DR, Makriyannis A (March 2008). "Pharmacotherapeutic targeting of the endocannabinoid signaling system: drugs for obesity and the metabolic syndrome". Physiology & Behavior. 93 (4–5): 671–86. doi:10.1016/j.physbeh.2007.11.012. PMC 3681125. PMID 18155257. The etiology of many appetitive disorders is characterized by a pathogenic component of reward-supported craving, be it for substances of abuse (including alcohol and nicotine) or food. Such maladies affect large numbers of people as prevalent socioeconomic and healthcare burdens. Yet in most instances drugs for their safe and effective pharmacotherapeutic management are lacking despite the attendant medical needs, collateral adverse physical and psychological effects, and enormous global market potential. The endocannabinoid signaling system plays a critical role in motivational homeostasis as a conduit for reward stimuli and a positive modulator of brain reward circuits. Endocannabinoid-system hyperactivity through CB1 receptor transmission is considered contributory to a range of appetitive disorders and, hence, is a major focus of contemporary pharmaceutical research.
The good news is that if you suspect you might have metabolic damage there are real answers and solutions and even tests to tell you what is going wrong in your body. For those looking to get answers on how to fix metabolism problems and metabolic damage we have created a FREE 3 part Metabolic Repair Video Course that walks you through all the steps. From how to get the correct tests to a done for you comprehensive metabolism assessment we cover it all in the course. The course will teach you:
Recent research indicates prolonged chronic stress can contribute to metabolic syndrome by disrupting the hormonal balance of the hypothalamic-pituitary-adrenal axis (HPA-axis). A dysfunctional HPA-axis causes high cortisol levels to circulate, which results in raising glucose and insulin levels, which in turn cause insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension, with direct effects on the bone, causing "low turnover" osteoporosis. HPA-axis dysfunction may explain the reported risk indication of abdominal obesity to cardiovascular disease (CVD), type 2 diabetes and stroke. Psychosocial stress is also linked to heart disease. http://www.sandysidhumedia.com/wp-content/uploads/2012/12/nailahquote.png
Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin. https://www.clairekerslake.com/wp-content/uploads/2011/10/young-woman-planning-in-calendar-app-on-white-iphone-picjumbo-com-1024x683.jpg