Eat anti-inflammatory foods and take less medications

Dr. Weeks’ Comment:  People ask “Will my anti-inflammatory diet – rich with nutrient-dense, anti-inflammatory,  whole,crushed ,organic, non-GMO seeds help with this ailment or that?  With my cancer or my grandson’t ADHD or my daughter’s PMS or my wife’s diabetes? What about my cousin’s PTSD or my other cousin’s gout or my niece’s migraines? You name it: from A – Z  (arthritis to zits) since all chronic degenerative illnesses are driven and made worse by inflammation, YES  – eat the seed!  Cancer, for example, spreads by inflammation so all cancer patients needs to eat the anti-inflammatory diet to prevent metastasis.  It will help.  Not because the anti-inflammatory foods including seeds are drugs. Not so. In stead, think of them as improvements in your lifestyle (diet, exercise, sleep, prayer and medication) which make your body healthy enough that it needs fewer synthetic, patented drugs.  That is a good thing. A very good thing. By improving your lifestyle, you can get healthy enough to require fewer and less powerful medications.  Any good doctor would support that.
For the entire article , click HERE 

Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes.

Review article

Esser N, et al. Diabetes Res Clin Pract. 2014.


It is recognized that a chronic low-grade inflammation and an activation of the immune system are involved in the pathogenesis of obesity-related insulin resistance and type 2 diabetes. Systemic inflammatory markers are risk factors for the development of type 2 diabetes and its macrovascular complications. Adipose tissue, liver, muscle and pancreas are themselves sites of inflammation in presence of obesity. An infiltration of macrophages and other immune cells is observed in these tissues associated with a cell population shift from an anti-inflammatory to a pro-inflammatory profile. These cells are crucial for the production of pro-inflammatory cytokines, which act in an autocrine and paracrine manner to interfere with insulin signaling in peripheral tissues or induce β-cell dysfunction and subsequent insulin deficiency. Particularly, the pro-inflammatory interleukin-1β is implicated in the pathogenesis of type 2 diabetes through the activation of the NLRP3 inflammasome. The objectives of this review are to expose recent data supporting the role of the immune system in the pathogenesis of insulin resistance and type 2 diabetes and to examine various mechanisms underlying this relationship. If type 2 diabetes is an inflammatory disease, anti-inflammatory therapies could have a place in prevention and treatment of type 2 diabetes.

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