Dr. Weeks’ Comment: Insulin saves lives but it is the most toxic of the diabetes medications because it is toxic to small blood vessels. SOUL, CORE, Berberine Plus, Gymnema, Metformin and Glyburide (both prescription drugs) are safer. Read below about the toxicity of insulin and use it carefully. My friend Dr. Majid Ali is quite articulate on this topic!
Majid Ali, M.D. (see this link)
In matters of life span, I summarize the lessons learned from my patients with the following simple words:
Keep insulin low without drugs and live longer,
or keep blood sugar low with drugs and die young.
The pandemic of diabetes can be neither understood nor addressed with knowing the fundamentals of the molecular biology of insulin, a subject that is sadly and regularly neglected in the prevailing model of medicine. I wrote Insulin Toxicity Series to shed light on the various faces of this pandemic.
Research and my patients helped me recognize seven stages of insulin toxicity:
☞ The first stage of insulin toxicity is without apparent negative health effects recognized by the person.
☞ The second stage of insulin toxicity is with negative health effects recognized by the person but unknown to the doctor.
☞ The third stage of insulin toxicity is tissue injury (in the liver, kidneys, skin, and other organs) unrecognized by a doctor who is clueless about molecular biology of insulin.
☞ The fourth stage of insulin toxicity is prediabetes without tests to detect insulin waste and damages.
☞ The fifth stage of insulin toxicity is Type 2 diabetes with the use of diabetes drugs that add to the insulin activity, hence its toxicity, with the blessings of the American Diabetic Association).
☞ The sixth stage of insulin toxicity is toxicity created by peaks of insulin caused by insulin injections (the end-stage of insulin depletion which is called insulin-dependent diabetes).
☞ The seventh stage of insulin toxicity is loss of vision and blindness (diabetic retinopathy), dialysis (diabetic nephropathy), and increased risk of heart attacks, strokes, autoimmune diseases, inflammatory disorders, and all degenerative states.
AND here are some peer-reviewed scientific articles…
The effects of insulin on the endothelium.
Recent data suggest that diabetes in general, and particularly diabetes in association with insulin resistance, obesity, and hyperglycemia, results in inflammatory changes including the production of cytokines, adhesion molecules, and reactive oxygen species that are toxic to the endothelium and could lead to vascular damage. Insulin suppresses these effects, either indirectly by decreasing glucose levels or directly by stimulating nitric oxide production and inhibiting important pathways in the inflammatory cascade. In addition, insulin directly reduces plasma concentrations of adhesion molecule production in endothelial cells and thus may decrease vascular inflammation. Some of these effects of insulin may be attenuated in patients with insulin resistance, and this finding may provide a mechanistic link for the increase in vascular disease seen in patients with insulin resistance. Doses of insulin adequate to restore normoglycemia may help overcome these abnormalities, although some patients may require insulin sensitization with lifestyle changes or pharmacologic therapy.
Effects of insulin resistance on endothelial progenitor cells and vascular repair.
Insulin resistance, a key feature of obesity, the metabolic syndrome and Type 2 diabetes mellitus, results in an array of metabolic and vascular phenomena which ultimately promote the development of atherosclerosis. Endothelial dysfunction is intricately related to insulinresistance through the parallel stimulatory effects of insulin on glucose disposal in metabolic tissues and NO production in the endothelium. Perturbations characteristic of insulin resistance, including dyslipidaemia, inflammation and oxidative stress, may jeopardize the structural or functional integrity of the endothelium. Recent evidence suggests that endothelial damage is mitigated by endogenous reparative processes which mediate endothelial regeneration. EPCs (endothelial progenitor cells) are circulating cells which have been identified as mediators of endothelial repair. Several of the abnormalities associated with insulin resistance, including reduced NO bioavailability, increased production of ROS (reactive oxygen species) and down-regulation of intracellular signalling pathways, have the potential to disrupt EPC function. Improvement in the number and function of EPCs may contribute to the protective actions of evidence-based therapies to reduce cardiometabolic risk. In the present article, we review the putative effects of insulin resistance on EPCs, discuss the underlying mechanisms and highlight potential therapeutic manoeuvres which could improve vascular repair in individuals with insulin resistance.
Insulin resistance and endothelial cell dysfunction: studies in mammalian models.
Type 2 diabetes and obesity are major risk factors for the development of cardiovascular atherosclerosis. Resistance to the metabolic effects of insulin on its traditional target tissues (muscle, liver and adipose tissue) is a central pathogenic feature of these disorders. However, the role of insulin resistance in non-canonical tissues, such as the endothelium, is less clear. Several large studies support a role for insulinresistance in the development of premature cardiovascular atherosclerosis independent of type 2 diabetes and obesity. A key step in the initiation and progression of atherosclerosis is a reduction in the bioactivity of endothelial cell-derived nitric oxide. Nitric oxide is a signalling molecule which has a portfolio of potential antiatherosclerotic effects. The presence of insulin receptors on endothelial cells is well documented, and the endothelium has now emerged as a potentially important target tissue for insulin, with insulin-stimulated production of nitric oxide a feature of the action of insulin on endothelial cells. The role of insulin resistance at the level of the endothelial cell in vascular pathophysiology is unclear. A number of studies in humans and gene-modified mice have demonstrated a close association between insulin resistance and nitric oxide bioactivity. In this review, we discuss the link between insulin resistance and endothelial cell function in humans and demonstrate the complimentary information provided by murine models of obesity and insulin resistance in our understanding of the vasculopathy associated with type 2 diabetes and obesity.