\n<\/p>\n
Although their intervention reduces carbohydrate and sugar intake dramatically and it does lower blood glucose. The problem is that it\u00a0does not address the core issue in Type 2 diabetes.<\/strong><\/p>\n Type 2 diabetes is defined<\/em><\/strong>\u00a0by a blood glucose of 126 or higher or a hemoglobin A1c of 6.5 or higher. If you introduce sugar and carbohydrate restriction and cause weight loss, the glucose and hemoglobin A1c levels will fall below those numbers and so, by that definition, diabetes is \u201ccured.\u201d The patient no longer meets the criteria for a diabetes diagnosis.<\/p>\n But this premise ignores fundamental and important realities. High glucose levels cause changes in gene expression that\u00a0persist<\/a>\u00a0after the glucose returns to normal\u00a0causing<\/a>\u00a0atherosclerosis and other complications. This well-known phenomenon is called metabolic memory.<\/p>\n Metabolic memory<\/em><\/strong>\u00a0is a critical concept that points to the broader reality of people living with Type 2 diabetes. The high glucose levels found in people with the condition are only one part of the complex molecular biology that causes diabetic complications.<\/p>\n The cardiovascular complications of diabetes begin in the\u00a0fetus<\/a>\u00a0and\u00a0even in the lifestyle choices of\u00a0prior generations<\/a>.<\/em>\u00a0Overfeeding or underfeeding in the parental generation can produce infants that are too small or too large based on inappropriate activation or inactivation of genes (epigenetics). That inappropriate switching on or off is persistent and many genes are involved causing hypertension, diabetes, and cardiovascular complications in adults.<\/p>\n Patients may themselves switch these genes on or off later in life by gaining weight or smoking. These genes cause diabetes by killing insulin-producing cells in the pancreas and increasing insulin resistance leading to high glucose which further increases oxidative particles and switches on additional genes that cause diabetic complications.<\/p>\n These genes remain\u00a0switched on<\/a>\u00a0even when the glucose is lowered. Therefore, it is very important to continue to take medications that interfere very specifically with the signaling that these genes generate.<\/p>\n Promoting the message that cardiometabolic medication should be stopped when the glucose falls below the diabetic level is not in keeping with the latest science and contrary to diabetic guidelines.<\/p>\n The American Diabetes Association (ADA) guidelines recommend metformin use even in\u00a0prediabetic patients<\/a>\u00a0who have a BMI of 35 or greater, have a history of gestational diabetes, or an increasing fasting glucose or hemoglobin A1c. That is because metformin\u00a0reduces progression<\/a>\u00a0to diabetes by about 31%.<\/p>\n Roughly half of prediabetic patients will progress to diabetes despite weight loss. Even patients in the later stages of prediabetes may have lost 70-80% of their insulin-producing function.<\/p>\n These prediabetic patients\u00a0should not stop<\/em>\u00a0metformin when they have lost weight and their glucose improves. There is a tendency for diabetes to reappear with age. Certainly, metformin should not be stopped in patients who already have diabetes regardless of their glucose level.<\/p>\n Metformin reduces diabetic complications by\u00a0interfering with signaling<\/a>\u00a0that has nothing to do with blood glucose levels. It inhibits the same\u00a0master metabolic switch<\/a>\u00a0as the active ingredient in the\u00a0drug-eluting<\/a>\u00a0coronary artery stent.<\/p>\n The increased risk of major cardiovascular events does not disappear with diet and weight loss, however, metformin directly\u00a0reduces<\/a>\u00a0that risk. Type 2 diabetics lose about\u00a010 years<\/a>\u00a0of life. If they are on metformin, they\u00a0live a bit longer<\/a>\u00a0than normal people. Metformin is safe and costs only about $4 a month.\u00a0It is dangerous to recommend \u201cstopping diabetic medications once the glucose is controlled by lifestyle interventions.\u201d<\/em><\/strong><\/p>\n Controlling glucose levels has beneficial effects on microvascular events like retinopathy, neuropathy, and kidney damage but it does not reduce the problems that cause most serious cardiovascular complications, death, disability, and costs. Most diabetics die of cardiovascular disease.<\/p>\n Lowering the glucose with lifestyle or\u00a0any medication<\/a>\u00a0approved for the purpose does NOT reduce cardiovascular events. In fact, aggressive glucose lowering with medication and lifestyle caused more people to die.<\/p>\n This is especially important because cardiovascular event incidence and other complications can be dramatically mitigated with a\u00a0comprehensive solution<\/a>\u00a0that brings to bear lifestyle management and medications that interfere with the molecular biology that causes cardiometabolic complications.<\/p>\n Lowering the glucose by any means below the diabetic level, stopping the medication, and expecting complications to fall makes sense, but that idea is not supported by the evidence.<\/p>\n Take a look at the diagram below. Type 2 diabetes occurs mostly in patients with extra abdominal fat caused by poor diet. Increased nutrition and fat switches genes on\/off that increase\u00a0angiotensin II<\/a>, aldosterone,\u00a0HMG CoA Reductase<\/a>, and\u00a0mTOR activity<\/a>.<\/p>\n Angiotensin receptor blockers (ARBs), spironolactone, statins, and metformin interfere directly with the molecular signaling cascades that these genes activate. Blocking angiotensin II with an ARB, aldosterone with spironolactone, HMG CoA reductase with a statin, and mTOR with\u00a0metformin<\/a>\u00a0dramatically reduces cardiovascular events in multiple settings. The genes involved are switched on before diabetes develops.<\/p>\n In fact, these elements contribute to diabetes development. Increased mTOR activity directly increases insulin resistance. Blocking mTOR with metformin reduces progression to diabetes.<\/p>\n Elevated aldosterone levels make a strong contribution to\u00a0metabolic syndrome<\/a>\u00a0development.\u00a0Blocking angiotensin II<\/a>\u00a0reduces progression to diabetes.<\/p>\n Blocking HMG Co A reductase with a statin actually\u00a0increases<\/a>\u00a0the incidence of diabetes but has a powerful impact on cardiovascular events and other outcomes. Even that can likely be explained by a hard look at the molecular biology. Blocking HMG CoA reductase with a statin does lower LDL cholesterol but it also\u00a0reduces Coenzyme Q10<\/a>\u00a0production. Coenzyme Q10 is a powerful antioxidant and it is important for mitochondrial function. Impaired\u00a0mitochondrial function<\/a>\u00a0may be important in the modestly increased risk of diabetes in patients who take statins.<\/p>\n The best treatment for type 2 diabetes is not a matter of either lifestyle or medication. Effective treatment requires best practice implementation of lifestyle measures along with medications that interfere with the molecular biology causing disease. For most patients, medical treatment will include metformin, statins, and angiotensin receptor blockers.<\/p>\n It is important to move beyond a medical system focused on risk factors and organ systems.<\/p>\n<\/blockquote>\n There is a very complex interplay in the molecular biology that causes hypertension, diabetes, high cholesterol, and related complications. Reversing diabetes with weight loss and dietary interventions makes perfect sense but improving cardiovascular outcomes and reducing costs to the fullest extent requires a more comprehensive solution.\u00a0We can treat chronic disease with precision medicine and molecular biology now.<\/strong><\/p>\n<\/p><\/div>\n\n","protected":false},"excerpt":{"rendered":" Although their intervention reduces carbohydrate and sugar intake dramatically and it does lower blood glucose. The problem is that it\u00a0does not address the core issue in Type 2 diabetes. The definition of Type 2 diabetes Type 2 diabetes is defined\u00a0by a blood glucose of 126 or higher or a hemoglobin A1c of 6.5 or higher. […]<\/p>\n","protected":false},"author":1,"featured_media":7072246,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[124586,233094,12534],"tags":[43009,11425],"dealstore":[],"offerexpiration":[],"class_list":["post-7072245","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-medical-care","category-obesity-metabolic-health","category-weight-loss","tag-diabetes","tag-reverse"],"yoast_head":"\nThe definition of Type 2 diabetes<\/h2>\n
Metabolic memory<\/h2>\n
Metformin<\/h2>\n
How metformin works<\/h3>\n
Controlling glucose<\/h2>\n
Drugs that block epigenetic signaling<\/h2>\n
Type 2 Diabetes Treatment<\/h2>\n
\n