The extent of weight loss required to reverse type 2 diabetes is much greater than conventionally advised. A clear distinction must be made between weight loss that improves glucose control but leaves blood glucose levels abnormal and weight loss of sufficient degree to normalize pancreatic function. The Belfast diet study provides an example of moderate weight loss leading to reasonably controlled, yet persistent diabetes. This study showed that a mean weight loss of 11 kg decreased fasting blood glucose levels from 10.4 to 7.0 mmol/L but that this abnormal level presaged the all-too-familiar deterioration of control (87).

It is also known as insulin-dependent diabetes mellitus (IDDM) and results from body's inability to produce insulin. Usually, it occurs in childhood or adolescence, but can surface up at any age. In this, the patient needs to take insulin injections on regular intervals (generally daily) in order to absorb glucose in the body. Type 1 diabetes mellitus is also referred to as juvenile diabetes, at times.

One of the biggest hits in type 2 diabetes treatment is glucagon-like peptide (GLP)-1 receptor agonists, which induce insulin production in beta-pancreatic cells while suppressing the secretion of glucagon. All big pharma have GLP-1 drugs on the market or their pipelines, including Sanofi, Eli Lilly, Roche, AstraZeneca and Boehringer Ingelheim. But Novo Nordisk is going a step further with the first oral version of a GLP-1 drug, which is now close to the market.
The physician can also make referrals to a wide variety of professionals for additional health care support. In the UK a patient training course is available for newly diagnosed diabetics (see DESMOND). In big cities, there may be diabetes centers where several specialists, such as diabetes educators and dietitians, work together as a team. In smaller towns, the health care team may come together a little differently depending on the types of practitioners in the area. By working together, doctors and patients can optimize the healthcare team to successfully manage diabetes over the long term.

Reduce Stress–  Stress raises cortisol and can lead to hormone imbalance, insulin issues and increases risk for certain types of disease. Work to reduce your sources of stress from lack of sleep, exposure to toxins, mental and emotional sources and poor diet. Getting quality sleep every night can help reduce stress hormone levels and is great for blood sugar.
Given the consequences of diabetes, self-management is something I want to encourage, not discourage. Without a commitment from the patient to take an active role in managing their diabetes, any treatment plan is doomed to fail. So is self-treatment with supplements a wise idea?  There’s an array available, and patients regularly ask about the latest treatment “Big Pharma doesn’t want you to know about”. That treatment used to be chromium. Ginseng was popular for a time, too. Fenugreek and bitter melon are used as well. The treatment that seems most popular now is cinnamon. Like any other herbal remedy, most sources will tell you that it’s been used for “thousands of years” as a medicinal herb. As a treatment for diabetes, I have my doubts. While reports of diabetes go back to 1552 BCE, the ability to effectively measure any diabetes treatment only goes back a few decades. Interest in cinnamon as a treatment seems to have started with in vitro tests but gained some plausibility in 2003, when a study from Alam Khan suggested several grams of cassia cinnamon per day could lower fasting blood glucose. Khan randomized Type 2 diabetes to 1g, 3g, or 6g of cinnamon for 40 days. All three groups improved their fasting blood glucose, and blood lipid levels, but there was no effect on A1C.
So you go to your doctor. What does he do? Instead of getting rid of the toxic sugar load, he doubles the dose of the medication. If the luggage doesn’t close, the solution is to empty it out, not use more force to . The higher dose of medication helps, but only for a time. Blood sugars go down as you force your body to gag down even more sugar. But eventually, this dose fails as well. So then your doctor gives you a second medication, then a third one and then eventually insulin injections.
Articles and information on this website may only be copied, reprinted, or redistributed with written permission (but please ask, we like to give written permission!) The purpose of this Blog is to encourage the free exchange of ideas. The entire contents of this website is based upon the opinions of Dave Asprey, unless otherwise noted. Individual articles are based upon the opinions of the respective authors, who may retain copyright as marked. The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the personal research and experience of Dave Asprey and the community. We will attempt to keep all objectionable messages off this site; however, it is impossible to review all messages immediately. All messages expressed on The Bulletproof Forum or the Blog, including comments posted to Blog entries, represent the views of the author exclusively and we are not responsible for the content of any message.
The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).
These are a relatively new class of drugs used to treat type 2 diabetes. They are oral medications that work by blocking the kidneys' reabsorption of glucose, leading to increased glucose excretion and reduction of blood sugar levels. The US FDA approved the SGLT2 inhibitors canagliflozin (Invokana) in March 2013 and dapagliflozin (Farxiga) in January 2014.
×