This essentially means that the type 2 diabetes is being managed at a level that seems as if the diabetes isn’t there at all. Choosing a healthy diet, exercising regularly and maintaining a healthy weight is the key. Eventually, what will likely happen is that blood glucose levels will increase again at a later time, as the person gets older, or if the person returns to an inactive and unhealthy lifestyle and regains weight because the beta cells of the pancreas have already been stressed.
All carbohydrates – to some degree at least – will raise your blood insulin levels. That is why I consider type 2 diabetes a form of “carbohydrate intolerance”. Protein can also raise levels but to a much lesser degree. The only macronutrient that keeps your insulin levels and, therefore, your blood sugar stable is FAT! Therefore, if you are trying to reduce insulin levels, you need to reduce your amount of certain carbohydrates and replace them instead with healthy, natural fats.
Clearly separate from the characteristic lack of acute insulin secretion in response to increase in glucose supply is the matter of total mass of β-cells. The former determines the immediate metabolic response to eating, whereas the latter places a long-term limitation on total possible insulin response. Histological studies of the pancreas in type 2 diabetes consistently show an ∼50% reduction in number of β-cells compared with normal subjects (66). β-Cell loss appears to increase as duration of diabetes increases (67). The process is likely to be regulated by apoptosis, a mechanism known to be increased by chronic exposure to increased fatty acid metabolites (68). Ceramides, which are synthesized directly from fatty acids, are likely mediators of the lipid effects on apoptosis (10,69). In light of new knowledge about β-cell apoptosis and rates of turnover during adult life, it is conceivable that removal of adverse factors could result in restoration of normal β-cell number, even late in the disease (66,70). Plasticity of lineage and transdifferentiation of human adult β-cells could also be relevant, and the evidence for this has recently been reviewed (71). β-Cell number following reversal of type 2 diabetes remains to be examined, but overall, it is clear that at least a critical mass of β-cells is not permanently damaged but merely metabolically inhibited.
Thank you for explaining just how things work. I have just (2months ago)gone off Diabetes Type 2 medication. BGLs around 7-10 now. It looks like I replace the rolled oats for cauliflower for breakfast and the three slices of wholegrain sourdough bread for veggies. Those two items were the continued delaying function. I’ll be on my way to decreasing the BGLs to normal, now. I have lots of fat from cold pressed virgin olive oil in my home-made hummus and over the veggies. I can look forward to the soya coffee with no guilt.
If you have type 2 diabetes and your body mass index (BMI) is greater than 35, you may be a candidate for weight-loss surgery (bariatric surgery). Blood sugar levels return to normal in 55 to 95 percent of people with diabetes, depending on the procedure performed. Surgeries that bypass a portion of the small intestine have more of an effect on blood sugar levels than do other weight-loss surgeries.
For people with either type of diabetes, exercise can lower the chance of having a heart attack or stroke and can improve circulation. It may offer stress relief, as well. People with type 2 diabetes who need to lose weight can benefit from moderate exercise. Most people with diabetes are encouraged to get at least 150 minutes each week of moderate-intensity aerobic physical activity, like walking. Strength training is often recommended at least twice a week. Talk to your doctor about what type of exercise is right for you.
Some studies show that certain plant foods may help your body fight inflammation and use insulin, a hormone that controls blood sugar. Cinnamon extracts can improve sugar metabolism, triggering insulin release, which also boosts cholesterol metabolism. Clove oil extracts (eugenol) have been found to help insulin work and to lower glucose, total cholesterol, LDL, and triglycerides. An unidentified compound in coffee (not caffeine) may enhance insulin sensitivity and lower the chances of developing type 2 diabetes.
Drugs that increase insulin production by the pancreas or its blood levels and/or reduce sugar production from the liver, including alogliptin (Nesina), dulaglutide (Trulicity), linagliptin (Tradjenta), exenatide (Byetta, Bydureon), liraglutide (Victoza), lixisenatide (Adlyxin), saxagliptin (Onglyza), sitagliptin (Januvia), and semaglutide (Ozempic)
Gene therapy can be used to turn duodenum cells and duodenum adult stem cells into beta cells which produce insulin and amylin naturally. By delivering beta cell DNA to the intestine cells in the duodenum, a few intestine cells will turn into beta cells, and subsequently adult stem cells will develop into beta cells. This makes the supply of beta cells in the duodenum self replenishing, and the beta cells will produce insulin in proportional response to carbohydrates consumed.
For our very insulin resistant patients with type 2 diabetes, after starting out at 30 grams, a few months later most of our patients find that they can increase their daily carb intake to 40 or 50 grams. Fifty grams of total carbohydrate typically allows 4-5 servings of non-starchy vegetables, 2 oz of nuts, and 3 oz of berry fruit (which includes avocado – but obviously you’d need to share it with someone unless it’s a tiny one!)”
In that analysis, the Khan study looks like an outlier. More studies have emerged since then: Crawford in 2009 found 1g of cinnamon per day reduced A1C levels compared to placebo. Suppapitiporn found no effect on any measure with 1.5g per day. Akilen, in 2010, found an effect with 2g per day. Another meta-analysis, published in 2012 and included 6 studies, concluded the opposite of Baker, and made positive conclusions:
Although a defect in mitochondrial function is associated with extremes of insulin resistance in skeletal muscle (30), this does not appear to be relevant to the etiology of type 2 diabetes. No defect is present in early type 2 diabetes but rather is directly related to ambient plasma glucose concentration (31). Observed rates of mitochondrial ATP production can be modified by increasing or decreasing plasma fatty acid concentration (32,33). Additionally, the onset of insulin stimulation of mitochondrial ATP synthesis is slow, gradually increasing over 2 h, and quite distinct from the acute onset of insulin’s metabolic effects (34). Although it remains possible that secondary mitochondrial effects of hyperglycemia and excess fatty acids exist, there is no evidence for a primary mitochondrial defect underlying type 2 diabetes.
Over a year ago I was diagnosed with DT2. I was devastated… I told that I needed to take medication and eat according to the ADA recommendations. I never did anything that I was told. I refused to take the medication and went to a LCHF diet. My A1C has never been above a 4.7 for an entire year and I lost 80 pounds with doing nothing but eating. I feel great and my labs are stellar…
Studies funded by the National Institutes of Health (NIH) have demonstrated that face-to-face training programs designed to help individuals with type 1 diabetes better anticipate, detect, and prevent extreme BG can reduce the occurrence of future hypoglycemia-related driving mishaps. An internet-version of this training has also been shown to have significant beneficial results. Additional NIH funded research to develop internet interventions specifically to help improve driving safety in drivers with type 1 diabetes is currently underway.
People with type 1 diabetes (T1D) can live long, happy lives with proper care and disease management. Advancements in medication types and delivery methods give people the freedom to choose which treatment options work best with their particular circumstance. T1D prognoses can be greatly improved with a combination of treatments and lifestyle choices.
Levels which are significantly above or below this range are problematic and can in some cases be dangerous. A level of <3.8 mmol/L (<70 mg/dL) is usually described as a hypoglycemic attack (low blood sugar). Most diabetics know when they are going to "go hypo" and usually are able to eat some food or drink something sweet to raise levels. A patient who is hyperglycemic (high glucose) can also become temporarily hypoglycemic, under certain conditions (e.g. not eating regularly, or after strenuous exercise, followed by fatigue). Intensive efforts to achieve blood sugar levels close to normal have been shown to triple the risk of the most severe form of hypoglycemia, in which the patient requires assistance from by-standers in order to treat the episode. In the United States, there were annually 48,500 hospitalizations for diabetic hypoglycemia and 13,100 for diabetic hypoglycemia resulting in coma in the period 1989 to 1991, before intensive blood sugar control was as widely recommended as today. One study found that hospital admissions for diabetic hypoglycemia increased by 50% from 1990–1993 to 1997–2000, as strict blood sugar control efforts became more common. Among intensively controlled type 1 diabetics, 55% of episodes of severe hypoglycemia occur during sleep, and 6% of all deaths in diabetics under the age of 40 are from nocturnal hypoglycemia in the so-called 'dead-in-bed syndrome,' while National Institute of Health statistics show that 2% to 4% of all deaths in diabetics are from hypoglycemia. In children and adolescents following intensive blood sugar control, 21% of hypoglycemic episodes occurred without explanation. In addition to the deaths caused by diabetic hypoglycemia, periods of severe low blood sugar can also cause permanent brain damage. Although diabetic nerve disease is usually associated with hyperglycemia, hypoglycemia as well can initiate or worsen neuropathy in diabetics intensively struggling to reduce their hyperglycemia.
The diabetes looks better, since you can only see the blood sugars. Doctors can congratulate themselves on a illusion of a job well done, even as the patient gets continually sicker. Patients require ever increasing doses of medications and yet still suffer with heart attacks, congestive heart failure, strokes, kidney failure, amputations and blindness. “Oh well” the doctor tells himself, “It’s a chronic, progressive disease”.
We live in a world where prescription medicine is getting more and more expensive as well as controversial. Alternative medicine is gaining momentum and with good reason! The same is true for treatments for diabetes type 2. You have therapies that can reverse diabetes through lifestyle and diet changes, natural supplements that can help stabilize blood sugar levels, and also herbs that lower blood sugar. Not only are these alternative therapies safer, but they are also easier on your pocket, on your body and mind.
The primary issue requiring management is that of the glucose cycle. In this, glucose in the bloodstream is made available to cells in the body; a process dependent upon the twin cycles of glucose entering the bloodstream, and insulin allowing appropriate uptake into the body cells. Both aspects can require management. Another issue that ties along with the glucose cycle is getting a balanced amount of the glucose to the major organs so they are not affected negatively.
Insulin is a naturally occurring hormone in your pancreas that helps your body use blood sugar and keeps blood sugar within a healthy range. But in the case of type 2 diabetes, a person’s body doesn’t use insulin properly, leading to insulin resistance. When your pancreas simply can't make enough insulin or use it well enough to control blood sugar, your doctor is likely to prescribe insulin injections.
Many manufacturers offer pen delivery systems. Such systems resemble the ink cartridge in a fountain pen. A small, pen-sized device holds an insulin cartridge (usually containing 300 units). Cartridges are available for the most widely used insulin formulations. The amount of insulin to be injected is dialed in, by turning the bottom of the pen until the required number of units is seen in the dose-viewing window. The tip of the pen consists of a needle that is replaced with each injection. A release mechanism allows the needle to penetrate just under the skin and deliver the required amount of insulin.