All of the above contributing factors don’t usually happen by themselves. Since the body functions as a whole, a problem in one area will usually correlate to problems in others. A combination of the factors above can be the catalyst for a full blown case of diabetes (or a lot of other diseases). While researchers often look at a single variable when trying to discover a cure for a disease, often the best approach is one that addresses the body as a whole. As with all diseases, the best cure is good prevention, but certain measures can help reverse disease once it has occurred.
An aromatic herb that is used commonly to add flavor and aroma to meats and soups, Rosemary also helps normalize blood sugar levels naturally. It promotes weight loss as well, which is a double boon for many diabetics who struggle with weight issues. A research conducted in Jordan to study the effects of rosemary on lipid profile in diabetic rats proved that rosemary has no significant influence on serum glucose level and lipid profile of normal rats. But when rosemary extract was administered to diabetic rats for 4 weeks, their blood sugar levels reduced by 20%, cholesterol levels by 22%, triglyceride levels by 24%, and LDL by 27% while HDL increased by 18% respectively. The study was published in African Journal of Plant Science Vol. 6 in 2012.
After two months under the care of the naturopath, John returned to his primary care doctor to discover that his hemoglobin A1c had dropped from 8.9% to 4.9%—a nondiabetic range. For eight months and counting, he’s been off all his diabetes medication. His last A1c reading was 5.1%. With the help of his naturopath, John seems to have reversed his diabetes.
If you'd like some proof that diabetes is a disease you can live well with, consider the accomplishments of these prolific people with diabetes: jazz musician Dizzy Gillespie, singer Ella Fitzgerald, actress Mary Tyler Moore, and baseball Hall-of-Famer Jim "Catfish" Hunter. Even before treatment was as sophisticated as it is today, author Ernest Hemingway and inventor Thomas Edison, both of whom had diabetes, managed to leave their marks on the world.
Most of us ignored the manual, just plugged it in and tried to figure out the rest. That’s why we all had the blinking 12:00 on. Today, most new electronics now come with a quick start guide which has the most basic 4 or 5 steps to get your machine working and then anything else you needed, you could reference the detailed instruction manual. Instruction manuals are just so much more useful this way.
It isn’t just keeping blood sugar levels down through insulin control that helps diabetes, but fixing the actual problem causing the diabetes. Addressing just one aspect of the problem (blood sugar or insulin) ignores all the other factors like poor diet, toxins, stress, gut problems, immune issues etc. Instead, this single focuses approach can contribute to the problem, making insulin resistance worse and eventually leading to insulin dependent diabetes when the pancreas shuts down completely. Many doctors and nutrition experts recommend the typical 6-11 servings of complex carbs from whole grain sources daily, suggesting that the fiber helps mitigate insulin response. As I have shown before, 6-11 servings of carbohydrates a day is bad for anyone, but is gasoline on a fire to anyone with an impaired insulin response.
Because blood sugar levels fluctuate throughout the day and glucose records are imperfect indicators of these changes, the percentage of hemoglobin which is glycosylated is used as a proxy measure of long-term glycemic control in research trials and clinical care of people with diabetes. This test, the hemoglobin A1c or glycosylated hemoglobin reflects average glucoses over the preceding 2–3 months. In nondiabetic persons with normal glucose metabolism the glycosylated hemoglobin is usually 4–6% by the most common methods (normal ranges may vary by method).
Any form of carbohydrate is eventually broken down by the body into glucose, a simple form of sugar. While the body can use glucose for fuel, levels that exceed what is needed are toxic to the body. In the long run, that whole wheat muffin, cup of millet, or bowl of oatmeal turns into the exact same thing as a cup of soda, a donut or a handful of candy.
Fasting plasma glucose concentration depends entirely on the fasting rate of hepatic glucose production and, hence, on its sensitivity to suppression by insulin. Hepatic insulin sensitivity cannot be inferred from observed postprandial change in hepatic glycogen concentration because glucose transport into the hepatocyte is not rate limiting, unlike in muscle, and hyperglycemia itself drives the process of glycogen synthesis irrespective of insulin action. Indeed, postprandial glycogen storage in liver has been shown to be moderately impaired in type 2 diabetes (50) compared with the marked impairment in skeletal muscle (51).
As of now, diabetes is classified as either Type I or Type II. New research suggests there are several more types of diabetes, which all require different treatment approaches, but that’s a developing area of knowledge. On an episode of Bulletproof Radio, Dr. Steven Masley explains why doctors are starting to view Altzheimer’s disease as “type III diabetes” and picks apart the relationship between insulin and brain degeneration. Listen to it on iTunes.
Currently, one goal for diabetics is to avoid or minimize chronic diabetic complications, as well as to avoid acute problems of hyperglycemia or hypoglycemia. Adequate control of diabetes leads to lower risk of complications associated with unmonitored diabetes including kidney failure (requiring dialysis or transplant), blindness, heart disease and limb amputation. The most prevalent form of medication is hypoglycemic treatment through either oral hypoglycemics and/or insulin therapy. There is emerging evidence that full-blown diabetes mellitus type 2 can be evaded in those with only mildly impaired glucose tolerance.
Glycemic control is a medical term referring to the typical levels of blood sugar (glucose) in a person with diabetes mellitus. Much evidence suggests that many of the long-term complications of diabetes, especially the microvascular complications, result from many years of hyperglycemia (elevated levels of glucose in the blood). Good glycemic control, in the sense of a "target" for treatment, has become an important goal of diabetes care, although recent research suggests that the complications of diabetes may be caused by genetic factors or, in type 1 diabetics, by the continuing effects of the autoimmune disease which first caused the pancreas to lose its insulin-producing ability.
A useful test that has usually been done in a laboratory is the measurement of blood HbA1c levels. This is the ratio of glycated hemoglobin in relation to the total hemoglobin. Persistent raised plasma glucose levels cause the proportion of these molecules to go up. This is a test that measures the average amount of diabetic control over a period originally thought to be about 3 months (the average red blood cell lifetime), but more recently[when?] thought to be more strongly weighted to the most recent 2 to 4 weeks. In the non-diabetic, the HbA1c level ranges from 4.0–6.0%; patients with diabetes mellitus who manage to keep their HbA1c level below 6.5% are considered to have good glycemic control. The HbA1c test is not appropriate if there has been changes to diet or treatment within shorter time periods than 6 weeks or there is disturbance of red cell aging (e.g. recent bleeding or hemolytic anemia) or a hemoglobinopathy (e.g. sickle cell disease). In such cases the alternative Fructosamine test is used to indicate average control in the preceding 2 to 3 weeks.
At his first visit, the naturopathic doctor told John he’d be “off medication and free of diabetes in three months.” John left the doctor’s office with instructions to eat a low-carb diet. He’d been on a low-fat diet for years because of heart problems, but while he’d cut the fat, his meals included many highly processed foods. His new diet included “a lot of salads and healthful, organic foods.” He was given several whole food supplements that he says were “simple to mix and tasted good.”
Called ALA for short, this vitamin-like substance neutralizes many types of free radicals. A build-up of free radicals, caused in part by high blood sugar, can lead to nerve damage and other problems. ALA may also help muscle cells take up blood sugar. In a German study, a team of scientists had 40 adults take either an ALA supplement or a placebo. At the end of the four-week study, the ALA group had improved their insulin sensitivity 27 percent. The placebo group showed no improvement. Other studies have shown a decrease in nerve pain, numbness, and burning.
Grains: Grains, especially gluten-containing grains like wheat, contain large amounts of carbohydrates that are broken down into sugar within only a few minutes of consumption. Gluten can cause intestinal inflammation, which affects hormones like cortisol and leptin, and can lead to spikes in blood sugar. I recommend removing all grains from your diet for 90 days as your body adjusts to this healing program. Then you can try bringing sprouted ancient grains back into your diet in small amounts.
Peripheral neuropathy is a problem with the functioning of the nerves outside of the spinal cord. Symptoms may include numbness, weakness, burning pain (especially at night), and loss of reflexes. Possible causes may include carpel tunnel syndrome, shingles, vitamin or nutritional deficiencies, and illnesses like diabetes, syphilis, AIDS, and kidney failure. Peripheral neuropathy is diagnosed with exams and tests. Treatment for the condition depends on the cause. Usually, the prognosis for peripheral neuropathy is good if the cause can be successfully treated or prevented.
Obesity is a disease, not something created by lack of character. It is a hormonal disease. There are many hormones involved, and one of the main ones is a hormone called insulin. The vast majority of obese individuals are resistant to insulin and that causes a lot of trouble. So, what does being insulin-resistant mean? Insulin resistance is essentially ‘pre-pre-type 2 diabetes.’ Insulin’s job is to drive glucose or blood sugar into cells where it can be used. In a nutshell, when someone has insulin resistance, they are having trouble getting glucose where it needs to go, into the cells. It can’t all hang out in the blood after we eat, or we would all have a diabetic crisis after every meal. When there is resistance to insulin, our bodies will just make more of it. The insulin levels rise and rise and for a while, years usually, this will keep up and blood sugar will stay normal. However, eventually it can’t keep up, and even elevate insulin levels are not enough to keep blood sugar normal, and blood sugar rises. And that is diabetes.
Within the hepatocyte, fatty acids can only be derived from de novo lipogenesis, uptake of nonesterified fatty acid and LDL, or lipolysis of intracellular triacylglycerol. The fatty acid pool may be oxidized for energy or may be combined with glycerol to form mono-, di-, and then triacylglycerols. It is possible that a lower ability to oxidize fat within the hepatocyte could be one of several susceptibility factors for the accumulation of liver fat (45). Excess diacylglycerol has a profound effect on activating protein kinase C epsilon type (PKCε), which inhibits the signaling pathway from the insulin receptor to insulin receptor substrate 1 (IRS-1), the first postreceptor step in intracellular insulin action (46). Thus, under circumstances of chronic energy excess, a raised level of intracellular diacylglycerol specifically prevents normal insulin action, and hepatic glucose production fails to be controlled (Fig. 4). High-fat feeding of rodents brings about raised levels of diacylglycerol, PKCε activation, and insulin resistance. However, if fatty acids are preferentially oxidized rather than esterified to diacylglycerol, then PKCε activation is prevented, and hepatic insulin sensitivity is maintained. The molecular specificity of this mechanism has been confirmed by use of antisense oligonucleotide to PKCε, which prevents hepatic insulin resistance despite raised diacylglycerol levels during high-fat feeding (47). In obese humans, intrahepatic diacylglycerol concentration has been shown to correlate with hepatic insulin sensitivity (48,49). Additionally, the presence of excess fatty acids promotes ceramide synthesis by esterification with sphingosine. Ceramides cause sequestration of Akt2 and activation of gluconeogenic enzymes (Fig. 4), although no relationship with in vivo insulin resistance could be demonstrated in humans (49). However, the described intracellular regulatory roles of diacylglycerol and ceramide are consistent with the in vivo observations of hepatic steatosis and control of hepatic glucose production (20,21).
Ideally, insulin should be administered in a manner that mimics the natural pattern of insulin secretion by a healthy pancreas. However, the complex pattern of natural insulin secretion is difficult to duplicate. Still, adequate blood glucose control can be achieved with careful attention to diet, regular exercise, home blood glucose monitoring, and multiple insulin injections throughout the day..