The more intense the exercise, the better. According to the British diabetes association diabetes.co.uk, high-intensity interval training (HIIT) may be better for weight loss and glucose control than continuous aerobic activity like jogging. HIIT involves alternating between short bursts of increased intensity exercise and rest — for instance, running and then walking on and off throughout the workout.

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!)”
A wide scatter of absolute levels of pancreas triacylglycerol has been reported, with a tendency for higher levels in people with diabetes (57). This large population study showed overlap between diabetic and weight-matched control groups. These findings were also observed in a more recent smaller study that used a more precise method (21). Why would one person have normal β-cell function with a pancreas fat level of, for example, 8%, whereas another has type 2 diabetes with a pancreas fat level of 5%? There must be varying degrees of liposusceptibility of the metabolic organs, and this has been demonstrated in relation to ethnic differences (72). If the fat is simply not available to the body, then the susceptibility of the pancreas will not be tested, whereas if the individual acquires excess fat stores, then β-cell failure may or may not develop depending on degree of liposusceptibility. In any group of people with type 2 diabetes, simple inspection reveals that diabetes develops in some with a body mass index (BMI) in the normal or overweight range, whereas others have a very high BMI. The pathophysiologic changes in insulin secretion and insulin sensitivity are not different in obese and normal weight people (73), and the upswing in population rates of type 2 diabetes relates to a right shift in the whole BMI distribution. Hence, the person with a BMI of 24 and type 2 diabetes would in a previous era have had a BMI of 21 and no diabetes. It is clear that individual susceptibility factors determine the onset of the condition, and both genetic and epigenetic factors may contribute. Given that diabetes cannot occur without loss of acute insulin response to food, it can be postulated that this failure of acute insulin secretion could relate to both accumulation of fat and susceptibility to the adverse effect of excess fat in the pancreas.
Diabetes is a well-established problem and a multi-billion dollar industry. It is medically characterized by Fasting Blood Glucose higher than 126 mg/dL , which ranges between 100-125 mg/dL are considered pre-diabetic and ranges below 99 mg/dL are considered normal. Studies are finding that a fasting blood glucose below 83 mg/dL is actually a better benchmark, as risk of heart disease begins to increase at anything above that.
Magnesium deficiency is common in diabetic patients, as magnesium can be lost in the urine with hyperglycemia. A study in Diabetes Care reported that low magnesium status is common in Type 2 Diabetes Mellitus (T2DM) and showed that when low-magnesium Type 2 Diabetes Mellitus patients were given an oral dose of magnesium daily for sixteen weeks, the mineral reduced insulin resistance, fasting glucose, and A1C levels.
The medical professionals at the Diabetes Treatment Center at Desert Springs Hospital Medical Center provide inpatient and outpatient evaluation, treatment and ongoing education for adults with Type 1 or Type 2 diabetes, as well as pre-diabetes conditions. The interdisciplinary team includes certified diabetes educators and nurses who work closely with patients' primary care physicians to work toward a common goal — to help patients lead longer, healthier lives.
Alternative: “I’m a fat-atarian,” says DeLaney, who tells her patients to avoid low-fat foods. She encourages them to eat whole-fat dairy products, egg yolks, butter, olive oil, and avocado. “Restoring healthful fats to our diets as well as eliminating trans fats and all refined oils that help deplete our fat and vitamin stores will help nourish the body and reduce the need for diabetes medication.”
Cinnamon’s effectiveness as a treatment for diabetes has not been established. A prescription drug as ineffective as cinnamon likely wouldn’t pass FDA muster. Existing drug treatments for diabetes, on the other hand, are cheap, effective, and generally well tolerated. Compared to drug therapy, we don’t know if cinnamon can reduce the risk of mortality due to diabetes, or the progression to any of the other serious outcomes of diabetes.   For my patients that insist on trying cinnamon, I’d caution them of the risks, and reinforce that cinnamon is no alternative for lifestyle changes and medication if necessary. It may be natural, sure, but that doesn’t mean it’s either safe or effective.
Curcumin is a bright yellow chemical produced by the spice turmeric, among other plants. Curcumin seems to have multiple benefits for diabetes symptoms. It has been shown to be a marked inhibitor of reactive oxygen species that promote oxidation damage in cells. Curcumin lowers inflammatory chemicals like tumor necrosis factor-alpha, and that’s good because TNF-a causes insulin resistance and irritates fatty livers. Curcumin can reduce another pro-inflammatory chemical called NF-KB. The above-mentioned actions provide a benefit in diabetes protection and reduce the risk of developing diabetes symptoms and complications. Curcumin has also been shown to enhance pancreatic beta cell functioning and reduce fatty liver deposition. It reduces high blood sugar, A1C, and insulin resistance. It was also shown to reduce the onset of Alzheimer’s disease, and that is a higher risk in diabetic patients than in nondiabetic patients. A good dose is 200 to 3,000 mg a day.

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.


The earliest predictor of the development of type 2 diabetes is low insulin sensitivity in skeletal muscle, but it is important to recognize that this is not a distinct abnormality but rather part of the wide range expressed in the population. Those people in whom diabetes will develop simply have insulin sensitivity, mainly in the lowest population quartile (29). In prediabetic individuals, raised plasma insulin levels compensate and allow normal plasma glucose control. However, because the process of de novo lipogenesis is stimulated by higher insulin levels (38), the scene is set for hepatic fat accumulation. Excess fat deposition in the liver is present before the onset of classical type 2 diabetes (43,74–76), and in established type 2 diabetes, liver fat is supranormal (20). When ultrasound rather than magnetic resonance imaging is used, only more-severe degrees of steatosis are detected, and the prevalence of fatty liver is underestimated, with estimates of 70% of people with type 2 diabetes as having a fatty liver (76). Nonetheless, the prognostic power of merely the presence of a fatty liver is impressive of predicting the onset of type 2 diabetes. A large study of individuals with normal glucose tolerance at baseline showed a very low 8-year incidence of type 2 diabetes if fatty liver had been excluded at baseline, whereas if present, the hazard ratio for diabetes was 5.5 (range 3.6–8.5) (74). In support of this finding, a temporal progression from weight gain to raised liver enzyme levels and onward to hypertriglyceridemia and then glucose intolerance has been demonstrated (77).
Poor glycemic control refers to persistently elevated blood glucose and glycosylated hemoglobin levels, which may range from 200–500 mg/dl (11–28 mmol/L) and 9–15% or higher over months and years before severe complications occur. Meta-analysis of large studies done on the effects of tight vs. conventional, or more relaxed, glycemic control in type 2 diabetics have failed to demonstrate a difference in all-cause cardiovascular death, non-fatal stroke, or limb amputation, but decreased the risk of nonfatal heart attack by 15%. Additionally, tight glucose control decreased the risk of progression of retinopathy and nephropathy, and decreased the incidence peripheral neuropathy, but increased the risk of hypoglycemia 2.4 times.[21]
They would often say to me, “Doctor. You’ve always said that weight loss is the key to reversing diabetes. Yet you prescribed me a drug that made me gain 25 pounds. How is that good?” I never had a good answer, because none existed. It was not good. The key was weight loss, whereupon the diabetes often goes away or at least gets significantly better. So, logically, insulin does not help reverse the disease, but actually worsens it.
Jump up ^ Qaseem A, Vijan S, Snow V, Cross JT, Weiss KB, Owens DK; Vijan; Snow; Cross; Weiss; Owens; Clinical Efficacy Assessment Subcommittee of the American College of Physicians (September 2007). "Glycemic control and type 2 diabetes mellitus: the optimal hemoglobin A1c targets. A guidance statement from the American College of Physicians". Annals of Internal Medicine. 147 (6): 417–22. doi:10.7326/0003-4819-147-6-200709180-00012. PMID 17876024. Retrieved 19 July 2008.

If your carb consumption is on the high side (once you add sugar into the mix, you’re most certainly on the high side), it’s stored as fat and you end up with insulin resistance or non-alcoholic fatty liver disease.[14] The reason behind it is that carbs metabolize into glucose, and limiting carbs helps your body control blood sugar more efficiently.[15][16] It improves overall blood sugar profiles, insulin sensitivity, and hemoglobin A1c, which is a diabetes marker.[17] Going low-carb is especially effective if you’re in the early stages when you do not yet need to administer insulin.[18]
If you have gestational diabetes, you should first try to control your blood glucose level by making healthy food choices and getting regular physical activity. If you can’t reach your blood glucose target, your health care team will talk with you about diabetes medicines, such as insulin or the diabetes pill metformin, that may be safe for you to take during pregnancy. Your health care team may start you on diabetes medicines right away if your blood glucose is very high.
A popular spice used in Indian cooking, and the main ingredient of ‘curry’ that has taken the world by storm, turmeric has antibacterial, anti-inflammatory and antioxidant properties that all come together to help diabetics manage more stable blood sugar levels. It helps boost immunity and prevent infections that diabetics are often vulnerable to. Studies conducted on rats prove that curcumin, the active ingredient in turmeric, is effective in reducing plasma glucose level and HbA1C as well as improving the lipid profile. Many diabetics also suffer from arthritis, since the sugar laden blood and inflammatory processes typical to diabetes often damage joints. Turmeric, with its anti-inflammatory abilities, also helps with these joint pains.

Once you have diabetes, it is there for life. I help people to get their blood glucose levels back to or as near as possible the normal range. Firstly this will help you to feel better in the short term but it also helps to protect your blood vessels which can become very irritated and damaged by high glucose levels. Focussing on healthy eating, limiting unprocessed foods and getting a wide variety of fruits and vegetables in the diet helps.
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.
As a result of his research and his success stories, Taylor encourages other doctors to stop turning to diabetes medicines right away and more strongly encourage weight loss as the first step for their patients newly diagnosed with type 2 diabetes. And the sooner, the better, he says. While Maher reversed his diabetes decades later, that's not typical, Taylor says. The ideal management, he says, is to start serious weight loss efforts right away.
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.
Other medications such as metformin or the DPP4 drug class are weight neutral. While this won’t make things worse, they won’t make things better either. Since weight loss is the key to reversing type 2 diabetes, medications won’t make things better. Medications make blood sugars (the symptom) better, but not the diabetes (the actual disease). We’ve been pretending that the symptom is the disease.We can pretend the disease is better, but that doesn’t make it true. That’s the reason most doctors think type 2 diabetes a chronic and progressive disease. We’ve been using the wrong treatment. We’ve been prescribing drugs for a dietary disease. No wonder it doesn’t work.
Optimal management of diabetes involves patients measuring and recording their own blood glucose levels. By keeping a diary of their own blood glucose measurements and noting the effect of food and exercise, patients can modify their lifestyle to better control their diabetes. For patients on insulin, patient involvement is important in achieving effective dosing and timing.
Studies conducted in the United States[43] and Europe[44] showed that drivers with type 1 diabetes had twice as many collisions as their non-diabetic spouses, demonstrating the increased risk of driving collisions in the type 1 diabetes population. Diabetes can compromise driving safety in several ways. First, long-term complications of diabetes can interfere with the safe operation of a vehicle. For example, diabetic retinopathy (loss of peripheral vision or visual acuity), or peripheral neuropathy (loss of feeling in the feet) can impair a driver’s ability to read street signs, control the speed of the vehicle, apply appropriate pressure to the brakes, etc.
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).
Isobel Murray, 65 from North Ayrshire, was one of those who took part. Over two years she lost three and a half stone (22kg) and no longer needs medication. “It has transformed my life,” she said. “I had type 2 diabetes for two to three years before the study. I was on various medications which were constantly increasing and I was becoming more and more ill every day.

Other medications such as metformin or the DPP4 drug class are weight neutral. While this won’t make things worse, they won’t make things better either. Since weight loss is the key to reversing type 2 diabetes, medications won’t make things better. Medications make blood sugars (the symptom) better, but not the diabetes (the actual disease). We’ve been pretending that the symptom is the disease.We can pretend the disease is better, but that doesn’t make it true. That’s the reason most doctors think type 2 diabetes a chronic and progressive disease. We’ve been using the wrong treatment. We’ve been prescribing drugs for a dietary disease. No wonder it doesn’t work.


Maintaining normal blood sugar levels is necessary for the body’s overall health. Erratic blood sugar levels can affect the body’s ability to function normally and even lead to complications if left unchecked. Some herbs and spices found in nature do a tremendous job of naturally lowering blood sugar levels, making them a boon for diabetics and pre-diabetics. What’s more, being nature’s multi-taskers, herbs and spices also produce overall health benefits beyond just helping balance blood sugar.
The aptly named bitter melon is thought to help cells use glucose more effectively and block sugar absorption in the intestine. When Philippine researchers had men and women take bitter melon in capsule form for three months, they had slight, but consistently, lower blood sugar than those taking a placebo. Gastrointestinal problems are possible side effects. You can reverse diabetes with these science-backed strategies.
Exenatide (Byetta) was the first drug of the GLP-1 agonist group. It originated from an interesting source, the saliva of the Gila monster. Scientists observed that this small lizard could go a long time without eating. They discovered a substance in its saliva that slowed stomach emptying, thus making the lizard feel fuller for a longer time. This substance resembled the hormone GLP-1.
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