But is John “free of diabetes”? This is where the lines become blurred. Medically speaking, the term “cure” is usually associated with acute disease—a temporary medical condition, such as bacterial pneumonia, that can be cured with antibiotics. For diabetes, which is a chronic disease, it may be more accurate to use the term “remission” rather than cure. Particularly when considering the pathology associated with diabetes and the individual’s genetic predisposition, relapse is always possible. In a consensus statement issued by the ADA, the term remission is defined based on the following definitions:2
The review affirmed how effective surgery is at treating diabetes (possibly even type 1 diabetes). Around two-thirds of patients with diabetes experience a full remission soon after surgery, while the rest are often better able to control their blood sugar through diet, exercise and medication. Other studies have shown that diabetics who have surgery outlive those who haven’t. Some longer-term research has suggested that one-third of these successes slide back into having active diabetes after five years, but to a lesser degree than they might have without surgery. By contrast, a 2014 study found that fewer than 2 percent of diabetes patients given standard care experienced any remission within a seven-year span.
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).

Why do people develop prediabetes? Prediabetes develops through a combination of factors that are still being investigated. For sure, lifestyle factors (food, exercise, stress, sleep) play a role, but family history and genetics certainly do as well. It is easy to assume that prediabetes is the result of being overweight, but the relationship is not that simple. While obesity is one underlying cause of insulin resistance, many overweight individuals may never develop prediabetes or type 2 diabetes, and a minority of people with prediabetes have never been overweight. To make matters worse, it can be increasingly difficult to make healthy choices in today’s toxic food environment that steers all of us to make the wrong food choices, and there are many factors that can contribute to weight gain in addition to diet.
Oral diabetes medications may also come in combination tablets such as Metaglip (glipizide/metformin), Prandimet (repaglinide/metformin), Glucovance (glyburide/metformin), Janumet (sitagliptin/metformin), Avandamet (rosiglitazone/metformin), Avandaryl (rosiglitazone/ glimepiride), Duetact (pioglitazone/glimepiride), Actoplus Met (pioglitazone/metformin).
It would be a mistake to assume that the diabetes has gone away, however. Basically, type 1 diabetes occurs when about 90 percent of the body's insulin-producing cells have been destroyed. At the time that type 1 diabetes is diagnosed, most patients still are producing some insulin. If obvious symptoms of type 1 diabetes emerge when the patient has an illness, virus or cold, for example, once the illness subsides the body's insulin needs may decrease. At this point, the number of insulin-producing cells remaining may be enough — for the moment — to meet the person's insulin needs again.
Yuri Elkaim is one of the world’s most trusted health and fitness experts. A former pro soccer player turned NYT bestselling author of The All-Day Energy Diet and The All-Day Fat Burning Diet, his clear, science-backed advice has transformed the lives of more than 500,000 men and women and he’s on a mission to help 100 million people by 2040. Read his inspiring story, “From Soccer to Bed to No Hair on My Head” that started it all.

The study, published in Diabetes Care, measured C-peptide, which is produced at the same time and in the same quantities as the insulin that regulates our blood sugar. By measuring C-peptide levels in blood or in urine, scientists can tell how much insulin a person is producing themselves, even if they are taking insulin injections as treatment. The team studied 1,549 people with Type 1 diabetes from Exeter, England and Tayside, Scotland in the UNITED study.

This seems hard to do, but really it’s not if you know one secret: Replace snacking with something far more satisfying — fat. That’s right, the government is wrong to recommend a low fat diet. Fat is what makes you feel full until your next meal. Take away the fat, take away the full. Don’t go to an extreme, but do lean strongly toward a high-fat low-carb diet.
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