Type 2 diabetes has long been known to progress despite glucose-lowering treatment, with 50% of individuals requiring insulin therapy within 10 years (1). This seemingly inexorable deterioration in control has been interpreted to mean that the condition is treatable but not curable. Clinical guidelines recognize this deterioration with algorithms of sequential addition of therapies. Insulin resistance and β-cell dysfunction are known to be the major pathophysiologic factors driving type 2 diabetes; however, these factors come into play with very different time courses. Insulin resistance in muscle is the earliest detectable abnormality of type 2 diabetes (2). In contrast, changes in insulin secretion determine both the onset of hyperglycemia and the progression toward insulin therapy (3,4). The etiology of each of these two major factors appears to be distinct. Insulin resistance may be caused by an insulin signaling defect (5), glucose transporter defect (6), or lipotoxicity (7), and β-cell dysfunction is postulated to be caused by amyloid deposition in the islets (8), oxidative stress (9), excess fatty acid (10), or lack of incretin effect (11). The demonstration of reversibility of type 2 diabetes offers the opportunity to evaluate the time sequence of pathophysiologic events during return to normal glucose metabolism and, hence, to unraveling the etiology.
Some people with type 2 diabetes can manage their disease by making healthy food choices and being more physically active. Many people with type 2 diabetes need diabetes medicines as well. These medicines may include diabetes pills or medicines you inject under your skin, such as insulin. In time, you may need more than one diabetes medicine to control your blood glucose. Even if you do not take insulin, you may need it at special times, such as during pregnancy or if you are in the hospital.
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.
Low blood sugar (hypoglycemia). If your blood sugar level drops below your target range, it's known as low blood sugar (hypoglycemia). Your blood sugar level can drop for many reasons, including skipping a meal, inadvertently taking more medication than usual or getting more physical activity than normal. Low blood sugar is most likely if you take glucose-lowering medications that promote the secretion of insulin or if you're taking insulin.
One of my patients, aged 58, had an initial hemoglobin A1c of 7.2%. She was taking oral hypoglycemic agents, statins, and proton pump inhibitors—the basic treatment for every diabetes diagnosis. The patient was 28 lbs overweight and worked long hours. She didn’t exercise, mostly ate a processed food diet, and was sleep deprived. The patient had a family history of diabetes, and ultimately her lifestyle expressed her genetic tendencies.
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).
Benefits of control and reduced hospital admission have been reported. However, patients on oral medication who do not self-adjust their drug dosage will miss many of the benefits of self-testing, and so it is questionable in this group. This is particularly so for patients taking monotherapy with metformin who are not at risk of hypoglycaemia. Regular 6 monthly laboratory testing of HbA1c (glycated haemoglobin) provides some assurance of long-term effective control and allows the adjustment of the patient's routine medication dosages in such cases. High frequency of self-testing in type 2 diabetes has not been shown to be associated with improved control. The argument is made, though, that type 2 patients with poor long term control despite home blood glucose monitoring, either have not had this integrated into their overall management, or are long overdue for tighter control by a switch from oral medication to injected insulin.
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.
Over a period of years, you went from pre-diabetes, to diabetes, to taking one medication, then two then three and then finally large doses of insulin. Here’s the thing. If you are taking more and more medications to keep your blood sugars at the same level, your diabetes is getting worse! Even if your blood sugars get better, your diabetes is getting worse. This is unfortunately what happens to virtually every patient. The body is already overflowing with sugar. The medications only hide the blood sugar by cramming it into the engorged body.
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.
There is no prescribed diet plan for diabetes and no single “diabetes diet”. Eating plans are tailored to fit each individual's needs, schedules, and eating habits. Each diabetes diet plan must be balanced with the intake of insulin and other diabetes medications. In general, the principles of a healthy diabetes diet are the same for everyone. Consumption of various foods in a healthy diet includes whole grains, fruits, non-fat dairy products, beans, lean meats, vegetarian substitutes, poultry, or fish.