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A patient diagnosed with type 2 diabetes (HbA1c of 6.5% or above) will always have type 2 diabetes. Interventions such as medication (including insulin), staying active and making good diet choices must be maintained to prevent the disease from progressing further. However, even if the patient undergoes strict medication, diet and exercise adherence and manages to lower the HbA1c they will still have type 2 diabetes.
The main goal of diabetes management is, as far as possible, to restore carbohydrate metabolism to a normal state. To achieve this goal, individuals with an absolute deficiency of insulin require insulin replacement therapy, which is given through injections or an insulin pump. Insulin resistance, in contrast, can be corrected by dietary modifications and exercise. Other goals of diabetes management are to prevent or treat the many complications that can result from the disease itself and from its treatment.
Diabetics often find their bodies swinging wildly out of equilibrium. In Type 1 Diabetes, the body attacks insulin-producing cells in the pancreas, causing a rise in blood sugar levels. In Type 2 Diabetes there is insufficient insulin produced in the pancreas, which slows the metabolism and elevates blood sugar levels. Both conditions, if not treated correctly, can cause a host of unpleasant side effects including high blood pressure, neuropathy, kidney damage, and in extreme cases amputation and even death.
The essential feature of type 2 diabetes and pre-diabetes is that our bodies are completely filled with sugar. It’s not just too much sugar in the blood. That’s only part of the problem. There’s too much sugar in our entire body. Imagine our bodies to be a sugar bowl. A bowl of sugar. When we are young, our sugar bowl is empty. Over decades, we eat too much of the wrong things — sugary cereals, desserts and white bread. The sugar bowl gradually fills up with sugar until completely full. The next time you eat, sugar comes into the body, but the bowl is full, so it spills out into the blood.
Focus on low glycemic index foods: While reducing fat and increasing fiber can significantly improve insulin sensitivity, low glycemic index (GI) foods reduce after-meal blood glucose levels. Low GI foods include pumpernickel or rye bread, oats, beans, bran cereals, most fruit, and sweet potatoes, compared to higher GI foods such as white potatoes, processed foods, and cold cereals.

Dr. Sarah Hallberg is a Medical Director at Virta Health. She also created the Medically Supervised Weight Loss Program at Indiana University Health Arnett and serves as its Medical Director. She is an adjunct Clinical Professor of Medicine at Indiana University School of Medicine. Dr. Hallberg is an expert in diabetes care and is board certified in Internal Medicine, Obesity Medicine, and Clinical Lipidology and also a Registered Clinical Exercise Physiologist from the ACSM.


Yes. The combination of insulin and an oral medication, when taken as directed by your doctor, is very safe and effective in controlling blood sugar. A typical combination therapy consists of taking an oral medication during the day and insulin at night. Once you begin taking insulin, you will need to monitor your blood sugar more often to reduce the risk of low blood sugar reactions.Combination therapies are often helpful for people who have Type 2 diabetes (adult onset diabetes). If you have been taking an oral medication, your doctor may change your treatment plan to include insulin injections. This change is often made to help people with Type 2 diabetes gain better control of their blood sugar.
The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).
Normally, blood glucose levels are tightly controlled by insulin, a hormone produced by the pancreas. Insulin lowers the blood glucose level. When the blood glucose elevates (for example, after eating food), insulin is released from the pancreas. This release of insulin promotes the uptake of glucose into body cells. In patients with diabetes, the absence of insufficient production of or lack of response to insulin causes hyperglycemia. Diabetes is a chronic medical condition, meaning that although it can be controlled, it lasts a lifetime.
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