In Type 2 diabetes, the insulin that is produced does not work effectively. This is referred to as “insulin resistance.” Previously referred to as “adult-onset diabetes,” Type 2 diabetes is the most common form and occurs most frequently in inactive, overweight adults. With rising rates of childhood obesity, we are now seeing Type 2 diabetes diagnosed in more children and teens. Type 2 diabetes is usually treated with a diet that promotes weight loss, exercise and oral medications. Over time, most with Type 2 diabetes produce less insulin. Because of this,insulin may also be required to treat Type 2 diabetes. 

1. Avoid toxins as much as possible: There is no doubt that we live in a polluted world, and it is next to impossible to avoid all toxins, however, recent research suggests that environmental toxins such as pesticides in our food and drinking water can be factors in causing or worsening Type 1 Diabetes. To lessen the amount of toxins that enter the body, try to buy “green” cleaners, organic fruits and vegetables, and dairy that is from organic or grass-fed cows. Although these items may be a bit more expensive, the health benefits are well-worth the higher price tag.
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).
Although the promises are big, these technologies are still far from the market. First, clinical trials will have to show they do work. Then, the price could be steep, as cell therapy precedents for other applications, such as oncology, come with price tags that reach the six figures and are finding difficulties to get reimbursed. Considering that compared to cancer, diabetes is not an immediately life-threatening disease, health insurers in some countries might be reluctant to cover the treatment.

Over a year ago I was diagnosed with DT2. I was devastated… I told that I needed to take medication and eat according to the ADA recommendations. I never did anything that I was told. I refused to take the medication and went to a LCHF diet. My A1C has never been above a 4.7 for an entire year and I lost 80 pounds with doing nothing but eating. I feel great and my labs are stellar…
Eating right and exercising more often is good for everyone. But it's especially important for people with type 2 diabetes. When people put on too much body fat, it's because they're eating more calories than they use each day. The body stores that extra energy in fat cells. Over time, gaining pounds of extra fat can lead to obesity and diseases related to obesity, like type 2 diabetes.
Relying on their own perceptions of symptoms of hyperglycemia or hypoglycemia is usually unsatisfactory as mild to moderate hyperglycemia causes no obvious symptoms in nearly all patients. Other considerations include the fact that, while food takes several hours to be digested and absorbed, insulin administration can have glucose lowering effects for as little as 2 hours or 24 hours or more (depending on the nature of the insulin preparation used and individual patient reaction). In addition, the onset and duration of the effects of oral hypoglycemic agents vary from type to type and from patient to patient.
Insulin therapy creates risk because of the inability to continuously know a person's blood glucose level and adjust insulin infusion appropriately. New advances in technology have overcome much of this problem. Small, portable insulin infusion pumps are available from several manufacturers. They allow a continuous infusion of small amounts of insulin to be delivered through the skin around the clock, plus the ability to give bolus doses when a person eats or has elevated blood glucose levels. This is very similar to how the pancreas works, but these pumps lack a continuous "feed-back" mechanism. Thus, the user is still at risk of giving too much or too little insulin unless blood glucose measurements are made.
Drugs of this class decrease the absorption of carbohydrates from the intestine. Before being absorbed into the bloodstream, enzymes in the small intestine must break down carbohydrates into smaller sugar particles, such as glucose. One of the enzymes involved in breaking down carbohydrates is called alpha-glucosidase. By inhibiting this enzyme, carbohydrates are not broken down as efficiently, and glucose absorption is delayed.