This type of discussion occurs all the time. A patient has been assessed by their physician, and informed that they have a medical problem of some sort. The patient, reluctant to accept the physician’s evaluation, heads to the pharmacy for a second opinion. In some cases, the patient may question the physician’s advice: “All my physician wants to do is prescribe drugs.” Yet there’s a disconnect when it comes to strategies for management. More often than not, non-drug approaches are rejected out-of-hand (probably because the sample I speak with have already made the decision to buy something). And in those that are leery of medical management, there’s often a willingness to consider anything that’s available without a prescription – particularly if it’s perceived as “natural.” Natural products are gentle, safe, and effective, while medicine is thought of as unnatural, harsh, and potentially dangerous. This is the appeal to nature fallacy, nothing more. Purveyors of supplements leverage the appeal to nature fallacy into the marketing strategy of choice for almost all supplements and “alternative” medicines. And it leads to bad health care decisions.
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The first step is to eliminate all sugar and refined starches from your diet. Sugar has no nutritional value and can therefore be eliminated. Starches are simply long chains of sugars. Highly refined starches such as flour or white rice are quickly broken down by digestion into glucose. This is quickly absorbed into the blood and raises blood sugar. For example, eating white bread increases blood sugars very quickly.
These three are the axis of evil in the nutrition world. They are all new introductions to the human diet, especially in the forms they are most eaten in (processed flour, table sugar and High Fructose Corn Syrup and vegetable oils).As we already know, grains (especially in a highly processed form) not only raise insulin levels but can damage the lining of the gut, even in those with no official celiac disease. Grains also cause inflammation in the body and can initiate an immune response.
^ Jump up to: a b Cox DJ, Kovatchev BP, Anderson SM, Clarke WL, Gonder-Frederick LA (November 2010). "Type 1 diabetic drivers with and without a history of recurrent hypoglycemia-related driving mishaps: physiological and performance differences during euglycemia and the induction of hypoglycemia". Diabetes Care. 33 (11): 2430–35. doi:10.2337/dc09-2130. PMC 2963507. PMID 20699432.
Levels which are significantly above or below this range are problematic and can in some cases be dangerous. A level of <3.8 mmol/L (<70 mg/dL) is usually described as a hypoglycemic attack (low blood sugar). Most diabetics know when they are going to "go hypo" and usually are able to eat some food or drink something sweet to raise levels. A patient who is hyperglycemic (high glucose) can also become temporarily hypoglycemic, under certain conditions (e.g. not eating regularly, or after strenuous exercise, followed by fatigue). Intensive efforts to achieve blood sugar levels close to normal have been shown to triple the risk of the most severe form of hypoglycemia, in which the patient requires assistance from by-standers in order to treat the episode. In the United States, there were annually 48,500 hospitalizations for diabetic hypoglycemia and 13,100 for diabetic hypoglycemia resulting in coma in the period 1989 to 1991, before intensive blood sugar control was as widely recommended as today. One study found that hospital admissions for diabetic hypoglycemia increased by 50% from 1990–1993 to 1997–2000, as strict blood sugar control efforts became more common. Among intensively controlled type 1 diabetics, 55% of episodes of severe hypoglycemia occur during sleep, and 6% of all deaths in diabetics under the age of 40 are from nocturnal hypoglycemia in the so-called 'dead-in-bed syndrome,' while National Institute of Health statistics show that 2% to 4% of all deaths in diabetics are from hypoglycemia. In children and adolescents following intensive blood sugar control, 21% of hypoglycemic episodes occurred without explanation. In addition to the deaths caused by diabetic hypoglycemia, periods of severe low blood sugar can also cause permanent brain damage. Although diabetic nerve disease is usually associated with hyperglycemia, hypoglycemia as well can initiate or worsen neuropathy in diabetics intensively struggling to reduce their hyperglycemia.
Whole-body insulin resistance is the earliest predictor of type 2 diabetes onset, and this mainly reflects muscle insulin resistance (26). However, careful separation of the contributions of muscle and liver have shown that early improvement in control of fasting plasma glucose level is associated only with improvement in liver insulin sensitivity (20,21). It is clear that the resumption of normal or near-normal diurnal blood glucose control does not require improvement in muscle insulin sensitivity. Although this finding may at first appear surprising, it is supported by a wide range of earlier observations. Mice totally lacking in skeletal muscle insulin receptors do not develop diabetes (27). Humans who have the PPP1R3A genetic variant of muscle glycogen synthase cannot store glycogen in muscle after meals but are not necessarily hyperglycemic (28). Many normoglycemic individuals maintain normal blood glucose levels with a degree of muscle insulin resistance identical to those with type 2 diabetes (29).
Parslane seeds have strong medicinal value and have been used to keep a check on blood sugar since ages. The compounds of parslane seeds help the body to produce insulin in a natural manner. Just consume a teaspoonful of parslane seeds with half a coup of water on a regular basis (everyday) for 4-5 months. It is one of the simpler, but effective home remedies for diabetes.
The accepted view has been that the β-cell dysfunction of established diabetes progresses inexorably (79,82,83), whereas insulin resistance can be modified at least to some extent. However, it is now clear that the β-cell defect, not solely hepatic insulin resistance, may be reversible by weight loss at least early in the course of type 2 diabetes (21,84). The low insulin sensitivity of muscle tissue does not change materially either during the onset of diabetes or during subsequent reversal. Overall, the information on the inhibitory effects of excess fat on β-cell function and apoptosis permits a new understanding of the etiology and time course of type 2 diabetes.
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.