Thank you for including me in the forum. We all agree that a low-glycemic, nutrient-packed diet—coupled with a healthful lifestyle—is the best way to treat and prevent type 2 diabetes. One of the easiest ways to start is by moving colorful plant-based foods to the center of the plate. If you’re interested in learning more about or test-driving a healthful vegan diet, please visit http://www.PhysiciansCommittee.org/diabetes.
“A major difference from other studies is that we advised a period of dietary weight loss with no increase in physical activity, but during the long-term follow up increased daily activity is important. Bariatric surgery can achieve remission of diabetes in about three-quarters of people, but it is more expensive and risky, and is only available to a small number of patients.”
Enriched with phytosterols, aloe vera can have an anti-hyperglycemic effect on the people with type 2 diabetics. Nutritionists suggest that it is a safe and natural source to alleviate fasting sugar levels in your blood. Also, you can prepare a mixture of turmeric, bay leaves, and aloe vera, this herbal medicine is said to control glucose in the blood.
FEED YOUR GUT BUGS, not just yourself. There are trillions of bugs that live in your gut – their health is critical in determining your health. Many studiesshow links between the state of your gut bugs (your microbiota) and type 2 diabetes. Start improving the health of your gut immediately by eating five servings of different coloured vegetables each day. The non digestible fibre in vegetables is the preferred food for your gut bacteria and when your gut bugs are happy, you will be happy. The wider the variety of colours, the more phytonutrients you will be getting.
Besides going raw and eliminating sugar out of your life, you must switch to raw milk or its alternatives. In the book, The Devil in the Milk, Dr. Kevin Woodford explains how the type of milk we drink, directly reflects of the high incidence of many diseases, including diabetes and cancers. There are many substitutes available from almond milk to oat milk. They are extremely healthy and easy to make.
The information on this website is provided as general health guidelines and may not be applicable to your particular health condition. Your individual health status and any required medical treatments can only be properly addressed by a professional healthcare provider of your choice. Remember: There is no adequate substitution for a personal consultation with your physician. Neither Desert Springs Hospital Medical Center, or any of their affiliates, nor any contributors shall have any liability for the content or any errors or omissions in the information provided by this website.
A wide scatter of absolute levels of pancreas triacylglycerol has been reported, with a tendency for higher levels in people with diabetes (57). This large population study showed overlap between diabetic and weight-matched control groups. These findings were also observed in a more recent smaller study that used a more precise method (21). Why would one person have normal β-cell function with a pancreas fat level of, for example, 8%, whereas another has type 2 diabetes with a pancreas fat level of 5%? There must be varying degrees of liposusceptibility of the metabolic organs, and this has been demonstrated in relation to ethnic differences (72). If the fat is simply not available to the body, then the susceptibility of the pancreas will not be tested, whereas if the individual acquires excess fat stores, then β-cell failure may or may not develop depending on degree of liposusceptibility. In any group of people with type 2 diabetes, simple inspection reveals that diabetes develops in some with a body mass index (BMI) in the normal or overweight range, whereas others have a very high BMI. The pathophysiologic changes in insulin secretion and insulin sensitivity are not different in obese and normal weight people (73), and the upswing in population rates of type 2 diabetes relates to a right shift in the whole BMI distribution. Hence, the person with a BMI of 24 and type 2 diabetes would in a previous era have had a BMI of 21 and no diabetes. It is clear that individual susceptibility factors determine the onset of the condition, and both genetic and epigenetic factors may contribute. Given that diabetes cannot occur without loss of acute insulin response to food, it can be postulated that this failure of acute insulin secretion could relate to both accumulation of fat and susceptibility to the adverse effect of excess fat in the pancreas.
The term diabetes includes several different metabolic disorders that all, if left untreated, result in abnormally high concentration of a sugar called glucose in the blood. Diabetes mellitus type 1 results when the pancreas no longer produces significant amounts of the hormone insulin, usually owing to the autoimmune destruction of the insulin-producing beta cells of the pancreas. Diabetes mellitus type 2, in contrast, is now thought to result from autoimmune attacks on the pancreas and/or insulin resistance. The pancreas of a person with type 2 diabetes may be producing normal or even abnormally large amounts of insulin. Other forms of diabetes mellitus, such as the various forms of maturity onset diabetes of the young, may represent some combination of insufficient insulin production and insulin resistance. Some degree of insulin resistance may also be present in a person with type 1 diabetes.
12. Consult a naturopathic, homeopathic, and/or Chinese medical doctor: Alternative practitioners are trained to treat the patient as a whole, organic being — not just their disease. This may help you develop a well-rounded treatment approach, as well as provide you with new information and perspectives on the disease and form of natural remedies for diabetes.
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.
In the twentieth century, insulin was available only in an injectable form that required carrying syringes, needles, vials of insulin, and alcohol swabs. Clearly, patients found it difficult to take multiple shots each day; as a result, good blood sugar control was often difficult. Many pharmaceutical companies now offer discreet and convenient methods for delivering insulin.
Although a close relationship exists among raised liver fat levels, insulin resistance, and raised liver enzyme levels (52), high levels of liver fat are not inevitably associated with hepatic insulin resistance. This is analogous to the discordance observed in the muscle of trained athletes in whom raised intramyocellular triacylglycerol is associated with high insulin sensitivity (53). This relationship is also seen in muscle of mice overexpressing the enzyme DGAT-1, which rapidly esterifies diacylglycerol to metabolically inert triacylglycerol (54). In both circumstances, raised intracellular triacylglycerol stores coexist with normal insulin sensitivity. When a variant of PNPLA3 was described as determining increased hepatic fat levels, it appeared that a major factor underlying nonalcoholic fatty liver disease and insulin resistance was identified (55). However, this relatively rare genetic variant is not associated with hepatic insulin resistance (56). Because the responsible G allele of PNPLA3 is believed to code for a lipase that is ineffective in triacylglycerol hydrolysis, it appears that diacylglycerol and fatty acids are sequestered as inert triacylglycerol, preventing any inhibitory effect on insulin signaling.
Another study published in the same journal, however, examined the effect of chromium on glycemic control in insulin-dependent people with type 2 diabetes. People were given either 500 or 1,000 mcg a day of chromium or a placebo for six months. There was no significant difference in glycosylated hemoglobin, body mass index, blood pressure, or insulin requirements across the three groups.
Storage of liver fat can only occur when daily calorie intake exceeds expenditure. Sucrose overfeeding for 3 weeks has been shown to cause a 30% increase in liver fat content (37). The associated metabolic stress on hepatocytes was reflected by a simultaneous 30% rise in serum alanine aminotransferase (ALT) levels, and both liver fat and serum ALT returned to normal levels during a subsequent hypocaloric diet. Superimposed upon a positive calorie balance, the extent of portal vein hyperinsulinemia determines how rapidly conversion of excess sugars to fatty acid occurs in the liver. In groups of both obese and nonobese subjects, it was found that those with higher plasma insulin levels have markedly increased rates of hepatic de novo lipogenesis (2,38,39). Conversely, in type 1 diabetes the relatively low insulin concentration in the portal vein (as a consequence of insulin injection into subcutaneous tissue) is associated with subnormal liver fat content (40). Initiation of subcutaneous insulin therapy in type 2 diabetes brings about a decrease in portal insulin delivery by suppression of pancreatic insulin secretion and, hence, a decrease in liver fat (41). Hypocaloric diet (42), physical activity (43), or thiazolidinedione use (23,44) each reduces insulin secretion and decreases liver fat content. Newly synthesized triacylglycerol in the liver will be either oxidized, exported, or stored as hepatic triacylglycerol. Because transport of fatty acid into mitochondria for oxidation is inhibited by the malonyl-CoA produced during de novo lipogenesis, newly synthesized triacylglycerol is preferentially directed toward storage or export. Hence, hepatic fat content and plasma VLDL triacylglycerol levels are increased.