Currently, there is no cure for Type 1 diabetes, but it can be treated successfully by administering insulin, either by an injection or pump, and by following a healthy, balanced diet and getting regular physical activity. Looking after diabetes requires planning and attention, which may feel overwhelming at times, especially when your child is first diagnosed. However, there’s no reason for it to stop your child living the healthy, happy and successful life you had hoped for them.
When evaluating patients with a chronic illness such as diabetes, TCM practitioners take a detailed, multi-system case history and supplement this information with observations that give information about the state of the patient’s health. These observations include the shape, color, and coating of the tongue; the color and expression of the face; the odor of the breath and body; and the strength, rhythm, and quality of the pulse. Many practitioners will palpate along meridians to detect points of tenderness that may indicate a blockage in the flow of Qi at that point.6
Some of the above drugs are available in compound form, and there are many patients taking three to four of them to control their blood sugar. But again, "the most common duo is metformin and a sulfonylurea,” says Arti Bhan, MD, division head of endocrinology at Henry Ford Health System in Detroit. “Metformin makes the body utilize insulin more effectively, and the sulfonylurea works on the pancreas to make more insulin in response to food consumption. Another common combination is metformin and insulin.”

Meanwhile, American Diabetes Scientist Zhen Gu, PhD, a professor in the Joint University of North Carolina/North Carolina State University Department of Biomedical Engineering, is working to develop a “smart insulin” patch that imitates the body's beta cells by both sensing blood glucose levels and releasing insulin using a nanotechnology that leverages bioengineering, biochemistry and materials science.


The fact these improvements can happen independently of weight loss should also signify a shift in how we conceptualize both obesity and diabetes, according to Peter Billings, the Seattle bariatric surgeon who operated on Benari. Billings, a nearly 20-year veteran in the field, has started to perform surgery on other lower-BMI patients similar to Benari, though they often pay out of pocket.

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).
The new study showed that a diet of 825–853 calories per day over a period of 3 to 5 months, followed by a gradual reintroduction of food in the next two to eight weeks, could have a profound impact. “Our findings suggest that even if you have had type 2 diabetes for six years, putting the disease into remission is feasible,” University of Glasgow professor Michael Lean, co-lead researcher, explained to The Guardian. “In contrast to other approaches, we focus on the need for long-term maintenance of weight loss through diet and exercise and encourage flexibility to optimize individual results.”
So, are Tory MPs still going to bury their collective heads in the sand and pretend that this deal:1) In any way resembles 'LEAVE THE EU', as we voted for? 2) Does not deliver the UK to EU vassalage, and by doing so sells out the integrity of the union?3) Does not surrender so many key UK rights, such as fishing territories and the ability to make trade deals, as to WORSEN our current situation, which itself was unacceptable to the people?
Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.
Change in fasting plasma glucose (A), 2 h post-oral glucose tolerance test (B), and homeostasis model assessment (HOMA-B) insulin secretion (C) during the 16-year follow-up in the Whitehall II study. Of the 6,538 people studied, diabetes developed in 505. Time 0 was taken as the diagnosis of diabetes or as the end of follow-up for those remaining normoglycemic. Redrawn with permission from Tabák et al. (80).
Green tea contains the bioflavinoid epigallocatechin gallate (EGCG), which has been shown to be a safe and effective antioxidant. In a study in Japan, green tea was shown to reduce the risk for Type 2 Diabetes Mellitus onset. It has been shown to improve glucose tolerance in patients, and decrease blood sugar production and over-secretion in Type 2 Diabetes Mellitus patients. Green tea has also been shown to have an effective anti-angiogenesis factor, that is, it reduces problematic overgrowth of blood vessels, which may have a significant effect on preventing diabetic retinopathy. It has also been shown to promote fat oxidation and thermogenesis. Last, green tea can provide antioxidant protection for the pancreas and the fatty liver. A good dose is 200 to 400 mg a day. It’s also beneficial to drink organic green tea.

There are many drugs available to treat type 2 diabetes. Your diabetes care team can help you understand the differences among the types of medication on this long list, and will explain how you take them, what they do, and what side effects they may cause. Your doctor will discuss your specific situation and your options for adding one or more types of medication to your treatment.


The study, published in Diabetes Care, measured C-peptide, which is produced at the same time and in the same quantities as the insulin that regulates our blood sugar. By measuring C-peptide levels in blood or in urine, scientists can tell how much insulin a person is producing themselves, even if they are taking insulin injections as treatment. The team studied 1,549 people with Type 1 diabetes from Exeter, England and Tayside, Scotland in the UNITED study.
Trick (most important): Go for longer periods of time without eating (yes, yes, fasting). Consume water only for days or weeks at a time. Your fat will literally dissolve away, and with it your type 2 diabetes and other ailments. The definitive book here is Dr. Joel Fuhrman’s book, Fasting and Eating for Health: A Medical Doctor’s Program for Conquering Disease. I highly recommend it; if you’re skeptical, read the 200+ testimonial comments on Amazon. I and at least 20 of my friends have tried fasts lasting days to weeks. It works, and it is amazing.
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