According to TCM, the major activity of the blood is to circulate through the body, nourishing and moistening the various organs and tissues. Disharmonies of the blood may manifest as “deficient” blood or “congealed” blood. If deficient blood exists and affects the entire body, the patient may present with dry skin, dizziness, and a dull complexion. Congealed blood may manifest as sharp, stabbing pains accompanied by tumors, cysts, or swelling of the organs (i.e., the liver).4 The key organs associated with blood are the heart, liver, and spleen.

But does Darkes' story really mean type 1 diabetes can be cured? Darkes declined to provide his medical records, and the experts Live Science spoke to said there were several missing or confusing pieces of information in his story. Usually, incredible medical stories like this one are reported as case reports in the medical literature, the experts said. And even if the details of his story can ultimately be confirmed, the experts emphasized that it's extremely unlikely that Darkes' case would lead to a widespread cure for type 1 diabetes, as reports in the media have wrongly suggested.
Type 2 diabetes is by far the most common form (around 90% of all cases) and the one which is increasing the most. It primarily affects overweight people in middle age or later. It’s not uncommon for the affected person to also have a high blood pressure and an abnormal lipid profile. Gestational diabetes is a temporary special case of type 2 diabetes.
"What is interesting is that some patients retain beta cell function for over 50 years," he said. "And, it seems if you retain some, that's a lot better." So, for Darkes to still have some functioning beta cells would not be impossible, but it wouldn't eliminate the disease, Von Herrath said. "Depending on how many beta cells he has, maybe his form of type 1 diabetes was not very severe."
“The field has suffered from a checkered history 20, 30 years ago, when there were operations that were dangerous. But modern metabolic surgery is very safe,” Cummings said. “The risk of dying from a laparoscopic gastric bypass is a little bit less than the risk of dying from having your gallbladder or appendix removed. But we never consider those risky surgeries; they’re totally bread-and-butter procedures.”
It is great to read these columns of Diabetes. I have tried feenugreek but it raises my blood pressure. Since, I am a patient of High Blood pressure, this does not help me. I am 65, control my diet, walk daily for 6-7 km too and take my medication regularly but still blood sugar is out of control. Fasting is usually 150. Any suggestions from friends. Thanks and Cheers for all.
The bionic pancreas is another project from Boston University and Massachusetts General Hospital in a joint effort to create a bionic pancreas, a type of artificial pancreas which not only includes insulin but also glucagon to raise blood sugar. The system is intended to use an algorithm that checks every 5 minutes to calculate the amount of insulin or glucagon needed. The project has recently formed into a public benefit corporation called Beta Bionics. This newer structure allows it to serve not just shareholders, but also the public good. Beta Bionics also became the first American company to raise over a $1 million from small investors under new public investing rules!

One of the biggest hits in type 2 diabetes treatment is glucagon-like peptide (GLP)-1 receptor agonists, which induce insulin production in beta-pancreatic cells while suppressing the secretion of glucagon. All big pharma have GLP-1 drugs on the market or their pipelines, including Sanofi, Eli Lilly, Roche, AstraZeneca and Boehringer Ingelheim. But Novo Nordisk is going a step further with the first oral version of a GLP-1 drug, which is now close to the market.
So, let's understand why a cell does not accept the Insulin fast enough. A healthy cell has a Sodium:Potassium ratio of 1:8. This varies a little from person to person depending on the amount of activity he/she does. A diabetic cell on the other hand has a very bad ratio. Any naturally available food always has more Potassium and less Sodium. When heated, Potassium is lost but Sodium is retained. And we add more Sodium to the food in the form of salt. We only require about 500mg of Sodium per day for normal activities which is naturally available in all types of food even without adding in the form of salt. A person who does more physical activity as part of his job or is an athlete etc. will require more Sodium not exceeding 2000mg. On the other hand, Potassium requirement is around 4700mg.
Dr. Nyitray established Encellin soon after she received her PhD in chemistry and chemical biology from the University of California San Francisco in 2015. Her work at UCSF, with advisor Tejal Desai, PhD, chair of the Department of Bioengineering and Therapeutic Sciences in UCSF’s schools of Pharmacy and Medicine, focused on developing a packaging system for islet cells.
Whenever this seasonal fruit is available in the market, try to include it in your diet as it can be very effective for the pancreas. Else you can make a powder of dried seeds of Jambul fruit and eat this powder with water twice a day. This fruit is native to India and its neighboring countries but you can find it at Asian markets and herbal shops.

In obese young people, decreased β-cell function has recently been shown to predict deterioration of glucose tolerance (4,78). Additionally, the rate of decline in glucose tolerance in first-degree relatives of type 2 diabetic individuals is strongly related to the loss of β-cell function, whereas insulin sensitivity changes little (79). This observation mirrors those in populations with a high incidence of type 2 diabetes in which transition from hyperinsulinemic normal glucose tolerance to overt diabetes involves a large, rapid rise in glucose levels as a result of a relatively small further loss of acute β-cell competence (3). The Whitehall II study showed in a large population followed prospectively that people with diabetes exhibit a sudden rise in fasting glucose as β-cell function deteriorates (Fig. 5) (80). Hence, the ability of the pancreas to mount a normal, brisk insulin response to an increasing plasma glucose level is lost in the 2 years before the detection of diabetes, although fasting plasma glucose levels may have been at the upper limit of normal for several years. This was very different from the widely assumed linear rise in fasting plasma glucose level and gradual β-cell decompensation but is consistent with the time course of markers of increased liver fat before the onset of type 2 diabetes observed in other studies (81). Data from the West of Scotland Coronary Prevention Study demonstrated that plasma triacylglycerol and ALT levels were modestly elevated 2 years before the diagnosis of type 2 diabetes and that there was a steady rise in the level of this liver enzyme in the run-up to the time of diagnosis (75).


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 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.
Clearly separate from the characteristic lack of acute insulin secretion in response to increase in glucose supply is the matter of total mass of β-cells. The former determines the immediate metabolic response to eating, whereas the latter places a long-term limitation on total possible insulin response. Histological studies of the pancreas in type 2 diabetes consistently show an ∼50% reduction in number of β-cells compared with normal subjects (66). β-Cell loss appears to increase as duration of diabetes increases (67). The process is likely to be regulated by apoptosis, a mechanism known to be increased by chronic exposure to increased fatty acid metabolites (68). Ceramides, which are synthesized directly from fatty acids, are likely mediators of the lipid effects on apoptosis (10,69). In light of new knowledge about β-cell apoptosis and rates of turnover during adult life, it is conceivable that removal of adverse factors could result in restoration of normal β-cell number, even late in the disease (66,70). Plasticity of lineage and transdifferentiation of human adult β-cells could also be relevant, and the evidence for this has recently been reviewed (71). β-Cell number following reversal of type 2 diabetes remains to be examined, but overall, it is clear that at least a critical mass of β-cells is not permanently damaged but merely metabolically inhibited.
In 1991, the National Institutes of Health issued a consensus statement, cautiously recommending surgery as a treatment for people living with morbid obesity, meaning they have a body mass index, or BMI, over 40. For people who have health complications connected to obesity, such as type 2 diabetes, the limit goes down to a BMI of 35. Relying on these guidelines, insurance companies and public payers like Medicaid and Medicare typically only cover surgery for people living with diabetes who fall into that category.
Mechanism of interaction between excess amounts of fatty acids, diacylglycerol, and ceramide and insulin action within the hepatocyte. Diacylglycerol activates PKCε and inhibits activation of IRS-1 by the insulin receptor. Ceramides cause sequestration of Akt2 by PKCζ and inhibit insulin control of gluconeogenesis. These mechanisms have recently been reviewed (99). FFA, free-fatty acid; TG, triacylglycerol.
Complete with success stories featuring people who followed the plan and not only lost weight (up to 50 pounds) but were also no longer diagnosed as diabetic, the Diabetes Cure teaches readers what's really causing their diabetes, shows them how to banish cravings once and for all, and provides the tools to help them take back control of their lives.
There are many promising studies suggesting chromium supplementation may be effective, but they are far from conclusive. For example, a small study published in the journal Diabetes Care compared the diabetes medication sulfonylurea taken with 1,000 mcg of chromium to sulfonylurea taken with a placebo. After 6 months, people who did not take chromium had a significant increase in body weight, body fat, and abdominal fat, whereas people taking the chromium had significant improvements in insulin sensitivity.
It’s long been believed that the condition is manageable, but not curable. According to findings published in the journal The Lancet, however, type 2 diabetes can be reversed through weight loss. More specifically, by reducing the amount of fat being carried in and around the abdomen, as accumulated fat in this region impedes the function of the pancreas.
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.

Oral diabetes medications may also come in combination tablets such as Metaglip (glipizide/metformin), Prandimet (repaglinide/metformin), Glucovance (glyburide/metformin), Janumet (sitagliptin/metformin), Avandamet (rosiglitazone/metformin), Avandaryl (rosiglitazone/ glimepiride), Duetact (pioglitazone/glimepiride), Actoplus Met (pioglitazone/metformin).

Use any combination of the tricks below to accelerate your weight loss and return to good health. If you use all five wisely, you can get to your ideal weight in 6–12 months or less — even if that means losing 100 pounds or more. Yes, think about your weight 10, 20, 30 years ago. Another friend of mine started on this journey last year weighing 270 pounds. He’s in his mid-thirties and about to reach his college wrestling weight class of 197 pounds and just ran his fastest 2 miles ever. He got to this point by following the two rules above and just 3 of the 5 tricks below.
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