The BAS colesevelam (Welchol) is a cholesterol-lowering medication that also reduces blood glucose levels in patients with diabetes.  BASs help remove cholesterol from the body, particularly LDL cholesterol, which is often elevated in people with diabetes.  The medications reduce LDL cholesterol by binding with bile acids in the digestive system; the body in turn uses cholesterol to replace the bile acids, which lowers cholesterol levels. The mechanism by which colesevelam lowers glucose levels is not well understood. Because BASs are not absorbed into the bloodstream, they are usually safe for use by patients who may not be able to use other medications because of liver problems. Because of the way they work, side effects of BASs can include flatulence and constipation.
Diabetes is a group of diseases characterized by elevated blood glucose levels due to defects in insulin secretion, insulin action, or both. According to the American Diabetes Association (ADA), type 2 diabetes usually begins with insulin resistance. For those people whose bodies resist insulin, the pancreas secretes extra insulin to maintain normal glucose levels. As the condition progresses, insulin production gradually decreases and eventually reaches a level of deficiency that can no longer maintain blood glucose in the normal range. But how type 2 diabetes presents and progresses can vary considerably, as noted by the ADA, and methods of treatment can vary from patient to patient.
“I am extremely pleased to see that technology developed in Tejal Desai’s group is getting to the point that we can explore this for therapeutic purposes,” Matthias Hebrok, PhD, the director of the Diabetes Center at UCSF and a member of Encellin’s scientific advisory board, noted on the UCSF website. “Encapsulation and protection of islet cells remain a critical hurdle that needs to be overcome before cell therapy becomes a reality in type 1 diabetes.”
In adults, a rare side effect of taking diabetes pills is lactic acidosis, a very serious condition caused by a buildup of lactic acid in the blood. Lactic acidosis can cause symptoms like rapid breathing, muscle pain, cool and clammy skin, sweet-smelling breath, nausea, and vomiting. This problem has mostly happened in elderly people who have other medical problems in addition to their diabetes.
A new study from the Faustman Lab at Massachusetts General Hospital suggests that a nearly 100 year old tuberculosis vaccine called BCG may hold cure-like promise  for people  with Type 1 diabetes. The bacillus Calmette-Guérin (BCG) vaccine, one of the oldest vaccines in the world, was developed for tuberculosis protection and for early stage bladder cancer therapy. 
High blood sugar (hyperglycemia). Your blood sugar level can rise for many reasons, including eating too much, being sick or not taking enough glucose-lowering medication. Check your blood sugar level often, and watch for signs and symptoms of high blood sugar — frequent urination, increased thirst, dry mouth, blurred vision, fatigue and nausea. If you have hyperglycemia, you'll need to adjust your meal plan, medications or both.
All you need to know about insulin sensitivity factor Insulin sensitivity factor is a measurement that describes how blood sugar levels are affected by taking 1 unit of insulin. It can help a person with type 1 diabetes regulate their blood sugar levels. Learn more about what insulin sensitivity factor is, who should test and when, and what the results mean. Read now
The study included 298 patients, aged 20 to 65, who had been diagnosed with type 2 diabetes within the previous six years. Half of the patients were put on a low-calorie diet and lost an average of 10 to 15 kg (22 to 33 pounds). The other half of patients, who served as a control group, received the best diabetes management available — but that did not include a weight loss program.
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Random blood sugar test. A blood sample will be taken at a random time. Blood sugar values are expressed in milligrams per deciliter (mg/dL) or millimoles per liter (mmol/L). Regardless of when you last ate, a random blood sugar level of 200 mg/dL (11.1 mmol/L) or higher suggests diabetes, especially when coupled with any of the signs and symptoms of diabetes, such as frequent urination and extreme thirst.

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.


Who is at risk of developing prediabetes? A well-known paper published in the Lancet in 2010 recommends screening for type 2 diabetes (which would also screen for prediabetes) every 3-5 years in all adults over the age of 45, regardless of other risk factors. Overweight and obese adults (a BMI >25 kg/m2) are also at significantly greater risk for developing prediabetes, as well as people with a family history of type 2 diabetes.
A newer class of diabetes medication, SGLT2 includes three medicines: canagliflozin, dapagliflozin, and empagliflozin. These drugs remove extra sugar from your body by blocking it from the kidneys. It also causes your body to be more sensitive to insulin. The most common side effects caused by SGLT2 are vaginal yeast infections and urinary tract infections.
During this 8-week study, β-cell function was tested by a gold standard method that used a stepped glucose infusion with subsequent arginine bolus (21). In type 2 diabetes, the glucose-induced initial rapid peak of insulin secretion (the first phase insulin response) typically is absent. This was confirmed at baseline in the study, but the first phase response increased gradually over 8 weeks of a very-low-calorie diet to become indistinguishable from that of age- and weight-matched nondiabetic control subjects. The maximum insulin response, as elicited by arginine bolus during hyperglycemia, also normalized. Pancreas fat content decreased gradually during the study period to become the same as that in the control group, a time course matching that of the increase in both first phase and total insulin secretion (Fig. 3). Fat content in the islets was not directly measured, although it is known that islets take up fat avidly (24) and that islet fat content closely reflects total pancreatic fat content in animal models (25). Although a cause-and-effect relationship between raised intraorgan fat levels and metabolic effect has not yet been proven, the time course data following the dietary intervention study are highly suggestive of a causal link (21).
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).
I think I may have the link to the original article and will post back here. I am actually going to meet Denise Faustman on 8/13 at 3:00 to learn more about the study It’s a clinical trial that is being held at mass general. I am surprised by the rather negative comments on here. I have lupus and type 1for 32years. I have no complications but lupus puts the same organs at risk as diabetes does. If I can barely take any insulin and have normal ranges without doing barely any work I will try it. I don’t see… Read more »

A new class of medications called DPP-4 inhibitors help improve A1C without causing hypoglycemia. They work by by preventing the breakdown of a naturally occurring compound in the body, GLP-1. GLP-1 reduces blood glucose levels in the body, but is broken down very quickly so it does not work well when injected as a drug itself. By interfering in the process that breaks down GLP-1, DPP-4 inhibitors allow it to remain active in the body longer, lowering blood glucose levels only when they are elevated. DPP-4 inhibitors do not tend to cause weight gain and tend to have a neutral or positive effect on cholesterol levels. Alogliptin (Nesina), linagliptin (Tradjenta), saxagliptin (Onglyza), and sitagliptin (Januvia) are the DPP-4 inhibitors currently on the market in the US.
What can people with prediabetes do to avoid the progression from prediabetes to type 2 diabetes? The most important action people diagnosed with prediabetes can take is to focus on living a healthy lifestyle. This includes making healthy food choices, controlling portions, and increasing physical activity. Regarding weight control, research shows losing 5-7% (often about 10–20 lbs.) from your initial body weight and keeping off as much of that weight over time as possible is critical to lowering the risk of type 2 diabetes. This task is of course easier said than done, but sustained weight loss over time can be key to improving health and delaying or preventing the onset of type 2 diabetes.
We live in a world where prescription medicine is getting more and more expensive as well as controversial. Alternative medicine is gaining momentum and with good reason! The same is true for treatments for diabetes type 2. You have therapies that can reverse diabetes through lifestyle and diet changes, natural supplements that can help stabilize blood sugar levels, and also herbs that lower blood sugar. Not only are these alternative therapies safer, but they are also easier on your pocket, on your body and mind.
Initial clinical trial results, published in a 2012 PLOS One paper, reported that two doses of BCG spaced four weeks apart led to reductions in autoreactive T cells, an increase in Tregs and what turned out to be a transient increase in insulin production. But by the end of that short, 20-week trial, there was no reduction in HbA1c, the established measure of blood sugar levels over time. An extension and expansion of that trial with long term follow-up, the current results are based on data from 282 human study participants – 52 with type 1 diabetes who participated in the BCG clinical trials and 230 who contributed blood samples for mechanistic studies.
There are numerous studies of botanical medicines and herbs for diabetes that speak to the effectiveness of natural and home remedies for diabetes. I have listed the most useful herbs with the most documented benefits. A patient does not need to take one hundred bottles a day of everything out on the market, but rather it is important to focus on a few botanicals backed by the most impressive studies and the best clinical evidence. The botanicals listed below are safe and effective.

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It was the same endorsement the first Diabetes Surgery Summit, also organized by Cummings in 2007, had made, but the landscape had changed since then. In addition to more accumulated research, this time, their stance was backed by over 50 international professional organizations, including the American Diabetes Association. And while other medical societies and organizations had long backed surgery as an option for diabetes, the DSS-II guidelines are the first meant to guide clinical practice.
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.

Online diabetes prevention programs: The CDC has now given pending recognition status to three digital prevention programs: DPS Health, Noom Health, and Omada Health. These offer the same one year long educational curriculum as the DPP study, but in an online format. Some insurance companies and employers cover these programs, and you can find more information at the links above. These digital versions are excellent options for those who live far away from NDPP locations or who prefer the anonymity and convenience of doing the program online.
"You only need 10 percent of your beta cells to supply sufficient insulin," Roep said. He said there have been a couple of rare cases where a patient had typical type 1 diabetes but could go through long periods without insulin injections. "Insulin needs can be a moving target, and if you have a lifestyle change it's very plausible that you have a lesser need for insulin, and you can deal with [diabetes] with the beta cells you have," Roep said.
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).
How to prevent type 2 diabetes: Six useful steps What are the risks factors for developing type 2 diabetes, and how can we prevent it? Some factors such as blood sugar levels, body weight, fiber intake, and stress can be controlled to some extent, but others, such as age and family history cannot. Find out more about reducing the risk of developing this condition. Read now

Meanwhile, other scientists are studying fenugreek seeds, a folk remedy for diabetes. Several studies, including one published in 1990 in the European Journal of Clinical Nutrition suggest that this herb can lower blood sugar. Researchers found that type 1 diabetics who took 50 grams of fenugreek seed powder twice daily had significantly lower blood sugar levels than those who took a placebo.
Herbal products are not well controlled by government. They may not be what the bottle says they are. According to Rodale Press, research by the U.S. Food and Drug Administration and the Canadian government both found that many combination herbal capsules contained NONE of the herbs listed on the label. That’s why I mainly recommend plants you can buy and use in their whole form, such as ginger, cinnamon, bitter melon, and okra.
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This class of drugs pulls double-duty. The medicine in this class, colesevelam, lowers cholesterol and reduces blood sugar levels. So it could be a good choice if you have diabetes and high cholesterol levels. And because these drugs are not absorbed in the blood stream, they may be the best choice for someone who also has liver problems and cannot take some of the other diabetes medicines. Side effects from bile acid sequestrants can include constipation and flatulence (gas).

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.
The earliest predictor of the development of type 2 diabetes is low insulin sensitivity in skeletal muscle, but it is important to recognize that this is not a distinct abnormality but rather part of the wide range expressed in the population. Those people in whom diabetes will develop simply have insulin sensitivity, mainly in the lowest population quartile (29). In prediabetic individuals, raised plasma insulin levels compensate and allow normal plasma glucose control. However, because the process of de novo lipogenesis is stimulated by higher insulin levels (38), the scene is set for hepatic fat accumulation. Excess fat deposition in the liver is present before the onset of classical type 2 diabetes (43,74–76), and in established type 2 diabetes, liver fat is supranormal (20). When ultrasound rather than magnetic resonance imaging is used, only more-severe degrees of steatosis are detected, and the prevalence of fatty liver is underestimated, with estimates of 70% of people with type 2 diabetes as having a fatty liver (76). Nonetheless, the prognostic power of merely the presence of a fatty liver is impressive of predicting the onset of type 2 diabetes. A large study of individuals with normal glucose tolerance at baseline showed a very low 8-year incidence of type 2 diabetes if fatty liver had been excluded at baseline, whereas if present, the hazard ratio for diabetes was 5.5 (range 3.6–8.5) (74). In support of this finding, a temporal progression from weight gain to raised liver enzyme levels and onward to hypertriglyceridemia and then glucose intolerance has been demonstrated (77).
In investigating how BCG administration produces its beneficial effects, the research team identified a mechanism never previously seen in humans in response to treatment with any drug – a shifting of the process of glucose metabolism from oxidative phosphorylation, the most common pathway by which cells convert glucose into energy, to aerobic glycolysis, a process that involves significantly greater glucose consumption by cells. The researchers also found that BCG could reduce blood sugar elevations in mice that were caused by means other than autoimmune attack, raising the possibility that BCG vaccines could also be beneficial against type 2 diabetes.”
Type 2 diabetes is a completely preventable and reversible condition, and with diet and lifestyle changes, you can greatly reduce your chances of getting the disease or reverse the condition if you’ve already been diagnosed. If you are one of the millions of Americans struggling with diabetes symptoms, begin the steps to reverse diabetes naturally today. With my diabetic diet plan, suggested supplements and increased physical activity, you can quickly regain your health and reverse diabetes the natural way.
The researchers concluded that the herb might help treat or prevent type 2 diabetes. They noted that S. oblonga appears to act in the same way as today’s oral diabetes drugs (alpha-glucoside inhibitors) in interfering with the absorption of carbohydrates. S. oblonga is not free of side effects, however. It can cause the same gas and cramping as the prescription drugs, particularly in higher doses.
John’s naturopath, Susan DeLaney, ND, RN, from The Wellness Alliance in Carrboro, North Carolina, considers diabetes to be reversed when an individual is no longer dependent on medication to maintain blood glucose levels within a fairly normal range. Kathie Madonna Swift, MS, RD, LDN, owner of Swift Nutrition and author of The Inside Tract: Your Good Gut Guide to Great Digestive Health, describes reversal of diabetes as “restoring function and bringing the body back into glycemic balance.”
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.
Diabetes is a group of diseases characterized by elevated blood glucose levels due to defects in insulin secretion, insulin action, or both. According to the American Diabetes Association (ADA), type 2 diabetes usually begins with insulin resistance. For those people whose bodies resist insulin, the pancreas secretes extra insulin to maintain normal glucose levels. As the condition progresses, insulin production gradually decreases and eventually reaches a level of deficiency that can no longer maintain blood glucose in the normal range. But how type 2 diabetes presents and progresses can vary considerably, as noted by the ADA, and methods of treatment can vary from patient to patient.
You might hear of alternative or complementary treatments, such as herbal remedies and vitamin or mineral supplements. Although research continues into their possible benefits, studies thus far haven't proved their effectiveness. They also could be dangerous for kids and teens with type 1 diabetes, especially if used to replace medically recommended treatments. Talk to the diabetes health care team if you have questions.
In some kids with diabetes, repeated insulin injections can cause a thickening or lumpiness of the fatty tissue beneath the skin, called lipodystrophy (or lipohypertrophy). This is more likely if injections are given in the same area again and again rather than in different injection sites as recommended. Usually, this is only a cosmetic problem. But in some cases, insulin injected in areas of skin with lipodystrophy may not be absorbed into the bloodstream as it should. This can make the insulin dose take longer than usual to work.
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).
People with diabetes are unable to control the level of sugar in their blood, usually due to a breakdown in how their bodies use the hormone insulin. It’s not completely clear how obesity can contribute to diabetes, but it is known that excess weight is associated with chronic inflammation and a dysfunctional metabolism. And these factors in turn make it easier for someone to stop responding to the presence of insulin as easily as they once did. So by using surgery to help very obese people with diabetes lose weight, the logic goes, you can indirectly treat or prevent the condition. But doctors such as David Cummings, a senior investigator at the University of Washington’s Diabetes & Obesity Center of Excellence, are pushing back against this way of thinking.
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