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).
Rosanna Keyes is a writer, editor, yoga teacher, and office manager extraordinaire living in the Asheville, NC area. She has a B.S.S. from Ohio University with concentrations in English Literature, Creative Writing, and Geography. She has been practicing yoga for over ten years and received her 200-hour teaching certification in 2013. Over the years yoga and writing have been important mainstays in her life. She is continually amazed and humbled at the deep healing, balance, and peace that comes from these practices, and she is grateful to be able to share those experiences with others.
In the study, Fung and his team randomly recruited three men, ages 40 to 67, with type 2 diabetes, who also had high cholesterol and high blood pressure. At the start of the study, the authors recorded the participants’ vitals, including their A1C (a three-month average of their blood sugar levels), their fasting blood glucose levels, their waist circumference, and their weight. All three men were on insulin and oral medication.
There has been a slew of studies done on the topic of alternative and naturopathic treatments and natural remedies for diabetes, and many of them exhibit long-lasting, beneficial results. While conventional medicine tends to treat only the symptoms of disease, alternative medicine focuses on both the underlying causes of the ailment, as well as the symptoms, evaluating the body as an interconnected whole.

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.
I'v seen the great importance of natural herbs and the wonderful work they have done. I wonder why people still spend thier resources on injection and drugs each time they are sick. There are some illness injection. Natural herbs can cure herpes, diabetics, asthma etc. Ive seen it with my own eyes. I known of a herbalist doctor who uses natural herbs to cure different kind of illness, i am a living testimony of it. If anyone here is suffering from any of the listed illness, let me know, i will direct you to where you will get your cure. Even if you are suffering with something you believe it has no cure, just email me on [email protected], You will be surprised by the positive result you will get from using natural herbs.
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.

In a person with carbohydrate intolerance, type 2 diabetes or prediabetes, this system breaks down. The body loses its insulin sensitivity and more and more insulin is required to remove the excess blood sugar. As a result, blood sugar levels remain high and insulin levels are high as well, and these high insulin levels can make your body even less sensitive to insulin.
Diabetes is a well-established problem and a multi-billion dollar industry. It is medically characterized by Fasting Blood Glucose higher than 126 mg/dL , which ranges between 100-125 mg/dL are considered pre-diabetic and ranges below 99 mg/dL are considered normal. Studies are finding that a fasting blood glucose below 83 mg/dL is actually a better benchmark, as risk of heart disease begins to increase at anything above that.
Ideally, insulin should be administered in a manner that mimics the natural pattern of insulin secretion by a healthy pancreas. However, the complex pattern of natural insulin secretion is difficult to duplicate. Still, adequate blood glucose control can be achieved with careful attention to diet, regular exercise, home blood glucose monitoring, and multiple insulin injections throughout the day..
Late in the 19th century, sugar in the urine (glycosuria) was associated with diabetes. Various doctors studied the connection. Frederick Madison Allen studied diabetes in 1909–12, then published a large volume, Studies Concerning Glycosuria and Diabetes, (Boston, 1913). He invented a fasting treatment for diabetes called the Allen treatment for diabetes. His diet was an early attempt at managing diabetes.
All carbohydrates – to some degree at least – will raise your blood insulin levels. That is why I consider type 2 diabetes a form of “carbohydrate intolerance”. Protein can also raise levels but to a much lesser degree. The only macronutrient that keeps your insulin levels and, therefore, your blood sugar stable is FAT! Therefore, if you are trying to reduce insulin levels, you need to reduce your amount of certain carbohydrates and replace them instead with healthy, natural fats.
How long will diabetes stay away after weight loss? Long-term normal blood glucose control in previously diabetic individuals after bariatric surgery demonstrates that diabetes does not recur for up to 10 years, unless substantial weight gain occurs (86). These observations are consistent with the twin cycle hypothesis and the existence of a trigger level for adverse metabolic effects of fat in the pancreas. Hence, for a given individual with type 2 diabetes, reducing the liver and pancreas fat content below his or her personal trigger levels would be expected to result in a release from the fatty acid–mediated dysfunction. Individual tolerance of different degrees of fat exposure vary, and understanding this liposusceptibility will underpin the future understanding of genetically determined risk in any given environment. However, this should not obscure the central point: If a person has type 2 diabetes, there is more fat in the liver and pancreas than he or she can cope with.
Cutting out the refined, processed starches and sugars, BG rebound into a normal range very quickly. My experience is when people begin to be more conscious of their food intake and physical activity, which happens immediately after being diagnosed with pre diabetes or diabetes, they begin to make better food choices and cut out the foods they know are not healthy.
Formal recommendations on how to reverse type 2 diabetes in clinical practice must await further studies. In the meantime, it will be helpful for all individuals with newly diagnosed type 2 diabetes to know that they have a metabolic syndrome that is reversible. They should know that if it is not reversed, the consequences for future health and cost of life insurance are dire, although these serious adverse effects must be balanced against the difficulties and privations associated with a substantial and sustained change in eating patterns. For many people, this may prove to be too high a price to pay, but for those who are strongly motivated to escape from type 2 diabetes, the new understanding gives clear direction. Physicians need to accept that long-term weight loss is achievable for a worthwhile proportion of patients (96). In the United States, diabetes costs $174 billion annually (97), and in the United Kingdom, it accounts for 10% of National Health Service expenditure. Even if only a small proportion of patients with type 2 diabetes return to normal glucose control, the savings in disease burden and economic cost will be enormous.
It’s like packing your clothes into a suitcase. At first, the clothes go without any trouble. After a certain point, though, it is just impossible to jam in those last 2 T-shirts. You can’t close the suitcase. The luggage is now ‘resistant’ to the clothes. It’s waaayyy harder to put those last 2 T-shirts than the first 2. It’s the same overflow phenomenon. The cell is filled to bursting with glucose, so trying to force more in is difficult and requires much higher doses of insulin.
The diabetes market is expected to reach a massively big €86Bn by 2025 combining both type 1 (€32Bn) and type 2 (€54Bn) treatments, and we can expect all sort of revolutionary technologies to come forward and claim their market share. Researchers are already speculating about microchips that can diagnose diabetes type 1 before the symptoms appear or nanorobots traveling in the bloodstream while they measure glucose and deliver insulin.
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).
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).

Primary Care Provider: Your primary care provider is the provider you see for general checkups or when you get sick. Your primary care provider may also be the one who refers you to specialists or other team members. Other health care providers who provide primary care include nurse practitioners and physician assistants, who typically work with a physician.
Among several home remedies for controlling diabetes, perhaps most vital is the bitter gourd. Bitter gourd contains a hypoglycemic or insulin-like principle, designated as 'plantinsulin', which is beneficial in lowering the blood and urine sugar levels. This property of bitter gourd it an excellent anti-diabetes agent. Consuming a glassful of bitter gourd juice first thing in the morning proves to be highly beneficial for diabetics. Also, it should be included generously in the diet of the diabetic. Remedy is also beneficial in long term and shows instant results. It is one of the best home remedies for diabetes.
Low blood sugar (hypoglycemia). If your blood sugar level drops below your target range, it's known as low blood sugar (hypoglycemia). Your blood sugar level can drop for many reasons, including skipping a meal, inadvertently taking more medication than usual or getting more physical activity than normal. Low blood sugar is most likely if you take glucose-lowering medications that promote the secretion of insulin or if you're taking insulin.
If your carb consumption is on the high side (once you add sugar into the mix, you’re most certainly on the high side), it’s stored as fat and you end up with insulin resistance or non-alcoholic fatty liver disease.[14] The reason behind it is that carbs metabolize into glucose, and limiting carbs helps your body control blood sugar more efficiently.[15][16] It improves overall blood sugar profiles, insulin sensitivity, and hemoglobin A1c, which is a diabetes marker.[17] Going low-carb is especially effective if you’re in the early stages when you do not yet need to administer insulin.[18]

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).

Type 1 diabetes is commonly called “juvenile diabetes” because it tends to develop at a younger age, typically before a person turns 20 years old. Type 1 diabetes is an autoimmune disease where the immune system attacks the insulin-producing beta cells in the pancreas. The damage to the pancreatic cells leads to a reduced ability or complete inability to create insulin. Some of the common causes that trigger this autoimmune response may include a virus, genetically modified organisms, heavy metals, vaccines, or foods like wheat, cow’s milk and soy. (4)
Focus on low glycemic index foods: While reducing fat and increasing fiber can significantly improve insulin sensitivity, low glycemic index (GI) foods reduce after-meal blood glucose levels. Low GI foods include pumpernickel or rye bread, oats, beans, bran cereals, most fruit, and sweet potatoes, compared to higher GI foods such as white potatoes, processed foods, and cold cereals.
When islet cells have been transplanted via the Edmonton protocol, insulin production (and glycemic control) was restored, but at the expense of continued immunosuppression drugs. Encapsulation of the islet cells in a protective coating has been developed to block the immune response to transplanted cells, which relieves the burden of immunosuppression and benefits the longevity of the transplant.[72]
Rosanna Keyes is a writer, editor, yoga teacher, and office manager extraordinaire living in the Asheville, NC area. She has a B.S.S. from Ohio University with concentrations in English Literature, Creative Writing, and Geography. She has been practicing yoga for over ten years and received her 200-hour teaching certification in 2013. Over the years yoga and writing have been important mainstays in her life. She is continually amazed and humbled at the deep healing, balance, and peace that comes from these practices, and she is grateful to be able to share those experiences with others.
"Perfect glycemic control" would mean that glucose levels were always normal (70–130 mg/dl, or 3.9–7.2 mmol/L) and indistinguishable from a person without diabetes. In reality, because of the imperfections of treatment measures, even "good glycemic control" describes blood glucose levels that average somewhat higher than normal much of the time. In addition, one survey of type 2 diabetics found that they rated the harm to their quality of life from intensive interventions to control their blood sugar to be just as severe as the harm resulting from intermediate levels of diabetic complications.[17]
NOTE: Do not eat or drink anything else during the three hours of testing. You may be able to get an accurate baseline of your insulin response after only a few days, but a week provides more data. If you are already diabetic, you probably have close ideas on these numbers, but take readings at the suggested times anyway to figure out your baseline.

These are a relatively new class of drugs used to treat type 2 diabetes. They are oral medications that work by blocking the kidneys' reabsorption of glucose, leading to increased glucose excretion and reduction of blood sugar levels. The US FDA approved the SGLT2 inhibitors canagliflozin (Invokana) in March 2013 and dapagliflozin (Farxiga) in January 2014.
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