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.
Omega 6 oils are also a relatively new addition to the diet, making their appearance in the early 1900s. Oils in this category include vegetable, canola, cottonseed, soybean, corn, safflower, sunflower, etc. Consumption of these oils increased in the 1950s when they were promoted as a “healthy” alternative to saturated fats (they weren’t). Research is now showing that consumption of these oils increases risk for obesity and can damage thyroid function. They contribute to insulin resistance and inflammation, further aggravating the poor pancreas.
Type 2 diabetes is the most common form of diabetes, and unlike type 1 diabetes, it usually occurs in people over the age of 40, especially those who are overweight. Type 2 diabetes is caused by insulin resistance, which means that the hormone insulin is being released, but a person doesn’t respond to it appropriately. Type 2 diabetes is a metabolic disorder that’s caused by high blood sugar. The body can keep up for a period of time by producing more insulin, but over time the insulin receptor sites burn out. Eventually, diabetes can affect nearly every system in the body, impacting your energy, digestion, weight, sleep, vision and more. (5)
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).
Sugars raise insulin levels, and over extended periods of time, damage the pancreas and cause insulin resistance, a precursor for diabetes. Fructose is the top offender in the sugar world, as it is recognized as a toxin the body and has no proven benefit to the body. Fructose is immediately taken to the liver, where it must be processed, and some doctors now suggest that this may be a large factor in development of fatty liver disease. Excess sugar in the bloodstream also increases the release of cortisol and adrenaline (more on those in a minute), slows the immune response, decreases necessary Leptin levels and promotes fat storage. There are various types of sugar and sweeteners, and while all should be limited, some are worse than others:
Diabetes is a costly disease, placing a high financial burden on the patient and the healthcare system. If poorly managed or left untreated, it can cause blindness, loss of kidney function, and conditions that require the amputation of digits or limbs. The CDC reports that it’s also a major cause of heart disease and stroke and the seventh leading cause of death in the United States.
The only way to effectively reverse type 2 diabetes (or even pre-diabetes) is to deal with the underlying cause – Insulin Resistance. Trying to address the blood sugar levels (with medication) without addressing the insulin levels is treating the symptoms, not treating the root cause. It is similar to using a bucket to remove water from an overflowing sink rather than actually turning off the tap!
As of now, diabetes is classified as either Type I or Type II. New research suggests there are several more types of diabetes, which all require different treatment approaches, but that’s a developing area of knowledge. On an episode of Bulletproof Radio, Dr. Steven Masley explains why doctors are starting to view Altzheimer’s disease as “type III diabetes” and picks apart the relationship between insulin and brain degeneration. Listen to it on iTunes.
Jump up ^ Qaseem A, Vijan S, Snow V, Cross JT, Weiss KB, Owens DK; Vijan; Snow; Cross; Weiss; Owens; Clinical Efficacy Assessment Subcommittee of the American College of Physicians (September 2007). "Glycemic control and type 2 diabetes mellitus: the optimal hemoglobin A1c targets. A guidance statement from the American College of Physicians". Annals of Internal Medicine. 147 (6): 417–22. doi:10.7326/0003-4819-147-6-200709180-00012. PMID 17876024. Retrieved 19 July 2008.
Jump up ^ Inzucchi, SE; Bergenstal, RM; Buse, JB; Diamant, M; Ferrannini, E; Nauck, M; Peters, AL; Tsapas, A; Wender, R; Matthews, DR (March 2015). "Management of hyperglycaemia in type 2 diabetes, 2015: a patient-centred approach. Update to a Position Statement of the American Diabetes Association and the European Association for the Study of Diabetes". Diabetologia. 58 (3): 429–42. doi:10.1007/s00125-014-3460-0. PMID 25583541.
I’m glad you talk about personal tolerance. My doc wants me to go on a ketogenic diet, but even when on the Autoimmune Paleo Diet, my adrenals would go a bit nuts. I can’t go any longer than 6 hours without food overnight…my adrenals start pumping out the adrenalin after about 3 to 6 hours of sleep (no matter what I eat or don’t eat before bed) and I wake up with anxiety. Adding a bit of carbs (3/4 cup at dinner and 1/2 cup at lunch) has allowed me to go a full 6 hours (would love 7 or 8) but it still feels terrible when I wake up.
“Our findings suggest that even if you have had type 2 diabetes for six years, putting the disease into remission is feasible”, says Prof Michael Lean from the University of Glasgow who co-led the study. “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 optimise individual results.”
Even if you don’t have any underlying glucose issues, testing your blood sugar occasionally will help you pin point which carbohydrates you tolerate well and which you don’t. It can help you have a better understanding of your body’s reaction to foods and take control of your health. It is also an accurate alternative to the pregnancy test for gestational diabetes, so talk to your doctor if you’d prefer to test yourself, though you may have to explain your reasons!
These substances are not considered to be medications by the US FDA and are therefore not regulated as such. This means that there are no standards in place to ensure that a given product contains the substance or dose as described on the label. There are also no requirements to perform studies showing that the products are safe or effective. Side effects of supplements are typically not well understood, and some supplements can interfere with the action of medications.
Another crucial element in a treatment program for diabetes is exercise. With either type of diabetes, check with your doctor before starting an exercise program. Exercise improves your body's use of insulin and may lower blood sugar levels. To prevent your blood sugar from falling to dangerously low levels, check your blood sugar and, if necessary, eat a carbohydrate snack about half an hour before exercising. If you start to feel symptoms of low blood sugar (called hypoglycemia), stop exercising and have a carbohydrate snack or drink. Wait 15 minutes and check again. Have another snack again if it is still too low.
Grains: Grains, especially gluten-containing grains like wheat, contain large amounts of carbohydrates that are broken down into sugar within only a few minutes of consumption. Gluten can cause intestinal inflammation, which affects hormones like cortisol and leptin, and can lead to spikes in blood sugar. I recommend removing all grains from your diet for 90 days as your body adjusts to this healing program. Then you can try bringing sprouted ancient grains back into your diet in small amounts.
If I could only prescribe one supplement for a diabetes patient, I would prescribe R-alpha-lipoic acid. Alpha-lipoic acid has numerous benefits to the diabetic patient. It is a water- and fat-soluble antioxidant and has been shown to protect patients with fatty liver from liver disease progression. It can help reduce insulin resistance and has been shown to protect people with diabetes from developing complications in their nerves, eyes, and kidneys. R-ALA can prevent glycosylation of proteins, which reduces the A1C level. It is safe, although very rarely it can cause stomach upset. Alpha-lipoic acid is listed either as ALA or R-ALA. When listed as ALA, this means it contains two forms—the S isomer form and the R isomer form, in a 50:50 ratio. The key is to find a product that says it contains “R-ALA” instead of just “ALA.” A good daily working dose of R-ALA is 300 to 1,200 mg a day, which is the equivalent of 600 to 2,400 mg a day of regular ALA, if you buy a regular ALA listed product.
Big pharma are in the early stages of developing their own cell therapy approaches for diabetes. Novo Nordisk, one of the largest providers of diabetes treatments, is bidding for stem cells and an encapsulation device, stating that the first clinical trial could take place in the “next few years.” Sanofi, also a big name in diabetes, is working with the German Evotec in a beta cell replacement therapy for diabetics.
Dr. Sarah Hallberg is a Medical Director at Virta Health. She also created the Medically Supervised Weight Loss Program at Indiana University Health Arnett and serves as its Medical Director. She is an adjunct Clinical Professor of Medicine at Indiana University School of Medicine. Dr. Hallberg is an expert in diabetes care and is board certified in Internal Medicine, Obesity Medicine, and Clinical Lipidology and also a Registered Clinical Exercise Physiologist from the ACSM.
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Patients with type 1 diabetes mellitus require direct injection of insulin as their bodies cannot produce enough (or even any) insulin. As of 2010, there is no other clinically available form of insulin administration other than injection for patients with type 1: injection can be done by insulin pump, by jet injector, or any of several forms of hypodermic needle. Non-injective methods of insulin administration have been unattainable as the insulin protein breaks down in the digestive tract. There are several insulin application mechanisms under experimental development as of 2004, including a capsule that passes to the liver and delivers insulin into the bloodstream. There have also been proposed vaccines for type I using glutamic acid decarboxylase (GAD), but these are currently not being tested by the pharmaceutical companies that have sublicensed the patents to them.
A spice that is popular for soothing your stomach and aiding digestion, Ginger also has the ability to normalize blood sugar levels. Multiple studies conducted on rats show that ginger extract can have a significant anti-hyperglycemic effect. It lowers serum total cholesterol, triglycerides and increases the HDL-cholesterol levels. Diabetes is a digestive disorder. Diabetics often face issues with acid reflux. Ginger soothes the entire digestive tract, giving diabetics another reason to add ginger to their supplement regimen.
The diagnosis of diabetes, and the effectiveness of treatments can be objectively measured. Fasting plasma glucose (FPG) measurements and then the oral glucose tolerance test accurately measure insulin function, and guide diagnosis. While routine blood sugar monitoring (with test strips) is generally unnecessary in Type 2 diabetes, measurement gives a point estimate of blood sugar levels. Glyclated hemoglobin (A1C) levels reflect overall blood sugar trends, with higher levels associated with more complications of the disease. Interestingly, super-intensive blood glucose lowering isn’t associated with additional risk reduction, and it increases the risk of side effects due to too-low blood sugar. Treatment goals are individualized (hey, it’s “holistic”), balancing a number of factors including risks as well as a patient’s ability to manage complex treatment plans.
Recent research shows that the first step in Diabetes management should be for patients to be put on a low carb diet. Patients that are put on a high carb diet find it very difficult to maintain normal blood glucose levels. Patients that are put on a low carb or restricted carbohydrate diet, manage to maintain near normal blood glucose levels and A1cs.
The medications only hide the blood sugar by cramming it into the engorged body. The diabetes looks better, since you can only see the blood sugars. Doctors can congratulate themselves on a illusion of a job well done, even as the patient gets continually sicker. Patients require ever increasing doses of medications and yet still suffer with heart attacks, congestive heart failure, strokes, kidney failure, amputations and blindness. “Oh well” the doctor tells himself, “It’s a chronic, progressive disease”.
He emphasizes lifestyle changes and weight loss as a first step. "We give them a 3-month trial of diet and lifestyle [modification] before starting medications," he says. "A lot of times, for many patients newly diagnosed, we will see the sugars melt back into the normal range" after the weight loss and other changes. He has seen it happen after a weight loss of 7% to 10% of their starting weight.
These are two lifestyle changes that are easy to do if you put your mind into it. Does it work though? If it does, how can you go about doing this or where should you start? We reached out to 28 experts in the field who spilled the beans to us about the reversal of diabetes type 2 and whether it is a myth or a reality. To find out more, please keep reading.
Like trials with any other supplement or herbal product, the primary question we must answer is “What exactly was studied?”. The cinnamon you have in your kitchen may be a single species of plant or a mix of different cultivars. Ceylon cinnamon (Cinnamommum verum) is more commonly found in the West. Cassia cinnamon (Cinnamomum aromaticum) is the version of cinnamon that’s been studied in trials. The chemical hydroxychalcone has been identified as a potential active ingredient, which is believed to modify the sensitivity of cells to insulin, enhancing their uptake. If that’s the true mechanism of action, then it would work in a manner similar to that of the drugs Avandia, Actos, and metformin (Glucophage). Given the active ingredient (or ingredients) have not yet been definitively isolated, the issue of studying cinnamon is problematic. There’s no way to assess the potency of any batch, which complicates any evaluation. And that may be a reason why the research with cinnamon is inconsistent and largely disappointing.
I would love to hear what you have to say about a person that is 5’5″ and 110 lbs. My blood sugar was was in the 90s to 112 when fasting. My A1C was 5.7. So I started to eat less carbs but my A1C stayed elevated. I was then diagnosed with Glucose intolerance and prescribed Tradjenta 5mg. I also read several books on the subject and came across your TEDTalk video. I then adjusted my low carb eating and on the meds since 2017. I still need the meds to maintain my A1C at 5.2.
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).
Robert Ferry Jr., MD, is a U.S. board-certified Pediatric Endocrinologist. After taking his baccalaureate degree from Yale College, receiving his doctoral degree and residency training in pediatrics at University of Texas Health Science Center at San Antonio (UTHSCSA), he completed fellowship training in pediatric endocrinology at The Children's Hospital of Philadelphia.