I have been suffering with diabetes since 2008. In the beginning of my being diagnosed I was in control of it. but now it seems that nothing works. I have lost 36 lbs. and still nothing. I can drink one soda one eat a cookie and my sugar will sky rocket. Please tell me what I can do the get this under control. There is a lot of good info here. I will be starting with the gooseberry juice tomorrow
Diabetes type 1 is caused by the destruction of enough beta cells to produce symptoms; these cells, which are found in the Islets of Langerhans in the pancreas, produce and secrete insulin, the single hormone responsible for allowing glucose to enter from the blood into cells (in addition to the hormone amylin, another hormone required for glucose homeostasis). Hence, the phrase "curing diabetes type 1" means "causing a maintenance or restoration of the endogenous ability of the body to produce insulin in response to the level of blood glucose" and cooperative operation with counterregulatory hormones.
As diabetes management is affected by an individual's emotional and cognitive state, there has been evidence suggesting the self-management of diabetes is negatively affected by diabetes-related distress and depression. There is growing evidence that there is higher levels of clinical depression in patients with diabetes compared to the non-diabetic population. Depression in individuals with diabetes has been found to be associated with poorer self-management of symptoms. This suggests that it may be important to target mood in treatment.
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.
Several types of plants are referred to as ginseng, but most studies have used American ginseng. They've shown some sugar-lowering effects in fasting and after-meal blood sugar levels, as well as in A1c results (average blood sugar levels over a 3-month period). But we need larger and more long-term studies. Researchers also found that the amount of sugar-lowering compound in ginseng plants varies widely.
The big news with the use of fig leaves is that they have anti-diabetic properties. The diabetic needs less insulin when on a treatment of using the fig leaf extract. The diabetic should take the extract with breakfast, first thing in the morning. An additional remedy is to boil the leaves of the fig in some freshly filtered waster and drink this as a tea. Read the whole article on fig leaves and diabetes:
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.
Can somebody at Virta help us find the actual presentation at the 2017 world polyphenol conference on lectins and polyphenols and artery flexibility? I can only find the agenda where the title of the presentation and time is made. He described what he was going to say in an interview a few weeks earlier, more rigidity of arteries with re-introduction of lectins, but I cannot find the actual presentation. He had a publication in 2013 on the reversal of endothelial dysfunction, is why I think we should take this other publication seriously:
This healthy lifestyle we refer to is being active 150 minutes or more each week and eating a meal plan low in fat and processed sugar with 3-5 vegetables and 2-3 fruits a day most days. It does not require low or no carbohydrate diet like Atkins or counting carbohydrates every meal. Most folks do better when they spread the carbohydrates out evenly over the day.
After you are diagnosed with diabetes, by following a healthy lifestyle, which includes a healthy diet along with exercise, you may be able to decrease your blood glucose levels to within normal range. Utilizing SMBG (self monitoring of blood glucose), you can see how different foods, as well as meals, influence your blood glucose levels. Doing SMBG along with a healthy diet and exercise is key to getting your diabetes under good control.
Pancreatic islet transplantation is an experimental treatment for poorly controlled type 1 diabetes. Pancreatic islets are clusters of cells in the pancreas that make the hormone insulin. In type 1 diabetes, the body’s immune system attacks these cells. A pancreatic islet transplant replaces destroyed islets with new ones that make and release insulin. This procedure takes islets from the pancreas of an organ donor and transfers them to a person with type 1 diabetes. Because researchers are still studying pancreatic islet transplantation, the procedure is only available to people enrolled in research studies. Learn more about islet transplantation studies.
It was once assumed that environmental factors took generations to affect a gene change, but research is now finding that a bad enough toxin or environmental stress can alter genes in a single generation. While genes can pre-dispose us to disease, the disease will only present itself in the presence of factors like toxins, poor diet or stress. A predisposition to diabetes, for instance, might be activated from toxins in foods, pesticides, herbicides, chemicals, or from a poor diet, especially when any of the above factors are also present.
A further danger of insulin treatment is that while diabetic microangiopathy is usually explained as the result of hyperglycemia, studies in rats indicate that the higher than normal level of insulin diabetics inject to control their hyperglycemia may itself promote small blood vessel disease. While there is no clear evidence that controlling hyperglycemia reduces diabetic macrovascular and cardiovascular disease, there are indications that intensive efforts to normalize blood glucose levels may worsen cardiovascular and cause diabetic mortality.
A wide scatter of absolute levels of pancreas triacylglycerol has been reported, with a tendency for higher levels in people with diabetes (57). This large population study showed overlap between diabetic and weight-matched control groups. These findings were also observed in a more recent smaller study that used a more precise method (21). Why would one person have normal β-cell function with a pancreas fat level of, for example, 8%, whereas another has type 2 diabetes with a pancreas fat level of 5%? There must be varying degrees of liposusceptibility of the metabolic organs, and this has been demonstrated in relation to ethnic differences (72). If the fat is simply not available to the body, then the susceptibility of the pancreas will not be tested, whereas if the individual acquires excess fat stores, then β-cell failure may or may not develop depending on degree of liposusceptibility. In any group of people with type 2 diabetes, simple inspection reveals that diabetes develops in some with a body mass index (BMI) in the normal or overweight range, whereas others have a very high BMI. The pathophysiologic changes in insulin secretion and insulin sensitivity are not different in obese and normal weight people (73), and the upswing in population rates of type 2 diabetes relates to a right shift in the whole BMI distribution. Hence, the person with a BMI of 24 and type 2 diabetes would in a previous era have had a BMI of 21 and no diabetes. It is clear that individual susceptibility factors determine the onset of the condition, and both genetic and epigenetic factors may contribute. Given that diabetes cannot occur without loss of acute insulin response to food, it can be postulated that this failure of acute insulin secretion could relate to both accumulation of fat and susceptibility to the adverse effect of excess fat in the pancreas.
Well, I don’t know much about VCRs, but I do know about type 2 diabetes. I could write an entire book about obesity (oh, wait, I did that already), or fasting (oh, wait, done too) or type 2 diabetes (next up for 2018). But many of you will not want to go through the entire instruction manual. So this is your quick start guide for reversing your type 2 diabetes.
I made a mistake in an earlier comment that I need to correct. I thought the VLDL represented the very small particles, and that is totally wrong. Here are the actual test results of the very small particles from a Quest Diagnostics after about 18 months on a ketogenic diet, with abundant use of MCT oil as caprylic acid. If the administrator deletes that comment, to avoid confusion, that would be fine with me. I can also provide much more data, as that test is pretty comprehensive.
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.
1. Avoid toxins as much as possible: There is no doubt that we live in a polluted world, and it is next to impossible to avoid all toxins, however, recent research suggests that environmental toxins such as pesticides in our food and drinking water can be factors in causing or worsening Type 1 Diabetes. To lessen the amount of toxins that enter the body, try to buy “green” cleaners, organic fruits and vegetables, and dairy that is from organic or grass-fed cows. Although these items may be a bit more expensive, the health benefits are well-worth the higher price tag.
A 2012 review of ginseng in animals and human beings found that not only does ginseng reduce insulin resistance, it also lowers HbA1C levels. It’s been used in traditional Chinese medicine for centuries as one of the most potent herbs for blood sugar control. Indian ginseng, also called Ashwagandha, offers fantastic all round benefits. Scientists are also researching the connection between diabetes and Alzhiemer’s. Panax Ginseng is a type of ginseng that is able to help with both diabetes and Alzheimer’s.
Although the relationship between magnesiumand diabetes has been studied for decades, we still don't fully understand it. Low magnesium may worsen blood sugar control in type 2 diabetes. Scientists say that it interrupts insulin secretion in the pancreas and builds insulin resistance in the body's tissues. And evidence suggests that a magnesium deficiency may contribute to some diabetes complications. People who get more magnesium in their diet (by eating whole grains, nuts, and green leafy vegetables) have a lower risk of type 2 diabetes.
Storage of liver fat can only occur when daily calorie intake exceeds expenditure. Sucrose overfeeding for 3 weeks has been shown to cause a 30% increase in liver fat content (37). The associated metabolic stress on hepatocytes was reflected by a simultaneous 30% rise in serum alanine aminotransferase (ALT) levels, and both liver fat and serum ALT returned to normal levels during a subsequent hypocaloric diet. Superimposed upon a positive calorie balance, the extent of portal vein hyperinsulinemia determines how rapidly conversion of excess sugars to fatty acid occurs in the liver. In groups of both obese and nonobese subjects, it was found that those with higher plasma insulin levels have markedly increased rates of hepatic de novo lipogenesis (2,38,39). Conversely, in type 1 diabetes the relatively low insulin concentration in the portal vein (as a consequence of insulin injection into subcutaneous tissue) is associated with subnormal liver fat content (40). Initiation of subcutaneous insulin therapy in type 2 diabetes brings about a decrease in portal insulin delivery by suppression of pancreatic insulin secretion and, hence, a decrease in liver fat (41). Hypocaloric diet (42), physical activity (43), or thiazolidinedione use (23,44) each reduces insulin secretion and decreases liver fat content. Newly synthesized triacylglycerol in the liver will be either oxidized, exported, or stored as hepatic triacylglycerol. Because transport of fatty acid into mitochondria for oxidation is inhibited by the malonyl-CoA produced during de novo lipogenesis, newly synthesized triacylglycerol is preferentially directed toward storage or export. Hence, hepatic fat content and plasma VLDL triacylglycerol levels are increased.
Ordinary calorie restriction through any diet can lead to weight loss and make it easier to manage blood sugar. Intermittent fasting is thought to go a step further by lowering serum insulin, which triggers the body to burn stored sugar, called glycogen, along with fat, in the absence of glucose from food, Dr. Fung says. These processes (called glycogenolysis and lipolysis, respectively) can temporarily lower blood sugar and cause weight loss.
Mr. Tutty said he jumped at the chance, becoming one of 30 men and women ages 25 to 80 to sign up. Mr. Tutty was one of 13 participants whose fasting plasma glucose dropped, and during the six-month follow-up remained below the seven millimole per liter (or 126 milligrams per deciliter) that defines diabetes. Although Mr. Tutty completed the study nearly three years ago, his fasting blood sugars continue to range from 5.2 to 5.6 mmol/L, he said.
According to studies, cinnamon may have a positive effect on the glycemic control and the lipid profile in patients with diabetes mellitus type 2. This is because it contains 18% polyphenol content in dry weight. This popular Indian spice can improve insulin sensitivity and blood glucose control. According to a study published in Journal Of The American Board Of Family Medicine, “cinnamon lowered HbA1C by 0.83% compared with standard medication alone lowering HbA1C 0.37%. Taking cinnamon could be useful for lowering serum HbA1C in type 2 diabetics with HbA1C >7.0 in addition to usual care.”
One such study, published in July 2018 in the Journal of the American Medical Association, found that intermittent fasting was no better at improving type 2 diabetes participants’ blood sugar levels than regular caloric restriction after one year. Previous studies on mice suggest intermittent fasting may improve memory, reduce disease risk, and aid with weight loss, according to an article published in June 2013 in the journal CMAJ, but, as Dr. Gabbay points out, “That doesn’t always translate to people.”
You also might hear about alternative treatments for diabetes, such as herbal remedies and vitamin or mineral supplements. These practices can be risky, especially when people stop following the treatment plan their doctor has given them. So get the facts by talking to your diabetes health care team. They keep track of the latest research developments, and will introduce new products as they become available.
That is the goal of Imcyse, a French company running a clinical trial with an immunotherapy designed to stop type 1 diabetes. Patients that have been diagnosed within the last 6 months, who still retain some insulin-producing cells, are given a treatment designed to make the immune system destroy the specific immune cells that are attacking insulin-producing cells. Results are expected later this year and will reveal whether the treatment has the potential to become a cure.
This modality can be contrasted with the emphasis of conventional medicine, which is to cure or mitigate disease, as reported by the American Holistic Health Association. For example, a conventional practitioner will follow an established algorithm for diabetes management that includes a medically established protocol centered on monitoring blood sugar and prescribing medications to balance it. An alternative medicine provider takes a personalized, whole-person approach that may include a prescription for changes in diet and exercise habits, stress reduction, and other lifestyle considerations. (The table below offers a comparison of alternative medicine with conventional medicine.)
In 2003, ephedrine -- also known as ma huang -- became the first herbal stimulant ever banned by the FDA. It was a popular component of over-the-counter weight loss drugs. Ephedrine had some benefits, but it could cause far more harm, especially in high doses: insomnia (difficulty falling and staying asleep), high blood pressure, glaucoma, and urinary retention. This herbal supplement has also been associated with numerous cases of stroke.
The problem, of course, has not been solved – the sugar bowl is still overflowing. You’ve only moved sugar from the blood (where you could see it) into the body (where you couldn’t see it). So, the very next time you eat, the exact same thing happens. Sugar comes in, spills out into the blood and you take metformin to cram the sugar back into the body. This works for a while, but eventually, the body fills up with sugar, too. Now, that same dose of metformin cannot force any more sugar into the body.
Some studies suggest that low magnesium levels may worsen blood glucose control in type 2 diabetes. There is also some evidence that magnesium supplementation may help with insulin resistance. For example, a study examined the effect of magnesium or placebo in 63 people with type 2 diabetes and low magnesium levels who were taking the medication glibenclamide. After 16 weeks, people who took magnesium had improved insulin sensitivity and lower fasting glucose levels.
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.