The way you take insulin may depend on your lifestyle, insurance plan, and preferences. You may decide that needles are not for you and prefer a different method. Talk with your doctor about the options and which is best for you. Most people with diabetes use a needle and syringe, pen, or insulin pump. Inhalers, injection ports, and jet injectors are less common.
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 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.


Given the prevalence of diabetes and the chronic nature of the disease, it’s no surprise that CAM is a popular treatment option. I don’t see a lot of CAM use in Type 1 diabetics. Insulin is the primary treatment, it works well, and patients can objectively measure their own blood sugar. Type 1 diabetics don’t seem to experiment with supplements that might alter their blood sugars. Those patients end up hospitalized or dead.
Pramlintide (Symlin) was the first in a class of injectable, anti-hyperglycemic medications for use in addition to insulin for type 1 diabetes or type 2 diabetes. Pramlintide is a synthetic analog of human amylin, a naturally occurring hormone made by the pancreas to help control glucose after meals. Similar to insulin, amylin is absent or deficient in person with diabetes.
The information on this website is provided as general health guidelines and may not be applicable to your particular health condition. Your individual health status and any required medical treatments can only be properly addressed by a professional healthcare provider of your choice. Remember: There is no adequate substitution for a personal consultation with your physician. Neither Desert Springs Hospital Medical Center, or any of their affiliates, nor any contributors shall have any liability for the content or any errors or omissions in the information provided by this website.            

Although a defect in mitochondrial function is associated with extremes of insulin resistance in skeletal muscle (30), this does not appear to be relevant to the etiology of type 2 diabetes. No defect is present in early type 2 diabetes but rather is directly related to ambient plasma glucose concentration (31). Observed rates of mitochondrial ATP production can be modified by increasing or decreasing plasma fatty acid concentration (32,33). Additionally, the onset of insulin stimulation of mitochondrial ATP synthesis is slow, gradually increasing over 2 h, and quite distinct from the acute onset of insulin’s metabolic effects (34). Although it remains possible that secondary mitochondrial effects of hyperglycemia and excess fatty acids exist, there is no evidence for a primary mitochondrial defect underlying type 2 diabetes.
The American Diabetes Association publishes treatment guidelines for physicians based on all available scientific evidence. In the 2018 guidelines document, Standard of Medical Care in Diabetes, the ADA states that there is not sufficient evidence to support the use of any of the proposed alternative treatments for diabetes. These guidelines state that:
Miscarriage is the medical term for the spontaneous loss of pregnancy from conception to 20 weeks gestation. Risk factors for a woman having a miscarriage include cigarette smoking, older maternal age, radiation exposure, previous miscarriage, maternal weight, illicit drug use, use of NSAIDs, and trauma or anatomical abnormalities to the uterus. There are five classified types of miscarriage: 1) threatened abortion; 2) incomplete abortion; 3) complete abortion; 4) missed abortion; and (5 septic abortion. While there are no specific treatments to stop a miscarriage, a woman's doctor may advise avoiding certain activities, bed rest, etc. If a woman believes she has had a miscarriage, she needs to seek prompt medical attention.
As time goes on, however, blood sugar levels can begin to rise again. Diabetes is a progressive disease which means that what is done today to care for it, may not work as well a year or two from now. A key to keeping blood sugar levels under control is to be active, watch portions of all foods, include all food groups and visit your doctor to make sure the blood sugar levels are staying at a safe level.
This essentially means that the type 2 diabetes is being managed at a level that seems as if the diabetes isn’t there at all. Choosing a healthy diet, exercising regularly and maintaining a healthy weight is the key. Eventually, what will likely happen is that blood glucose levels will increase again at a later time, as the person gets older, or if the person returns to an inactive and unhealthy lifestyle and regains weight because the beta cells of the pancreas have already been stressed.
Testosterone replacement therapy may improve glucose tolerance and insulin sensitivity in diabetic hypogonadal men. The mechanisms by which testosterone decreases insulin resistance is under study.[81] Moreover, testosterone may have a protective effect on pancreatic beta cells, which is possibly exerted by androgen-receptor-mediated mechanisms and influence of inflammatory cytokines.[82]
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.
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). It’s putting a band-aid over a bullet hole. So, the very next time you eat, the exact same thing happens. Sugar comes in, spills out into the blood and you take medication 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 medication cannot force any more sugar into the body.
If the T2DM has been recently diagnosed, there is a greater likelihood of being able to reverse the disease. Doing this requires losing approximately 5-10% of current body weight, balancing carbs and protein and engaging in daily physical exercise. A diabetes educator (C.D.E.) is the expert who can help put together a plan for realistic and permanent lifestyle changes.

Imagine our bodies to be a sugar bowl. A bowl of sugar. When we are young, our sugar bowl is empty. Over decades, we eat too much of the wrong things – sugary cereals, desserts and white bread. The sugar bowl gradually fills up with sugar until completely full. The next time you eat, sugar comes into the body, but the bowl is full, so it spills out into the blood.

Exercise– Even the mainstream medical community recognizes the advantage of exercise, as it increases the muscles ability to use insulin and over time can help fix insulin resistance. All exercise isn’t created equal though and fortunately, smaller amounts of high intensity exercise have been shown to have a better effect on insulin levels (and weight loss) than an hour of daily moderate cardio. According to the Healthy Skeptic: “A pair of studies done at McMaster University found that “6-minutes of pure, hard exercise once a week could be just as effective as an hour of daily moderate activity“, according to the June 6, 2005 CNN article reporting on the study.” I recommend high intensity exercise anyway for its various health advantages, and it is great for diabetes control. too.

An injection port has a short tube that you insert into the tissue beneath your skin. On the skin’s surface, an adhesive patch or dressing holds the port in place. You inject insulin through the port with a needle and syringe or an insulin pen. The port stays in place for a few days, and then you replace the port. With an injection port, you no longer puncture your skin for each shot—only when you apply a new port.
Change in fasting plasma glucose (A), 2 h post-oral glucose tolerance test (B), and homeostasis model assessment (HOMA-B) insulin secretion (C) during the 16-year follow-up in the Whitehall II study. Of the 6,538 people studied, diabetes developed in 505. Time 0 was taken as the diagnosis of diabetes or as the end of follow-up for those remaining normoglycemic. Redrawn with permission from Tabák et al. (80).
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.[67] There is growing evidence that there is higher levels of clinical depression in patients with diabetes compared to the non-diabetic population.[68][69] Depression in individuals with diabetes has been found to be associated with poorer self-management of symptoms.[70] This suggests that it may be important to target mood in treatment.
However, the observation that normalization of glucose in type 2 diabetes occurred within days after bariatric surgery, before substantial weight loss (15), led to the widespread belief that surgery itself brought about specific changes mediated through incretin hormone secretion (16,17). This reasoning overlooked the major change that follows bariatric surgery: an acute, profound decrease in calorie intake. Typically, those undergoing bariatric surgery have a mean body weight of ∼150 kg (15) and would therefore require a daily calorie intake of ∼13.4 MJ/day (3,200 kcal/day) for weight maintenance (18). This intake decreases precipitously at the time of surgery. The sudden reversal of traffic into fat stores brings about a profound change in intracellular concentration of fat metabolites. It is known that under hypocaloric conditions, fat is mobilized first from the liver and other ectopic sites rather than from visceral or subcutaneous fat stores (19). This process has been studied in detail during more moderate calorie restriction in type 2 diabetes over 8 weeks (20). Fasting plasma glucose was shown to be improved because of an 81% decrease in liver fat content and normalization of hepatic insulin sensitivity with no change in the insulin resistance of muscle.
According to the American Diabetes Association, nearly 21 million people in the United States have diabetes, with about 90 percent to 95 percent having type 2 diabetes. Sugar, in the form of glucose, is the main source of fuel for body cells. The hormone insulin allows glucose in the blood to enter cells. In type 2 diabetes, either the body doesn't produce enough insulin or cells are resistant to effects of insulin.
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.
Together with evidence of normalization of insulin secretion after bariatric surgery (84), insights into the behavior of the liver and pancreas during hypocaloric dieting lead to a hypothesis of the etiology and pathogenesis of type 2 diabetes (Fig. 6): The accumulation of fat in liver and secondarily in the pancreas will lead to self-reinforcing cycles that interact to bring about type 2 diabetes. Fatty liver leads to impaired fasting glucose metabolism and increases export of VLDL triacylglycerol (85), which increases fat delivery to all tissues, including the islets. The liver and pancreas cycles drive onward after diagnosis with steadily decreasing β-cell function. However, of note, observations of the reversal of type 2 diabetes confirm that if the primary influence of positive calorie balance is removed, then the processes are reversible (21).
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.
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).
O-3 oils, with both EPA and DHA, can help patients by lowering lipid panels (reduce triglycerides and cholesterol); reducing insulin resistance; reducing pain and inflammation so exercise and sleep are easier; reducing the risk of cardiovascular disease by lowering blood pressure; reducing the risk of dementia and Alzheimer’s disease; preventing and treating anxiety and depression; and promoting antioxidant actions in the body and brain to help reduce developing diabetic complications.
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.

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.
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”.
Does acupuncture for diabetes work? Acupuncture has many uses, and some research has suggested that it may work for diabetes, although how it would help has not yet been explained. Find out about the types of acupuncture that might help, the risks, and some evidence of its benefits. Anyone considering acupuncture should first check with their doctor. Read now

But look closer. The results may be statistically significant, but they’re not that impressive compared to medication. Cinnamon lowered A1C by 0.09%, versus the usual 1% with medication. Give A1c reflects overall glucose trends, cinnamon doesn’t look that impressive. Even at the extreme of the confidence interval, cinnamon has, at best, 10% of the efficacy of drug treatments. At worst, it’s completely ineffective.


I was diabetic for 13 years and was taking metformin 1000 mg twice daily. Last A1C was 15. My symptoms have always been stomach and bowels. I am a 54 year old male. the metformin wasn’t really working so this year, our family doctor started me on Natural Herbal Gardens Diabetes Disease Herbal mixture, With the help of Natural Herbal Garden natural herbs I have been able to reverse my symptoms using herbs, my symptoms totally declined over a 7 weeks use of the Natural Herbal Gardens Diabetes disease natural herbal formula. My diabetes is totally reversed! Visit their website www . naturalherbalgardens . com I am thankful to nature
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Diabetics often find their bodies swinging wildly out of equilibrium. In Type 1 Diabetes, the body attacks insulin-producing cells in the pancreas, causing a rise in blood sugar levels. In Type 2 Diabetes there is insufficient insulin produced in the pancreas, which slows the metabolism and elevates blood sugar levels. Both conditions, if not treated correctly, can cause a host of unpleasant side effects including high blood pressure, neuropathy, kidney damage, and in extreme cases amputation and even death.
Healthy fats: Medium-chained fatty acids found in coconut and red palm oil can help balance blood sugar levels, and they serve as the preferred fuel source for your body rather than sugar. Using coconut milk, ghee and grass-fed butter can also help balance out your blood sugar levels, so include these foods into your meals and smoothies. Some research actually suggests that a high-fat, low carb diet known as the keto diet may be a novel approach to reverse diabetes naturally, although you don’t technically have to go into ketosis to achieve the benefits of healthy fats in treating diabetes. (12)
“Whether it be the patient saying for the fifth time ‘I will start watching my diet and start exercising,’ or a physician saying ‘the A1c is close to goal and I don’t really want to add yet another medication and copay, we will wait and see what happens in another 3 months,’ the end result is lack of intensification and A1c goal attainment,” Pantalone said.

Imagine that you hide your kitchen garbage under the rug instead throwing it outside in the trash. You can’t see it, so you can pretend your house is clean. When there’s no more room underneath the rug, you throw the garbage into your bedroom, and bathroom, too. Anywhere where you don’t have to see it. Eventually, it begins to smell. Really, really bad. You needed to throw out the garbage, not hide it away. If we understand that too much sugar in the blood is toxic, why can’t we understand that too much sugar in the body is toxic too?


Hyperglycemic hyperosmolar nonketotic syndrome (HHNS). Signs and symptoms of this life-threatening condition include a blood sugar reading higher than 600 mg/dL (33.3 mmol/L), dry mouth, extreme thirst, fever greater than 101 F (38 C), drowsiness, confusion, vision loss, hallucinations and dark urine. Your blood sugar monitor may not be able to give you an exact reading at such high levels and may instead just read "high."
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:
As self-management of diabetes typically involves lifestyle modifications, adherence may pose a significant self-management burden on many individuals.[65] For example, individuals with diabetes may find themselves faced with the need to self-monitor their blood glucose levels, adhere to healthier diets and maintain exercise regimens regularly in order to maintain metabolic control and reduce the risk of developing cardiovascular problems. Barriers to adherence have been associated with key psychological mechanisms: knowledge of self-management, beliefs about the efficacy of treatment and self-efficacy/perceived control.[65] Such mechanisms are inter-related, as one's thoughts (e.g. one's perception of diabetes, or one's appraisal of how helpful self-management is) is likely to relate to one's emotions (e.g. motivation to change), which in turn, affects one's self-efficacy (one's confidence in their ability to engage in a behaviour to achieve a desired outcome).[66]
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.

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).
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.

In order to reverse diabetes naturally, remove foods like refined sugar, grains, conventional cow’s milk, alcohol, GMO foods and hydrogenated oils from your diet; incorporate healthy foods like foods high in fiber, chromium, magnesium, healthy fats and clean protein, along with foods with low glycemic loads; take supplements for diabetes; follow my diabetic eating plan; and exercise to balance blood sugar.
A series of studies from Newcastle University in Newcastle upon Tyne, United Kingdom, starting in 2011 have supported this notion, including a new report published online August 2 in the journal Cell Metabolism. This current investigation examined reasons why substantial weight loss in some patients produces type 2 diabetes remission, which is a state in which most or all signs and symptoms of diabetes disappear.
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).
So, can you “reverse” diabetes? No – but you can manage it very well with the help of a Certified Diabetes Educator (CDE) and a knowledgeable primary care physician or endocrinologist. There are even prescription apps available to bridge the care that your clinicians can give you between visits and apps that offer virtual CDE’s for greater assistance.
Miscarriage is the medical term for the spontaneous loss of pregnancy from conception to 20 weeks gestation. Risk factors for a woman having a miscarriage include cigarette smoking, older maternal age, radiation exposure, previous miscarriage, maternal weight, illicit drug use, use of NSAIDs, and trauma or anatomical abnormalities to the uterus. There are five classified types of miscarriage: 1) threatened abortion; 2) incomplete abortion; 3) complete abortion; 4) missed abortion; and (5 septic abortion. While there are no specific treatments to stop a miscarriage, a woman's doctor may advise avoiding certain activities, bed rest, etc. If a woman believes she has had a miscarriage, she needs to seek prompt medical attention.
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