Transform your smartphone into a glucometer and get useful insights on blood sugar changes so you can best manage your diabetes. BeatO offers the resources and analytics to provide custom monitoring for all of your diabetes needs. It comes with the ability to contact a free diabetes educator service during the first three months when you purchase a BeatO Smartphone Glucometer.
The development of type 2 diabetes is caused by a combination of lifestyle and genetic factors.[24][26] While some of these factors are under personal control, such as diet and obesity, other factors are not, such as increasing age, female gender, and genetics.[10] Obesity is more common in women than men in many parts of Africa.[27] A lack of sleep has been linked to type 2 diabetes.[28] This is believed to act through its effect on metabolism.[28] The nutritional status of a mother during fetal development may also play a role, with one proposed mechanism being that of DNA methylation.[29] The intestinal bacteria Prevotella copri and Bacteroides vulgatus have been connected with type 2 diabetes.[30]

^ Palmer SC, Mavridis D, Nicolucci A, Johnson DW, Tonelli M, Craig JC, Maggo J, Gray V, De Berardis G, Ruospo M, Natale P, Saglimbene V, Badve SV, Cho Y, Nadeau-Fredette AC, Burke M, Faruque L, Lloyd A, Ahmad N, Liu Y, Tiv S, Wiebe N, Strippoli GF (July 2016). "Comparison of Clinical Outcomes and Adverse Events Associated With Glucose-Lowering Drugs in Patients With Type 2 Diabetes: A Meta-analysis". JAMA. 316 (3): 313–24. doi:10.1001/jama.2016.9400. PMID 27434443.
[1] Diabetes Prevention Program Research Group. Long-term effects of lifestyle intervention or metformin on diabetes development and microvascular complications over 15-year follow-up: the Diabetes Prevention Program Outcomes Study. The Lancet Diabetes & Endocrinology. 2015;3(11):866‒875. You can find more information about this study on the Diabetes Prevention Program Outcomes Study website.
Kidney damage from diabetes is called diabetic nephropathy. The onset of kidney disease and its progression is extremely variable. Initially, diseased small blood vessels in the kidneys cause the leakage of protein in the urine. Later on, the kidneys lose their ability to cleanse and filter blood. The accumulation of toxic waste products in the blood leads to the need for dialysis. Dialysis involves using a machine that serves the function of the kidney by filtering and cleaning the blood. In patients who do not want to undergo chronic dialysis, kidney transplantation can be considered.
A great app to add to the list is Wellocity Health. It helps you manage chronic conditions such as heart disease and diabetes by addressing key risk factors. This free app allows users to track medications, vitals and activity and share reports of your progress with your doctor or coach. Actionable insights and realistic goals make it easy to monitor progress and improve. The app also has a built-in community that allow users to share experiences.
Our bodies break down the foods we eat into glucose and other nutrients we need, which are then absorbed into the bloodstream from the gastrointestinal tract. The glucose level in the blood rises after a meal and triggers the pancreas to make the hormone insulin and release it into the bloodstream. But in people with diabetes, the body either can't make or can't respond to insulin properly.
Diabetes mellitus type 2 is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency.[52] This is in contrast to diabetes mellitus type 1 in which there is an absolute insulin deficiency due to destruction of islet cells in the pancreas and gestational diabetes mellitus that is a new onset of high blood sugars associated with pregnancy.[13] Type 1 and type 2 diabetes can typically be distinguished based on the presenting circumstances.[49] If the diagnosis is in doubt antibody testing may be useful to confirm type 1 diabetes and C-peptide levels may be useful to confirm type 2 diabetes,[53] with C-peptide levels normal or high in type 2 diabetes, but low in type 1 diabetes.[54]
Morris AP, Voight BF, Teslovich TM, Ferreira T, Segrè AV, Steinthorsdottir V, Strawbridge RJ, Khan H, Grallert H, Mahajan A, Prokopenko I, Kang HM, Dina C, Esko T, Fraser RM, Kanoni S, Kumar A, Lagou V, Langenberg C, Luan J, Lindgren CM, Müller-Nurasyid M, Pechlivanis S, Rayner NW, Scott LJ, Wiltshire S, Yengo L, Kinnunen L, Rossin EJ, Raychaudhuri S, Johnson AD, Dimas AS, Loos RJ, Vedantam S, Chen H, Florez JC, Fox C, Liu CT, Rybin D, Couper DJ, Kao WH, Li M, Cornelis MC, Kraft P, Sun Q, van Dam RM, Stringham HM, Chines PS, Fischer K, Fontanillas P, Holmen OL, Hunt SE, Jackson AU, Kong A, Lawrence R, Meyer J, Perry JR, Platou CG, Potter S, Rehnberg E, Robertson N, Sivapalaratnam S, Stančáková A, Stirrups K, Thorleifsson G, Tikkanen E, Wood AR, Almgren P, Atalay M, Benediktsson R, Bonnycastle LL, Burtt N, Carey J, Charpentier G, Crenshaw AT, Doney AS, Dorkhan M, Edkins S, Emilsson V, Eury E, Forsen T, Gertow K, Gigante B, Grant GB, Groves CJ, Guiducci C, Herder C, Hreidarsson AB, Hui J, James A, Jonsson A, Rathmann W, Klopp N, Kravic J, Krjutškov K, Langford C, Leander K, Lindholm E, Lobbens S, Männistö S, Mirza G, Mühleisen TW, Musk B, Parkin M, Rallidis L, Saramies J, Sennblad B, Shah S, Sigurðsson G, Silveira A, Steinbach G, Thorand B, Trakalo J, Veglia F, Wennauer R, Winckler W, Zabaneh D, Campbell H, van Duijn C, Uitterlinden AG, Hofman A, Sijbrands E, Abecasis GR, Owen KR, Zeggini E, Trip MD, Forouhi NG, Syvänen AC, Eriksson JG, Peltonen L, Nöthen MM, Balkau B, Palmer CN, Lyssenko V, Tuomi T, Isomaa B, Hunter DJ, Qi L; Wellcome Trust Case Control Consortium; Meta-Analyses of Glucose and Insulin-related traits Consortium (MAGIC) Investigators; Genetic Investigation of ANthropometric Traits (GIANT) Consortium; Asian Genetic Epidemiology Network–Type 2 Diabetes (AGEN-T2D) Consortium; South Asian Type 2 Diabetes (SAT2D) Consortium, Shuldiner AR, Roden M, Barroso I, Wilsgaard T, Beilby J, Hovingh K, Price JF, Wilson JF, Rauramaa R, Lakka TA, Lind L, Dedoussis G, Njølstad I, Pedersen NL, Khaw KT, Wareham NJ, Keinanen-Kiukaanniemi SM, Saaristo TE, Korpi-Hyövälti E, Saltevo J, Laakso M, Kuusisto J, Metspalu A, Collins FS, Mohlke KL, Bergman RN, Tuomilehto J, Boehm BO, Gieger C, Hveem K, Cauchi S, Froguel P, Baldassarre D, Tremoli E, Humphries SE, Saleheen D, Danesh J, Ingelsson E, Ripatti S, Salomaa V, Erbel R, Jöckel KH, Moebus S, Peters A, Illig T, de Faire U, Hamsten A, Morris AD, Donnelly PJ, Frayling TM, Hattersley AT, Boerwinkle E, Melander O, Kathiresan S, Nilsson PM, Deloukas P, Thorsteinsdottir U, Groop LC, Stefansson K, Hu F, Pankow JS, Dupuis J, Meigs JB, Altshuler D, Boehnke M, McCarthy MI; DIAbetes Genetics Replication And Meta-analysis (DIAGRAM) Consortium. Large-scale association analysis provides insights into the genetic architecture and pathophysiology of type 2 diabetes. Nat Genet. 2012 Sep;44(9):981-90. doi: 10.1038/ng.2383. Epub 2012 Aug 12.
The classic symptoms of untreated diabetes are unintended weight loss, polyuria (increased urination), polydipsia (increased thirst), and polyphagia (increased hunger).[20] Symptoms may develop rapidly (weeks or months) in type 1 DM, while they usually develop much more slowly and may be subtle or absent in type 2 DM. Other symptoms of diabetes mellitus include weight loss and tiredness.[21]
Diabetes Educational Services (DES) has established this website to provide information and education to health care professionals. Nothing in this website constitutes medical advice nor is it a substitute for medical advice. References in this website to any and all specific products, services or processes do not constitute or imply an endorsement or recommendation by Diabetes Educational Services.
[1] Diabetes Prevention Program Research Group. Long-term effects of lifestyle intervention or metformin on diabetes development and microvascular complications over 15-year follow-up: the Diabetes Prevention Program Outcomes Study. The Lancet Diabetes & Endocrinology. 2015;3(11):866‒875. You can find more information about this study on the Diabetes Prevention Program Outcomes Study website.

Disclaimer: The entire contents of this website are based upon the opinions of Dr. Mercola, unless otherwise noted. Individual articles are based upon the opinions of the respective author, who retains copyright as marked. The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the research and experience of Dr. Mercola and his community. Dr. Mercola encourages you to make your own health care decisions based upon your research and in partnership with a qualified health care professional. If you are pregnant, nursing, taking medication, or have a medical condition, consult your health care professional before using products based on this content.
Findings from the Diabetes Control and Complications Trial (DCCT) and the United Kingdom Prospective Diabetes Study (UKPDS) have clearly shown that aggressive and intensive control of elevated levels of blood sugar in patients with type 1 and type 2 diabetes decreases the complications of nephropathy, neuropathy, retinopathy, and may reduce the occurrence and severity of large blood vessel diseases. Aggressive control with intensive therapy means achieving fasting glucose levels between 70-120 mg/dl; glucose levels of less than 160 mg/dl after meals; and a near normal hemoglobin A1c levels (see below).
Type 2 diabetes was also previously referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult-onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs, particularly in the face of insulin resistance as discussed above. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells).
Enter your weight, blood pressure, HbA1c levels, and more into Glucose Buddy and see why people with diabetes find this app effective and easy to use. It also lets you track carb intake and workouts, and monitor trends so you get a better idea of how to best manage your condition. Subscriptions are $14.99 per month or $59.99 per year and give users access to premium features such as other fitness apps, advanced graphs, and custom tagging tools.
Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.
In type 2 diabetes (adult onset diabetes), the pancreas makes insulin, but it either doesn't produce enough, or the insulin does not work properly. Nine out of 10 people with diabetes have type 2. This type occurs most often in people who are over 40 years old but can occur even in childhood if there are risk factors present. Type 2 diabetes may sometimes be controlled with a combination of diet, weight management and exercise. However, treatment also may include oral glucose-lowering medications (taken by mouth) or insulin injections (shots).
Though not routinely used any longer, the oral glucose tolerance test (OGTT) is a gold standard for making the diagnosis of type 2 diabetes. It is still commonly used for diagnosing gestational diabetes and in conditions of pre-diabetes, such as polycystic ovary syndrome. With an oral glucose tolerance test, the person fasts overnight (at least eight but not more than 16 hours). Then first, the fasting plasma glucose is tested. After this test, the person receives an oral dose (75 grams) of glucose. There are several methods employed by obstetricians to do this test, but the one described here is standard. Usually, the glucose is in a sweet-tasting liquid that the person drinks. Blood samples are taken at specific intervals to measure the blood glucose.
As of 2017, an estimated 425 million people had diabetes worldwide,[8] with type 2 DM making up about 90% of the cases.[16][17] This represents 8.8% of the adult population,[8] with equal rates in both women and men.[18] Trend suggests that rates will continue to rise.[8] Diabetes at least doubles a person's risk of early death.[2] In 2017, diabetes resulted in approximately 3.2 to 5.0 million deaths.[8] The global economic cost of diabetes related health expenditure in 2017 was estimated at US$727 billion.[8] In the United States, diabetes cost nearly US$245 billion in 2012.[19]
Dietary factors also influence the risk of developing type 2 DM. Consumption of sugar-sweetened drinks in excess is associated with an increased risk.[45][46] The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk.[44] Eating lots of white rice, and other starches, also may increase the risk of diabetes.[47] A lack of physical activity is believed to cause 7% of cases.[48]
Your doctor may recommend working with a registered dietitian and a personal trainer to help you set up a diabetes weight loss plan. "Diet and exercise is always encouraged as the first line of therapy, but it works better for some people than others," says Sullivan. If you’re obese and having trouble losing weight with diet and exercise alone, your doctor may recommend medications to suppress your appetite and promote weight loss, or even gastric bypass surgery.ause of nontraumatic blindness and kidney failure.[24] It has also been associated with an increased risk of cognitive dysfunction and dementia through disease processes such as Alzheimer's disease and vascular dementia.[25] Other complications include acanthosis nigricans, sexual dysfunction, and frequent infections.[23]

There is no known preventive measure for type 1 diabetes.[2] Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet.[2] Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%.[71] Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish.[72] Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes.[72] Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.[73]

The development of type 2 diabetes is caused by a combination of lifestyle and genetic factors.[24][26] While some of these factors are under personal control, such as diet and obesity, other factors are not, such as increasing age, female gender, and genetics.[10] Obesity is more common in women than men in many parts of Africa.[27] A lack of sleep has been linked to type 2 diabetes.[28] This is believed to act through its effect on metabolism.[28] The nutritional status of a mother during fetal development may also play a role, with one proposed mechanism being that of DNA methylation.[29] The intestinal bacteria Prevotella copri and Bacteroides vulgatus have been connected with type 2 diabetes.[30]
Monogenic diabetes is caused by mutations, or changes, in a single gene. These changes are usually passed through families, but sometimes the gene mutation happens on its own. Most of these gene mutations cause diabetes by making the pancreas less able to make insulin. The most common types of monogenic diabetes are neonatal diabetes and maturity-onset diabetes of the young (MODY). Neonatal diabetes occurs in the first 6 months of life. Doctors usually diagnose MODY during adolescence or early adulthood, but sometimes the disease is not diagnosed until later in life.
×