Cons: Glucose Buddy does not sync with meters, continuous glucose monitors (CGMs), or pumps. Both Android and Apple users can access glucosebuddy.com, but only Apple users can sync their app with the website; Android users have to manually input their log on the web portal. There is no way to back up your data, so if you lose your phone and you haven’t manually entered logbook data on the website (or if your Apple device didn’t sync), you’ll have to start over. A built-in calorie tracker and food database is planned, but no release date has been set yet.
Researchers looked at 5,185 apps for phones running Google’s Android software or Apple’s iOS system. Out of this total, they found 371 apps that claimed to provide several key components for type 2 diabetes management: recording blood sugar data; reminding patients when they need to do specific things to manage the illness; and educating patients on how to handle conditions like dangerously low or high blood sugar.
The apps on Apple's list aren't all from the US, and they don't all target diabetes specifically. While many are tracking and management apps for blood glucose and insulin levels, others are more general purpose apps for eating specific diets, which people with diabetes could benefit from. The list includes mostly consumer-facing apps but one app for doctors, as well as one for kids and one for pregnant women with diabetes.
The connection may be hard to imagine. But the primary reason that regularly skimping on shuteye can increase your risk of type 2 diabetes is because your hormone levels get thrown out of whack. Specifically, with ongoing sleep loss, less insulin (a hormone that regulates blood sugar) is released in the body after you eat. Meanwhile, your body secretes more stress hormones (such as cortisol), which helps you stay awake but makes it harder for insulin to do its job effectively. The net effect: Too much glucose stays in the bloodstream, which can increase your risk of developing type 2 diabetes.
Fuchsberger C, Flannick J, Teslovich TM, Mahajan A, Agarwala V, Gaulton KJ, Ma C, Fontanillas P, Moutsianas L, McCarthy DJ, Rivas MA, Perry JRB, Sim X, Blackwell TW, Robertson NR, Rayner NW, Cingolani P, Locke AE, Tajes JF, Highland HM, Dupuis J, Chines PS, Lindgren CM, Hartl C, Jackson AU, Chen H, Huyghe JR, van de Bunt M, Pearson RD, Kumar A, Müller-Nurasyid M, Grarup N, Stringham HM, Gamazon ER, Lee J, Chen Y, Scott RA, Below JE, Chen P, Huang J, Go MJ, Stitzel ML, Pasko D, Parker SCJ, Varga TV, Green T, Beer NL, Day-Williams AG, Ferreira T, Fingerlin T, Horikoshi M, Hu C, Huh I, Ikram MK, Kim BJ, Kim Y, Kim YJ, Kwon MS, Lee J, Lee S, Lin KH, Maxwell TJ, Nagai Y, Wang X, Welch RP, Yoon J, Zhang W, Barzilai N, Voight BF, Han BG, Jenkinson CP, Kuulasmaa T, Kuusisto J, Manning A, Ng MCY, Palmer ND, Balkau B, Stančáková A, Abboud HE, Boeing H, Giedraitis V, Prabhakaran D, Gottesman O, Scott J, Carey J, Kwan P, Grant G, Smith JD, Neale BM, Purcell S, Butterworth AS, Howson JMM, Lee HM, Lu Y, Kwak SH, Zhao W, Danesh J, Lam VKL, Park KS, Saleheen D, So WY, Tam CHT, Afzal U, Aguilar D, Arya R, Aung T, Chan E, Navarro C, Cheng CY, Palli D, Correa A, Curran JE, Rybin D, Farook VS, Fowler SP, Freedman BI, Griswold M, Hale DE, Hicks PJ, Khor CC, Kumar S, Lehne B, Thuillier D, Lim WY, Liu J, van der Schouw YT, Loh M, Musani SK, Puppala S, Scott WR, Yengo L, Tan ST, Taylor HA Jr, Thameem F, Wilson G Sr, Wong TY, Njølstad PR, Levy JC, Mangino M, Bonnycastle LL, Schwarzmayr T, Fadista J, Surdulescu GL, Herder C, Groves CJ, Wieland T, Bork-Jensen J, Brandslund I, Christensen C, Koistinen HA, Doney ASF, Kinnunen L, Esko T, Farmer AJ, Hakaste L, Hodgkiss D, Kravic J, Lyssenko V, Hollensted M, Jørgensen ME, Jørgensen T, Ladenvall C, Justesen JM, Käräjämäki A, Kriebel J, Rathmann W, Lannfelt L, Lauritzen T, Narisu N, Linneberg A, Melander O, Milani L, Neville M, Orho-Melander M, Qi L, Qi Q, Roden M, Rolandsson O, Swift A, Rosengren AH, Stirrups K, Wood AR, Mihailov E, Blancher C, Carneiro MO, Maguire J, Poplin R, Shakir K, Fennell T, DePristo M, de Angelis MH, Deloukas P, Gjesing AP, Jun G, Nilsson P, Murphy J, Onofrio R, Thorand B, Hansen T, Meisinger C, Hu FB, Isomaa B, Karpe F, Liang L, Peters A, Huth C, O'Rahilly SP, Palmer CNA, Pedersen O, Rauramaa R, Tuomilehto J, Salomaa V, Watanabe RM, Syvänen AC, Bergman RN, Bharadwaj D, Bottinger EP, Cho YS, Chandak GR, Chan JCN, Chia KS, Daly MJ, Ebrahim SB, Langenberg C, Elliott P, Jablonski KA, Lehman DM, Jia W, Ma RCW, Pollin TI, Sandhu M, Tandon N, Froguel P, Barroso I, Teo YY, Zeggini E, Loos RJF, Small KS, Ried JS, DeFronzo RA, Grallert H, Glaser B, Metspalu A, Wareham NJ, Walker M, Banks E, Gieger C, Ingelsson E, Im HK, Illig T, Franks PW, Buck G, Trakalo J, Buck D, Prokopenko I, Mägi R, Lind L, Farjoun Y, Owen KR, Gloyn AL, Strauch K, Tuomi T, Kooner JS, Lee JY, Park T, Donnelly P, Morris AD, Hattersley AT, Bowden DW, Collins FS, Atzmon G, Chambers JC, Spector TD, Laakso M, Strom TM, Bell GI, Blangero J, Duggirala R, Tai ES, McVean G, Hanis CL, Wilson JG, Seielstad M, Frayling TM, Meigs JB, Cox NJ, Sladek R, Lander ES, Gabriel S, Burtt NP, Mohlke KL, Meitinger T, Groop L, Abecasis G, Florez JC, Scott LJ, Morris AP, Kang HM, Boehnke M, Altshuler D, McCarthy MI. The genetic architecture of type 2 diabetes. Nature. 2016 Aug 4;536(7614):41-47. doi: 10.1038/nature18642. Epub 2016 Jul 11.

^ Sarwar N, Gao P, Seshasai SR, Gobin R, Kaptoge S, Di Angelantonio E, Ingelsson E, Lawlor DA, Selvin E, Stampfer M, Stehouwer CD, Lewington S, Pennells L, Thompson A, Sattar N, White IR, Ray KK, Danesh J (June 2010). "Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies". Lancet. 375 (9733): 2215–22. doi:10.1016/S0140-6736(10)60484-9. PMC 2904878. PMID 20609967.
You can manually enter your blood glucose values in the app or buy their special cable to upload your glucometer readings to the app. For every glucose entry, add notes about medications, mood, exercise, and meals (you can even add a photo of your meal for a quick record), and then track your trends over the course of the day and long term. This app also has features for tracking blood pressure, weight, and A1C.
Threshold for diagnosis of diabetes is based on the relationship between results of glucose tolerance tests, fasting glucose or HbA1c and complications such as retinal problems.[10] A fasting or random blood sugar is preferred over the glucose tolerance test, as they are more convenient for people.[10] HbA1c has the advantages that fasting is not required and results are more stable but has the disadvantage that the test is more costly than measurement of blood glucose.[51] It is estimated that 20% of people with diabetes in the United States do not realize that they have the disease.[10]
Insulin serves as a “key” to open your cells, to allow the glucose to enter -- and allow you to use the glucose for energy.  Without insulin, there is no “key.”   So, the sugar stays -- and builds up-- in the blood. The result: the body’s cells starve from the lack of glucose.  And, if left untreated, the high level of “blood sugar” can damage eyes, kidneys, nerves, and the heart, and can also lead to coma and death. 

Other potentially important mechanisms associated with type 2 diabetes and insulin resistance include: increased breakdown of lipids within fat cells, resistance to and lack of incretin, high glucagon levels in the blood, increased retention of salt and water by the kidneys, and inappropriate regulation of metabolism by the central nervous system.[10] However, not all people with insulin resistance develop diabetes, since an impairment of insulin secretion by pancreatic beta cells is also required.[13]
There are a number of rare cases of diabetes that arise due to an abnormality in a single gene (known as monogenic forms of diabetes or "other specific types of diabetes").[10][13] These include maturity onset diabetes of the young (MODY), Donohue syndrome, and Rabson–Mendenhall syndrome, among others.[10] Maturity onset diabetes of the young constitute 1–5% of all cases of diabetes in young people.[39]
Weight loss surgery in those who are obese is an effective measure to treat diabetes.[103] Many are able to maintain normal blood sugar levels with little or no medication following surgery[104] and long-term mortality is decreased.[105] There however is some short-term mortality risk of less than 1% from the surgery.[106] The body mass index cutoffs for when surgery is appropriate are not yet clear.[105] It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.[107][108]
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]
Rates of diabetes in 1985 were estimated at 30 million, increasing to 135 million in 1995 and 217 million in 2005.[18] This increase is believed to be primarily due to the global population aging, a decrease in exercise, and increasing rates of obesity.[18] The five countries with the greatest number of people with diabetes as of 2000 are India having 31.7 million, China 20.8 million, the United States 17.7 million, Indonesia 8.4 million, and Japan 6.8 million.[111] It is recognized as a global epidemic by the World Health Organization.[1]
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).

Prevention and treatment involve maintaining a healthy diet, regular physical exercise, a normal body weight, and avoiding use of tobacco.[2] Control of blood pressure and maintaining proper foot care are important for people with the disease.[2] Type 1 DM must be managed with insulin injections.[2] Type 2 DM may be treated with medications with or without insulin.[12] Insulin and some oral medications can cause low blood sugar.[13] Weight loss surgery in those with obesity is sometimes an effective measure in those with type 2 DM.[14] Gestational diabetes usually resolves after the birth of the baby.[15]

BlueStar Diabetes is an FDA-approved, Class 2 medical app which provides approved diabetics with 24/7, real-time coaching from a certified diabetes specialist. This comprehensive app is available only by prescription and offers an impressive range of tools tailored to the individual. When registered, users can receive personalized guidance based on their blood glucose, medications, current health, and a review of lifestyle factors.
Some kids and teens are already using devices that make blood glucose testing and insulin injections easier, less painful, and more effective. One of these is the insulin pump, a mechanical device that can deliver insulin more like the pancreas does. There's also been progress toward the development of a wearable or implantable "artificial pancreas." This consists of an insulin pump linked to a device that measures the person's blood glucose level continuously.

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]
The pain of diabetic nerve damage may respond to traditional treatments with certain medications such as gabapentin (Neurontin), phenytoin (Dilantin), and carbamazepine (Tegretol) that are traditionally used in the treatment of seizure disorders. Amitriptyline (Elavil, Endep) and desipramine (Norpraminine) are medications that are traditionally used for depression. While many of these medications are not indicated specifically for the treatment of diabetes related nerve pain, they are used by physicians commonly.
Lifestyle change has been proven effective in preventing or delaying the onset of type 2 diabetes in high-risk individuals. Based on this, new public health approaches are emerging that may deserve monitoring at the national level. For example, the Diabetes Prevention Program research trial demonstrated that lifestyle intervention had its greatest impact in older adults and was effective in all racial and ethnic groups. Translational studies of this work have also shown that delivery of the lifestyle intervention in group settings at the community level are also effective at reducing type 2 diabetes risk. The National Diabetes Prevention Program has now been established to implement the lifestyle intervention nationwide.

Type 2 diabetes can occur at any age, but it most commonly begins in middle age or later. Signs and symptoms develop slowly over years. They include frequent urination (polyuria), excessive thirst (polydipsia), fatigue, blurred vision, tingling or loss of feeling in the hands and feet (diabetic neuropathy), sores that do not heal well, and weight loss. If blood sugar levels are not controlled through medication or diet, type 2 diabetes can cause long-lasting (chronic) health problems including heart disease and stroke; nerve damage; and damage to the kidneys, eyes, and other parts of the body.
Diabetes is a metabolic disorder that occurs when your blood sugar (glucose), is too high (hyperglycemia). Glucose is what the body uses for energy, and the pancreas produces a hormone called insulin that helps convert the glucose from the food you eat into energy. When the body either does not produce enough insulin, does not produce any at all, or your body becomes resistant to the insulin, the glucose does not reach your cells to be used for energy. This results in the health condition termed diabetes.

Type 2 diabetes is partly preventable by staying a normal weight, exercising regularly, and eating properly.[1] Treatment involves exercise and dietary changes.[1] If blood sugar levels are not adequately lowered, the medication metformin is typically recommended.[7][14] Many people may eventually also require insulin injections.[9] In those on insulin, routinely checking blood sugar levels is advised; however, this may not be needed in those taking pills.[15] Bariatric surgery often improves diabetes in those who are obese.[8][16]


^ Cheng J, Zhang W, Zhang X, Han F, Li X, He X, Li Q, Chen J (May 2014). "Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on all-cause mortality, cardiovascular deaths, and cardiovascular events in patients with diabetes mellitus: a meta-analysis". JAMA Internal Medicine. 174 (5): 773–85. doi:10.1001/jamainternmed.2014.348. PMID 24687000.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/l (110 to 125 mg/dl) are considered to have impaired fasting glucose.[67] people with plasma glucose at or above 7.8 mmol/l (140 mg/dl), but not over 11.1 mmol/l (200 mg/dl), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease.[68] The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/l (100 to 125 mg/dl).[69]

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]

Hypoglycemia means abnormally low blood sugar (glucose). In patients with diabetes, the most common cause of low blood sugar is excessive use of insulin or other glucose-lowering medications, to lower the blood sugar level in diabetic patients in the presence of a delayed or absent meal. When low blood sugar levels occur because of too much insulin, it is called an insulin reaction. Sometimes, low blood sugar can be the result of an insufficient caloric intake or sudden excessive physical exertion.


Diabetes mellitus is a disease in which a person's blood sugar (blood glucose) is either too high (hyperglycemia) or too low (hypoglycemia) due to problems with insulin regulation in the body. There are two main types of diabetes mellitus, type 1 and type 2. Type 1 diabetes usually occurs during childhood, while type 2 diabetes usually occurs during adulthood, however, rates of both types of diabetes in children, adolescents, and teens is increasing. More men than women have diabetes in the US, and the disease can affect men differently than women.
^ Boussageon R, Bejan-Angoulvant T, Saadatian-Elahi M, Lafont S, Bergeonneau C, Kassaï B, Erpeldinger S, Wright JM, Gueyffier F, Cornu C (July 2011). "Effect of intensive glucose lowering treatment on all cause mortality, cardiovascular death, and microvascular events in type 2 diabetes: meta-analysis of randomised controlled trials". BMJ. 343: d4169. doi:10.1136/bmj.d4169. PMC 3144314. PMID 21791495.

Exposure to certain viral infections (mumps and Coxsackie viruses) or other environmental toxins may serve to trigger abnormal antibody responses that cause damage to the pancreas cells where insulin is made. Some of the antibodies seen in type 1 diabetes include anti-islet cell antibodies, anti-insulin antibodies and anti-glutamic decarboxylase antibodies. These antibodies can be detected in the majority of patients, and may help determine which individuals are at risk for developing type 1 diabetes.

×