A1C: Your A1C, also called glycated hemoglobin, reflects your average blood glucose levels for the past 2 to 3 months. If your A1C is 6.5% or greater, your doctor may diagnose diabetes. If your A1C is between 6.0% and 6.4%, your doctor may diagnose prediabetes. Of note, A1C cannot be used to diagnose type 1 diabetes, diabetes in children, adolescents, or pregnant women.
The problem with sweetened drinks is that, due to their liquid form, they’re among the fastest simple carbs to be digested in the body, causing blood sugar levels to spike even more than a simple carb in solid-food form would. Research supports this idea: A review published in November 2010 in the journal Diabetes Care suggested adding only one serving of a sweetened beverage to your diet may increase your risk for type 2 diabetes by 15 percent.

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]

Diabetes mellitus is a chronic disease caused by inherited and/or acquired deficiency in production of insulin by the pancreas, or by the ineffectiveness of the insulin produced. Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
As of 2015, an estimated 415 million people had diabetes worldwide,[8] with type 2 DM making up about 90% of the cases.[16][17] This represents 8.3% of the adult population,[17] with equal rates in both women and men.[18] As of 2014, trends suggested the rate would continue to rise.[19] Diabetes at least doubles a person's risk of early death.[2] From 2012 to 2015, approximately 1.5 to 5.0 million deaths each year resulted from diabetes.[8][9] The global economic cost of diabetes in 2014 was estimated to be US$612 billion.[20] In the United States, diabetes cost $245 billion in 2012.[21]
In type 2 diabetes, there also is a steady decline of beta cells that adds to the process of elevated blood sugars. Essentially, if someone is resistant to insulin, the body can, to some degree, increase production of insulin and overcome the level of resistance. After time, if production decreases and insulin cannot be released as vigorously, hyperglycemia develops.
Diabetes mellitus is classified into four broad categories: type 1, type 2, gestational diabetes, and "other specific types".[11] The "other specific types" are a collection of a few dozen individual causes.[11] Diabetes is a more variable disease than once thought and people may have combinations of forms.[37] The term "diabetes", without qualification, usually refers to diabetes mellitus.
To explain what hemoglobin A1c is, think in simple terms. Sugar sticks, and when it's around for a long time, it's harder to get it off. In the body, sugar sticks too, particularly to proteins. The red blood cells that circulate in the body live for about three months before they die off. When sugar sticks to these hemoglobin proteins in these cells, it is known as glycosylated hemoglobin or hemoglobin A1c (HBA1c). Measurement of HBA1c gives us an idea of how much sugar is present in the bloodstream for the preceding three months. In most labs, the normal range is 4%-5.9 %. In poorly controlled diabetes, its 8.0% or above, and in well controlled patients it's less than 7.0% (optimal is <6.5%). The benefits of measuring A1c is that is gives a more reasonable and stable view of what's happening over the course of time (three months), and the value does not vary as much as finger stick blood sugar measurements. There is a direct correlation between A1c levels and average blood sugar levels as follows.
No single environmental trigger has been identified as causing diabetes mellitus, however both infectious agents and dietary factors are thought to be important. Various viruses have been implicated in the development of type I DM. They may act by initiating or modifying the autoimmune process. In particular, the rubella virus and coxsackie viruses have been closely studied. In particular, congenital rubella infection has shown direct relationships with the development of type 1 diabetes mellitus. This is presumably due to the virus (or antibodies against it) damaging the beta cells of the pancreas. Some research has looked at dietary factors that may be associated with type 1 diabetes. In particular, cow’s milk proteins (such as bovine serum albumin) which may have some similarities to pancreatic islet cell markers may be able to trigger the autoimmune process. Other chemicals including nitrosamines have been identified as causes of diabetes mellitus in animal models, but not in humans.
Your body is like a car—it needs fuel to function. Its primary source of fuel is glucose (sugar), which is gained from foods that contain carbohydrates that get broken down. Insulin, a hormone produced by the pancreas, takes sugar from your blood to your cells to use for energy. However, when you have diabetes, either your pancreas isn't making enough insulin or the insulin that your body is making isn't being used the way it's supposed to be, typically because the cells become resistant to it.

Sugary breath isn’t as sweet as it seems.  Diabetics often notice that they’ve developed sweet or nail-polish-like breath before they’re diagnosed. However, if you’re dealing with this strange symptom, time is of the essence. Sweet breath is often a sign of diabetic ketoacidosis, a condition in which your body can’t effectively convert glucose into energy, keeping your blood sugar at dangerous—potentially fatal—levels if untreated.
Insulin is vital to patients with type 1 diabetes - they cannot live without a source of exogenous insulin. Without insulin, patients with type 1 diabetes develop severely elevated blood sugar levels. This leads to increased urine glucose, which in turn leads to excessive loss of fluid and electrolytes in the urine. Lack of insulin also causes the inability to store fat and protein along with breakdown of existing fat and protein stores. This dysregulation, results in the process of ketosis and the release of ketones into the blood. Ketones turn the blood acidic, a condition called diabetic ketoacidosis (DKA). Symptoms of diabetic ketoacidosis include nausea, vomiting, and abdominal pain. Without prompt medical treatment, patients with diabetic ketoacidosis can rapidly go into shock, coma, and even death may result.
After eating carbohydrates, the carbs break down into sugar, trigger the pancreas to produce insulin and are then stored in liver and muscles. However, there is a limit to the amount of sugar the liver and muscles can store. The easiest way to understand this is to think of your liver and muscles as small closets without much storage space. If sugar keeps coming in, the closet will quickly fill up.
Progression toward type 2 diabetes may even be self-perpetuating. Once a person begins to become insulin resistant, for whatever reason, things may snowball from there. The increased levels of circulating insulin required to compensate for resistance encourage the body to pack on pounds. That extra weight will in turn make the body more insulin resistant. Furthermore, the heavier a person is, the more difficult it can be to exercise, continuing the slide toward diabetes.
Clinistix and Diastix are paper strips or dipsticks that change color when dipped in urine. The test strip is compared to a chart that shows the amount of glucose in the urine based on the change in color. The level of glucose in the urine lags behind the level of glucose in the blood. Testing the urine with a test stick, paper strip, or tablet that changes color when sugar is present is not as accurate as blood testing, however it can give a fast and simple reading.
The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.[74]

There is no single gene that “causes” type 1 diabetes. Instead, there are a large number of inherited factors that may increase an individual’s likelihood of developing diabetes. This is known as multifactorial inheritance. The genes implicated in the development of type 1 diabetes mellitus control the human leukocyte antigen (HLA) system. This system is involved in the complex process of identifying cells which are a normal part of the body, and distinguishing them from foreign cells, such as those of bacteria or viruses. In an autoimmune disease such as diabetes mellitus, this system makes a mistake in identifying the normal ‘self’ cells as ‘foreign’, and attacks the body.  
Creatinine is a chemical waste molecule that is generated from muscle metabolism. Creatinine is produced from creatine, a molecule of major importance for energy production in muscles. Creatinine has been found to be a fairly reliable indicator of kidney function. As the kidneys become impaired the creatinine level in the blood will rise. Normal levels of creatinine in the blood vary from gender and age of the individual.
A healthy lifestyle can prevent almost all cases of type 2 diabetes. A large research study called the Diabetes Prevention Program, found that patients who made intensive changes including diet and exercise, reduced their risk of developing diabetes by 58%. Patients who were over 60 years old seemed to experience extra benefit; they reduced their risk by 71%. In comparison, patients who were given the drug metformin for prevention only reduced their risk by 31%.
Type 1 diabetes has some connection to your family genes, but that doesn't mean you'll get it if one of your parents had it. "Since not all identical twins get diabetes, we do think that exposure to an additional environmental factor may trigger an immune response that ultimately causes destruction of the insulin-producing cells of the pancreas," says Dr. Sarah R. Rettinger, an endocrinologist with Providence Saint John's Health Center in Santa Monica, California.
In ‘type 2 diabetes’ (previously called non-insulin-dependent diabetes mellitus), which accounts for 90% of all diabetes, the beta cells do not stop making insulin completely, but the insulin produced does not work properly so it struggles to store the sugar found in the blood. As a consequence, the pancreas has to produce more insulin to compensate for this reduction in insulin function. This is called insulin resistance and is commonly linked to obesity. This type of diabetes is seen more commonly over the age of 40 years but can occur at any age.  
With type 1, a disease that often seems to strike suddenly and unexpectedly, the effects of environment and lifestyle are far less clear. But several theories attempt to explain why cases of type 1 have increased so dramatically in recent decades, by around 5 percent per year since 1980. The three main suspects now are too little sun, too good hygiene, and too much cow's milk.
A study by Dabelea et al found that in teenagers and young adults in whom diabetes mellitus had been diagnosed during childhood or adolescence, diabetes-related complications and comorbidities—including diabetic kidney disease, retinopathy, and peripheral neuropathy (but not arterial stiffness or hypertension)—were more prevalent in those with type 2 diabetes than in those with type 1 disease. [44]

In type 2 diabetes (formerly called non– insulin-dependent diabetes or adult-onset diabetes), the pancreas often continues to produce insulin, sometimes even at higher-than-normal levels, especially early in the disease. However, the body develops resistance to the effects of insulin, so there is not enough insulin to meet the body’s needs. As type 2 diabetes progresses, the insulin-producing ability of the pancreas decreases.
In addition to learning about diabetes itself, older people may have to learn how to fit management of diabetes in with their management of other disorders. Learning about how to avoid complications, such as dehydration, skin breakdown, and circulation problems, and to manage factors that can contribute to complications of diabetes, such as high blood pressure and high cholesterol levels, is especially important. Such problems become more common as people age, whether they have diabetes or not.

It is clearly established that diabetes mellitus is not a single disease but a genetically heterogeneous group of disorders that share glucose intolerance in common (4–7). The concept of genetic heterogeneity (i.e. that different genetic and/or environmental etiologic factors can result in similar phenotypes) has significantly altered the genetic analysis of this common disorder. Diabetes and glucose intolerance are not diagnostic terms, but, like anemia, simply describe symptoms and/or laboratory abnormalities that can have a number of distinct etiologies.
Periodontal Disease. Periodontal disease is a commonly observed dental problem for patients with diabetes. It is similar to the periodontal disease encountered among nondiabetic patients. However, as a consequence of the impaired immunity and healing associated with diabetes, it may be more severe and progress more rapidly (see Right). The potential for these changes points to the need for periodic professional evaluation and treatment.
Type 2 diabetes, which is often diagnosed when a person has an A1C of at least 7 on two separate occasions, can lead to potentially serious issues, like neuropathy, or nerve damage; vision problems; an increased risk of heart disease; and other diabetes complications. A person’s A1C is the two- to three-month average of his or her blood sugar levels.
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