Older people may have a difficult time adding exercise to their daily life, particularly if they have not been active or if they have a disorder that limits their movement, such as arthritis. However, they may be able to add exercise to their usual routine. For example, they can walk instead of drive or climb the stairs instead of take the elevator. Also, many community organizations offer exercise programs designed for older people.
Yet carbs are processed differently in the body based on their type: While simple carbs are digested and metabolized quickly, complex carbs take longer to go through this system, resulting in more stable blood sugar. “It comes down to their chemical forms: A simple carbohydrate has a simpler chemical makeup, so it doesn’t take as much for it to be digested, whereas the complex ones take a little longer,” Grieger explains.
; DM multiaetiology metabolic disease due to reduced/absent production of pancreatic insulin, and/or insulin resistance by peripheral tissue insulin receptors; characterized by reduced carbohydrate metabolism and increased fat and protein metabolism, leading to hyperglycaemia, increasing glycosuria, water and electrolyte imbalance, ketoacidosis, coma and death if left untreated; chronic long-term complications of DM include nephropathy, retinopathy, neuropathy and generalized degenerative changes in large and small arteries; treatment (with insulin/oral hypoglycaemic agents/diet) aims to stabilize blood glucose levels to the normal range (difficult to achieve fully; patients may tend to hyperglycaemia or hypoglycaemia due to mismanagement of glycaemic control); Tables D4-D7
If you are symptomatic (e.g., increased thirst or urination, unexplained weight loss), your doctor may only use a single test to diagnose diabetes/prediabetes. If you don't have any symptoms, one high blood glucose test doesn't necessarily mean you have diabetes/prediabetes. Your doctor will repeat one of the blood tests again on another day (generally 1 week later) to confirm the diagnosis.
Jump up ^ Picot, J; Jones, J; Colquitt, JL; Gospodarevskaya, E; Loveman, E; Baxter, L; Clegg, AJ (September 2009). "The clinical effectiveness and cost-effectiveness of bariatric (weight loss) surgery for obesity: a systematic review and economic evaluation". Health Technology Assessment. Winchester, England. 13 (41): iii–iv, 1–190, 215–357. doi:10.3310/hta13410. PMID 19726018.
"We know that there is a very large genetic component," Rettinger says. "A person with a first-degree relative with Type 2 diabetes has a five to 10 time higher risk of developing diabetes than a person the same age and weight without a family history of Type 2 diabetes." Heredity actually plays a larger role in Type 2 diabetes than Type 1, Rettinger says.

Family or personal history. Your risk increases if you have prediabetes — a precursor to type 2 diabetes — or if a close family member, such as a parent or sibling, has type 2 diabetes. You're also at greater risk if you had gestational diabetes during a previous pregnancy, if you delivered a very large baby or if you had an unexplained stillbirth.


Infections. Poorly controlled diabetes can lead to a variety of tissue infections. The most commonly encountered is a yeast infection (Candida) and the presence of dry mouth further increases one’s risk (see PATIENT INFORMATION SHEET – Oral Yeast Infections). Typically, affected areas appear redder than the surrounding tissue and commonly affected sites include the tongue, palate, cheeks, gums, or corners of the mouth (see Right). There is conflicting data regarding cavity risk in the diabetic patient, but those who have dry mouth are clearly at increased risk for developing cavities.
In Type II diabetes, the pancreas may produce enough insulin, however, cells have become resistant to the insulin produced and it may not work as effectively. Symptoms of Type II diabetes can begin so gradually that a person may not know that he or she has it. Early signs are lethargy, extreme thirst, and frequent urination. Other symptoms may include sudden weight loss, slow wound healing, urinary tract infections, gum disease, or blurred vision. It is not unusual for Type II diabetes to be detected while a patient is seeing a doctor about another health concern that is actually being caused by the yet undiagnosed diabetes.
Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels.[76][77] The goal of treatment is an HbA1C level of 6.5%, but should not be lower than that, and may be set higher.[78] Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise.[78] Specialized footwear is widely used to reduce the risk of ulceration, or re-ulceration, in at-risk diabetic feet. Evidence for the efficacy of this remains equivocal, however.[79]
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.

Normally, blood glucose levels are tightly controlled by insulin, a hormone produced by the pancreas. Insulin lowers the blood glucose level. When the blood glucose elevates (for example, after eating food), insulin is released from the pancreas to normalize the glucose level by promoting the uptake of glucose into body cells. In patients with diabetes, the absence of insufficient production of or lack of response to insulin causes hyperglycemia. Diabetes is a chronic medical condition, meaning that although it can be controlled, it lasts a lifetime.


Which came first: the diabetes or the PCOS? For many women, a diagnosis of polycystic ovary syndrome means a diabetes diagnosis isn’t far behind. PCOS and diabetes are both associated with insulin resistance, meaning there are similar hormonal issues at play in both diseases. Fortunately, managing your PCOS and losing weight may help reduce your risk of becoming diabetic over time.
Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly.[2] As the disease progresses, a lack of insulin may also develop.[12] This form was previously referred to as "non insulin-dependent diabetes mellitus" (NIDDM) or "adult-onset diabetes".[2] The most common cause is excessive body weight and insufficient exercise.[2]
Diabetes mellitus results mainly from a deficiency or diminished effectiveness of insulin that is normally produced by the beta cells of the pancreas. It is characterised by high blood sugar, altered sugar and glucose metabolism and this affects blood vessels and causes several organ damage. Causes of diabetes can be classified according to the types of diabetes.
The body will attempt to dilute the high level of glucose in the blood, a condition called hyperglycemia, by drawing water out of the cells and into the bloodstream in an effort to dilute the sugar and excrete it in the urine. It is not unusual for people with undiagnosed diabetes to be constantly thirsty, drink large quantities of water, and urinate frequently as their bodies try to get rid of the extra glucose. This creates high levels of glucose in the urine.
FIGURE 19-1 ■. This figure shows the hyperbolic relationship of insulin resistance and beta cell function. On the y-axis is beta cell function as reflected in the first-phase insulin response during intravenous (IV) glucose infusion; on the x-axis is insulin sensitivity and its mirror image resistance. In a subject with normal glucose tolerance (NGT) and beta-cell reserve, an increase in insulin resistance results in increased insulin release and normal glucose tolerance. In an individual for whom the capacity to increase insulin release is compromised, increasing insulin resistance with partial or no beta-cell compensation results in progression from normal glucose tolerance, to impaired glucose tolerance (IGT), and finally to diabetes (T2D). Differences between these categories are small at high insulin sensitivity, which may be maintained by weight reduction, exercise, and certain drugs. At a critical degree of insulin resistance, due to obesity or other listed factors, only a further small increment in resistance requires a large increase in insulin output. Those that can increase insulin secretion to this extent retain normal glucose tolerance; those who cannot achieve this degree of insulin secretion (e.g., due to a mild defect in genes regulating insulin synthesis, insulin secretion, insulin action, or an ongoing immune destruction of beta cells) now unmask varying degrees of carbohydrate intolerance. The product of insulin sensitivity (the reciprocal of insulin resistance) and acute insulin response (a measurement beta-cell function) has been called the “disposition index.” This index remains constant in an individual with normal beta cell compensation in response to changes in insulin resistance. IGT, impaired glucose tolerance; NGT, normal glucose tolerance; T2D, type 2 diabetes.

The American Diabetes Association recommends that blood sugars be 80mg/dL-130mg/dL before meals and less than or equal to 180mg/dL two hours after meals. Blood sugar targets are individualized based on a variety of factors such as age, length of diagnosis, if you have other health issues, etc. For example, if you are an elderly person, your targets maybe a bit higher than someone else. Ask your physician what targets are right for you.
Polyuria is defined as an increase in the frequency of urination. When you have abnormally high levels of sugar in your blood, your kidneys draw in water from your tissues to dilute that sugar, so that your body can get rid of it through the urine. The cells are also pumping water into the bloodstream to help flush out sugar, and the kidneys are unable to reabsorb this fluid during filtering, which results in excess urination.

The word mellitus (/məˈlaɪtəs/ or /ˈmɛlɪtəs/) comes from the classical Latin word mellītus, meaning "mellite"[114] (i.e. sweetened with honey;[114] honey-sweet[115]). The Latin word comes from mell-, which comes from mel, meaning "honey";[114][115] sweetness;[115] pleasant thing,[115] and the suffix -ītus,[114] whose meaning is the same as that of the English suffix "-ite".[116] It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a diabetic had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.
It is recommended that all people with type 2 diabetes get regular eye examination.[13] There is weak evidence suggesting that treating gum disease by scaling and root planing may result in a small short-term improvement in blood sugar levels for people with diabetes.[79] There is no evidence to suggest that this improvement in blood sugar levels is maintained longer than 4 months.[79] There is also not enough evidence to determine if medications to treat gum disease are effective at lowering blood sugar levels.[79]

The classic symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss.[23] Other symptoms that are commonly present at diagnosis include a history of blurred vision, itchiness, peripheral neuropathy, recurrent vaginal infections, and fatigue.[13] Many people, however, have no symptoms during the first few years and are diagnosed on routine testing.[13] A small number of people with type 2 diabetes mellitus can develop a hyperosmolar hyperglycemic state (a condition of very high blood sugar associated with a decreased level of consciousness and low blood pressure).[13]
Some older people cannot control what they eat because someone else is cooking for them—at home or in a nursing home or other institution. When people with diabetes do not do their own cooking, the people who shop and prepare meals for them must also understand the diet that is needed. Older people and their caregivers usually benefit from meeting with a dietitian to develop a healthy, feasible eating plan.
Which came first: the diabetes or the PCOS? For many women, a diagnosis of polycystic ovary syndrome means a diabetes diagnosis isn’t far behind. PCOS and diabetes are both associated with insulin resistance, meaning there are similar hormonal issues at play in both diseases. Fortunately, managing your PCOS and losing weight may help reduce your risk of becoming diabetic over time.
a broadly applied term used to denote a complex group of syndromes that have in common a disturbance in the oxidation and utilization of glucose, which is secondary to a malfunction of the beta cells of the pancreas, whose function is the production and release of insulin. Because insulin is involved in the metabolism of carbohydrates, proteins and fats, diabetes is not limited to a disturbance of glucose homeostasis alone.
Medications used to treat diabetes do so by lowering blood sugar levels. There is broad consensus that when people with diabetes maintain tight glucose control (also called "tight glycemic control") -- keeping the glucose levels in their blood within normal ranges - that they experience fewer complications like kidney problems and eye problems.[84][85] There is however debate as to whether this is cost effective for people later in life.[86]

Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.

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