Diabetes may have symptoms in some people, and no symptoms in others. Generally, people with Type 1 diabetes have increased thirst (polydipsia), frequent urination (polyuria), and increased hunger (polyphagia). Symptoms may develop over weeks to months. Untreated, this condition may cause a person to lose consciousness and become very ill (diabetic ketoacidosis).
Elevated homocysteine levels in the blood called hyperhomocysteinemia, is a sign that the body isn't producing enough of the amino acid homocysteine. is a rare and serious condition that may be inherited (genetic). People with homocystinuria die at an early age. Symptoms of hyperhomocysteinemia include developmental delays, osteoporosis, blood clots, heart attack, heart disease, stroke, and visual abnormalities.
Onset of type 2 diabetes can be delayed or prevented through proper nutrition and regular exercise. Intensive lifestyle measures may reduce the risk by over half. The benefit of exercise occurs regardless of the person's initial weight or subsequent weight loss. High levels of physical activity reduce the risk of diabetes by about 28%. Evidence for the benefit of dietary changes alone, however, is limited, with some evidence for a diet high in green leafy vegetables and some for limiting the intake of sugary drinks. In those with impaired glucose tolerance, diet and exercise either alone or in combination with metformin or acarbose may decrease the risk of developing diabetes. Lifestyle interventions are more effective than metformin. A 2017 review found that, long term, lifestyle changes decreased the risk by 28%, while medication does not reduce risk after withdrawal. While low vitamin D levels are associated with an increased risk of diabetes, correcting the levels by supplementing vitamin D3 does not improve that risk.
The levels of glucose in the blood vary normally throughout the day. They rise after a meal and return to pre-meal levels within about 2 hours after eating. Once the levels of glucose in the blood return to premeal levels, insulin production decreases. The variation in blood glucose levels is usually within a narrow range, about 70 to 110 milligrams per deciliter (mg/dL) of blood in healthy people. If people eat a large amount of carbohydrates, the levels may increase more. People older than 65 years tend to have slightly higher levels, especially after eating.
While many experts believe that most type 1 genes have been identified, the situation with type 2 diabetes is much different. A recent study found that the known genetic links to type 2 probably account for only about 6 percent of the genetic predisposition for that form of diabetes. This could mean either that some of the genes discovered have a bigger effect than is currently believed or that "we are still missing 94 percent of the genes," says Atul Butte, MD, PhD, an assistant professor of pediatrics at Stanford University.
People with type 1 diabetes and certain people with type 2 diabetes may use carbohydrate counting or the carbohydrate exchange system to match their insulin dose to the carbohydrate content of their meal. "Counting" the amount of carbohydrate in a meal is used to calculate the amount of insulin the person takes before eating. However, the carbohydrate-to-insulin ratio (the amount of insulin taken for each gram of carbohydrate in the meal) varies for each person, and people with diabetes need to work closely with a dietician who has experience in working with people with diabetes to master the technique. Some experts have advised use of the glycemic index (a measure of the impact of an ingested carbohydrate-containing food on the blood glucose level) to delineate between rapid and slowly metabolized carbohydrates, although there is little evidence to support this approach.
The body’s immune system is responsible for fighting off foreign invaders, like harmful viruses and bacteria. In people with type 1 diabetes, the immune system mistakes the body’s own healthy cells for foreign invaders. The immune system attacks and destroys the insulin-producing beta cells in the pancreas. After these beta cells are destroyed, the body is unable to produce insulin.
Clinical Manifestations. Diabetes mellitus can present a wide variety of symptoms, from none at all to profound ketosis and coma. If the disease manifests itself late in life, patients may not know they have it until it is discovered during a routine examination, or when the symptoms of chronic vascular disease, insidious renal failure, or impaired vision cause them to seek medical help.
Diabetes is a chronic condition, and it can last an entire lifetime. The goal of treating diabetes is to keep blood glucose levels as close to a normal range as possible. This prevents the symptoms of diabetes and the long-term complications of the condition. If you've been diagnosed with diabetes, your doctor – working with the members of your diabetes care team – will help you find your target blood glucose levels.
Insulin is a hormone that is produced by specialized cells (beta cells) of the pancreas. (The pancreas is a deep-seated organ in the abdomen located behind the stomach.) In addition to helping glucose enter the cells, insulin is also important in tightly regulating the level of glucose in the blood. After a meal, the blood glucose level rises. In response to the increased glucose level, the pancreas normally releases more insulin into the bloodstream to help glucose enter the cells and lower blood glucose levels after a meal. When the blood glucose levels are lowered, the insulin release from the pancreas is turned down. It is important to note that even in the fasting state there is a low steady release of insulin than fluctuates a bit and helps to maintain a steady blood sugar level during fasting. In normal individuals, such a regulatory system helps to keep blood glucose levels in a tightly controlled range. As outlined above, in patients with diabetes, the insulin is either absent, relatively insufficient for the body's needs, or not used properly by the body. All of these factors cause elevated levels of blood glucose (hyperglycemia).
Patients with type 1 DM, unless they have had a pancreatic transplant, require insulin to live; intensive therapy with insulin to limit hyperglycemia (“tight control”) is more effective than conventional therapy in preventing the progression of serious microvascular complications such as kidney and retinal diseases. Intensive therapy consists of three or more doses of insulin injected or administered by infusion pump daily, with frequent self-monitoring of blood glucose levels as well as frequent changes in therapy as a result of contacts with health care professionals. Some negative aspects of intensive therapy include a three times more frequent occurrence of severe hypoglycemia, weight gain, and an adverse effect on serum lipid levels, i.e., a rise in total cholesterol, LDL cholesterol, and triglycerides and a fall in HDL cholesterol. Participation in an intensive therapy program requires a motivated patient, but it can dramatically reduce eye, nerve, and renal complications compared to conventional therapy. See: insulin pump for illus.
How does type 2 diabetes progress over time? Type 2 diabetes is a progressive disease, meaning that the body’s ability to regulate blood sugar gets worse over time, despite careful management. Over time, the body’s cells become increasingly less responsive to insulin (increased insulin resistance) and beta cells in the pancreas produce less and less insulin (called beta-cell burnout). In fact, when people are diagnosed with type 2 diabetes, they usually have already lost up to 50% or more of their beta cell function. As type 2 diabetes progresses, people typically need to add one or more different types of medications. The good news is that there are many more choices available for treatments, and a number of these medications don’t cause as much hypoglycemia, hunger and/or weight gain (e.g., metformin, pioglitazone, DPP-4 inhibitors, GLP-1 agonists, SGLT-2 inhibitors, and better insulin). Diligent management early on can help preserve remaining beta cell function and sometimes slow progression of the disease, although the need to use more and different types of medications does not mean that you have failed.
American Diabetes Association Joslin Diabetes Center Mayo Clinic International Diabetes Federation Canadian Diabetes Association National Institute of Diabetes and Digestive and Kidney Diseases Diabetes Daily American Heart Association Diabetes Forecast Diabetic Living American Association of Clinical Endocrinologists European Association for the Study of Diabetes
On behalf of the millions of Americans who live with or are at risk for diabetes, we are committed to helping you understand this chronic disease. Help us set the record straight and educate the world about diabetes and its risk factors by sharing the common questions and answers below. If you're new to type 2 diabetes, join our Living With Type 2 Diabetes program to get more facts.
Jump up ^ Ahlqvist, Emma; Storm, Petter; Käräjämäki, Annemari; Martinell, Mats; Dorkhan, Mozhgan; Carlsson, Annelie; Vikman, Petter; Prasad, Rashmi B; Aly, Dina Mansour (2018). "Novel subgroups of adult-onset diabetes and their association with outcomes: a data-driven cluster analysis of six variables". The Lancet Diabetes & Endocrinology. 0 (5): 361–369. doi:10.1016/S2213-8587(18)30051-2. ISSN 2213-8587. PMID 29503172.
observations The onset of type 1 diabetes mellitus is sudden in children. Type 2 diabetes often begins insidiously. Characteristically the course is progressive and includes polyuria, polydipsia, weight loss, polyphagia, hyperglycemia, and glycosuria. The eyes, kidneys, nervous system, skin, and circulatory system may be affected by the long-term complications of either type of diabetes; infections are common; and atherosclerosis often develops. In type 1 diabetes mellitus, when no endogenous insulin is being secreted, ketoacidosis is a constant danger. The diagnosis is confirmed by fasting plasma glucose and history.
Most cases (95%) of type 1 diabetes mellitus are the result of environmental factors interacting with a genetically susceptible person. This interaction leads to the development of autoimmune disease directed at the insulin-producing cells of the pancreatic islets of Langerhans. These cells are progressively destroyed, with insulin deficiency usually developing after the destruction of 90% of islet cells.