In people with type 1 diabetes, the symptoms often begin abruptly and dramatically. A serious condition called diabetic ketoacidosis, a complication in which the body produces excess acid, may quickly develop. In addition to the usual diabetes symptoms of excessive thirst and urination, the initial symptoms of diabetic ketoacidosis also include nausea, vomiting, fatigue, and—particularly in children—abdominal pain. Breathing tends to become deep and rapid as the body attempts to correct the blood’s acidity (see Acidosis), and the breath smells fruity and like nail polish remover. Without treatment, diabetic ketoacidosis can progress to coma and death, sometimes very quickly.
The causes of diabetes mellitus are unclear, however, there seem to be both hereditary (genetic factors passed on in families) and environmental factors involved. Research has shown that some people who develop diabetes have common genetic markers. In Type I diabetes, the immune system, the body's defense system against infection, is believed to be triggered by a virus or another microorganism that destroys cells in the pancreas that produce insulin. In Type II diabetes, age, obesity, and family history of diabetes play a role.
Low blood sugar (hypoglycemia), is common in people with type 1 and type 2 DM. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and (rarely) permanent brain damage or death in severe cases. Moderately low blood sugar may easily be mistaken for drunkenness; rapid breathing and sweating, cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in sugar. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
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.
Unexplained weight loss can happen for lots of reasons, and diabetes is one of them. Goundan explains that insulin helps your body move sugar from your blood to your cells, so when you have an insulin resistance, you don’t get enough energy into your cells despite all that sugar flowing through your body. “Because you’re unable to get enough energy from sugar, your body burns your own fat and muscle for energy," Kellis says. "Weight loss can be pretty significant, sometimes 10 to 20 pounds."
Endocrinology A chronic condition which affects ±10% of the general population, characterized by ↑ serum glucose and a relative or absolute ↓ in pancreatic insulin production, or ↓ tissue responsiveness to insulin; if not properly controlled, the excess glucose damages blood vessels of the eyes, kidneys, nerves, heart Types Insulin dependent–type I and non-insulin dependent–type II diabetes Symptoms type 1 DM is associated with ↑ urine output, thirst, fatigue, and weight loss (despite an ↑ appetite), N&V; type 2 DM is associated with, in addition, non-healing ulcers, oral and bladder infections, blurred vision, paresthesias in the hands and feet, and itching Cardiovascular MI, stoke Eyes Retinal damage, blindness Legs/feet Nonhealing ulcers, cuts leading to gangrene and amputation Kidneys HTN, renal failure Neurology Paresthesias, neuropathy Diagnosis Serum glucose above cut-off points after meals or when fasting; once therapy is begun, serum levels of glycosylated Hb are measured periodically to assess adequacy of glucose control Management Therapy reflects type of DM; metformin and triglitazone have equal and additive effects on glycemic control Prognosis A function of stringency of glucose control and presence of complications. See ABCD Trial, Brittle diabetes, Bronze diabetes, Chemical diabetes, Gestational diabetes, Insulin-dependent diabetes, Metformin, MODY diabetes, Nephrogenic diabetes insipidus, Non-insulin-dependent diabetes mellitus, Pseudodiabetes, Secondary diabetes, Starvation diabetes, Troglitazone.
Several tests are helpful in identifying DM. These include tests of fasting plasma glucose levels, casual (randomly assessed) glucose levels, or glycosylated hemoglobin levels. Diabetes is currently established if patients have classic diabetic symptoms and if on two occasions fasting glucose levels exceed 126 mg/dL (> 7 mmol/L), random glucose levels exceed 200 mg/dL (11.1 mmol/L), or a 2-hr oral glucose tolerance test is 200 mg/dL or more. A hemoglobin A1c test that is more than two standard deviations above normal (6.5% or greater) is also diagnostic of the disease.
When you have diabetes, it’s important to avoid eating many packaged, processed snacks such as cookies, chips, cake, granola bars, and the like, in lieu of fresh, whole foods, like fiber-rich fruits, veggies, and whole grains. (27) Eating foods high in fiber can help keep blood sugar levels steady and fill you up, potentially promoting weight loss and improving insulin sensitivity. (28)
Hyperglycemia (ie, random blood glucose concentration of more than 200 mg/dL or 11 mmol/L) results when insulin deficiency leads to uninhibited gluconeogenesis and prevents the use and storage of circulating glucose. The kidneys cannot reabsorb the excess glucose load, causing glycosuria, osmotic diuresis, thirst, and dehydration. Increased fat and protein breakdown leads to ketone production and weight loss. Without insulin, a child with type 1 diabetes mellitus wastes away and eventually dies due to DKA. The effects of insulin deficiency are shown in the image below.
Get to Know Your Medications: If you have diabetes, it is important to know and understand what your medications do. This can help to keep blood sugars controlled and prevent low and high blood sugars. Certain medicines need to be taken with food, or they will cause your blood sugar will drop. There are so many diabetes medications out there. Being your own advocate can help you. Make sure to tell your doctor if your medications are too expensive or if they are causing any side effects. If your medication regimen is not working for you, odds are your doctor can find a new medicine that might work better.
The problem with sugar, regardless of type, is the sheer amount of it that’s found in the Standard American Diet (SAD), which is the typical eating plan many people in the United States — as well as those in an increasing number of modernized countries — have developed a taste for. When consumed in excess, foods in this category can lead to heart disease, stroke, and other serious health issues. “Often, foods with added sugar also contain fat,” explains Grieger, noting that these components go hand in hand when it comes to the risk for insulin resistance, the hallmark of type 2 diabetes.
Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
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Type 2 diabetes is a preventable disease that affects more than 9 percent of the U.S. population, or about 29 million people. According to the Centers for Disease Control and Prevention, more than a quarter — some 8 million people — remain undiagnosed. With complications including nerve damage, kidney damage, poor blood circulation, and even death, it’s important for us all to know the early signs of type 2 diabetes.