The prevalence of type 2 diabetes has increased dramatically over the past decade. From 1985 to 2010, the total number of people with diabetes worldwide increased from 30 million to 285 million, and this number is expected to reach 438 million by 2030. Although both type 1 and type 2 diabetes have increased, the increase in type 2 diabetes has been much more rapid and pronounced, which may be due to increasing obesity rates, decreasing physical activity levels, and aging populations. Today, diabetes is a major cause of death worldwide, ranking as the seventh leading cause of death in 2007 and the fifth leading cause of death in 2010.<\/p>\n
The criteria for diagnosing type 2 diabetes based on the latest scientific conventions are as follows:<\/p>\n
Diabetes symptoms + a random blood sugar above 200 mg\/dl (random sugar is sugar that is taken without regard to the last meal eaten.)
\nUndetected sugar above 126 mg\/dl (fasting sugar should be taken after at least 8 hours of fasting)
\nTwo-hour sugar above 200 mg\/dl (sample is taken two hours after eating 75 grams of glucose dissolved in water.)
\nHbA1C above 6.5<\/p>\n
Fasting sugar between 100 and 125 mg\/dl
\nTwo-hour sugar between 140 and 199
\n<6.4 HbA1C <7.5<\/p>\n
People with impaired blood sugar homeostasis are not considered diabetic but have a higher risk of developing type 2 diabetes and in In fact, people are called prediabetics. These people have an increased risk of cardiovascular diseases.<\/p>\n
Today, it is recommended that all people over the age of 45 be screened for type 2 diabetes every three years, and if a person is overweight (BMI>25Kg\/m2) or has a risk factor for type 2 diabetes, screening should begin at age 45.<\/p>\n
The importance of screening:<\/p>\n
Many people have had their disease for years (even a decade) when they are diagnosed with diabetes.<\/p>\n
Many people have no symptoms when they are diagnosed.<\/p>\n
Many people have complications of diabetes (diabetic retinopathy) at the time of diagnosis.<\/p>\n
Early treatment and prevention of type 2 diabetes can change the nature and outcome of the disease in these people.<\/p>\n
Family history of type 2 diabetes (parent, brother or sister)
\nBMI>25Kg\/m2
\nInactivity
\nRace
\nImpaired fasting glucose or HbA1C or impaired 2-hour glucose
\nHistory of gestational diabetes or history of giving birth to a baby weighing more than 4 kg
\nHigh blood pressure BP>140\/90
\nImpaired HDL cholesterol<35 or TG>250
\nPolycystic ovary syndrome
\nCardiovascular disease<\/p>\n
Insulin resistance and abnormal insulin secretion are the two main factors known to cause this disease. It seems that although both of the above factors are effective in the development of this disease, the first step is resistance to the hormone insulin, but the disease occurs when the amount of insulin secretion is not sufficient.<\/p>\n
Deficiency in insulin secretion 2) Insulin resistance 3) Increased glucose production in the liver 4) Impaired fat metabolism<\/p>\n
In the early stages of the disease, glucose levels are normal despite the fact that there is insulin resistance in the cells. Therefore, maintaining normal blood sugar occurs at the expense of increasing insulin production in the pancreatic beta cells. As this situation continues, the pancreatic beta cells are no longer able to compensate for this resistance, while insulin resistance also progresses, resulting in impaired 2-hour blood sugar, and gradually the person moves towards clear diabetes and increased fasting blood sugar. In fact, when there is insulin resistance, the uptake of insulin by the body’s cells, in the presence of insulin, is reduced compared to normal people (30-60%), and this causes glucose-sensitive cells to force the liver to produce more glucose, so despite the presence of unused glucose in the bloodstream, more glucose is produced by the liver and enters the bloodstream, and the person now suffers from fasting hyperglycemia (increased blood sugar).<\/p>\n
Just as an abnormal and pathological increase in sugar production by the liver causes an increase in fasting sugar. The failure of the body’s cells to absorb sugar due to resistance to the hormone insulin causes an increase in blood sugar after a meal.<\/p>\n
The origin of insulin resistance in diabetes is not yet fully understood, but two factors, genetics and obesity, are known to play a significant role.<\/p>\n
Obesity, especially central and visceral types, is known to be very effective in the pathogenesis of type 2 diabetes. Increased fat cell mass increases the level of circulating fatty acids and some adipokines. Adipokines are substances that play a role in controlling weight, appetite, and energy content. In addition to the above, adipokines also regulate insulin sensitivity. Increased levels of fatty acids and adipokines can increase insulin resistance in muscle tissue and liver, and therefore increased adipokines cause decreased glucose uptake by muscle cells, increased glucose production in the liver, and impaired pancreatic beta cell function. In contrast, the production of adiponectin (a peptide that plays a role in increasing the sensitivity of cell receptors to insulin) by fat cells is reduced in obesity.<\/p>\n
On the other hand, fat cell products and adipokines cause an inflammatory state in which inflammatory factors such as IL6 and CRP are increased in patients with type 2 diabetes.<\/p>\n
The reason why the compensatory capacity of pancreatic beta cells decreases over time in people with type 2 diabetes is still unknown, but pathological studies have suggested some hypotheses. For example, it is possible that a genetic defect adds to the above problems and causes beta cell loss. In people with fully established diabetes, the number of pancreatic beta cells decreases to less than 50%.<\/p>\n
Amyloid polypeptides of pancreatic islets, or amylin, are also secreted from beta cells simultaneously with insulin, and amyloid fibrils or strands deposited in the pancreatic islets are seen in people with diabetes.<\/p>\n
On the other hand, the metabolic status of people with type 2 diabetes can also be effective in beta cell dysfunction. For example, hyperglycemia or high blood sugar causes beta cell dysfunction (glucose toxicity), which causes blood sugar to rise (due to decreased insulin secretion), and consequently, it has been seen that better blood sugar control improves insulin secretion from beta cells.<\/p>\n
On the other hand, an increase in free fatty acids in the bloodstream, or in other words, lipid toxicity, can also cause further dysfunction in pancreatic beta cell function.<\/p>\n
Insulin resistance causes hepatic gluconeogenesis (production of glucose in the liver) to not be suppressed despite high blood sugar levels, and this is what causes fasting blood sugar levels to increase in diabetics.<\/p>\n
On the other hand, insulin resistance in adipose tissue causes the production of free fatty acids by adipose tissue to increase and their release into the blood from adipose tissue to increase, especially VLDL, which causes triglyceride production in the liver, which causes the phenomenon of non-alcoholic fatty liver in diabetics, while dyslipidemia also occurs in these people.<\/p>\n
Type 2 diabetes often occurs after a period of impaired fasting or 2-hour blood sugar, and some medications and lifestyle adjustments can delay or even prevent its onset.<\/p>\n
A diabetes prevention program that includes major lifestyle changes (i.e., exercise for at least 30 minutes, 5 times a week + a low-fat, low-carb diet) delays or eliminates the onset of diabetes by up to 85%. These lifestyle changes have had a similar effect in all age, gender, and race groups.<\/p>\n
Metformin, as a drug, has been shown to prevent or delay the onset of diabetes by up to 31% compared to placebo in studies.<\/p>\n
Therefore, individuals with a positive and specific history of type 2 diabetes in their first-degree relatives (father, mother, siblings) or individuals with a history of impaired fasting or 2-hour glucose should be included in the diabetes prevention program and are strongly encouraged to do so.<\/p>\n
Adopting a drug program for diabetes prevention is still debated in the scientific community and there is still no evidence of their cost-effectiveness. The benefit of using this drug against its harm has not yet been carefully monitored. However, the American Diabetes Association has recommended that for individuals with impaired fasting or 2-hour glucose and at high risk for developing diabetes, namely age less than 60 years, BMI <35 and a positive family history, high TG, low HDL, HTN and HbA1C>6, it is better to undergo drug prevention with metformin.<\/p>\n
Diabetic ketoacidosis and hyperosmolar hyperglycemia are two emergencies or acute complications that may occur in people with diabetes.
\nDKA or diabetic ketoacidosis is often considered an emergency of type 1 diabetes, but it has now been proven that it may occur in some types of type 2 diabetes and some races in certain cases. Hyperosmolar hyperglycemia is only seen in type 2 diabetes. In both cases, there is a lack or deficiency of insulin, loss of body water volume for any reason and a disturbance in acid-base homeostasis, and in most cases, both of these conditions occur following an undiagnosed acute pre-existing condition in a diabetic person.<\/p>\n
In diabetic ketoacidosis following an acute illness, symptoms such as nausea and vomiting, acute abdominal pain similar to that of pancreatitis or visceral rupture, glucosuria (presence of glucose in the urine), dehydration, and tachycardia (increased heart rate). Hypotension in these patients may be due to volume depletion and vascular dilation. A fruity odor is present from the patient’s breath, which is due to metabolic acidosis and increased acetone. Cosmic respiration (rapid and shallow secondary to metabolic acidosis) and ultimately lethargy or CNS depression and cerebral edema, which is a dangerous and severe complication that is often seen in children who are newly diagnosed with type 1 diabetes due to lack of timely treatment.<\/p>\n
Some conditions that can cause DKA or HHS in type 1 or type 2 diabetes include: Insufficient insulin use Infectious diseases such as pneumonia, UTI, gastroenteritis, sepsis SEPSIS Cerebral, coronary, mesenteric and peripheral vascular strokes Narcotics Pregnancy<\/p>\n
The typical face of these patients is an elderly person with type 2 diabetes with a history of several weeks of polyuria (increased urination), weight loss, and decreased food and fluid intake for any reason (usually seen in elderly people with brain problems).<\/p>\n
Clinical examination reveals dehydration (dehydration), hyperosmolarity, hypotension, tachycardia (increased heart rate), and altered state of consciousness (loss of consciousness).<\/p>\n
Infectious diseases such as pneumonia, urinary tract infection, heart and stroke, sepsis, dementia, or any factor in which a diabetic person intentionally or unintentionally avoids eating and drinking can lead him to hyperosmolar hyperglycemia.<\/p>\n
Treatment of both acute complications of diabetes, HHS and DKA, is considered a medical emergency and must be performed by experienced specialists in a hospital setting, following hospitalization, and outpatient treatment is not possible.<\/p>\n
Chronic complications of diabetes can involve many organs and cause many disabilities and disorders in the quality of life of people with diabetes.<\/p>\n
Chronic complications are divided into two groups: vascular and non-vascular. Vascular complications are divided into two groups: microvascular complications (retinopathy, neuropathy and nephropathy) and macrovascular (coronary artery disease (CHD), peripheral artery disease (PAD), cerebrovascular complications)<\/p>\n
Non-vascular complications include gastroparesis (paralysis and decreased efficiency of the stomach nerves), infections, skin changes, hearing loss in very long-standing diabetes, cataracts and gum disease.<\/p>\n
The probability and risk of chronic complications of diabetes are related to two indicators: the duration of diabetes and the severity of hyperglycemia (high blood sugar), and these two factors are often inseparable from each other.<\/p>\n
In people with type 2 diabetes, chronic complications of the disease are often established before the diagnosis of the disease (during the asymptomatic period of the disease).<\/p>\n
According to studies, it seems that the risk of microvascular complications of diabetes increases significantly with chronic hyperglycemia. However, according to studies, this increased susceptibility to some of these complications may have a genetic basis, meaning that two people with similar blood sugar monitoring (before and after meals and HbA1C) have different chances of developing microvascular complications. Regarding macrovascular complications, a clear relationship between the level of chronic hyperglycemia and the occurrence of complications has not been found, although in some studies, the incidence of heart attacks and strokes has been reported to be two to four times higher than in normal people. Of course, risk factors such as high blood pressure or impaired blood lipid profile are known to be contributing factors in the occurrence of these complications (macrovascular) in people with diabetes.<\/p>\n
Blood sugar control is generally possible in two ways:<\/p>\n
Very intensive control or in other words Intensive diabetes management<\/p>\n
Conventional and normal blood sugar control<\/p>\n
In the first method, they receive insulin several times a day, undergo careful training and are under intensive and precise clinical support. In this method, the target HbA1C is less than 7.3%.<\/p>\n
In the traditional method, blood sugar is done solely with the aim of preventing complications. They receive insulin twice a day, receive less nutritional education and are less screened for chronic complications. In this method, the target HbA1C is less than 9.1%.<\/p>\n
In a study, people whose only risk factor for micro- and macrovascular diseases was diabetes and who were relatively young and without complications were divided into two groups. Each group was treated with one of the above methods. The results of the studies show that intensive blood sugar control can significantly reduce the risk of microvascular complications, improve the quality of life of the individual and increase his life expectancy (HbA1C <7.3), but the risk of macrovascular complications did not show a significant difference in this study.<\/p>\n
In general, it is believed that each number that is reduced from the HbA1C of the individuals can reduce the risk of microvascular complications by about 30% and the goal of control for every diabetic individual is to reach a HbA1C close to normal. Therefore, it is important to note that the ability of the individuals to carry out this treatment program must be considered. In many people, intensive diabetes management is not possible, so today it is recommended that you bring your blood sugar, and especially your HbA1C, as close to normal as possible.<\/p>\n
On the other hand, studies have proven that controlling blood pressure and keeping BP below 144\/82 is as important as controlling blood sugar, and even more so, in preventing micro- and macrovascular complications.<\/p>\n","protected":false},"excerpt":{"rendered":"
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