Hypertension develops secondary to environmental factors, as well as multiple genes, whose inheritance appears to be complex. [12, 21] Furthermore, obesity, diabetes, and heart disease also have genetic components and contribute to hypertension. Epidemiological studies using twin data and data from Framingham Heart Study families reveal that BP has a substantial heritable component, ranging from 33-57%. [22, 23, 24]
Renovascular hypertension (RVHT) causes 0.2-4% of cases. Since the seminal experiment in 1934 by Goldblatt et al, [28] RVHT has become increasingly recognized as an important cause of clinically atypical hypertension and chronic kidney disease—the latter by virtue of renal ischemia. The coexistence of renal arterial vascular (ie, renovascular) disease and hypertension roughly defines this type of nonessential hypertension. More specific diagnoses are made retrospectively when hypertension is improved after intravascular intervention.
If you don't take your high blood pressure medications exactly as directed, your blood pressure can pay the price. If you skip doses because you can't afford the medications, because you have side effects or because you simply forget to take your medications, talk to your doctor about solutions. Don't change your treatment without your doctor's guidance.

Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/l (110 to 125 mg/dl) are considered to have impaired fasting glucose.[67] people with plasma glucose at or above 7.8 mmol/l (140 mg/dl), but not over 11.1 mmol/l (200 mg/dl), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease.[68] The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/l (100 to 125 mg/dl).[69]
Stress reduction techniques such as biofeedback or transcendental meditation may be considered as an add-on to other treatments to reduce hypertension, but do not have evidence for preventing cardiovascular disease on their own.[125][126][127] Self-monitoring and appointment reminders might support the use of other strategies to improve blood pressure control, but need further evaluation.[128]
Dietary changes: The health care provider might recommend a diet that includes more vegetables (especially leafy green vegetables), fruits, low-fat dairy products, and fiber-rich foods, and fewer carbohydrates, fats, processed foods, and sugary drinks. He or she also might recommend preparing low-sodium dishes and not adding salt to foods. Watch out for foods with lots of hidden salt (like bread, sandwiches, pizza, and many restaurant and fast-food options).
Type 1 diabetes occurs because the insulin-producing cells of the pancreas (beta cells) are damaged. In type 1 diabetes, the pancreas makes little or no insulin, so sugar cannot get into the body's cells for use as energy. People with type 1 diabetes must use insulin injections to control their blood glucose. Type 1 is the most common form of diabetes in people who are under age 30, but it can occur at any age. Ten percent of people with diabetes are diagnosed with type 1.
Moreover, it is estimated that 1 death is prevented per 11 patients treated for stage 1 hypertension and other cardiovascular risk factors when a sustained reduction of 12 mm Hg in systolic BP over 10 years is achieved. [2] However, for the same reduction is systolic BP reduction, it is estimated that 1 death is prevented per 9 patients treated when cardiovascular disease or end-organ damage is present. [2]
In type 2 diabetes (adult onset diabetes), the pancreas makes insulin, but it either doesn't produce enough, or the insulin does not work properly. Nine out of 10 people with diabetes have type 2. This type occurs most often in people who are over 40 years old but can occur even in childhood if there are risk factors present. Type 2 diabetes may sometimes be controlled with a combination of diet, weight management and exercise. However, treatment also may include oral glucose-lowering medications (taken by mouth) or insulin injections (shots). https://i.ytimg.com/vi/LcWFI9Xawl8/maxresdefault.jpg
Some people may ask: Why not just have liposuction of the abdomen and remove the large amount of abdominal fat that is a big part of the problem? Data thus far shows no benefit in liposuction on insulin sensitivity, blood pressure, or cholesterol. As the saying goes, "If it's too good to be true, it probably is." Diet and exercise are still the preferred primary treatment of metabolic syndrome.
As the name implies, combo training is a combination of resistance training and aerobic exercise. This is probably the most demanding of all the MRT techniques; it's sure to leave you physically drained by the end of your session. That said: the results are worth it. I've used this extensively with private clients over the years and can attest that it skyrockets fat burning.

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.

I think it's better to look at total work than just reps in a given set, as not all drills are created equal.  For example, if you do a barbell complex consisting of five snatches, five cleans, five front squats, five barbell rows, and five deadlifts, you've done a ton more work than if you just did 25 medicine ball throws.  The loading capabilities are greater with the barbell complex, and the bar travels over a greater distance.  Since work equals force times distance, it's a more powerful stimulus than the medicine ball throws.
Because the population of the U.S. is aging, and because metabolic syndrome is more likely the older you are, the American Heart Association (AHA) has estimated that metabolic syndrome soon will become the main risk factor for cardiovascular disease, ahead of cigarette smoking. Experts also think that increasing rates of obesity are related to the increasing rates of metabolic syndrome.
It has not been contested that cardiovascular risk factors tend to cluster together; the matter of contention has been the assertion that the metabolic syndrome is anything more than the sum of its constituent parts. Phenotypic heterogeneity (for example, represented by variation in metabolic syndrome factor combinations among individuals with metabolic syndrome) has fueled that debate. However, more recent evidence suggests that common triggers (for example, excessive sugar-intake in the environment of overabundant food) can contribute to the development of multiple metabolic abnormalities at the same time, supporting the commonality of the energy utilization and storage pathways in metabolic syndrome.

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.
It is common for there to be a development of visceral fat, after which the adipocytes (fat cells) of the visceral fat increase plasma levels of TNF-α and alter levels of a number of other substances (e.g., adiponectin, resistin, and PAI-1). TNF-α has been shown not only to cause the production of inflammatory cytokines, but also possibly to trigger cell signaling by interaction with a TNF-α receptor that may lead to insulin resistance.[31] An experiment with rats fed a diet with 33% sucrose has been proposed as a model for the development of metabolic syndrome. The sucrose first elevated blood levels of triglycerides, which induced visceral fat and ultimately resulted in insulin resistance. The progression from visceral fat to increased TNF-α to insulin resistance has some parallels to human development of metabolic syndrome. The increase in adipose tissue also increases the number of immune cells present within, which play a role in inflammation. Chronic inflammation contributes to an increased risk of hypertension, atherosclerosis and diabetes.[32]
It has not been contested that cardiovascular risk factors tend to cluster together; the matter of contention has been the assertion that the metabolic syndrome is anything more than the sum of its constituent parts. Phenotypic heterogeneity (for example, represented by variation in metabolic syndrome factor combinations among individuals with metabolic syndrome) has fueled that debate. However, more recent evidence suggests that common triggers (for example, excessive sugar-intake in the environment of overabundant food) can contribute to the development of multiple metabolic abnormalities at the same time, supporting the commonality of the energy utilization and storage pathways in metabolic syndrome.
The second hormone that becomes involved when you begin to lose weight is a hormone known as leptin. Leptin is a hormone that is released from the fat cells to signal to the brain about how much fat we have in storage. To our body this is kind of like the indicator on a car telling us how much fuel we have in the tank. Leptin is also a messenger that is involved with controlling your metabolic rate AND your appetite.
Push-ups would be another example.  We've all seen the classic push-up form deterioration under fatigued conditions: a sagging, excessively arched lower back; forward head posture; and elbows flaring out.  It's the classic "panic mode" strategy employed by beginners.  However, you never see it in experienced lifters; they'll simply fail before the technique breaks down.  Part of this comes from technical proficiency, but it's also related to the fact that the limiting factor shifts from anterior core stability to upper body strength/endurance as an individual gets more experienced.

Cycle the diet in a way that has periods of reduced energy intake and periods of increased energy intake. This helps offset the leptin decline that occurs with dieting. There is individual variation with this, but for those who respond well, a day or a few days of overeating can set the metabolic rate back to a higher level. This cycling approach may be more effective for fat loss than the traditional approach

Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH is a member of the following medical societies: Alpha Omega Alpha, American Chemical Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Society for Pharmacology and Experimental Therapeutics, American Society of Hypertension, American Thoracic Society, Heart Failure Society of America, National Lipid Association, Southern Society for Clinical Investigation


The device being used is known as a “sphygmomanometer”, which uses an air-filled cuff wrapped around the upper arm, to obstruct the bloodflow into the arm. By releasing the air pumped into the cuff in small, incremental quantities, eventually blood is permitted to flow back into the arm, at which point, the pressure inside the cuff is measured, and which will equate to the pressure inside the arteries. This pressure, known as the systolic pressure, represents the pressure in the arteries during contraction of the heart. When the heart relaxes between beats the pressure drops, and is known as the diastolic pressure. Together, these two pressures are written as a ratio, and represents ones “blood pressure”.

Most people who have metabolic syndrome have insulin resistance. The body makes insulin to move glucose (sugar) into cells for use as energy. Obesity, commonly found in people with metabolic syndrome, makes it more difficult for cells in the body to respond to insulin. If the body can’t make enough insulin to override the resistance, the blood sugar level increases, causing type 2 diabetes. Metabolic syndrome may be a start of the development of type 2 diabetes.


Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/l (110 to 125 mg/dl) are considered to have impaired fasting glucose.[67] people with plasma glucose at or above 7.8 mmol/l (140 mg/dl), but not over 11.1 mmol/l (200 mg/dl), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease.[68] The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/l (100 to 125 mg/dl).[69]

Doctors may also prescribe medications to lower blood pressure, control cholesterol or help you lose weight. Insulin sensitizers like Glucophage (Metformin) may be prescribed to help your body use insulin more effectively. It lowers blood sugar, which also seems to help lower cholesterol and triglycerides as well as decreasing appetite. The side effects of Metformin (often temporary) include nausea, stomach pain, bloating and diarrhea. A more serious side effect, lactic acidosis, can affect those with kidney or liver disease, severe heart failure or a history of alcohol abuse and is potentially, though rarely, fatal. Aspirin therapy is often given to help reduce risk of heart attack and stroke.
The metabolic syndrome quintuples the risk of type 2 diabetes mellitus. Type 2 diabetes is considered a complication of metabolic syndrome. In people with impaired glucose tolerance or impaired fasting glucose, presence of metabolic syndrome doubles the risk of developing type 2 diabetes.[28] It is likely that prediabetes and metabolic syndrome denote the same disorder, defining it by the different sets of biological markers.
Though it may be transient, untreated GDM can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.[51]
Hypertension, the medical term for high blood pressure, is known as "the silent killer." More than 80 million Americans (33%) have high blood pressure, and as many as 16 million of them do not even know they have the condition. If left untreated, high blood pressure greatly increases your risk for heart attack and stroke. Hypertension is projected to increase about 8 percent between 2013 and 2030.

Hypertensive retinopathy was associated with an increased long-term risk of stroke, even in patients with well-controlled BP, in a report of 2907 adults with hypertension participating in the Atherosclerosis Risk in Communities (ARIC) study. [39, 40] Increasing severity of hypertensive retinopathy was associated with an increased risk of stroke; the stroke risk was 1.35 in the mild retinopathy group and 2.37 in the moderate/severe group.
On physical examination, hypertension may be associated with the presence of changes in the optic fundus seen by ophthalmoscopy.[22] The severity of the changes typical of hypertensive retinopathy is graded from I to IV; grades I and II may be difficult to differentiate.[22] The severity of the retinopathy correlates roughly with the duration or the severity of the hypertension.[20]
Hypertension is a worldwide epidemic; accordingly, its epidemiology has been well studied. Data from National Health and Nutrition Examination Survey (NHANES) spanning 2011-2014 in the United States found that in the population aged 20 years or older, an estimated 86 million adults had hypertension, with a prevalence of 34%. [1] Hypertension affects US men and women nearly equally, affecting an estimated 40.8 million men and 44.9 million women. [1]
A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test.[66] According to the current definition, two fasting glucose measurements above 7.0 mmol/l (126 mg/dl) is considered diagnostic for diabetes mellitus.

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
While there is a strong genetic component to developing this form of diabetes, there are other risk factors - the most significant of which is obesity. There is a direct relationship between the degree of obesity and the risk of developing type 2 diabetes, and this holds true in children as well as adults. It is estimated that the chance to develop diabetes doubles for every 20% increase over desirable body weight.
Optimally, the management approach results in weight loss based on a healthy diet and regular physical activity, which includes a combination of aerobic activity and resistance training, reinforced with behavioral therapy. Metformin, an insulin sensitizer, or a thiazolidinedione (eg, rosiglitazone, pioglitazone) may be useful. Weight loss of ≈ 7% may be sufficient to reverse the syndrome, but if not, each feature of the syndrome should be managed to achieve recommended targets; available drug treatment is very effective.

^ O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos JA, Ettinger SM, Fang JC, Fesmire FM, Franklin BA, Granger CB, Krumholz HM, Linderbaum JA, Morrow DA, Newby LK, Ornato JP, Ou N, Radford MJ, Tamis-Holland JE, Tommaso CL, Tracy CM, Woo YJ, Zhao DX, Anderson JL, Jacobs AK, Halperin JL, Albert NM, Brindis RG, Creager MA, DeMets D, Guyton RA, Hochman JS, Kovacs RJ, Kushner FG, Ohman EM, Stevenson WG, Yancy CW (January 2013). "2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Circulation. 127 (4): e362–425. doi:10.1161/CIR.0b013e3182742cf6. PMID 23247304.
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.[53] http://www.sandysidhumedia.com/wp-content/uploads/2012/12/clairequote1.jpg
As evident from the above, younger individuals may present with hypertension associated with an elevated cardiac output (high-output hypertension). High-output hypertension results from volume and sodium retention by the kidney, leading to increased stroke volume and, often, with cardiac stimulation by adrenergic hyperactivity. Systemic vascular resistance is generally not increased at such earlier stages of hypertension. As hypertension is sustained, however, vascular adaptations including remodeling, vasoconstriction, and vascular rarefaction occur, leading to increased systemic vascular resistance. In this situation, cardiac output is generally normal or slightly reduced, and circulating blood volume is normal.
Type 2 diabetes, a form of diabetes mellitus, is likely one of the better-known chronic diseases in the world — and that's no surprise. Data from the Centers for Disease Control and Prevention suggest in the United States alone, 30.3 million people, or 9.4 percent of the U.S. population, has diabetes, and the majority of these people have type 2. (1)
Hypertension (HTN or HT), also known as high blood pressure (HBP), is a long-term medical condition in which the blood pressure in the arteries is persistently elevated.[10] High blood pressure typically does not cause symptoms.[1] Long-term high blood pressure, however, is a major risk factor for coronary artery disease, stroke, heart failure, atrial fibrillation, peripheral vascular disease, vision loss, chronic kidney disease, and dementia.[2][3][4][11]
The prevalence of metabolic syndrome increases with age, with about 40% of people older than 60 years meeting the criteria. [26] However, metabolic syndrome can no longer be considered a disease of only adult populations. Alarmingly, metabolic syndrome and diabetes mellitus are increasingly prevalent in the pediatric population, again in parallel with a rise in obesity. [50]
The AHA/ASA recommends a diet that is low in sodium, is high in potassium, and promotes the consumption of fruits, vegetables, and low-fat dairy products for reducing BP and lowering the risk of stroke. Other recommendations include increasing physical activity (30 minutes or more of moderate intensity activity on a daily basis) and losing weight (for overweight and obese persons).
Diabetes: The differences between types 1 and 2 There are fundamental differences between diabetes type 1 and type 2, including when they might occur, their causes, and how they affect someone's life. Find out here what distinguishes the different forms of the disease, the various symptoms, treatment methods, and how blood tests are interpreted. Read now
Type 2 DM is primarily due to lifestyle factors and genetics.[45] A number of lifestyle factors are known to be important to the development of type 2 DM, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization.[16] Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders.[11] Even those who are not obese often have a high waist–hip ratio.[11]
In the Framingham Heart Study, the age-adjusted risk of congestive heart failure was 2.3 times higher in men and 3 times higher in women when the highest BP was compared to the lowest BP. [44] Multiple Risk Factor Intervention Trial (MRFIT) data showed that the relative risk for coronary artery disease mortality was 2.3 to 6.9 times higher for persons with mild to severe hypertension than it was for persons with normal BP. [45] The relative risk for stroke ranged from 3.6 to 19.2. The population-attributable risk percentage for coronary artery disease varied from 2.3 to 25.6%, whereas the population-attributable risk for stroke ranged from 6.8-40%.
The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation of diabetes with other diseases, and he discussed differential diagnosis from the snakebite which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.[110]
As the name implies, combo training is a combination of resistance training and aerobic exercise. This is probably the most demanding of all the MRT techniques; it's sure to leave you physically drained by the end of your session. That said: the results are worth it. I've used this extensively with private clients over the years and can attest that it skyrockets fat burning.
Diabetes mellitus occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries,[101] where more than 80% of diabetic deaths occur.[105] The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030.[106] The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet).[101][106] The global prevalence of diabetes might increase by 55% between 2013 and 2035.[101]

In the Framingham Heart Study, the age-adjusted risk of congestive heart failure was 2.3 times higher in men and 3 times higher in women when the highest BP was compared to the lowest BP. [44] Multiple Risk Factor Intervention Trial (MRFIT) data showed that the relative risk for coronary artery disease mortality was 2.3 to 6.9 times higher for persons with mild to severe hypertension than it was for persons with normal BP. [45] The relative risk for stroke ranged from 3.6 to 19.2. The population-attributable risk percentage for coronary artery disease varied from 2.3 to 25.6%, whereas the population-attributable risk for stroke ranged from 6.8-40%. https://i.ytimg.com/vi/54Ep_LFJ9Wc/3.jpg
I think it's better to look at total work than just reps in a given set, as not all drills are created equal.  For example, if you do a barbell complex consisting of five snatches, five cleans, five front squats, five barbell rows, and five deadlifts, you've done a ton more work than if you just did 25 medicine ball throws.  The loading capabilities are greater with the barbell complex, and the bar travels over a greater distance.  Since work equals force times distance, it's a more powerful stimulus than the medicine ball throws.
Because the population of the U.S. is aging, and because metabolic syndrome is more likely the older you are, the American Heart Association (AHA) has estimated that metabolic syndrome soon will become the main risk factor for cardiovascular disease, ahead of cigarette smoking. Experts also think that increasing rates of obesity are related to the increasing rates of metabolic syndrome.
When the glucose concentration in the blood remains high over time, the kidneys will reach a threshold of reabsorption, and glucose will be excreted in the urine (glycosuria).[62] This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst (polydipsia).[60]
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/l (110 to 125 mg/dl) are considered to have impaired fasting glucose.[67] people with plasma glucose at or above 7.8 mmol/l (140 mg/dl), but not over 11.1 mmol/l (200 mg/dl), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease.[68] The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/l (100 to 125 mg/dl).[69]
Doctors, pharmacists, and other health-care professionals use abbreviations, acronyms, and other terminology for instructions and information in regard to a patient's health condition, prescription drugs they are to take, or medical procedures that have been ordered. There is no approved this list of common medical abbreviations, acronyms, and terminology used by doctors and other health- care professionals. You can use this list of medical abbreviations and acronyms written by our doctors the next time you can't understand what is on your prescription package, blood test results, or medical procedure orders. Examples include:
Exposure to certain viral infections (mumps and Coxsackie viruses) or other environmental toxins may serve to trigger abnormal antibody responses that cause damage to the pancreas cells where insulin is made. Some of the antibodies seen in type 1 diabetes include anti-islet cell antibodies, anti-insulin antibodies and anti-glutamic decarboxylase antibodies. These antibodies can be detected in the majority of patients, and may help determine which individuals are at risk for developing type 1 diabetes.
Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.[61] https://www.clairekerslake.com/wp-content/uploads/2011/10/young-woman-planning-in-calendar-app-on-white-iphone-picjumbo-com-1024x683.jpg
×