The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.[74]

Type 1 diabetes is caused by an autoimmune reaction (the body attacks itself by mistake) that stops your body from making insulin. About 5% of the people who have diabetes have type 1. Symptoms of type 1 diabetes often develop quickly. It’s usually diagnosed in children, teens, and young adults. If you have type 1 diabetes, you’ll need to take insulin every day to survive. Currently, no one knows how to prevent type 1 diabetes.

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]
Staphylococcus or staph is a group of bacteria that can cause a multitude of diseases. Staph infections can cause illness directly by infection or indirectly by the toxins they produce. Symptoms and signs of a staph infection include redness, swelling, pain, and drainage of pus. Minor skin infections are treated with an antibiotic ointment, while more serious infections are treated with intravenous antibiotics.

However, medication is needed to sufficiently reduce blood pressure for most stage 1 and almost all stage 2 hypertension cases. There are a vast number of prescription medications that have been approved for the treatment of hypertension, and guidelines have been developed to help doctors quickly find an effective and well-tolerated treatment regimen for almost anyone with this concern.
When you are first diagnosed with hypertension, you can expect a period of time when you will be seeing your doctor more often than usual. You will need some baseline testing to look for an underlying cause for your hypertension, and you will probably need several medical visits to determine whether lifestyle adjustments or medication will be effective in helping you reach your optimal blood pressure.
Diabetes can occur temporarily during pregnancy, and reports suggest that it occurs in 2% to 10% of all pregnancies. Significant hormonal changes during pregnancy can lead to blood sugar elevation in genetically predisposed individuals. Blood sugar elevation during pregnancy is called gestational diabetes. Gestational diabetes usually resolves once the baby is born. However, 35% to 60% of women with gestational diabetes will eventually develop type 2 diabetes over the next 10 to 20 years, especially in those who require insulin during pregnancy and those who remain overweight after their delivery. Women with gestational diabetes are usually asked to undergo an oral glucose tolerance test about six weeks after giving birth to determine if their diabetes has persisted beyond the pregnancy, or if any evidence (such as impaired glucose tolerance) is present that may be a clue to a risk for developing diabetes.

Investigations into the pathophysiology of hypertension, both in animals and humans, have revealed that hypertension may have an immunological basis. Studies have revealed that hypertension is associated with renal infiltration of immune cells and that pharmacologic immunosuppression (such as with the drug mycophenolate mofetil) or pathologic immunosuppression (such as occurs with HIV) results in reduced blood pressure in animals and humans. Evidence suggests that T lymphocytes and T-cell derived cytokines (eg, interleukin 17, tumor necrosis factor alpha) play an important role in hypertension. [14, 15]

Now let’s say they are one of those people that has a very large metabolic compensation. So large that it equals or exceeds the 500 calorie deficit they were following. At this point not only will all progress stall, but the person may even start gaining weight. This is something the calorie zealots will never tell you, and if you don’t want to take my word for it, follow the links throughout this blog, or read the very nice free review article out of the International Journal of Obesity posted in the references.

Not so anymore. Thanks to the rising obesity epidemic in young people, kids and teens are getting these conditions — and they're getting them earlier than ever before. Some estimates say that nearly 1 in 10 teens — and over a third of obese teens — have metabolic syndrome. And a study of 375 second- and third-graders found that 5% had metabolic syndrome and 45% had one or two risk factors for it. https://i.ytimg.com/vi/-wDavU9u0rQ/hqdefault.jpg?sqp
Type 2 diabetes was also previously referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult-onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs, particularly in the face of insulin resistance as discussed above. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells). http://www.clairekerslake.com/wp-content/uploads/2014/03/ipad_new.png
^ Jump up to: a b Petzold A, Solimena M, Knoch KP (October 2015). "Mechanisms of Beta Cell Dysfunction Associated With Viral Infection". Current Diabetes Reports (Review). 15 (10): 73. doi:10.1007/s11892-015-0654-x. PMC 4539350. PMID 26280364. So far, none of the hypotheses accounting for virus-induced beta cell autoimmunity has been supported by stringent evidence in humans, and the involvement of several mechanisms rather than just one is also plausible. http://www.sandysidhumedia.com/wp-content/uploads/2012/12/bennyquote.png

Although treatment of sleep apnea with continuous airway positive pressure (CPAP) would logically seem to improve CV outcomes and hypertension, studies evaluating this mode of therapy have been disappointing. A 2016 review of several studies indicated that CPAP either had no effect or a modest BP-lowering effect. [29] Findings from the SAVE study showed no effect of CPAP therapy on BP above usual care. [30] It is likely that patients with sleep apnea have other etiologies of hypertension, including obesity, hyperaldosteronism, increased sympathetic drive, and activation of the renin/angiotensin system that contribute to their hypertension. Although CPAP remains an effective therapy for other aspects of sleep apnea, it should not be expected to normalize BP in the majority of patients.


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]
First-line medications for hypertension include thiazide-diuretics, calcium channel blockers, angiotensin converting enzyme inhibitors (ACE inhibitors), and angiotensin receptor blockers (ARBs).[13] These medications may be used alone or in combination (ACE inhibitors and ARBs are not recommended for use in combination); the latter option may serve to minimize counter-regulatory mechanisms that act to restore blood pressure values to pre-treatment levels.[13][129] Most people require more than one medication to control their hypertension.[111] Medications for blood pressure control should be implemented by a stepped care approach when target levels are not reached.[128]
Metabolic syndrome is quite common. Approximately 32% of the population in the U.S. has metabolic syndrome, and about 85% of those with type 2 diabetes have metabolic syndrome. Around 25% of adults in Europe and Latin America are estimated to have the condition, and rates are rising in developing East Asian countries. Within the US, Mexican Americans have the highest prevalence of metabolic syndrome. The prevalence of metabolic syndrome increases with age, and about 40% of people over 60 are affected.
Cortisol reactivity, an index of hypothalamic-pituitary-adrenal function, may be another mechanism by which psychosocial stress is associated with future hypertension. [20] In a prospective sub-study of the Whitehall II cohort, with 3 years follow-up of an occupational cohort in previously healthy patients, investigators reported 15.9% of the patient sample developed hypertension in response to laboratory-induced mental stressors and found an association between cortisol stress reactivity and incident hypertension. [20]
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