There is debate regarding whether obesity or insulin resistance is the cause of the metabolic syndrome or if they are consequences of a more far-reaching metabolic derangement. A number of markers of systemic inflammation, including C-reactive protein, are often increased, as are fibrinogen, interleukin 6, tumor necrosis factor-alpha (TNF-α), and others. Some have pointed to a variety of causes, including increased uric acid levels caused by dietary fructose.[18][19][20]

Approximately half of individuals with hypertension have OSA, and approximately half with OSA have hypertension. Ambulatory BP monitoring normally reveals a "dip" in BP of at least 10% during sleep. However, if a patient is a "nondipper," the chances that the patient has OSA is increased. Nondipping is thought to be caused by frequent apneic/hypopneic episodes that end with arousals associated with marked spikes in BP that last for several seconds. Apneic episodes are associated with striking increases in sympathetic nerve activity and enormous elevations of BP. Individuals with sleep apnea have increased cardiovascular mortality, in part likely related to the high incidence of hypertension.
According to the Centers for Disease Control and Prevention, more than 50% of people age 50 and older have high blood pressure. Women are about as likely as men to develop high blood pressure, though this varies somewhat by age. For people younger than age 45, more men than women are affected, while for those age 65 and older, more women than men are affected. Americans of African descent develop high blood pressure more often and at an earlier age than those of European and Hispanic descent.
One hypothesis is that prehypertension results in oxidation of lipids such as arachidonic acid that leads to the formation of isoketals or isolevuglandins, which function as neoantigens, which are then presented to T cells, leading to T-cell activation and infiltration of critical organs (eg, kidney, vasculature). [16] This results in persistent or severe hypertension and end organ damage. Sympathetic nervous system activation and noradrenergic stimuli have also been shown to promote T-lymphocyte activation and infiltration and contribute to the pathophysiology of hypertension. [17, 18, 19]
Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly.[2] As the disease progresses, a lack of insulin may also develop.[12] This form was previously referred to as "non insulin-dependent diabetes mellitus" (NIDDM) or "adult-onset diabetes".[2] The most common cause is a combination of excessive body weight and insufficient exercise.[2]
Between 2006 and 2011, there was a 25% increase in the number of people visiting US emergency rooms for essential hypertension, according to an analysis of data from the Nationwide Emergency Department Sample in 2014. [37] The reason for the increase, however, remained uncertain. The rate of emergency department visits also increased significantly, according to the study, rising from 190.1 visits per 100,000 population in 2006 to 238.5 visits per 100,000 population in 2011. Over the same period, however, admission rates decreased, from 10.47% in 2006 to 8.85% in 2011. [37]
Enlarged heart. High blood pressure increases the amount of work for your heart. Like any heavily exercised muscle in your body, your heart grows bigger (enlarges) to handle the extra workload. The bigger your heart is, the more it demands oxygen-rich blood but the less able it is to maintain proper blood flow. As a result, you feel weak and tired and are not able to exercise or perform physical activities. Without treatment, your heart failure will only get worse.

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]
Lipodystrophic disorders in general are associated with metabolic syndrome. Both genetic (e.g., Berardinelli-Seip congenital lipodystrophy, Dunnigan familial partial lipodystrophy) and acquired (e.g., HIV-related lipodystrophy in patients treated with highly active antiretroviral therapy) forms of lipodystrophy may give rise to severe insulin resistance and many of metabolic syndrome's components.[27]
According to the Mayo Clinic, doctors may use other tests to diagnose diabetes. For example, they may conduct a fasting blood glucose test, which is a blood glucose test done after a night of fasting. While a fasting blood sugar level of less than 100 milligrams per deciliter (mg/dL) is normal, one that is between 100 to 125 mg/dL signals prediabetes, and a reading that reaches 126 mg/dL on two separate occasions means you have diabetes.