These calorie counting fanatics are either unaware, or don’t want you to know about what we call the law of metabolic compensation. This law dictates that your metabolism is not like a calculator at all but more like a thermostat or see-saw. You eat less and exercise more to burn calories, and your body compensates by making you more hungry while at the same time decreasing the amount of calories you burn at rest (resting energy expenditure or REE).
Another common endocrine cause is oral contraceptive use. Activation of the renin-angiotensin-aldosterone system (RAAS) is the likely mechanism, because hepatic synthesis of angiotensinogen is induced by the estrogen component of oral contraceptives. Approximately 5% of women taking oral contraceptives may develop hypertension, which abates within 6 months after discontinuation. The risk factors for oral contraceptive–associated hypertension include mild renal disease, familial history of essential hypertension, age older than 35 years, and obesity. It would be better to group oral contraceptives and steroids with drug-induced hypertension (see Table 1, below).
High blood pressure is classified as either primary (essential) high blood pressure or secondary high blood pressure. About 90–95% of cases are primary, defined as high blood pressure due to nonspecific lifestyle and genetic factors. Lifestyle factors that increase the risk include excess salt in the diet, excess body weight, smoking, and alcohol use. The remaining 5–10% of cases are categorized as secondary high blood pressure, defined as high blood pressure due to an identifiable cause, such as chronic kidney disease, narrowing of the kidney arteries, an endocrine disorder, or the use of birth control pills.
Bhasin et al, as part of the Framingham Heart Study, found that sex hormone-binding globulin is independently associated with the risk of metabolic syndrome, whereas testosterone is not. Age, body mass index (BMI), and insulin sensitivity independently affect sex hormone-binding globulin and testosterone levels.  More recent studies have raised the possibility of an association between testosterone deficiency and metabolic syndrome. 
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.
Just briefly I want to mention something for the more savvy readers out there. Many, who are well versed in metabolism, will immediately point out that if you lose weight, then of course you are going to be burning less calories because you have less body tissue. True. But what research shows, and my clinical experience validates, is that the reduced rate of metabolic output goes far beyond what would be predicted from loss of fat mass or muscle mass.
As a clinician who works with weight loss and obesity, I can tell you with certainty that people can and do become weight loss resistant and can develop some degree of “metabolic damage”. Metabolic damage is a non-diagnostic term many in the weight loss industry use to describe a set of functional disturbances. These disturbances include severe metabolic compensations that result in a depressed metabolic rate, chronic fatigue, immune suppression, and multiple hormonal effects (i.e. suppressed thyroid function, adrenal stress maladaptation, and loss of libido and/or menses).
POPs primarily impact the thyroid gland by decreasing its ability to make thyroid hormone, disrupting thyroid hormones once they are made, and causing thyroid hormones to be removed from the body faster. If your metabolism is a large jumbo jetliner, the thyroid gland is one of the engines. POPs appear to work in part by blowing out the thyroid engine.
People with glucose levels between normal and diabetic have impaired glucose tolerance (IGT) or insulin resistance. People with impaired glucose tolerance do not have diabetes, but are at high risk for progressing to diabetes. Each year, 1% to 5% of people whose test results show impaired glucose tolerance actually eventually develop diabetes. Weight loss and exercise may help people with impaired glucose tolerance return their glucose levels to normal. In addition, some physicians advocate the use of medications, such as metformin (Glucophage), to help prevent/delay the onset of overt diabetes.
People with diabetes can benefit from education about the disease and treatment, good nutrition to achieve a normal body weight, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.
The pathogenesis of essential hypertension is multifactorial and complex.  Multiple factors modulate the blood pressure (BP) including humoral mediators, vascular reactivity, circulating blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation. A possible pathogenesis of essential hypertension has been proposed in which multiple factors, including genetic predisposition, excess dietary salt intake, and adrenergic tone, may interact to produce hypertension. Although genetics appears to contribute, the exact mechanisms underlying essential hypertension have not been established.
Cortisol reactivity, an index of hypothalamic-pituitary-adrenal function, may be another mechanism by which psychosocial stress is associated with future hypertension.  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. 
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. High blood pressure typically does not cause symptoms. 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.
Patients with metabolic syndrome can have several disorders of coagulation that make it easier for blood clots to form within blood vessels. These blood clots are often a precipitating factor in developing heart attacks. Patients with metabolic syndrome should generally be placed on daily aspirin therapy to help prevent such clotting events. You should speak to a doctor, of course, before starting any new medication regimen.
Normal blood pressure can differ substantially between breeds but hypertension in dogs is often diagnosed if systolic blood pressure is above 160 mm Hg particularly if this is associated with target organ damage. Inhibitors of the renin-angiotensin system and calcium channel blockers are often used to treat hypertension in dogs, although other drugs may be indicated for specific conditions causing high blood pressure.
Emerging data suggest an important correlation between metabolic syndrome and risk of stroke.  Each of the components of metabolic syndrome has been associated with elevated stroke risk, and evidence demonstrates a relationship between the collective metabolic syndrome and risk of ischemic stroke.  Metabolic syndrome may also be linked to neuropathy beyond hyperglycemic mechanisms through inflammatory mediators.