Dr Jacomien de Villiers qualified as a specialist physician at the University of Pretoria in 1995. She worked at various clinics at the Department of Internal Medicine, Steve Biko Hospital, these include General Internal Medicine, Hypertension, Diabetes and Cardiology. She has run a private practice since 2001, as well as a consultant post at the Endocrine Clinic of Steve Biko Hospital.

In most people with established essential hypertension, increased resistance to blood flow (total peripheral resistance) accounts for the high pressure while cardiac output remains normal.[52] There is evidence that some younger people with prehypertension or 'borderline hypertension' have high cardiac output, an elevated heart rate and normal peripheral resistance, termed hyperkinetic borderline hypertension.[53] These individuals develop the typical features of established essential hypertension in later life as their cardiac output falls and peripheral resistance rises with age.[53] Whether this pattern is typical of all people who ultimately develop hypertension is disputed.[54] The increased peripheral resistance in established hypertension is mainly attributable to structural narrowing of small arteries and arterioles,[55] although a reduction in the number or density of capillaries may also contribute.[56]
Mark A Silverberg, MD, MMB, FACEP Assistant Professor, Associate Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate Medical Center
^ Cheng J, Zhang W, Zhang X, Han F, Li X, He X, Li Q, Chen J (May 2014). "Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on all-cause mortality, cardiovascular deaths, and cardiovascular events in patients with diabetes mellitus: a meta-analysis". JAMA Internal Medicine. 174 (5): 773–85. doi:10.1001/jamainternmed.2014.348. PMID 24687000.
(As a side note, one tricky thing we are coming to find with leptin is that many obese people have very high circulating levels of leptin but some how their body still doesn’t listen to the signal. They are leptin resistant. This means that your metabolism slows and your hunger gets jacked up… even though you have plenty of fat stores on your body! Talk about frustrating… but solvable!)
Insulin is a hormone that is produced by specialized cells (beta cells) of the pancreas. (The pancreas is a deep-seated organ in the abdomen located behind the stomach.) In addition to helping glucose enter the cells, insulin is also important in tightly regulating the level of glucose in the blood. After a meal, the blood glucose level rises. In response to the increased glucose level, the pancreas normally releases more insulin into the bloodstream to help glucose enter the cells and lower blood glucose levels after a meal. When the blood glucose levels are lowered, the insulin release from the pancreas is turned down. It is important to note that even in the fasting state there is a low steady release of insulin than fluctuates a bit and helps to maintain a steady blood sugar level during fasting. In normal individuals, such a regulatory system helps to keep blood glucose levels in a tightly controlled range. As outlined above, in patients with diabetes, the insulin is either absent, relatively insufficient for the body's needs, or not used properly by the body. All of these factors cause elevated levels of blood glucose (hyperglycemia). https://i.ytimg.com/vi/03Ar9vo6VbM/hqdefault.jpg?sqp
Out of this whole article this quote from a participant was the thing that drove my emotions. For anyone who struggles with weight loss resistance this will stab you in the heart. It is so incredibly true. There is nothing quite like feeling like your body is failing you and that even starving yourself, restricting every delicious food and exercising to the max is not enough.
At the end of the twelve-week study both groups lost weight, but the difference in the amount of muscle vs. fat loss was telling. The aerobic group lost 37 pounds over the course of the study. Ten of those pounds came from muscle. In contrast, the resistance-training group lost 32 pounds. None of the weight they lost came from muscle. When the resting metabolic rate of each group was calculated, the aerobic group was shown to be burning 210 fewer calories per day. The resistance-training group avoided this metabolic decline and instead was burning 63 more calories per day.

Research has shown this is NOT an imaginary issue. As far back as 1975, researchers published a study in the journal Lancet that looked at the issue of weight loss resistance. 29 women who claimed they could not lose weight were studied. The researchers, like many of us, assumed these women simply were not compliant and wanted to test their metabolism by sequestering them in a house and controlling all food and exercise they did. Each woman was put on a strict 1500 calorie a day diet.
A sustainable exercise program, for example 30 minutes five days a week is reasonable to start, providing there is no medical contraindication. (If you have any special concerns in this regard, check with your doctor first.) There is a beneficial effect of exercise on blood pressure, cholesterol levels, and insulin sensitivity, regardless of whether weight loss is achieved or not. Thus, exercise in itself is a helpful tool in treating metabolic syndrome.
Lipase inhibitors can play a role. These are foods that have action in decreasing the digestion of fats so they move out of the body instead of getting absorbed. Since the digestive tract is the major place where POPs are both removed from the body and taken into the body, doing what is possible to NOT allow fat soluble compounds reentry is important. Some common lipase inhibitors include green tea, oolong tea, mate tea, and ginger root.

Recent research indicates prolonged chronic stress can contribute to metabolic syndrome by disrupting the hormonal balance of the hypothalamic-pituitary-adrenal axis (HPA-axis).[23] A dysfunctional HPA-axis causes high cortisol levels to circulate, which results in raising glucose and insulin levels, which in turn cause insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension, with direct effects on the bone, causing "low turnover" osteoporosis.[24] HPA-axis dysfunction may explain the reported risk indication of abdominal obesity to cardiovascular disease (CVD), type 2 diabetes and stroke.[25] Psychosocial stress is also linked to heart disease.[26]

The goal of treating metabolic syndrome is to prevent the development of diabetes, heart disease, and stroke. Your doctor will first suggest lifestyle modifications such as exercising for 30 minutes most days of the week. One study showed that individuals who are physically active (30 minutes of activity at least once per week) have half the risk of developing metabolic syndrome than those who are inactive. Your doctor may also suggest eating a healthy diet to promote weight loss and normal blood cholesterol and fat levels. https://www.healthshare.com.au/storage/e2d6972eb9e9fe519fb8847f9afe0d6f.png.60x60_q85_box-0,0,446,446.png
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