^ Jump up to: a b c Vemuri VK, Janero DR, Makriyannis A (March 2008). "Pharmacotherapeutic targeting of the endocannabinoid signaling system: drugs for obesity and the metabolic syndrome". Physiology & Behavior. 93 (4–5): 671–86. doi:10.1016/j.physbeh.2007.11.012. PMC 3681125. PMID 18155257. The etiology of many appetitive disorders is characterized by a pathogenic component of reward-supported craving, be it for substances of abuse (including alcohol and nicotine) or food. Such maladies affect large numbers of people as prevalent socioeconomic and healthcare burdens. Yet in most instances drugs for their safe and effective pharmacotherapeutic management are lacking despite the attendant medical needs, collateral adverse physical and psychological effects, and enormous global market potential. The endocannabinoid signaling system plays a critical role in motivational homeostasis as a conduit for reward stimuli and a positive modulator of brain reward circuits. Endocannabinoid-system hyperactivity through CB1 receptor transmission is considered contributory to a range of appetitive disorders and, hence, is a major focus of contemporary pharmaceutical research.
Mind/Body: It is important to attend to stress in positive ways. Rather than using alcohol, tobacco, or television, try breathing exercises. They are simple, free, and right under your nose. Dr. Weil has compiled ten ways to reduce stress and promote relaxation, calm and peace within yourself. Some techniques take practice, and most require some commitment on your part to achieve results. However, the results are well worth the effort.

The pressure generated by the beating heart forces the blood forward and stretches the elastic walls of the arteries. In between heartbeats, as the heart muscle relaxes, the arterial walls snap back to their original shape, moving the blood forward to the body’s tissues. With hypertension, the pressure in the arteries is high enough to eventually produce damage to the blood vessels.
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
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]
When it comes to laboratory values, numbers like blood glucose and A1C levels are commonly checked. Less often, doctors order a test for your fasting insulin level; yet this test can help predict your risk of developing prediabetes and metabolic syndrome. Insulin plays a key role in metabolism, and high insulin levels can promote obesity, stimulate hunger, and increase the storage of fat.
With self-limiting exercises, fatigue stops you from completing a rep before your technique can break down.  A perfect example would be sled pushing or dragging.  It's virtually impossible to have technique break down with these exercises, especially in a trained athlete, and even under considerable loading.  And, I can't say that I've ever seen anyone injured while using a sled.
Diabetes is a disease that occurs when your blood glucose, also called blood sugar, is too high. Blood glucose is your main source of energy and comes from the food you eat. Insulin, a hormone made by the pancreas, helps glucose from food get into your cells to be used for energy. Sometimes your body doesn’t make enough—or any—insulin or doesn’t use insulin well. Glucose then stays in your blood and doesn’t reach your cells.

The value of routine screening for hypertension in children over the age of 3 years is debated.[90][91] In 2004 the National High Blood Pressure Education Program recommended that children aged 3 years and older have blood pressure measurement at least once at every health care visit[89] and the National Heart, Lung, and Blood Institute and American Academy of Pediatrics made a similar recommendation.[92] However, the American Academy of Family Physicians[93] supports the view of the U.S. Preventive Services Task Force that the available evidence is insufficient to determine the balance of benefits and harms of screening for hypertension in children and adolescents who do not have symptoms.[94]
Leptin is considered by many to be THE most important metabolic hormone as far as setting metabolic output and weight regain. If you want to keep your metabolic rate up, you have to make sure leptin levels don’t fall too fast. One way to overcome this appears to be a short period of overeating of between 1 and 3 days. This technique raises leptin levels and has also been shown to substantially raise a depressed metabolic rate. This effect varies substantially from person to person with some people showing no effect from the brief overfeeding and others seeing a jump in resting calorie burn of several hundred calories per day.

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]
^ Xie, X; Atkins, E; Lv, J; Bennett, A; Neal, B; Ninomiya, T; Woodward, M; MacMahon, S; Turnbull, F; Hillis, GS; Chalmers, J; Mant, J; Salam, A; Rahimi, K; Perkovic, V; Rodgers, A (30 January 2016). "Effects of intensive blood pressure lowering on cardiovascular and renal outcomes: updated systematic review and meta-analysis". Lancet. 387 (10017): 435–43. doi:10.1016/S0140-6736(15)00805-3. PMID 26559744.

Let me give you an example of this. A person decides to follow a low calorie diet. They determine that their resting metabolic rate is 2000 calories per day. They decide, according to conventional wisdom, to reduce their daily calorie intake by 500 calories per day. Now they are consuming 1500 calories per day. They remain compliant and in a few weeks have lost a few pounds.
Insulin — the hormone that allows your body to regulate sugar in the blood — is made in your pancreas. Essentially, insulin resistance is a state in which the body’s cells do not use insulin efficiently. As a result, it takes more insulin than normal to transport blood sugar (glucose) into cells, to be used immediately for fuel or stored for later use. A drop in efficiency in getting glucose to cells creates a problem for cell function; glucose is normally the body’s quickest and most readily available source of energy.
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.
Emerging data suggest an important correlation between metabolic syndrome and risk of stroke. [58] 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. [59] Metabolic syndrome may also be linked to neuropathy beyond hyperglycemic mechanisms through inflammatory mediators. [60]
This explains why my attempts at a low fat, high protein, high carb diet left me gaining weight all while eating 1000 calories per day! Those 1000 calories were simply fueling my brain and then getting shuttled into my fat cells. If you are not insulin resistant, then this diet may be just the thing you need to shed some short term pounds (although I never recommend a 1000 calorie diet!- more on that later), but to me it caused metabolic chaos.

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.

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. [48] More recent studies have raised the possibility of an association between testosterone deficiency and metabolic syndrome. [49]

Events in early life, such as low birth weight, maternal smoking, and lack of breastfeeding may be risk factors for adult essential hypertension, although the mechanisms linking these exposures to adult hypertension remain unclear.[43] An increased rate of high blood urea has been found in untreated people with hypertension in comparison with people with normal blood pressure, although it is uncertain whether the former plays a causal role or is subsidiary to poor kidney function.[44] Average blood pressure may be higher in the winter than in the summer.[45] Periodontal disease is also associated with high blood pressure.[46]


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