A person who weighed 180 pounds who diets down to 150 pounds burns significantly less energy than another person of the same height who also weighs 150 pounds who did not diet. Something about dieting causes an exaggerated slow down in metabolic rate that goes beyond what would be predicted based on tissue loss. And, as pointed out previously, this comes along with strong and unrelenting biological sensations to seek food. That is a recipe for compensatory weight regain.
Effective lifestyle modification may lower blood pressure as much as an individual antihypertensive medication. Combinations of two or more lifestyle modifications can achieve even better results.[87] There is considerable evidence that reducing dietary salt intake lowers blood pressure, but whether this translates into a reduction in mortality and cardiovascular disease remains uncertain.[96] Estimated sodium intake ≥6g/day and <3g/day are both associated with high risk of death or major cardiovascular disease, but the association between high sodium intake and adverse outcomes is only observed in people with hypertension.[97] Consequently, in the absence of results from randomized controlled trials, the wisdom of reducing levels of dietary salt intake below 3g/day has been questioned.[96]
Great article, Roman. I bought LWF2 as soon as I saw that it was released. Typically, sequels are not as good as the first, but I knew Jen's would be the exception and she did not let me down! :) I have seen others ask about your manual if we have already invested in LWF2. How should we go about this? Shall we send you the order number or will it be uploaded to the LWF2 member site in the download section? Cheers and thanks for such epic content!

^ Jump up to: a b Gatta-Cherifi, Blandine; Cota, Daniela (2015). "Endocannabinoids and Metabolic Disorders". Endocannabinoids. Handbook of Experimental Pharmacology. 231. pp. 367–91. doi:10.1007/978-3-319-20825-1_13. ISBN 978-3-319-20824-4. PMID 26408168. The endocannabinoid system (ECS) is known to exert regulatory control on essentially every aspect related to the search for, and the intake, metabolism and storage of calories, and consequently it represents a potential pharmacotherapeutic target for obesity, diabetes and eating disorders. ... recent research in animals and humans has provided new knowledge on the mechanisms of actions of the ECS in the regulation of eating behavior, energy balance, and metabolism. In this review, we discuss these recent advances and how they may allow targeting the ECS in a more specific and selective manner for the future development of therapies against obesity, metabolic syndrome, and eating disorders.


The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body.[60] Insulin plays a critical role in balancing glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.[60]

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. https://www.healthshare.com.au/storage/avatars/True_Local_Shot.jpg.60x60_q85_box-0,140,558,697.jpg


In autoimmune diseases, such as type 1 diabetes, the immune system mistakenly manufactures antibodies and inflammatory cells that are directed against and cause damage to patients' own body tissues. In persons with type 1 diabetes, the beta cells of the pancreas, which are responsible for insulin production, are attacked by the misdirected immune system. It is believed that the tendency to develop abnormal antibodies in type 1 diabetes is, in part, genetically inherited, though the details are not fully understood.
What medication is available for diabetes? Diabetes causes blood sugar levels to rise. The body may stop producing insulin, the hormone that regulates blood sugar, and this results in type 1 diabetes. In people with type 2 diabetes, insulin is not working effectively. Learn about the range of treatments for each type and recent medical developments here. Read now
Diabetes mellitus is classified into four broad categories: type 1, type 2, gestational diabetes, and "other specific types".[11] The "other specific types" are a collection of a few dozen individual causes.[11] Diabetes is a more variable disease than once thought and people may have combinations of forms.[37] The term "diabetes", without qualification, usually refers to diabetes mellitus.
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.[51]
Because some medications, such as over-the-counter cold medicines, pain medications, antidepressants, birth control pills and others, can raise your blood pressure, it might be a good idea to bring a list of medications and supplements you take to your doctor's appointment. Don't stop taking any prescription medications that you think may affect your blood pressure without your doctor's advice.
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).
A joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity published a guideline to harmonize the definition of the metabolic syndrome.[39] This definition recognizes that the risk associated with a particular waist measurement will differ in different populations. Whether it is better at this time to set the level at which risk starts to increase or at which there is already substantially increased risk will be up to local decision-making groups. However, for international comparisons and to facilitate the etiology, it is critical that a commonly agreed-upon set of criteria be used worldwide, with agreed-upon cut points for different ethnic groups and sexes. There are many people in the world of mixed ethnicity, and in those cases, pragmatic decisions will have to be made. Therefore, an international criterion of overweight (BMI≥25) may be more appropriate than ethnic specific criteria of abdominal obesity for an anthropometric component of this syndrome which results from an excess lipid storage in adipose tissue, skeletal muscle and liver.
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.
Push-ups would be another example.  We've all seen the classic push-up form deterioration under fatigued conditions: a sagging, excessively arched lower back; forward head posture; and elbows flaring out.  It's the classic "panic mode" strategy employed by beginners.  However, you never see it in experienced lifters; they'll simply fail before the technique breaks down.  Part of this comes from technical proficiency, but it's also related to the fact that the limiting factor shifts from anterior core stability to upper body strength/endurance as an individual gets more experienced.

As waistlines expand, so does the epidemic of metabolic syndrome. It’s estimated that nearly one of every four American adults has this condition(1). If you’re one of them, it puts you on the track to developing type 2 diabetes and triples your risk for heart disease down the road. The identification of metabolic syndrome two decades ago(2) is now recognized as a turning point in our understanding of how metabolism can go awry, resulting in obesity, diabetes and cardiovascular disease.


The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature.[citation needed]
Secondary hypertension results from an identifiable cause. Kidney disease is the most common secondary cause of hypertension.[23] Hypertension can also be caused by endocrine conditions, such as Cushing's syndrome, hyperthyroidism, hypothyroidism, acromegaly, Conn's syndrome or hyperaldosteronism, renal artery stenosis (from atherosclerosis or fibromuscular dysplasia), hyperparathyroidism, and pheochromocytoma.[23][47] Other causes of secondary hypertension include obesity, sleep apnea, pregnancy, coarctation of the aorta, excessive eating of liquorice, excessive drinking of alcohol, and certain prescription medicines, herbal remedies, and illegal drugs such as cocaine and methamphetamine.[23][48] Arsenic exposure through drinking water has been shown to correlate with elevated blood pressure.[49][50]

MRT, a.k.a. "metabolic resistance training," might as well be called "madman training." It's no-holds-barred, haul-ass, maximum-effort, build-muscle, heave-weight, torch-fat, absolutely insane huff-n-puff training. It'll spike your metabolism, crush calories like beer cans, lift your lactate threshold, boost your ability to make muscle, and maximize your body's capacity for change.


^ Jump up to: a b Burt VL, Cutler JA, Higgins M, et al. (July 1995). "Trends in the prevalence, awareness, treatment, and control of hypertension in the adult US population. Data from the health examination surveys, 1960 to 1991". Hypertension. 26 (1): 60–69. doi:10.1161/01.HYP.26.1.60. PMID 7607734. Archived from the original on 2012-12-20. Retrieved 5 June 2009.

^ Jump up to: a b c d e f James, PA.; Oparil, S.; Carter, BL.; Cushman, WC.; Dennison-Himmelfarb, C.; Handler, J.; Lackland, DT.; Lefevre, ML.; et al. (Dec 2013). "2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults: Report From the Panel Members Appointed to the Eighth Joint National Committee (JNC 8)". JAMA. 311 (5): 507–20. doi:10.1001/jama.2013.284427. PMID 24352797.


An exception to this is those with very high blood pressure readings especially when there is poor organ function.[79] Initial assessment of the hypertensive people should include a complete history and physical examination. With the availability of 24-hour ambulatory blood pressure monitors and home blood pressure machines, the importance of not wrongly diagnosing those who have white coat hypertension has led to a change in protocols. In the United Kingdom, current best practice is to follow up a single raised clinic reading with ambulatory measurement, or less ideally with home blood pressure monitoring over the course of 7 days.[79] The United States Preventive Services Task Force also recommends getting measurements outside of the healthcare environment.[80] Pseudohypertension in the elderly or noncompressibility artery syndrome may also require consideration. This condition is believed to be due to calcification of the arteries resulting in abnormally high blood pressure readings with a blood pressure cuff while intra arterial measurements of blood pressure are normal.[81] Orthostatic hypertension is when blood pressure increases upon standing.[82]
But why does someone get to this point?  For the chronic dieter they arrive with metabolic damage because they hold tightly to the “Eat less, exercise more” mantras they were taught.  When weight loss slows down, they eat less and push harder in their exercise routine, pushing metabolism into the ground.  For the person with the unknown metabolism problem their road to metabolic damage is much more subtle.  This person simply isn’t feeling well, starts putting on weight, and progresses all the way to metabolic damage because no doctor was able to identify what was going wrong.

Metabolic syndrome is a serious health condition that affects about 23 percent of adults and places them at higher risk of cardiovascular disease, diabetes, stroke and diseases related to fatty buildups in artery walls. The underlying causes of metabolic syndrome include overweight and obesity, physical inactivity, genetic factors and getting older.
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. 
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