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.

^ Qaseem A, Wilt TJ, Rich R, Humphrey LL, Frost J, Forciea MA (17 January 2017). "Pharmacologic Treatment of Hypertension in Adults Aged 60 Years or Older to Higher Versus Lower Blood Pressure Targets: A Clinical Practice Guideline From the American College of Physicians and the American Academy of Family Physicians". Annals of Internal Medicine. 166 (6): 430–437. doi:10.7326/M16-1785. PMID 28135725.
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. http://www.sandysidhumedia.com/wp-content/uploads/2013/12/SSM_Logo_White.png
Place a Swiss ball in front of you on the floor. Place forearms and fists on the top of it and keep your body in a straight line from your ankles to head. Keep core engaged, elbows bent at 90 degrees, and naturally arch lower back as you roll the ball forward. Make sure your body doesn't collapse as you perform this movement. Pause here, then using your abs, pull the ball back toward knees to starting position.
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.
If someone has already had a heart attack, their LDL ("bad") cholesterol should be reduced below 70mg/dl. A person who has diabetes has a heart attack risk equivalent to that of someone who has already one and so should be treated in the same way. If you have metabolic syndrome, a detailed discussion about lipid therapy is needed between you and your doctor, as each individual is unique.
The distribution of adipose tissue appears to affect its role in metabolic syndrome. Fat that is visceral or intra-abdominal correlates with inflammation, whereas subcutaneous fat does not. There are a number of potential explanations for this, including experimental observations that omental fat is more resistant to insulin and may result in a higher concentration of toxic free fatty acids in the portal circulation. [21]
This is an incredibly important, but commonly overlooked factor that heavily influences a metabolic resistance training program's success. While you can usually get by with minimal equipment with a MRT program, body weight only can get old very quickly.  Fortunately, just adding a kettlebell, band, suspension trainer, barbell, or other implement can quickly expand your exercise selection pool.  It's important to realize that a little bit can go a long way, especially if you're training in a busy gym and can't monopolize pieces of equipment for too long without someone walking off with them! https://www.healthshare.com.au/storage/avatars/35489.png.60x60_q85_box-0,0,256,256.jpg
In the 19th and 20th centuries, before effective pharmacological treatment for hypertension became possible, three treatment modalities were used, all with numerous side-effects: strict sodium restriction (for example the rice diet[152]), sympathectomy (surgical ablation of parts of the sympathetic nervous system), and pyrogen therapy (injection of substances that caused a fever, indirectly reducing blood pressure).[152][158]

The clinical value of using "metabolic syndrome" as a diagnosis has previously been debated due to different sets of conflicting and incomplete diagnostic criteria. These concerns have led the American Diabetes Association and the European Association for the Study of Diabetes to issue a joint statement identifying eight major concerns on the clinical utility of the metabolic syndrome diagnosis.[69] The principal argument has been that when confounding factors such as obesity are accounted for, diagnosis of the metabolic syndrome has a negligible association with the risk of heart disease.[70]

^ Jump up to: a b Petzold A, Solimena M, Knoch KP (October 2015). "Mechanisms of Beta Cell Dysfunction Associated With Viral Infection". Current Diabetes Reports (Review). 15 (10): 73. doi:10.1007/s11892-015-0654-x. PMC 4539350. PMID 26280364. So far, none of the hypotheses accounting for virus-induced beta cell autoimmunity has been supported by stringent evidence in humans, and the involvement of several mechanisms rather than just one is also plausible.
Researchers assigned overweight subjects to three groups: diet-only, diet plus aerobics, diet plus aerobics plus weights. The diet group lost 14.6 pounds of fat in 12 weeks. The aerobic group lost only one more pound than the diet group. Their training was three times a week starting at 30 minutes and progressing to 50 minutes over the 12 weeks. Nothing special. But the weight training group lost over 21 pounds of fat. That's 44% and 35% more than diet and cardio-only groups respectively. The addition of aerobic training didn't result in significant fat loss over dieting alone. Thirty-six sessions of up to 50 minutes is a lot of work for one additional pound of fat loss. But the addition of resistance training greatly accelerated fat loss results.

The depth of this product really blew me away, as there are 138 pages of sample MRT workouts using all sorts of different equipment, or none at all. There are some great ideas in there for fitness professionals and fitness enthusiasts alike, and I'll certainly be implementing some of the techniques Jen describes in our programming at Cressey Performance.  It's on sale at a great introductory price this week, so be sure to check it out.

The approximate prevalence of the metabolic syndrome in patients with coronary artery disease (CAD) is 50%, with a prevalence of 37% in patients with premature coronary artery disease (age 45), particularly in women. With appropriate cardiac rehabilitation and changes in lifestyle (e.g., nutrition, physical activity, weight reduction, and, in some cases, drugs), the prevalence of the syndrome can be reduced.[27]
After reading a recent Time article entitled “The Weight loss trap” I quite literally jumped off of my office chair, frustrated, angry and delighted. (I also lit up my husband’s phone with a thousand messages). I am so over misinformation in the weight loss space, but even more, it kills me that people are made to feel out of control and hopeless in their own bodies. Why delighted? Well, I was not quite ready to announce my upcoming book but I just could not give up this opportunity to share with you all of the reasons why Time has great points, but doesn’t tell the whole story. You can finally overcome weight loss resistance! http://www.sandysidhumedia.com/wp-content/uploads/2012/03/Natalie-Sisson.jpg

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]

 Even the low-fat craze that kicked off in the late 1970s–which was based on the intuitively appealing but incorrect notion that eating fat will make you fat–depended on the calorie-counting model of weight loss. (Since fatty foods are more calorie-dense than, say, plants, logic suggests that if you eat less of them, you will consume fewer calories overall, and then you’ll lose weight.)

The pain of diabetic nerve damage may respond to traditional treatments with certain medications such as gabapentin (Neurontin), phenytoin (Dilantin), and carbamazepine (Tegretol) that are traditionally used in the treatment of seizure disorders. Amitriptyline (Elavil, Endep) and desipramine (Norpraminine) are medications that are traditionally used for depression. While many of these medications are not indicated specifically for the treatment of diabetes related nerve pain, they are used by physicians commonly.

When there is excess glucose present in the blood, as with type 2 diabetes, the kidneys react by flushing it out of the blood and into the urine. This results in more urine production and the need to urinate more frequently, as well as an increased risk of urinary tract infections (UTIs) in men and women. People with type 2 diabetes are twice as likely to get a UTI as people without the disease, and the risk is higher in women than in men.


There are two major types of diabetes, called type 1 and type 2. Type 1 diabetes was also formerly called insulin dependent diabetes mellitus (IDDM), or juvenile-onset diabetes mellitus. In type 1 diabetes, the pancreas undergoes an autoimmune attack by the body itself, and is rendered incapable of making insulin. Abnormal antibodies have been found in the majority of patients with type 1 diabetes. Antibodies are proteins in the blood that are part of the body's immune system. The patient with type 1 diabetes must rely on insulin medication for survival.
Type 2 diabetes was also previously referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult-onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs, particularly in the face of insulin resistance as discussed above. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells).
Most doctors do not make a final diagnosis of high blood pressure until they measure your blood pressure several times (at least 2 blood pressure readings on 3 different days). Some doctors ask their patients to wear a portable machine that measures their blood pressure over the course of several days. This machine may help the doctor find out whether a patient has true high blood pressure or what is known as “white-coat hypertension.” White-coat hypertension is a condition in which a patient’s blood pressure rises during a visit to a doctor when anxiety and stress probably play a role.
Although the first formal definition of metabolic syndrome entered medical textbooks not so long ago (1998), it is as widespread as pimples and the common cold . According to the American Heart Association, 47 million Americans have it. That's almost a staggering one out of every six people. The syndrome runs in families and is more common among African-Americans, Hispanics, Asians, and Native Americans. The risks of developing metabolic syndrome increases as you age. https://www.healthshare.com.au/storage/avatars/34553.png.60x60_q85_box-0,0,256,256.png

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]
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.
Metabolic syndrome (also known as metabolic syndrome X) is a grouping of cardiac risk factors that result from insulin resistance (when the body's tissues do not respond normally to insulin). A person with metabolic syndrome has a greatly increased risk of developing type 2 diabetes, cardiovascular disease and premature death. In fact, another name for metabolic syndrome is pre-diabetes. https://www.clairekerslake.com/wp-content/uploads/2011/11/candles.jpg
A 2015 review of several studies found that restoring blood vitamin D levels by using supplements (more than 1,000 IU per day) reduced blood pressure in hypertensive individuals when they had existing vitamin D deficiency.[167] The results also demonstrated a correlation of chronically low vitamin D levels with a higher chance of becoming hypertensive. Supplementation with vitamin D over 18 months in normotensive individuals with vitamin D deficiency did not significantly affect blood pressure.[167]
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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