This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.
Findings from the Diabetes Control and Complications Trial (DCCT) and the United Kingdom Prospective Diabetes Study (UKPDS) have clearly shown that aggressive and intensive control of elevated levels of blood sugar in patients with type 1 and type 2 diabetes decreases the complications of nephropathy, neuropathy, retinopathy, and may reduce the occurrence and severity of large blood vessel diseases. Aggressive control with intensive therapy means achieving fasting glucose levels between 70-120 mg/dl; glucose levels of less than 160 mg/dl after meals; and a near normal hemoglobin A1c levels (see below).
(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

Type 1 and type 2 diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with type 1 associated with youth and type 2 with being overweight.[108] The term "mellitus" or "from honey" was added by the Briton John Rolle in the late 1700s to separate the condition from diabetes insipidus, which is also associated with frequent urination.[108] Effective treatment was not developed until the early part of the 20th century, when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922.[108] This was followed by the development of the long-acting insulin NPH in the 1940s.[108]
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.

Nerve damage from diabetes is called diabetic neuropathy and is also caused by disease of small blood vessels. In essence, the blood flow to the nerves is limited, leaving the nerves without blood flow, and they get damaged or die as a result (a term known as ischemia). Symptoms of diabetic nerve damage include numbness, burning, and aching of the feet and lower extremities. When the nerve disease causes a complete loss of sensation in the feet, patients may not be aware of injuries to the feet, and fail to properly protect them. Shoes or other protection should be worn as much as possible. Seemingly minor skin injuries should be attended to promptly to avoid serious infections. Because of poor blood circulation, diabetic foot injuries may not heal. Sometimes, minor foot injuries can lead to serious infection, ulcers, and even gangrene, necessitating surgical amputation of toes, feet, and other infected parts.


Interestingly enough, some data suggests that consumption of sodas (diet or regular) and other products containing high-fructose corn syrup (HFCS) like salad dressings and ketchup, jams, jellies, ice cream and many more foods may be linked to obesity, insulin resistance, and metabolic syndrome in both adults and children. Interrupted sleep patterns (such as sleep apnea) may also be a factor in increasing the incidence of insulin resistance and metabolic syndrome in the adult population.
In a meta-analysis of pooled data from 19 prospective cohort studies involving 762,393 patients, Huang et al reported that, after adjustment for multiple cardiovascular risk factors, prehypertension was associated with a 66% increased risk for stroke, compared with an optimal blood pressure (< 120/80 mm Hg). [41, 42] Patients in the high range of prehypertension (130-139/85-89 mm Hg) had a 95% increased risk of stroke, compared with a 44% increased risk for those in the low range of prehypertension (120-129/80-84 mm Hg). [41, 42]

There is no known preventive measure for type 1 diabetes.[2] Type 2 diabetes – which accounts for 85–90% of all cases – can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and consuming a healthy diet.[2] Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%.[71] Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish.[72] Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes.[72] Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.[73]
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] http://media-cache-ec5.pinterest.com/upload/21110691974453216_0I4oS4Zs_c.jpg
Excess abdominal fat leads to excess free fatty acids in the portal vein, increasing fat accumulation in the liver. Fat also accumulates in muscle cells. Insulin resistance develops, with hyperinsulinemia. Glucose metabolism is impaired, and dyslipidemias and hypertension develop. Serum uric acid levels are typically elevated (increasing risk of gout), and a prothrombotic state (with increased levels of fibrinogen and plasminogen activator inhibitor I) and an inflammatory state develop.
Type 1 diabetes is caused by an autoimmune reaction (the body attacks itself by mistake) that stops your body from making insulin. About 5% of the people who have diabetes have type 1. Symptoms of type 1 diabetes often develop quickly. It’s usually diagnosed in children, teens, and young adults. If you have type 1 diabetes, you’ll need to take insulin every day to survive. Currently, no one knows how to prevent type 1 diabetes.
Various expert groups have produced guidelines regarding how low the blood pressure target should be when a person is treated for hypertension. These groups recommend a target below the range 140–160 / 90–100 mmHg for the general population.[13][99][100][101][102] Cochrane reviews recommend similar targets for subgroups such as people with diabetes[103] and people with prior cardiovascular disease.[104]

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).
Being undiagnosed celiac for decades definitely played into my weight loss struggles. This is counter to what current medical literature says but I see it all of the time. Food allergies, food sensitivities and the like can have a huge impact on weight loss resistance! They do this through inflammatory processes in the body but also through altering gut hormones and the types of bacteria that live in the gut. Study after study has shown that the blood sugar and insulin response to a food is incredibly individual BUT it can be predicted by the type of bacteria that are living in your gut. Yes, in the future we will be sequencing everyone’s gut bugs and using them to alter the course of every disease. I am sure of it!
Blood pressure rises and falls during the day depending on a person's level of activity and physical and emotional stress. Largely controlled by the autonomic nervous system (the part of the nervous system that controls involuntary actions), BP is also affected by several different hormones, including angiotensin II, aldosterone and catecholamines.
Both Metabolic Resistance Training workouts and Cardio Interval Training workouts offer an intense experience in a condensed timeframe. Both will torch fat and push you to the next level. And both will elevate your body's furnace, burning calories long after you've showered and crashed on the couch. But despite the fact both are advertised as such, only one (CRT) technically qualifies as HIIT training. So the next time your workout buddy suggests taking a HIIT course, double check on what type of workout experience they are aiming for.
Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.[61]
^ 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. http://www.sandysidhumedia.com/wp-content/uploads/2012/12/bennyquote.png
How to treat metabolic syndrome is controversial. Because there are several potential markers, the public health community has struggled with the decision of how best to define, diagnose and treat it. Nutritional approaches have generally been downplayed in favor of multiple medications that target the individual markers. Conventional recommendations tend to emphasize caloric restriction and reduced fat intake, even though metabolic syndrome can best be described as carbohydrate intolerance. The most effective treatment for metabolic syndrome is to control the intake of carbs, not fat. In fact, restricting dietary fat and replacing it with carbohydrate actually makes many of the problems of metabolic syndrome worse. The metabolic syndrome paradigm has therefore caused a great deal of distress—and pushback—among those advocating low-fat diets. For more on how to prevent metabolic syndrome, see How to Reduce Your Risk for Metabolic Syndrome.

When you go on a diet set your protein intake higher. Studies have shown that a higher protein diet, one that exceeds the RDA of .8g/kg body weight, helps offset the decline in metabolic rate that occurs with dieting. At Metabolic Effect, we set the protein level to 40% of total calories during fat reducing stages (i.e. 30:40:30 carbs:protein:fat). Another way to look at this is to make sure you are getting at least 1g of protein per pound of body weight (if you want to try to gain muscle) or 1g per pound of muscle mass (if you are trying to just maintain muscle).


Serum creatinine is measured to assess for the presence of kidney disease, which can be either the cause or the result of hypertension. Serum creatinine alone may overestimate glomerular filtration rate and recent guidelines advocate the use of predictive equations such as the Modification of Diet in Renal Disease (MDRD) formula to estimate glomerular filtration rate (eGFR).[27] eGFR can also provide a baseline measurement of kidney function that can be used to monitor for side effects of certain anti-hypertensive drugs on kidney function. Additionally, testing of urine samples for protein is used as a secondary indicator of kidney disease. Electrocardiogram (EKG/ECG) testing is done to check for evidence that the heart is under strain from high blood pressure. It may also show whether there is thickening of the heart muscle (left ventricular hypertrophy) or whether the heart has experienced a prior minor disturbance such as a silent heart attack. A chest X-ray or an echocardiogram may also be performed to look for signs of heart enlargement or damage to the heart.[23]
"Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used.[39] Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, frequently with ketosis, and sometimes with serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease).[39] These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.[40]
Okay, you've suffered through the particulars and are sufficiently MRT-educated. Let's get to the good stuff: three tried-and-true MRT strategies guaranteed to help strip away stubborn fat and heighten acid-buffering ability. You can stick with one strategy for a given timeframe or periodize strategies from one week to the next. Regardless of what you decide to do, it's best to insert an "unloading microcycle" (one week of light weight) every fourth week or so to avoid the potential for overtraining. During the unloading cycle, reduce the effort expended so you're not substantially challenging your muscles on the last few reps of each set (aim for about a 7 on an RPE scale of 1-10). As a general rule, limit metabolic training cycles to a maximum of about 8 weeks. Any longer and you risk compromising muscular gains.

^ Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents, National Heart, Lung, and Blood Institute (Dec 2011). "Expert panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents: summary report". Pediatrics. 128 Suppl 5: S213–56. doi:10.1542/peds.2009-2107C. PMC 4536582. PMID 22084329.
Current strategies for controlling cardiovascular disease (CVD) risk factors, such as high blood pressure and high cholesterol, are not widely used as standard practice. CDC developed this guide to provide health professionals with evidence-based strategies for effective and sustainable CVD prevention, including health and economic impact and potential for reducing health disparities.
Type 2 DM is primarily due to lifestyle factors and genetics.[45] A number of lifestyle factors are known to be important to the development of type 2 DM, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization.[16] Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders.[11] Even those who are not obese often have a high waist–hip ratio.[11]
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.
^ Mente, Andrew; O'Donnell, Martin; Rangarajan, Sumathy; Dagenais, Gilles; Lear, Scott; McQueen, Matthew; Diaz, Rafael; Avezum, Alvaro; Lopez-Jaramillo, Patricio; Lanas, Fernando; Li, Wei; Lu, Yin; Yi, Sun; Rensheng, Lei; Iqbal, Romaina; Mony, Prem; Yusuf, Rita; Yusoff, Khalid; Szuba, Andrzej; Oguz, Aytekin; Rosengren, Annika; Bahonar, Ahmad; Yusufali, Afzalhussein; Schutte, Aletta Elisabeth; Chifamba, Jephat; Mann, Johannes F E; Anand, Sonia S; Teo, Koon; Yusuf, S (July 2016). "Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies". The Lancet. 388 (10043): 465–75. doi:10.1016/S0140-6736(16)30467-6. PMID 27216139.
If lifestyle modifications are insufficient to achieve the goal BP, there are several drug options for treating and managing hypertension. Thiazide diuretics, an angiotensin-converting enzyme inhibitor (ACEI) /angiotensin receptor blocker (ARB), or calcium channel blocker (CCB) are the preferred agents in nonblack populations, whereas CCBs or thiazide diuretics are favored in black hypertensive populations. [8] These recommendations do not exclude the use of ACE inhibitors or ARBs in treatment of black patients, or CCBs or diuretics in non-black persons. Often, patients require several antihypertensive agents to achieve adequate BP control.
Cataracts and glaucoma are also more common among diabetics. It is also important to note that since the lens of the eye lets water through, if blood sugar concentrations vary a lot, the lens of the eye will shrink and swell with fluid accordingly. As a result, blurry vision is very common in poorly controlled diabetes. Patients are usually discouraged from getting a new eyeglass prescription until their blood sugar is controlled. This allows for a more accurate assessment of what kind of glasses prescription is required.
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