Diabetes was one of the first diseases described,[107] with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine".[108] The Ebers papyrus includes a recommendation for a drink to be taken in such cases.[109] The first described cases are believed to be of type 1 diabetes.[108] Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.[108][109]
The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves.[32] Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness.[32] Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that diabetics visit an eye doctor once a year.[33] Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation.[32] Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes.[32] The symptoms can include numbness, tingling, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
^ 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.
^ 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.
^ Qaseem, A; Wilt, TJ; Rich, R; Humphrey, LL; Frost, J; Forciea, MA; Clinical Guidelines Committee of the American College of Physicians and the Commission on Health of the Public and Science of the American Academy of Family, Physicians. (21 March 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.
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.
You can take additional magnesium if you do not think you’re getting enough in the diet. Dr. Weil recommends magnesium citrate, chelate, or glycinate. Avoid magnesium oxide, which can be irritating, and take half the amount of magnesium as the calcium you take in supplemental form. If you do not take any supplemental calcium, watch out for taking large amounts of magnesium, which can cause diarrhea.

Nope! Just as Time agreed, other research has shown that the low fat craze directly coincides with the increasing obesity epidemic. As you may have noticed above, fat is not on the list of insulin stimulating foods.. but sugar is! And sugar is just the thing that is added to low fat foods to make them taste better. So not only do you get a heightened insulin response to these low fat, low calorie foods leaving you in fat storing mode, but you are get an altered satiety response. That is right, fat is critical for the regulation of gut hormones and also the hormones that make you feel full after a meal and keep you feeling full between meals.

Most conventional practitioners recommend that patients follow a healthy eating plan like the American Dietary Association (ADA) diet, the Dietary Approaches to Stop Hypertension (DASH) diet or the Mediterranean Diet. All of these emphasize fruits, vegetables, and whole grains, while limiting unhealthy fats and promoting leaner protein foods like low-fat dairy and lean meats like chicken and fish.


Researchers used a circuit training protocol of 12 sets in 31 minutes. EPOC (Exercise Post Oxygen Consumption) was elevated significantly for 38 hours post-workout. That's a significant timeframe for metabolism to be elevated. If you trained for one hour on Monday morning, you'd still be burning more calories (without training) at midnight on Tuesday.
Another method is to have the individual wear a device that monitors and records the blood pressure at regular intervals during the day to evaluate blood pressure over time. This is especially helpful during the diagnostic process and can help rule out "white coat" hypertension, the high measurements that are sometimes present only when the person is in the doctor's office and not at other times. (See High Blood Pressure: Using an Ambulatory Blood Pressure Monitor on FamilyDoctor.org.)

Investigations into the pathophysiology of hypertension, both in animals and humans, have revealed that hypertension may have an immunological basis. Studies have revealed that hypertension is associated with renal infiltration of immune cells and that pharmacologic immunosuppression (such as with the drug mycophenolate mofetil) or pathologic immunosuppression (such as occurs with HIV) results in reduced blood pressure in animals and humans. Evidence suggests that T lymphocytes and T-cell derived cytokines (eg, interleukin 17, tumor necrosis factor alpha) play an important role in hypertension. [14, 15]
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!
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]

Kidney damage from diabetes is called diabetic nephropathy. The onset of kidney disease and its progression is extremely variable. Initially, diseased small blood vessels in the kidneys cause the leakage of protein in the urine. Later on, the kidneys lose their ability to cleanse and filter blood. The accumulation of toxic waste products in the blood leads to the need for dialysis. Dialysis involves using a machine that serves the function of the kidney by filtering and cleaning the blood. In patients who do not want to undergo chronic dialysis, kidney transplantation can be considered.

When the glucose concentration in the blood remains high over time, the kidneys will reach a threshold of reabsorption, and glucose will be excreted in the urine (glycosuria).[62] This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst (polydipsia).[60]


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.

When you have type 2 diabetes, your cells don't get enough glucose, which may cause you to lose weight. Also, if you are urinating more frequently because of uncontrolled diabetes, you may lose more calories and water, resulting in weight loss, says Daniel Einhorn, MD, medical director of the Scripps Whittier Diabetes Institute and clinical professor of medicine at the University of California in San Diego.
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