^ Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, Fruchart JC, James WP, Loria CM, Smith SC (October 2009). "Harmonizing the metabolic syndrome: 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" (PDF). Circulation. 120 (16): 1640–45. doi:10.1161/CIRCULATIONAHA.109.192644. PMID 19805654.
Again, the answer to why has already been discovered! We have a 24hr clock in our body, known as the circadian rhythm. This rhythm controls what hormones are released and when, it controls our wake sleep rhythm and when working properly signals what physiological processes happen during the day and at night. When you think about it, it is a pretty simple concept that we should be eating during the day and not eating during our biological night. People who are ‘night owls’ often eat during their biological night and it has been shown that the insulin and glucose response to a meal eaten at night is that of a DIABETIC! I was shocked when I first discovered this! This means that even a ‘healthy’ thin person is predisposed to weight gain and gets stuck in fat storage mode if they eat all night long. This is aggravated in people who are predisposed to insulin resistance and metabolic hormone chaos!
Research has shown this is NOT an imaginary issue. As far back as 1975, researchers published a study in the journal Lancet that looked at the issue of weight loss resistance. 29 women who claimed they could not lose weight were studied. The researchers, like many of us, assumed these women simply were not compliant and wanted to test their metabolism by sequestering them in a house and controlling all food and exercise they did. Each woman was put on a strict 1500 calorie a day diet.
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).
Enlarged heart. High blood pressure increases the amount of work for your heart. Like any heavily exercised muscle in your body, your heart grows bigger (enlarges) to handle the extra workload. The bigger your heart is, the more it demands oxygen-rich blood but the less able it is to maintain proper blood flow. As a result, you feel weak and tired and are not able to exercise or perform physical activities. Without treatment, your heart failure will only get worse.
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.
The brain is crucial in development of metabolic syndrome, modulating peripheral carbohydrate and lipid metabolism. The metabolic syndrome can be induced by overfeeding with sugar or fructose, particularly concomitantly with high-fat diet. The resulting oversupply of omega-6 fatty acids, particularly arachidonic acid (AA), is an important factor in the pathogenesis of metabolic syndrome.
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.
Some risks of the keto diet include low blood sugar, negative medication interactions, and nutrient deficiencies. (People who should avoid the keto diet include those with kidney damage or disease, women who are pregnant or breast-feeding, and those with or at a heightened risk for heart disease due to high blood pressure, high cholesterol, or family history. (40)
It has not been contested that cardiovascular risk factors tend to cluster together; the matter of contention has been the assertion that the metabolic syndrome is anything more than the sum of its constituent parts. Phenotypic heterogeneity (for example, represented by variation in metabolic syndrome factor combinations among individuals with metabolic syndrome) has fueled that debate. However, more recent evidence suggests that common triggers (for example, excessive sugar-intake in the environment of overabundant food) can contribute to the development of multiple metabolic abnormalities at the same time, supporting the commonality of the energy utilization and storage pathways in metabolic syndrome. http://www.sandysidhumedia.com/wp-content/uploads/2012/12/nataliequote.jpg
Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of the immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults, but was traditionally termed "juvenile diabetes" because a majority of these diabetes cases were found in children.
Arachidonic acid (with its precursor – linoleic acid) serve as a substrate to the production of inflammatory mediators known as eicosanoids, whereas the arachidonic acid-containing compound diacylglycerol (DAG) is a precursor to the endocannabinoid 2-arachidonoylglycerol (2-AG) while fatty acid amide hydrolase (FAAH) mediates the metabolism of anandamide into arachidonic acid. Anandamide can also be produced from N-acylphosphatidylethanolamine via several pathways. Anandamide and 2-AG can also be hydrolized into arachidonic acid, potentially leading to increased eicosanoid synthesis. Metabolic syndrome is a risk factor for neurological disorders. Metabolomic studies suggest an excess of organic acids, impaired lipid oxidation byproducts, essential fatty acids and essential amino acids in the blood serum of affected patients.
It has not been contested that cardiovascular risk factors tend to cluster together; the matter of contention has been the assertion that the metabolic syndrome is anything more than the sum of its constituent parts. Phenotypic heterogeneity (for example, represented by variation in metabolic syndrome factor combinations among individuals with metabolic syndrome) has fueled that debate. However, more recent evidence suggests that common triggers (for example, excessive sugar-intake in the environment of overabundant food) can contribute to the development of multiple metabolic abnormalities at the same time, supporting the commonality of the energy utilization and storage pathways in metabolic syndrome.
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. 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. 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. This was followed by the development of the long-acting insulin NPH in the 1940s.
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.
Medicines are available if these changes do not help control your blood pressure within 3 to 6 months. Diuretics help rid your body of water and sodium. ACE inhibitors block the enzyme that raises your blood pressure. Other types of medicines— beta blockers, calcium channel blockers, and other vasodilators—work in different ways, but their overall effect is to help relax and widen your blood vessels and reduce the pressure inside the vessel. [See also the free government publication “Medicines to Help You: High Blood Pressure” (PDF) from the US Food and Drug Administration.]
Epigenetic phenomena, such as DNA methylation and histone modification, have also been implicated in the pathogenesis of hypertension. For example, a high-salt diet appears to unmask nephron development caused by methylation. Maternal water deprivation and protein restriction during pregnancy increase renin-angiotensin expression in the fetus. Mental stress induces a DNA methylase, which enhances autonomic responsiveness. The pattern of serine protease inhibitor gene methylation predicts preeclampsia in pregnant women. 
If you are diagnosed with metabolic syndrome, the goal of treatment will be to reduce your risk of developing further health complications. Your doctor will recommend lifestyle changes that may include losing between 7 and 10 percent of your current weight and getting at least 30 minutes of moderate to intense exercise five to seven days a week. They may also suggest that you quit smoking.
Tyler played college basketball at Utah State from 2007-2011, and had the opportunity to play in three NCAA tournaments. His coaches and trainers always had Gatorade or candy on hand in case his blood glucose dropped during a game. Tyler tested his blood glucose right before training, and during halftime breaks. He says working out and playing basketball has helped him to better control his T1D.
^ Roerecke, Michael; Tobe, Sheldon W.; Kaczorowski, Janusz; Bacon, Simon L.; Vafaei, Afshin; Hasan, Omer S. M.; Krishnan, Rohin J.; Raifu, Amidu O.; Rehm, Jürgen (27 June 2018). "Sex‐Specific Associations Between Alcohol Consumption and Incidence of Hypertension: A Systematic Review and Meta‐Analysis of Cohort Studies". Journal of the American Heart Association. 7 (13): e008202. doi:10.1161/JAHA.117.008202.
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.
The primary problem in metabolic syndrome is insulin resistance. In the body's attempt to compensate for insulin resistance, extra insulin is produced, leading to elevated insulin levels. The elevated insulin levels can lead, directly or indirectly, to the characteristic metabolic abnormalities seen in these patients. Frequently, the insulin resistance will progress to overt type 2 diabetes, which further increases the risk of cardiovascular complications.
Triglycerides are a common form of fat that we digest. Triglycerides are the main ingredient in animal fats and vegetable oils. Elevated levels of triglycerides are a risk factor for heart disease, heart attack, stroke, fatty liver disease, and pancreatitis. Elevated levels of triglycerides are also associated with diseases like diabetes, kidney disease, and medications (for example, diuretics, birth control pills, and beta blockers). Dietary changes, and medication if necessary can help lower triglyceride blood levels.
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).
Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. The goal of treatment is an HbA1C level of 6.5%, but should not be lower than that, and may be set higher. Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise. Specialized footwear is widely used to reduce the risk of ulceration, or re-ulceration, in at-risk diabetic feet. Evidence for the efficacy of this remains equivocal, however.
Kids who have a family history of heart disease or diabetes are at greater risk for metabolic syndrome. But, as with many things in life, the lifestyle habits a child adopts can push things in one direction or another. So kids who are active, fit, and eat a lot of fruits and vegetables may drastically decrease their chances of developing metabolic syndrome — even if a close relative already has it.
Polycystic ovarian syndrome. Thought to be related to insulin resistance, this disorder involves the release of extra male hormones by the ovaries, which can lead to abnormal menstrual bleeding, excessive hair growth, acne, and fertility problems. It is also associated with an increased risk for obesity, hypertension, and — in the long-term — diabetes, heart disease, and cancer.
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