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Glycaemic Index

Definition:
The glycemic index or glycaemic index (GI) is a number associated with a particular type of food that indicates the food’s effect on a person’s blood glucose (also called blood sugar) level. The number typically ranges between 50 and 100, where 100 represents the standard, an equivalent amount of pure glucose.

The GI represents the total rise in a person’s blood sugar level following consumption of the food; it may or may not represent the rapidity of the rise in blood sugar. The steepness of the rise can be influenced by a number of other factors, such as the quantity of fat eaten with the food. The GI is useful for understanding how the body breaks down carbohydrates  and only takes into account the available carbohydrate (total carbohydrate minus fiber) in a food. Although the food may contain fats and other components that contribute to the total rise in blood sugar, these effects are not reflected in the GI.

The glycemic index is usually applied in the context of the quantity of the food and the amount of carbohydrate in the food that is actually consumed. A related measure, the glycemic load (GL), factors this in by multiplying the glycemic index of the food in question by the carbohydrate content of the actual serving. Watermelon has a high glycemic index, but a low glycemic load for the quantity typically consumed. Fructose, by contrast, has a low glycemic index, but can have a high glycemic load if a large quantity is consumed.

GI tables are available that list many types of foods and their GIs. Some tables also include the serving size and the glycemic load of the food per serving.

A practical limitation of the glycemic index is that it does not measure insulin production due to rises in blood sugar. As a result, two foods could have the same glycemic index, but produce different amounts of insulin. Likewise, two foods could have the same glycemic load, but cause different insulin responses. Furthermore, both the glycemic index and glycemic load measurements are defined by the carbohydrate content of food. For example when eating steak, which has no carbohydrate content but provides a high protein intake, up to 50% of that protein can be converted to glucose when there is little to no carbohydrate consumed with it.  But because it contains no carbohydrate itself, steak cannot have a glycemic index. For some food comparisons, the “insulin index” may be more useful.

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Glycemic index charts often give only one value per food, but variations are possible due to variety, ripeness (riper fruits contain more sugars increasing GI), cooking methods (the more cooked, or over cooked, a food the more its cellular structure is broken with a tendency for it to digest quickly and raise GI more), processing (e.g., flour has a higher GI than the whole grain from which it is ground as grinding breaks the grain’s protective layers) and the length of storage. Potatoes are a notable example, ranging from moderate to very high GI even within the same variety.

The glycemic response is different from one person to another, and also in the same person from day to day, depending on blood glucose levels, insulin resistance, and other factors.

Most of the values on the glycemic index do not show the impact on glucose levels after two hours. Some people with diabetes may have elevated levels after four hours.

Why  GI is so Important?
Over the past 15 years, low-GI diets have been associated with decreased risk of cardiovascular disease, type 2 diabetes, metabolic syndrome, stroke, depression, chronic kidney disease, formation of gall stones, neural tube defects, formation of uterine fibroids, and cancers of the breast, colon, prostate, and pancreas. Taking advantage of these potential health benefits can be as simple as sticking with whole, natural foods that are either low or very low in their GI value.

Determination of GI of a food:
Foods with carbohydrates that break down quickly during digestion and release glucose rapidly into the bloodstream tend to have a high GI; foods with carbohydrates that break down more slowly, releasing glucose more gradually into the bloodstream, tend to have a low GI. The concept was developed by Dr. David J. Jenkins and colleagues  in 1980–1981 at the University of Toronto in their research to find out which foods were best for people with diabetes. A lower glycemic index suggests slower rates of digestion and absorption of the foods’ carbohydrates and may also indicate greater extraction from the liver and periphery of the products of carbohydrate digestion. A lower glycemic response usually equates to a lower insulin demand but not always, and may improve long-term blood glucose control   and blood lipids. The insulin index is also useful for providing a direct measure of the insulin response to a food.

The glycemic index of a food is defined as the incremental area under the two-hour blood glucose response curve (AUC) following a 12-hour fast and ingestion of a food with a certain quantity of available carbohydrate (usually 50 g). The AUC of the test food is divided by the AUC of the standard (either glucose or white bread, giving two different definitions) and multiplied by 100. The average GI value is calculated from data collected in 10 human subjects. Both the standard and test food must contain an equal amount of available carbohydrate. The result gives a relative ranking for each tested food.

The current validated methods use glucose as the reference food, giving it a glycemic index value of 100 by definition. This has the advantages of being universal and producing maximum GI values of approximately 100. White bread can also be used as a reference food, giving a different set of GI values (if white bread = 100, then glucose ? 140). For people whose staple carbohydrate source is white bread, this has the advantage of conveying directly whether replacement of the dietary staple with a different food would result in faster or slower blood glucose response. A disadvantage with this system is that the reference food is not well-defined.

Classification:
GI values can be interpreted intuitively as percentages on an absolute scale and are commonly interpreted as follows:

Low GI…..(55 or less fructose;) …….Examples:beans (white, black, pink, kidney, lentil, soy, almond, peanut, walnut, chickpea); small seeds (sunflower, flax, pumpkin, poppy, sesame, hemp); most whole intact grains (durum/spelt/kamut wheat, millet, oat, rye, rice, barley); most vegetables, most sweet fruits (peaches, strawberries, mangos); tagatose; mushrooms; chilis.

Medium GI…..(56–69 Examples: white sugar or sucrose, not intact whole wheat or enriched wheat, pita bread, basmati rice, unpeeled boiled potato, grape juice, raisins, prunes, pumpernickel bread, cranberry juice,[10] regular ice cream, banana.

High GI….….(70 and above) Examples: glucose (dextrose, grape sugar), high fructose corn syrup, white bread (only wheat endosperm), most white rice (only rice endosperm), corn flakes, extruded breakfast cereals, maltose, maltodextrins, sweet potato , white potato , pretzels, bagels.

A low-GI food will release glucose more slowly and steadily, which leads to more suitable postprandial (after meal) blood glucose readings. A high-GI food causes a more rapid rise in blood glucose levels and is suitable for energy recovery after exercise or for a person experiencing hypoglycemia.

The glycemic effect of foods depends on a number of factors, such as the type of starch (amylose versus amylopectin), physical entrapment of the starch molecules within the food, fat and protein content of the food and organic acids or their salts in the meal — adding vinegar, for example, will lower the GI. The presence of fat or soluble dietary fiber can slow the gastric emptying rate, thus lowering the GI. In general, coarse, grainy breads with higher amounts of fiber have a lower GI value than white breads.  However, most breads made with 100% whole wheat or wholemeal flour have a GI not very different from endosperm only (white) bread.  Many brown breads are treated with enzymes to soften the crust, which makes the starch more accessible (high GI).

While adding fat or protein will lower the glycemic response to a meal, the relative differences remain. That is, with or without additions, there is still a higher blood glucose curve after a high-GI bread than after a low-GI bread such as pumpernickel.

Fruits and vegetables tend to have a low glycemic index. The glycemic index can be applied only to foods where the test relies on subjects consuming an amount of food containing 50 g of available carbohydrate.[citation needed] But many fruits and vegetables (not potatoes, sweet potatoes, corn) contain less than 50 g of available carbohydrate per typical serving. Carrots were originally and incorrectly reported as having a high GI.  Alcoholic beverages have been reported to have low GI values; however, beer was initially reported to have a moderate GI due to the presence of maltose. This has been refuted by brewing industry professionals, who say that all maltose sugar is consumed in the brewing process and that packaged beer has little to no maltose present. Recent studies have shown that the consumption of an alcoholic drink prior to a meal reduces the GI of the meal by approximately 15%.  Moderate alcohol consumption more than 12 hours prior to a test does not affect the GI.

Many modern diets rely on the glycemic index, including the South Beach Diet, Transitions by Market America and NutriSystem Nourish Diet. However, others have pointed out that foods generally considered to be unhealthy can have a low glycemic index, for instance, chocolate cake (GI 38), ice cream (37), or pure fructose (19), whereas foods like potatoes and rice have GIs around 100 but are commonly eaten in some countries with low rates of diabetes.

The GI Symbol Program is an independent worldwide GI certification program that helps consumers identify low-GI foods and drinks. The symbol is only on foods or beverages that have had their GI values tested according to standard and meet the GI Foundation’s certification criteria as a healthy choice within their food group, so they are also lower in kilojoules, fat and/or salt.

Weight control:
Recent animal research provides compelling evidence that high-GI carbohydrate is associated with increased risk of obesity. In one study,  male rats were split into high- and low-GI groups over 18 weeks while mean body weight was maintained. Rats fed the high-GI diet were 71% fatter and had 8% less lean body mass than the low-GI group. Postmeal glycemia and insulin levels were significantly higher, and plasma triglycerides were threefold greater in the high-GI-fed rats. Furthermore, pancreatic islet cells suffered “severely disorganized architecture and extensive fibrosis.” However, the GI of these diets was not experimentally determined. In a well controlled feeding study no improvement in weight loss was observed with a low glycemic index diet over calorie restriction.  Because high-amylose cornstarch (the major component of the assumed low-GI diet) contains large amounts of resistant starch, which is not digested and absorbed as glucose, the lower glycemic response and possibly the beneficial effects can be attributed to lower energy density and fermentation products of the resistant starch, rather than the GI.

In humans, a 2012 study shows that, after weight loss, the energy expenditure is higher on a low-glycemic index diet than on a low-fat diet (but lower than on the Atkins diet).

 Prevention of Diseases:
Several lines of recent [1999] scientific evidence have shown that individuals who followed a low-GI diet over many years were at a significantly lower risk for developing both type 2 diabetes, coronary heart disease, and age-related macular degeneration than others.  High blood glucose levels or repeated glycemic “spikes” following a meal may promote these diseases by increasing systemic glycative stress, other oxidative stress to the vasculature, and also by the direct increase in insulin levels.  The glycative stress sets up a vicious cycle of systemic protein glycation, compromised protein editing capacity involving the ubiquitin proteolytic pathway and autophagic pathways, leading to enhanced accumulation of glycated and other obsolete proteins.

In the past, postprandial hyperglycemia has been considered a risk factor associated mainly with diabetes. However, more recent evidence shows that it also presents an increased risk for atherosclerosis in the non-diabetic population   and that high GI diets,  high blood-sugar levels more generally,  and diabetes  are related to kidney disease as well.

Conversely, there are areas such as Peru and Asia where people eat high-glycemic index foods such as potatoes and high-GI rice without a high level of obesity or diabetes.  The high consumption of legumes in South America and fresh fruit and vegetables in Asia likely lowers the glycemic effect in these individuals. The mixing of high- and low-GI carbohydrates produces moderate GI values.

A study from the University of Sydney in Australia suggests that having a breakfast of white bread and sugar-rich cereals, over time, may make a person susceptible to diabetes, heart disease, and even cancer.

A study published in the American Journal of Clinical Nutrition found that age-related adult macular degeneration (AMD), which leads to blindness, is 42% higher among people with a high-GI diet, and concluded that eating a lower-GI diet would eliminate 20% of AMD cases.

The American Diabetes Association supports glycemic index but warns that the total amount of carbohydrate in the food is still the strongest and most important indicator, and that everyone should make their own custom method that works best for them.

The International Life Sciences Institute concluded in 2011 that because there are many different ways of lowering glycemic response, not all of which have the same effects on health, “It is becoming evident that modifying the glycemic response of the diet should not be seen as a stand-alone strategy but rather as an element of an overall balanced diet and lifestyle.”

A systematic review of few human trials examined the potential of low GI diet to improve pregnancy outcomes. Potential benefits were still seen despite no ground breaking findings in maternal glycemia or pregnancy outcomes. In this regard, more women under low GI diet achieved the target treatment goal for the postprandial glycemic level and reduced their need for insulin treatment. A low GI diet may also provide greater benefits to overweight and obese women. Interestingly, intervention at an early stage of pregnancy has shown a tendency to lower birth weight and birth centile in infants born to women with GDM.

Other factors:
The number of grams of carbohydrate can have a bigger impact than glycemic index on blood sugar levels, depending on quantities. Consuming fewer calories, losing weight, and carbohydrate counting can be better for lowering the blood sugar level. Carbohydrates impact glucose levels most profoundly,  and two foods with the same carbohydrate content are, in general, comparable in their effects on blood sugar.  A food with a low glycemic index may have a high carbohydrate content or vice versa; this can be accounted for with the glycemic load (GL). Consuming carbohydrates with a low glycemic index and calculating carbohydrate intake would produce the most stable blood sugar levels.

Criticism and alternatives:
The glycemic index does not take into account other factors besides glycemic response, such as insulin response, which is measured by the insulin index and can be more appropriate in representing the effects from some food contents other than carbohydrates. In particular, since it is based on the area under the curve of the glucose response over time from ingesting a subject food, the shape of the curve has no bearing on the corresponding GI value. The glucose response can rise to a high level and fall quickly, or rise less high but remain there for a longer time, and have the same area under the curve. For subjects with type 1 diabetes who do not have an insulin response, the rate of appearance of glucose after ingestion represents the absorption of the food itself. This glycemic response has been modeled, where the model parameters for the food enable prediction of the continuous effect of the food over time on glucose values, and not merely the ultimate effect that the GI represents.

Although the glycemic index provides some insights into the relative diabetic risk within specific food groups, it contains many counter-intuitive ratings. These include suggestions that bread generally has a higher glycemic ranking than sugar and that some potatoes are more glycemic than glucose. More significantly, studies such as that by Bazzano et al.  demonstrate a significant beneficial diabetic effect for fruit compared to a substantial detrimental impact for fruit juice despite these having similar “low GI” ratings.

From blood glucose curves presented by Brand-Miller et al.  the main distinguishing feature between average fruit and fruit juice blood glucose curves is the maximum slope of the leading edge of 4.38 mmol·L-1·h-1 for fruit and 6.71 mmol·L-1·h-1 for fruit juice. This raises the concept that the rate of increase in blood glucose may be a significant determinant particularly when comparing liquids to solids which release carbohydrates over time and therefore have an inherently greater area under the blood glucose curve.

If you were to restrict yourself to eating only low GI foods, your diet is likely to be unbalanced and may be high in fat and calories, leading to weight gain and increasing your risk of heart disease. It is important not to focus exclusively on GI and to think about the balance of your meals, which should be low in fat, salt and sugar and contain plenty of fruit and vegetables.

There are books that give a long list of GI values for many different foods. This kind of list does have its limitations. The GI value relates to the food eaten on its own and in practice we usually eat foods in combination as meals. Bread, for example is usually eaten with butter or margarine, and potatoes could be eaten with meat and vegetables.

An additional problem is that GI compares the glycaemic effect of an amount of food containing 50g of carbohydrate but in real life we eat different amounts of food containing different amounts of carbohydrate.

Note: The amount of carbohydrate you eat has a bigger effect on blood glucose levels than GI alone.

How to have lower GI?
*Choose basmati or easy cook rice, pasta or noodles.
*Switch baked or mashed potato for sweet potato or boiled new potatoes.
*Instead of white and wholemeal bread, choose granary, pumpernickel or rye bread.
*Swap frozen microwaveable French fries for pasta or noodles.
*Try porridge, natural muesli or wholegrain breakfast cereals.
*You can maximise the benefit of GI by switching to a low GI option food with each meal or snack

Resources:
http://en.wikipedia.org/wiki/Glycemic_index
https://www.diabetes.org.uk/Guide-to-diabetes/Managing-your-diabetes/Glycaemic-Index-GI/
http://www.whfoods.com/genpage.php?tname=faq&dbid=32

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Ailmemts & Remedies

Gastroparesis

Definition:
Gastroparesis (gastro-, “stomach” + -paresis, “partial paralysis”), also called delayed gastric emptying, is a medical condition consisting of a paresis (partial paralysis) of the stomach, resulting in food remaining in the stomach for an abnormally long time. Normally, the stomach contracts to move food down into the small intestine for additional digestion. The vagus nerve controls these contractions. Gastroparesis may occur when the vagus nerve is damaged and the muscles of the stomach and intestines do not properly function. Food then moves slowly or stops moving through the digestive tract….CLICK & SEE

YOU MAY CLICK & SEEOur Digestive System and How It Works 
Symptoms:
The most common symptoms of gastroparesis are the following:
*Chronic nausea (93%)
*Vomiting (especially of undigested food) (68-84%)
*Abdominal pain (46-90%)
*A feeling of fullness after eating just a few bites (60-86%)

Other symptoms include the following:
*Palpitations
*Heartburn
*Abdominal bloating
*Erratic blood glucose levels
*Lack of appetite
*Gastroesophageal reflux
*Spasms of the stomach wall
*Weight loss and malnutrition

Morning nausea may also indicate gastroparesis. Vomiting may not occur in all cases, as sufferers may adjust their diets to include only small amounts of food.

Symptoms may be aggravated by eating greasy or rich foods, large quantities of foods with fiber—such as raw fruits and vegetables—or drinking beverages high in fat or carbonation. Symptoms may be mild or severe, and they can occur frequently in some people and less often in others. The symptoms of gastroparesis may also vary in intensity over time in the same individual. Sometimes gastroparesis is difficult to diagnose because people experience a range of symptoms similar to those of other diseases.

Causes:
Transient gastroparesis may arise in acute illness of any kind, as a consequence of certain cancer treatments or other drugs which affect digestive action, or due to abnormal eating patterns.

It is frequently caused by autonomic neuropathy. This may occur in people with type 1 or type 2 diabetes. In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may affect chemical changes in the nerves.The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis. Other possible causes include anorexia nervosa and bulimia nervosa, which may also damage the vagus nerve. Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers-Danlos syndrome, and neurological conditions such as Parkinson’s disease. It may also occur as part of a mitochondrial disease.

Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery.  Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining.

Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection. “Stomach flu”, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.

Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men.A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest. Neither theory has been proven definitively.

Gastroparesis can also be connected to hypochlorhydria and be caused by chloride, sodium and/or zinc deficiency, as these minerals are needed for the stomach to produce adequate levels of gastric acid (HCL) in order to properly empty itself of a meal.

Other identifiable causes of gastroparesis include intestinal surgery and nervous system diseases such as Parkinson’s disease or multiple sclerosis. For reasons that are not very clear, gastroparesis is more commonly found in women than in men.

Complications:
The complications of gastroparesis can include

*severe dehydration due to persistent vomiting

*gastroesophageal reflux disease (GERD), which is GER that occurs more than twice a week for a few weeks; GERD can lead to esophagitis— irritation of the esophagus

*bezoars, which can cause nausea, vomiting, obstruction, or interfere with absorption of some medications in pill form

*difficulty managing blood glucose levels in people with diabetes

*malnutrition due to poor absorption of nutrients or a low calorie intake

*decreased quality of life, including work absences due to severe symptoms

Diagnosis:
Gastroparesis is diagnosed through a physical exam, medical history, blood tests, tests to rule out blockage or structural problems in the GI tract, and gastric emptying tests. Tests may also identify a nutritional disorder or underlying disease. To rule out any blockage or other structural problems, the doctor may perform one or more of the following tests:

*Upper gastrointestinal (GI) endoscopy. This procedure involves using an endoscope—a small, flexible tube with a light—to see the upper GI tract, which includes the esophagus, stomach, and duodenum—the first part of the small intestine. The test is performed at a hospital or outpatient center by a gastroenterologist—a doctor who specializes in digestive diseases. The endoscope is carefully fed down the esophagus and into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. A person may receive a liquid anesthetic that is gargled or sprayed on the back of the throat. An intravenous (IV) needle is placed in a vein in the arm if general anesthesia is given. The test may show blockage or large bezoars—solid collections of food, mucus, vegetable fiber, hair, or other material that cannot be digested in the stomach—that are sometimes softened, dissolved, or broken up during an upper GI endoscopy.

*

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Ailmemts & Remedies

Gestational Diabetes

Definition:
Gestational diabetes (or gestational diabetes mellitus, GDM) is a condition in which women without previously diagnosed diabetes exhibit high blood glucose levels during pregnancy (especially during their third trimester). Gestational diabetes is caused when insulin receptors do not function properly. This is likely due to pregnancy-related factors such as the presence of human placental lactogen that interferes with susceptible insulin receptors. This in turn causes inappropriately elevated blood sugar levels.

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Gestational diabetes generally has few symptoms and it is most commonly diagnosed by screening during pregnancy. Diagnostic tests detect inappropriately high levels of glucose in blood samples. Gestational diabetes affects 3-10% of pregnancies, depending on the population studied.

As with diabetes mellitus in pregnancy in general, babies born to mothers with untreated gestational diabetes are typically at increased risk of problems such as being large for gestational age (which may lead to delivery complications), low blood sugar, and jaundice. If untreated, it can also cause seizures or stillbirth. Gestational diabetes is a treatable condition and women who have adequate control of glucose levels can effectively decrease these risks. The food plan is often the first recommended target for strategic management of GDM.

Clasifications:
There are two subtypes of gestational diabetes:
Type A1: abnormal oral glucose tolerance test (OGTT), but normal blood glucose levels during fasting and two hours after meals; diet modification is sufficient to control glucose levels

Type A2: abnormal OGTT compounded by abnormal glucose levels during fasting and/or after meals; additional therapy with insulin or other medications is required

Approximately 7% of all pregnancies are complicated by GDM, resulting in more than 200,000 cases annually. The prevalence may range from 1 to 14% of all pregnancies, depending on the population studied and the diagnostic tests employed.

Symptoms:
Because gestational diabetes does not cause much symptoms, the patient need to be tested for the condition. This is usually done between the 24th and 28th weeks of pregnancy. It is surprised if your test shows a high blood sugar level and is important for the patient to be tested for gestational diabetes, because high blood sugar can cause problems for both the pregnent woman and the baby.Sometimes, a pregnant woman has been living with diabetes without knowing it. If she has the  symptoms of diabetes  and that may include:

*Increased thirst.
*Increased urination.
*Increased hunger.
*Blurred vision.

Pregnancy causes most women to urinate more often and to feel more hungry, so having these symptoms doesn’t always mean that a woman has diabetes.Doctor should be consulted wheather  these symptoms are for diabetes  and then he can suggest for the test of diabetes.

*Infections:
Since diabetes interferes with the body’s ability to fight infections, the pregnant woman may experience frequent infections in areas such as the bladder, vagina and skin. White blood cells defend the body against bacteria, but these cells aren’t able to function normally when a person has a high blood sugar. A woman with gestational diabetes may also complain of a yeast infection in the vagina or on the skin. Yeast cells are normally present in the vaginal area in small amounts. The vaginal secretions and urine contain more glucose when a woman has gestational diabetes. The yeast cells use the glucose as food, which causes the cells to multiply. With the body’s immune system compromised by the high level of glucose in the blood, this increase in yeast cells turns into a yeast infection.

*High Blood Sugar:
Since a woman may not have any noticeable symptoms of gestational diabetes and symptoms can mimic regular pregnancy symptoms, screening for this condition is part of prenatal care for at-risk women between weeks 24 and 28 of pregnancy. The doctor will initially order a blood test called a glucose challenge test. If the glucose challenge test indicates a high blood sugar level, the doctor may order a glucose tolerance test to confirm the diagnosis of gestational diabetes. Both tests involve drinking a sweet glucose solution and having your blood drawn after a prescribed amount of time.

Causes:
Almost all women have some degree of impaired glucose intolerance as a result of hormonal changes that occur during pregnancy. That means that their blood sugar may be higher than normal, but not high enough to have diabetes. During the later part of pregnancy (the third trimester), these hormonal changes place pregnant woman at risk for gestational diabetes.

During pregnancy, increased levels of certain hormones made in the placenta (the organ that connects the baby by the umbilical cord to the uterus) help shift nutrients from the mother to the developing fetus. Other hormones are produced by the placenta to help prevent the mother from developing low blood sugar.

They work by resisting the actions of insulin.
Over the course of the pregnancy, these hormones lead to progressive impaired glucose intolerance (higher blood sugar levels). To try to decrease blood sugar levels, the body makes more insulin to get glucose into cells to be used for energy.
Usually, the mother’s pancreas is able to produce more insulin (about three times the normal amount) to overcome the effect of the pregnancy hormones on blood sugar levels. If, however, the pancreas cannot produce enough insulin, blood sugar levels will rise, resulting in gestational diabetes.

Risk factors:
Any woman can develop gestational diabetes, but some women are at greater risk. Risk factors for gestational diabetes include:

*Age greater than 25. Women older than age 25 are more likely to develop gestational diabetes.
*Family or personal health history. the risk of developing gestational diabetes increases if the woman has prediabetes — slightly elevated blood sugar that may be a precursor to type 2 diabetes — or if a close family member, such as a parent or sibling, has type 2 diabetes.the woman is also more likely to develop gestational diabetes if she had it during a previous pregnancy, if the woman delivered a baby who weighed more than 9 pounds (4.1 kilograms), or if she had an unexplained stillbirth.
*Excess weight. You’re more likely to develop gestational diabetes if you’re significantly overweight with a body mass index (BMI) of 30 or higher.
*Race factor. For reasons that aren’t clear, women who are black, Hispanic, American Indian or Asian are more likely to develop gestational diabetes.

Complications:
Most women who have gestational diabetes deliver healthy babies. However, gestational diabetes that’s not carefully managed can lead to uncontrolled blood

sugar levels and cause problems for patient and the baby, including an increased likelihood of needing a C-section to deliver.

Complications that may affect the baby are:
1.Excessive birth weight. Extra glucose in your bloodstream crosses the placenta, which triggers your baby’s pancreas to make extra insulin. This can cause the baby to grow too large (macrosomia). Very large babies — those that weigh 9 pounds or more — are more likely to become wedged in the birth canal, sustain birth injuries or require a C-section birth.

2.Early (preterm) birth and respiratory distress syndrome. A mother’s high blood sugar may increase her risk of early labor and delivering her baby before its due date. Or her doctor may recommend early delivery because the baby is large.

3.Babies born early may experience respiratory distress syndrome — a condition that makes breathing difficult. Babies with this syndrome may need help breathing until their lungs mature and become stronger. Babies of mothers with gestational diabetes may experience respiratory distress syndrome even if they’re not born early.

4.Low blood sugar (hypoglycemia). Sometimes babies of mothers with gestational diabetes develop low blood sugar (hypoglycemia) shortly after birth because their own insulin production is high. Severe episodes of hypoglycemia may provoke seizures in the baby. Prompt feedings and sometimes an intravenous glucose solution can return the baby’s blood sugar level to normal.

5.Type 2 diabetes later in life. Babies of mothers who have gestational diabetes have a higher risk of developing obesity and type 2 diabetes later in life.
Untreated gestational diabetes can result in a baby’s death either before or shortly after birth.

Complications that may affect the patient are:
1.High blood pressure and preeclampsia. Gestational diabetes raises your risk of high blood pressure, as well as, preeclampsia — a serious complication of pregnancy that causes high blood pressure and other symptoms that can threaten the lives of both mother and baby.

2.Future diabetes. If the pregnent woman has gestational diabetes, she is more likely to get it again during a future pregnancy and also more likely to develop type 2 diabetes as she gets older. However, making healthy lifestyle choices such as eating healthy foods and exercising can help reduce the risk of future type 2 diabetes.Of those women with a history of gestational diabetes who reach their ideal body weight after delivery, fewer than 1 in 4 eventually develops type 2 diabetes.

Diagnosis:
Gestational diabetes usually starts halfway through the pregnancy. All pregnant women should receive an oral glucose tolerance test between the 24th and 28th week of pregnancy to screen for the condition. Women who have risk factors for gestational diabetes may have this test earlier in the pregnancy.

Once the pregnent woman is diagnosed with gestational diabetes, she can see how well she is doing by testing the glucose level at home. The most common way involves pricking her finger and putting a drop of the blood on a machine that will give her the glucose reading.

Treatment:
The goals of treatment are to keep blood sugar (glucose) levels within normal limits during the pregnancy, and to make sure that the growing baby is healthy.

Watching the baby:
1.The health care provider should closely check both the patient  and the baby throughout the pregnancy. Fetal monitoring will check the size and health of the fetus.

2.A nonstress test is a very simple, painless test for the patient and the baby.

3.A machine that hears and displays the baby’s heartbeat (electronic fetal monitor) is placed on the abdomen.
The health care provider can compare the pattern of the baby’s heartbeat to movements and find out whether the baby  is doing well.

Diet and exercise:
The best way to improve the pregnent woman’s diet is by eating a variety of healthy foods.She should learn how to read food labels, and check them when making food decisions.The doctor or dietitian  should advice the diet chart and that should be strictly followed  during pregnancy.

In general, when the pregnent woman has gestational diabetes the diet should:
*Be moderate in fat and protein.

#Provide  carbohydrates through foods that include fruits, vegetables, and complex carbohydrates (such as bread, cereal, pasta, and rice)
Be low in foods that contain a lot of sugar, such as soft drinks, fruit juices, and pastries.

#If managing the diet does not control blood sugar (glucose) levels, she may be prescribed diabetes medicine by mouth or insulin therapy.
Most women who develop gestational diabetes will not need diabetes medicines or insulin, but some will.

Prevention:
Theoretically, smoking cessation may decrease the risk of gestational diabetes among smokers.Physical exercise has not been found to have a significant effect of primary prevention of gestational diabetes in randomized controlled trials. It may be effective as tertiary prevention for women who have already developed the condition.
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Gestational_diabetes
http://www.webmd.com/diabetes/guide/gestational-diabetes-symptoms
http://www.ehow.com/list_6080912_signs-symptoms-gestational-diabetes.html
http://www.webmd.com/diabetes/guide/gestational_diabetes
http://www.mayoclinic.org/diseases-conditions/gestational-diabetes/basics/risk-factors/CON-20014854
http://www.nytimes.com/health/guides/disease/gestational-diabetes/overview.html

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Ailmemts & Remedies

Acanthosis nigricans

Definition:
Acanthosis nigricans is a fairly common skin pigmentation disorder.It is a brown to black, poorly defined, velvety hyperpigmentation of the skin. It is usually found in body folds, such as the posterior and lateral folds of the neck, the armpits, groin, navel, forehead, and other areas.

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Types:
This is conventionally divided into benign and malignant forms., although may be divided into syndromes according to cause.

*Benign This may include obesity-related, hereditary, and endocrine forms of acanthosis nigricans.

*Malignant. This may include forms that are associated with tumour products and insulin-like activity, or tumour necrosis factor.

An alternate classification system still used to describe acanthosis nigricans was proposed in 1994 by dermatologist Schwartz. This classification system delineates acanthosis nigricans syndromes according to their associated syndromes, including benign and malignant forms, forms associated with obesity and drugs, acral acanthosis nigricans, unilateral acanthosis nigricans, and mixed and syndromic forms.

Acanthosis nigricans may be a sign of a more serious health problem such as pre-diabetes. The most effective treatments focus on finding and resolving medical condition at the root of the problem. Fortunately, these skin patches tend to disappear after successfully treating the root condition.

Signs and symptoms:
Acanthosis nigricans may present with thickened, relatively darker areas of skin on the neck, armpit and in skin folds.These patches may also appear on the groin, elbows, knees, knuckles, or skin folds. Lips, palms, and soles of the feet.

Causes:
It typically occurs in individuals younger than age 40, may be genetically inherited, and is associated with obesity or endocrinopathies, such as hypothyroidism, acromegaly, polycystic ovary disease, insulin-resistant diabetes, or Cushing’s disease.

This occurs when epidermal skin cells begin to rapidly reproduce. This abnormal skin cell growth is most commonly triggered by high levels of insulin in the blood. In rare cases, the increase in skin cells may be caused by medications, cancer, or other medical conditions, as describe below.

*Too Much Insulin
The most frequent trigger for acanthosis nigricans is too much insulin in your bloodstream. Here’s why.

When you eat, your body converts carbohydrates into sugar molecules such as glucose. Some of this glucose is used for energy while the rest is stored. In order to use the glucose for energy, insulin must also be used. The insulin enables the glucose to enter the cells.

Overweight people tend to develop resistance to insulin over time. So although the pancreas is making insulin, the body cannot use it properly. This creates a buildup of glucose in the bloodstream, which can result in high levels of both blood glucose and insulin in your bloodstream.

Excess insulin causes normal skin cells to reproduce at a rapid rate. For those with dark skin, these new cells have more melanin. This increase in melanin produces a patch of skin that is darker than the skin surrounding it. Thus, the presence of acanthosis nigricans is a strong predictor of future diabetes. If this is indeed the cause, it is relatively easy to correct with proper diet, exercise, and blood sugar control.

*Medications:
Acanthosis nigricans can also be triggered by certain medications such as birth control pills, human growth hormones, thyroid medications, and even some body-building supplements. All of these medications can cause changes in insulin levels. Medications used to ease the side effects of chemotherapy have also been linked to acanthosis nigricans. In most cases, the condition clears up when the medications are discontinued.

Some Other Causes:(Potential but rare)

#stomach cancer (gastric adenocarcinoma)
#adrenal gland disorders such as Addison’s disease
#disorders of the pituitary gland
#low levels of thyroid hormones
#high doses of niacin

Diagnosis:
Acanthosis nigricans is typically diagnosed clinically.It is easy to recognize by sight. The doctor may want to check for diabetes or insulin resistance as the root cause. These tests may include blood glucose tests or fasting insulin tests. Your doctor may also review all your medications to see if they are a contributing factor.

It is important to inform the doctor of any dietary supplements, vitamins, or muscle-building supplements you may be taking in addition to your prescription medications.

In rare cases, the doctor may perform other tests such as a small skin biopsy to rule out other possible causes.

Treatment :
People with acanthosis nigricans should be screened for diabetes and, although rare, cancer. Controlling blood glucose levels through exercise and diet often improves symptoms. Acanthosis nigricans maligna may resolve if the causative tumor is successfully removed.

Cosmetic treatments exist for cases that are especially unsightly or embarrassing. Dark patches may be covered up with cosmetics or lightened with prescription skin lighteners. Although these treatments are not as effective as treating the root cause of the condition, they can provide some relief. Available skin lighteners include Retin-A, 20 percent urea, alpha hydroxy acids, and salicylic acid.

Prognosis:
Acanthosis nigricans often fades if the underlying cause can be determined and treated  properly.

Prevention:
Maintaining a healthy lifestyle & exercisIng regularly can usually prevent Acanthosis nigricans. Losing weight, controlling your diet, and, perhaps adjusting any medications that are contributing to the condition are all crucial steps. Healthier lifestyle choices will also reduce your risks for many other types of illnesses.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.healthline.com/health/acanthosis-nigricans#Definition
http://en.wikipedia.org/wiki/Acanthosis_nigricans

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Categories
Ailmemts & Remedies

Diabetics

Definition:
Diabetes mellitus, or simply diabetes, is a group of metabolic diseases in which a person has high blood sugar, either because the pancreas does not produce enough insulin, or because cells do not respond to the insulin that is produced.  This high blood sugar produces the classical symptoms of polyuria (frequent urination), polydipsia (increased thirst), and polyphagia (increased hunger).

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There are three main types of diabetes mellitus (DM).

*Type 1 DM results from the body’s failure to produce insulin, and currently requires the person to inject insulin or wear an insulin pump. This form was previously referred to as “insulin-dependent diabetes mellitus” (IDDM) or “juvenile diabetes”.

*Type 2 DM results from insulin resistance, a condition in which cells fail to use insulin properly, sometimes combined with an absolute insulin deficiency. This form was previously referred to as non insulin-dependent diabetes mellitus (NIDDM) or “adult-onset diabetes”.

*The third main form, gestational diabetes, occurs when pregnant women without a previous diagnosis of diabetes develop a high blood glucose level. It may precede development of type 2 DM.

Other forms of diabetes mellitus include congenital diabetes, which is due to genetic defects of insulin secretion, cystic fibrosis-related diabetes, steroid diabetes induced by high doses of glucocorticoids, and several forms of monogenic diabetes.
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Diabetes has no age bar. It can appear in a newborn, children, young adults, during pregnancy or in older people. If there are suspicious symptoms, tests should be done.

Some families have a tendency to develop diabetes, with many members being affected. This is because it is a genetic disease that an be inherited from both parents. Type 1 and 2 diabetes are inherited from multiple genes. In type 2 diabetes particularly, the environment and family’s dietary and exercise habits also influence these genes. Families that eat “well” and are sedentary with snacking and excessive TV viewing are more likely to develop type 2 diabetes. Sometimes type 1 diabetes can develop in persons without a family history or genetic predisposition. It may follow viral infections, especially with the mumps and coxsackie group of viruses. The virus attacks and destroys the cells in the pancreas responsible for manufacturing insulin.

There is now a third type of diabetes, where the mutation occurs in a single gene. This gene is dominant, so that if either parent carries it, then half the children (male and female) will be affected. It was called MODY (maturity onset diabetes of youth). The diabetes affecting newborn children is of this type.

Initially, MODY was called type 1.5 diabetes and it was presumed that it was caused by only one type of genetic defect. Recent research has shown that there are 13 defects that lead to MODY.

*It is likely to be present in people who have been diagnosed with diabetes before the age of 30.

*It is present in every generation of the family.

*It can be managed with diet, exercise and tablets. Insulin is usually not required (even in children).

*MODY (depending on the type) can result in the affected woman having small or large babies.

* There may be cysts in the kidney.

* Malabsorption can occur.

* Patients may be infertile.

The incidence of MODY is higher in areas where there is a great deal of consanguinity (marrying a close relative) and when people marry generation after generation from the same community.

It is now possible to test for MODY genes in many centres and identify high-risk individuals and families.

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Symptoms:
The classic symptoms of untreated diabetes are loss of weight, polyuria (frequent urination), polydipsia (increased thirst), and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 diabetes, while they usually develop much more slowly and may be subtle or absent in type 2 diabetes.

Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Blurred vision is a common complaint leading to a diabetes diagnosis. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.

Causes:
The cause of diabetes depends on the type.

Type 1

Type 1 diabetes is partly inherited, and then triggered by certain infections, with some evidence pointing at Coxsackie B4 virus. A genetic element in individual susceptibility to some of these triggers has been traced to particular HLA genotypes (i.e., the genetic “self” identifiers relied upon by the immune system). However, even in those who have inherited the susceptibility, type 1 DM seems to require an environmental trigger. The onset of type 1 diabetes is unrelated to lifestyle.

Type 2

Type 2 diabetes is due primarily to lifestyle factors and genetics.[16] A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than thirty), lack of physical activity, poor diet, stress, and urbanization.[4] 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. Those who are not obese often have a high waist–hip ratio.

Dietary factors also influence the risk of developing type 2 diabetes. Consumption of sugar-sweetened drinks in excess is associated with an increased risk.  The type of fats in the diet is also important, with saturated fats and trans fatty acids increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk.  Eating lots of white rice appears to also play a role in increasing risk.  A lack of exercise is believed to cause 7% of cases.

The following is a comprehensive list of other causes of diabetes:

*Genetic defects of ?-cell function
*Maturity onset diabetes of the young
*Mitochondrial DNA mutations

*Genetic defects in insulin processing or insulin action
*Defects in proinsulin conversion
*Insulin gene mutations
*Insulin receptor mutations

*Exocrine pancreatic defects
*Chronic pancreatitis
*Pancreatectomy
*Pancreatic neoplasia
*Cystic fibrosis
*Hemochromatosis
*Fibrocalculous pancreatopathy

Diabetes has no age bar. It can appear in a newborn, children, young adults, during pregnancy or in older people. If there are suspicious symptoms, tests should be done.

Some families have a tendency to develop diabetes, with many members being affected. This is because it is a genetic disease that an be inherited from both parents. Type 1 and 2 diabetes are inherited from multiple genes. In type 2 diabetes particularly, the environment and family’s dietary and exercise habits also influence these genes. Families that eat “well” and are sedentary with snacking and excessive TV viewing are more likely to develop type 2 diabetes. Sometimes type 1 diabetes can develop in persons without a family history or genetic predisposition. It may follow viral infections, especially with the mumps and coxsackie group of viruses. The virus attacks and destroys the cells in the pancreas responsible for manufacturing insulin.

Diagnosis:
Diabetes is diagnosed with blood tests. Blood sugar count after a 12 hour fast should be less than 100mg/dl and two hours after a full meal less than 140 mg/. Glycosolated haemoglobin (HbA1 c) should be 5.6.

A GTT (glucose tolerance test) can be done in suspect cases. In this the fasting blood glucose level is checked and 75gm glucose given. The blood is checked every 30 to 60 minutes after that. One hour later the blood glucose level should be lower than 180 mg/dL, two hours later less than 155 mg/dL, and three hours later lower than 140 mg/dL.

Complications:
Uncontrolled, untreated, neglected diabetes of all types causes complications with the nervous system, heart, kidneys, eyes and muscles affected.

All forms of diabetes increase the risk of long-term complications. These typically develop after many years (10–20), but may be the first symptom in those who have otherwise not received a diagnosis before that time. The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease. The main “macrovascular” diseases (related to atherosclerosis of larger arteries) are ischemic heart disease (angina and myocardial infarction), stroke, and peripheral vascular disease.

Diabetes also damages the capillaries (causes microangiopathy). Diabetic retinopathy, which affects blood vessel formation in the retina of the eye, can lead to visual symptoms including reduced vision and potentially blindness. Diabetic nephropathy, the impact of diabetes on the kidneys, can lead to scarring changes in the kidney tissue, loss of small or progressively larger amounts of protein in the urine, and eventually chronic kidney disease requiring dialysis.

Another risk is diabetic neuropathy, the impact of diabetes on the nervous system — most commonly causing numbness, tingling, and pain in the feet, and also increasing the risk of skin damage due to altered sensation. Together with vascular disease in the legs, neuropathy contributes to the risk of diabetes-related foot problems (such as diabetic foot ulcers) that can be difficult to treat and occasionally require amputation. Additionally, proximal diabetic neuropathy causes painful muscle wasting and weakness.

Several studies suggest a link between cognitive deficit and diabetes. Compared to those without diabetes, the research showed that those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function, and are at greater risk.

Treatment:
The major goal in treating diabetes is to minimize any elevation of blood sugar (glucose) without causing abnormally low levels of blood sugar. Type 1 diabetes is treated with insulin, exercise, and a diabetic diet. Type 2 diabetes is treated first with weight reduction, a diabetic diet, and exercise. When these measures fail to control the elevated blood sugars, oral medications are used. If oral medications are still insufficient, treatment with insulin is considered.

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A change in lifestyle goes a long way in preventing the onset of diabetes and controlling it after it sets in. These guidelines are particularly important if you have MODY or feel that you or your family members are in danger of developing it.

Prevention:
To prevent development of the disease as an adult, it is our children who need to be targeted for intervention. Lifestyle changes — a healthy diet and regular exercise — should be implemented at the school level.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Diabetes_mellitus
http://www.medicinenet.com/diabetes_treatment/article.htm
http://www.telegraphindia.com/1131118/jsp/knowhow/story_17579340.jsp#.UolfgL4o52Y

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