Tag Archives: Diabetes mellitus type 2

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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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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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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Gymnema silvestre

Botanical Name : Gymnema silvestre

Family: Asclepiadaceae
Genus: Gymnema
Species: G. sylvestre
Kingdom: Plantae
Order: Gentianales

Common Name :Gurmari, Gurmarbooti, Gurmar, periploca of the woods, meshasring.

Alternative names:
Despite the part used being the leaf, one common name of this species is miracle fruit, a name shared by two other species: Synsepalum dulcificum and Thaumatococcus daniellii. Both species are used to alter the perceived sweetness of foods.

In English the species is also known as gymnema, Cowplant and Australian cowplant.

This species also goes under many other names such as; Gurmari, Gurmarbooti, Gurmar, periploca of the woods and Meshasringa. The Hindi word Gur-mar (Madhunaashini in Sanskrit, Chakkarakolli in Malayalam,Podapatri in Telugu), literally means sugar destroyer. Meshasringa (Sanskrit) translates as “ram’s horn”, a name given to the plant from the shape of its fruits. Gymnema derives from the Greek words “gymnos”  and “n?ma” (????) meaning “naked” and “thread” respectively, the species epitheton sylvestre means “of the forest” in Latin.

Habitat :  Gymnema silvestre is   native to the tropical forests of southern and central India where it has been used as a natural treatment for diabetes for nearly two millennia.

Description:
Gudmar or Gymnema Sylvestre is Large climbers, rooting at nodes, leaves elliptic, acuminate, base acute to acuminate, glabrous above sparsely or densely tomentose beneath; Flowers small, in axillary and lateral umbel like cymes, pedicels long; Calyx-lobes long, ovate, obtuse, pubescent; Corolla pale yellow campanulate, valvate, corona single, with 5 fleshy scales. Scales adnate to throat of corolla tube between lobes; Anther connective produced into a membranous tip, pollinia 2, erect, carpels 2,unilocular; locules many ovuled; Follicle long, fusiform1.

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Chemical composition:
The major bioactive constituents of Gymnema sylvestris are a group of oleanane type triterpenoid saponins known as gymnemic acids. The latter contain several acylated (tigloyl, methylbutyroyl etc.,) derivatives of deacylgymnemic acid (DAGA) which is 3-O-glucuronide of gymnemagenin (3, 16, 21, 22, 23, 28-hexahydroxy-olean-12-ene)2. The individual gymnemic acids (saponins) include gymnemic acids I-VII, gymnemosides A-F, gymnemasaponins.

G. sylvestre leaves contain triterpene saponins belonging to oleanane and dammarene classes. Oleanane saponins are gymnemic acids and gymnemasaponins, while dammarene saponins are gymnemasides. Besides this, other plant constituents are flavones, anthraquinones, hentri-acontane, pentatriacontane, ? and ?- chlorophylls, phytin, resins, d-quercitol, tartaric acid, formic acid, butyric acid, lupeol, ?-amyrin related glycosides and stigmasterol. The plant extract also tests positive for alkaloids. Leaves of this species yield acidic glycosides and anthroquinones and their derivatives.

Gymnemic acids have antidiabetic, antisweetener and anti-inflammatory activities. The antidiabetic array of molecules has been identified as a group of closely related gymnemic acids after it was successfully isolated and purified from the leaves of Gymnema sylvestre. Later, the phytoconstituents of Gymnema sylvestre were isolated, and their chemistry and structures were studied and elucidated.

Medicinal Uses:
While it is still being studied, and the effects of the herb are not entirely known, the herb has been shown to reduce blood sugar levels when used for an extended period of time. Additionally, Gymnema reduces the taste of sugar when it is placed in the mouth, thus some use it to fight sugar cravings. From extract of the leaves were isolated glycosides known as Gymnemic acids, which exhibit anti-sweet activity.

This effect lasts up to about 2 hours. Some postulate that the herb actually reduces cravings for sugar by blocking sugar receptors in the tongue. This effect was observed in rats in a 2003 study conducted by CH Lemon, et al. It is currently being used in an all natural medication for diabetes with other ingredients such as cinnamon, chromium, zinc, biotin, banaba plant, huckleberry and bitter melon.

The active ingredients are thought to be the family of compounds related to gymnemic acid: purified gymnemic acids are widely used as experimental reagents in taste physiology and have also been shown to affect experimental diabetes, reduce intestinal transport of sugars. and fatty acids. Extracts of Gymnema is not only claimed to curb sweet tooths but also for treatment of as varied problems as hyperglycemia, obesity, high cholesterol levels, anemia and digestion. The leaves were also used for stomach ailments, constipation, water retention, and liver disease; historically these claims are not supported by scientific studies.[8] According to the Sushruta of the Ayurveda it helps to treat Madhumeha ie glycosuria.[citation needed]

In 2005, a study made by King’s College, London, United Kingdom, showed that a water-soluble extract of Gymnema Sylvestre, caused reversible increases in intracellular calcium and insulin secretion in mouse and human ?-cells when used at a concentration (0.125 mg/ml) without compromising cell viability. Hence forth these data suggest that extracts derived from Gymnema Sylvestre may be useful as therapeutic agents for the stimulation of insulin secretion in individuals with Type 2 Diabetes.[9] According to research done by Persaud and colleagues in 1999 the raise in insulin levels may be due to regeneration of the cells in the pancreas.  Gymnema can also help prevent adrenal hormones from stimulating the liver to produce glucose, thereby reducing blood sugar levels  Clinical trials with diabetics in India have used 400 mg per day of water-soluble acidic fraction of the gymnema leaves. However, Gymnema cannot be used in place of insulin to control blood sugar by people with either Type 1 or Type 2 Diabetes.

In 2010, King’s College, London, United Kingdom performed another study on Gymnema Sylvestre. OmSantal Adivasi extract, a high molecular weight extract from the plant Gymnema Sylvestre was found to improve the symptoms of type 2 diabetes mellitus. Glycemic control after OmSantal Adivasi administration was related to increased circulating levels of insulin and/or C-peptide. Experimenting with human islets in vitro, there was a rapid onset response to OmSantal Adivasi exposure, continued for extent of exposure to OmSantal Adivasi, and also a rapid reverse if there was a withdrawal of OmSantal Adivasi. OmSantal Adivasi created a biphasic pattern of glucose-induced insulin secretion. This resulted in enhanced rates of insulin secretion being maintained for length of exposure to OmSantal Adivasi. Other Gymnema Sylvestre extracts induce cell damage to the membrane causing pathological and unregulated release of insulin to BETA-cells. OmSantal Adivasi has a low concentration of saponin, what causes damage to cell membranes, which would be degraded during digestion. OmSantal Adivasi directly stimulates BETA-cells of the islets of Langerhans, reducing fasting and post-prandial blood glucose. OmSantal Adivasi experiments, in vitro, initiated insulin secretion at a sub-stimulatory concentration of glucose. OmSantal Adivasi has been shown to effectively reduce blood glucose and increase plasma insulin and C-peptide levels in humans

Indian physicians first used Gymnema to treat diabetes over 2,000 years ago.  . In the 1920s, preliminary scientific studies found some evidence that Gymnema leaves can reduce blood sugar levels, but nothing much came of this observation for decades.  It is a taste suppressant.  By topical application gymnema has been shown to block the sweet and some of the bitter taste, but not salt and acid taste.  By keeping off the sweet taste it helps to control a craving for sugar.  Responsible for this are considered saponins.  Gymnema has also shown mild hypoglycemic effect.  Topically (applied to the tongue, mainly to the tip or by chewing) it is used to control a craving for sugar, recommended as an aid to a weightloss diet and diabetes.  Internally it is used as an adjuvant (tea, h.p.) for diabetes. Gymnema leaves raise insulin levels, according to research in healthy volunteers. Based on animal studies, this may be due to regeneration of the cells in the pancreas that secrete insulin. Other animal research shows that Gymnema can also improve uptake of glucose into cells and prevent adrenaline from stimulating the liver to produce glucose, thereby reducing blood sugar levels. The leaves are also noted for lowering serum cholesterol and triglycerides.  In the past, powdered Gymnema root was used to treat snake bites, constipation, stomach complaints, water retention, and liver disease.

Gurmar, also known as Gymnema or Gymnema Sylvestre, is often referred to as “sugar destroyer” and has been used in Ayurveda since the 6th century BC. It has been used in Ayurvedic medicine for several centuries as a safe and natural approach to help regulate sugar metabolism. The key component of Gymnema – Gymnemic Acids – mimics glucose molecules, numbing receptor sites on the tongue. Gymnema contains Gymnemic acid, Quercitol, Lupeol, Beta-Amyrin and Stigmasterol, all of which are thought to help the body maintain healthy blood glucose levels.

Benefits of Gymnema Sylvestre (Gurmar)
Gymnema may:

*Help abolish the taste of sugar*
*Help manage sugar cravings and sugar addictions*
*Help support healthy glucose metabolism*
*Help maintain healthy blood sugar levels*
*Support healthy weight*

Disclaimer:
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Resources:
http://www.herbalprovider.com/gymnema-sylvestre.html?src=ggl&w=gymnema-sylvestre&gclid=CLjflMqo8qoCFQHf4AodDghbPA
http://en.wikipedia.org/wiki/Gymnema_sylvestre
http://www.herbnet.com/Herb%20Uses_FGH.htm

http://www.nutrasanus.com/gymnema-sylvestre.html

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Cajanus cajan (Pegion pea)

Botanical Name :Cajanus cajan (Linn) Millsp.
Other scientific names:  Cystisus cajan, Cystisus pseudo-cajan  ,Cajan inodorum  ,Cajanus bicolor,Cajanus indicus
Family :Fabaceae

Genus: Cajanus
Species: C. cajan
Kingdom: Plantae
Division: Magnoliophyta
Class: Magnoliopsida
Order: Fabales

Synonyms:Cajanus indicus Spreng. (Valder 1895) and Cytisus cajan (Crawfurd 1852)

Common Names :Arhar, Red gram, Pigeon pea, Gablos (Tag.) ,Kadios (Mang., Tag., P. Bis.) ,Kagyos (Tag.) ,Kaldis (Ig., Ilk.)   Kagyas (Tag.) ,Kalios (Tag.) , Kardis (Ibn., Ilk., Ig.) ,Kidis (Ilk., Bon.) ,Kusia (Ig., If.) , Tabios (Bik., C. Bis.) ,Guandu (Brazil) .Pigeon pea (Engl.),toor dal or arhar dal (India), Congo pea or gungo pea (in Jamaica), Pois Congo (in Haiti), gandul (in Puerto Rico), gunga pea, or no-eye pea.   arhar dal  in Bengali


Habitat :
Probably native to India, pigeon pea was brought millennia ago to Africa where different strains developed. These were brought to the new world in post-Columbian times. Truly wild Cajanus has never been found; they exist mostly as remnants of cultivations. In several places Cajanus persists in the forest. The closest wild relative, Atylosia cajanifolia Haines, has been found in some localities in East India. Most other Atylosias are found scattered throughout India, while in North Australia a group of endemic Atylosia species grow. In Africa Cajanus kerstingii grows in the drier belts of Senegal, Ghana, Togo, and Nigeria. Pigeon peas occur throughout the tropical and subtropical regions, as well as the warmer temperate regions (as North Carolina) from 30°N to 30°S (Duke, 1981a). In settled areas throughout the Philippines: cultivated, semicultivated, and in some places, spontaneous.

Description:

It is  is a perennial herb.An erect, branched, hairy shrub, 1-2 meters high. Leaves are oblong-lanceolate to oblanceolate with three leaflets. Flowers are yellow, in sparse peduncled racemes, about 1.5 cm long. Pod is hairy, 4-7 cm long, 1 cm wide, containing 2-7 seeds.

 

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Cultivation:
The cultivation of the pigeon pea goes back at least 3000 years. The centre of origin is most likely Asia, from where it traveled to East Africa and by means of the slave trade to the American continent. Today pigeon peas are widely cultivated in all tropical and semi-tropical regions of both the Old and the New World. Pigeon peas can be of a perennial variety, in which the crop can last 3–5 years (although the seed yield drops considerably after the first two years), or an annual variety more suitable for seed production.

Pigeon peas are an important legume crop of rainfed agriculture in the semi-arid tropics. The Indian subcontinent, Eastern Africa and Central America, in that order, are the world’s three main pigeon pea producing regions. Pigeon peas are cultivated in more than 25 tropical and sub-tropical countries, either as a sole crop or intermixed with cereals such as sorghum (Sorchum bicolor), pearl millet (Pennisetium glaucum), or maize (Zea mays), or with other legumes, such as peanuts (Arachis hypogaea). Being a legume, the pigeon pea enriches soil through symbiotic nitrogen fixation.

The crop is cultivated on marginal land by resource-poor farmers, who commonly grow traditional medium- and long-duration (5–11 months) landraces. Short-duration pigeon peas (3–4 months) suitable for multiple cropping have recently been developed. Traditionally, the use of such input as fertilizers, weeding, irrigation, and pesticides is minimal, so present yield levels are low (average = 700 kg/ha). Greater attention is now being given to managing the crop because it is in high demand at remunerative prices.

Pigeon peas are very drought resistant and can be grown in areas with less than 650 mm annual rainfall.

World production of pigeon peas is estimated at 46,000 km2. About 82% of this is grown in India. These days it is the most essential ingredient of animal feed used in West Africa, most especially in Nigeria where it is also grown

Edible Uses: Vegetable food crop ( seeds and pods) in South-East Asia.Pigeon peas are both a food crop (dried peas, flour, or green vegetable peas) and a forage/cover crop. They contain high levels of protein and the important amino acids methionine, lysine, and tryptophan.  In combination with cereals, pigeon peas make a well-balanced human food. The dried peas may be sprouted briefly, then cooked, for a flavor different from the green or dried peas. Sprouting also enhances the digestibility of dried pigeon peas via the reduction of indigestible sugars that would otherwise remain in the cooked dried peas.

In India, split pigeon peas (toor dal) are one of the most popular pulses, being an important source of protein in a mostly vegetarian diet. In regions where it grows, fresh young pods are eaten as vegetable in dishes such as sambhar.

In Ethiopia, not only the pods but the young shoots and leaves are cooked and eaten.

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In some places, such as the Dominican Republic and Hawaii, pigeon peas are grown for canning and consumption. A dish made of rice and green pigeon peas (called “Moro de Guandules”) is a traditional food in Dominican Republic. Pigeon peas are also made as a stew, with plantain balls. In Puerto Rico, arroz con gandules is made with rice and pigeon peas and is a typical dish.

In Thailand, pigeon peas are grown as a host for scale insects which produce lac.

Pigeon peas are in some areas an important crop for green manure, providing up to 40 kg nitrogen per hectare. The woody stems of pigeon peas can also be used as firewood, fencing and thatch.

Nutrition
Used mainly for its edible young pods and seeds.

Chemical constituents :
Roots are considered antihelminthic, expectorant, febrifuge, sedative, vulnerary.
Seeds are rich in carbohydrates (58%) and proteins (19%).
Fair source of calcium and iron; good source of vitamin B.
Chemical studies reveal: 2′-2’methylcajanone, 2′-hydroxygenistein, isoflavones, cajanin, cahanones, among many others.

Analysis of dhal (without husk) gave the following values: moisture, 15.2; protein, 22.3; fat (ether extract), 1.7; mineral matter, 3.6; carbohydrate, 57.2; Ca, 9.1; and P, 0.26%; carotene evaluated as vitamin A, 220 IU and vitamin B1, 150 IU per 100 g. Sun-dried seeds of Cajanus cajan are reported to contain (per 100 g) 345 calories, 9.9% moisture, 19.5 g protein, 1.3 g fat, 65.5 g carbohydrate, 1.3 g fiber, 3.8 g ash, 161 mg Ca, 285 mg P, 15.0 mg Fe, 55 mg b-carotene equivalent, 0.72 mg thiamine, 0.14 mg riboflavin, and 2.9 mg niacin. Immature seeds of Cajanus cajan are reported to contain per 100 g, 117 calories, 69.5% moisture, 7.2 g protein, 0.6 g fat, 21.3 g total carbohydrate, 3.3 g fiber, 1.4 g ash, 29 mg Ca, 135 mg P, 1.3 mg Fe, 5 mg Na, 563 mg K, 145 mg b-carotene equivalent, 0.40 mg thiamine, 0.25 mg riboflavin, 2.4 mg niacin, and 26 mg ascorbic acid/100 g. Of the total amino acids, 6.7% is arginine, 1.2% cystine, 3.4% histidine, 3.8% isoleucine, 7.6% leucine, 7.0% lysine, 1.5% methionine, 8.7% phenylalanine, 3.4% threonine, 2.2% tyrosine, 5.0% valine, 9.8 aspartic acid, 19.2% glutamic acid, 6.4% alanine, 3.6% glycine, 4.4% proline, 5.0% serine with 0 values for canavanine, citrulline and homoserine. Methionine, cystine, and tryptophane are the main limiting amino acids. However, in combination with cereals, as pigeon peas are always eaten, this legume contributes to a nutritionally balanced human food. The oil of the seeds contains 5.7% linolenic acid, 51.4% linoleic, 6.3% oleic, and 36.6% saturated fatty acids. Seeds are reported to contain trypsin inhibitors and chymotrypsin inhibitors. Fresh green forage contains 70.4% moisture, 7.1 crude protein, 10.7 crude fiber, 7.9 N-free extract, 1.6 fat, 2.3 ash. The whole plant, dried and ground contains 1,1.2% moisture, 14.8 crude protein, 28.9 crude fiber, 39.9 N-free extract, 1.7 fat, and 3.5 ash. (Duke, 1981a)

Medicinal Uses:
Parts used
Leaves, roots.

Folkloric:-
*Decoction or infusionn of leaves for coughs, diarrhea, abdominal pains.
*Tender leaves are chewed for aphthous stomatitis and spongy gums.
*Pulped or poulticed leaves used for sores.
*In Peru, leaves are used as an infusion for anemial, hepatitis, diabetes, urinary infections and yellow fever.
*In Argentina, leaves used for genital and skin problems; flowers used for bronchitis, cough and pneumonia.
*In China, as vermifuge, vulnerary; for tumors.
*In Panama, used for treatment of diabetes (See study below).
*In Indian folk medicine, used for a variety of liver disorders.



Other Uses:

As forage or hay.
Branches and stems for basket and fuel. (Source)

Often grown as a shade crop for tree crops or vanilla, a cover crop, or occasionally as a windbreak hedge. In Thailand and N. Bengal, pigeon pea serves as host for the scale insect which produces lac or sticklac. In Malagasy the leaves are used as food for the silkworm. Dried stalks serve for fuel, thatch and basketry. (Duke, 1981a).

Studies:-
RBC Sickling Inhibition: StudyClinical studies have reported seed extracts to inhibit red blood cell sickling and potential benefit for people with sickle cell anemia.

• Antiplasmodial constituents of Cajanus cajan: Study isolated two stilbenes, longistylin A and C and betulinic acid from the roots and leaves of CC and showed moderately high in vitro activity against Plasmodium falcifarum strain.

• Stilbenes / Neuroprotective / Alzheimer’s Disease: Study of stilbenes containing extract-fraction from C cajan showed significant amelioration of cognitive deficits and neuron apoptosis. Findings suggest sECC has a potential in the development of therapeutic agent to manage cognitive impairment associated with Alzheimer’s disease through increase choline acetyltransferase activity and anti-oxidative mechanism.

• Hypocholesterolemic Effect: Study on the stilbenes containing extract-fraction of CC showed a hypocholesterolemic effect possibly through enhancement of hepatic LDL-receptor and cholesterol 7-alpha-hydroxylase expression levels and bile acid synthesis.

Hyperglycemic Effect: Evaluation of traditional medicine: effects of Cajanus cajan L. and of Cassia fistula L. on carbohydrate metabolism in mice: Contradicting its traditional use for diabetes, CC did not have a hypoglycemic effect on sugar, instead at higher doses, it produced a hyperglycemic effect.

Antimicrobial: Study shows the organic solvent extracts to inhibit E coli, S aureus and S typhi and the aqueous extract were inhibitory to E coli and S aureus.

• Antimicrobial / Antifungal: Nigerian study on the antimicrobial effects of the ethanol and aqueous extracts of locally available plants, including C cajan, showerd inhibition against S aureus, P aeruginosa, E coli and C albicans. The extracts of C cajam produced wider zones of inhibition against C albicans.

• Hyperglycemic Effect: Study of the aqueous extract of C cajan leaves showed a hyperglycemic effect, suggesting a usefulness incontrolling hypoglycemia that may be due to excess of insulin or other hypoglycemic drugs.

• Hepatoprotective: (1) Study of the methanol-aqueous fraction of C cajan leaf extract showed it could prevent the chronically treated alcohol induced rat liver damage and presents a promise as a non-toxic herb for therapeutic use in alcohol-induced liver dysfunction. (2) Study in mice with carbon tetrachloride-induced liver damage showed the methanol extracts of B orellana, C cajan, G pentaphylla and C equisetifolia showed significant decrease in levels of serum markers, indicating the protection of hepatic cells in a dose-dependent manner.

Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider.

Resources:
http://en.wikipedia.org/wiki/Pigeon_pea
http://www.stuartxchange.com/Kadios.html
http://vaniindia.org.whbus12.onlyfordemo.com/herbal/plantdir.asp

http://www.hort.purdue.edu/newcrop/duke_energy/Cajanus_cajun.html

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