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The Quiet Cancers

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Three big dangers your doctor may not talk about and how to stay safe:

Your doctor has given you the lowdown on how to protect yourself against breast, colon, and lung cancer: Get yearly mammograms (check) and regular colonoscopies (check), and don’t smoke (double check).

But when was the last time she asked if you had any persistent mouth sores, unexplained fevers or joint pain, or discomfort during sex? These can be symptoms of three cancers—oral, leukemia, and endometrial—that don’t get the attention they deserve. Even though they are among the most common cancers affecting women over age 55, these diseases can fall through the cracks as doctors focus on the biggest killers hogging the health headlines, says Elmer Huerta, M.D., president of the American Cancer Society.

Oral Cancer

Your Risk:
1 in 98, with diagnoses peaking between the ages of 55 and 65. Oral cancer is lethal more often than it needs to be because people tend to ignore symptoms (it’s typically caught in late stages).

Stay healthy: Watch your mouth—see a dentist or doctor about any sore in your mouth or on your lips that doesn’t clear up in two weeks. A change in color or persistent pain, tenderness, or numbness anywhere in your mouth or on your lips should also prompt a fast visit.

Curb your vices: About 75 percent of oral cancers are caused by smoking and drinking alcohol. When such habits were considered unladylike, men with oral cancer outnumbered women 6 to 1, says Sol Silverman Jr., D.D.S., a professor of oral medicine at the University of California, San Francisco, School of Dentistry. “But in the last 50 years, the incidence in women has soared—now the ratio is two men to every woman.” Limit your intake to one drink per day.

Guard your lips: They need protection, too. Sunscreen isn’t exactly tasty, so choose a balm with SPF and then apply your favorite gloss or lipstick.

…………….

The good news: Researchers at Ohio State University recently found that phytochemicals extracted from Hass avocados could kill or stop the growth of oral cancer cells. The study was done in test tubes, but there’s no need to wait for confirmation—bring on the guacamole!

Leukemia

Your Risk: Many think of it as a children’s disease, but the biggest jump in cases occurs between ages 55 and 74.

Stay healthy: Note any symptoms If you find yourself extremely pale or bruising easily, or if your gums bleed (more than is normal if you neglect to floss), it’s time to get checked out. Extreme fatigue, unexplained fevers, and bone or joint pain are other common symptoms.

Avoid unnecessary scans: CT scans are a great diagnostic tool, but they deliver much more radiation than X-rays and may be overused, says Barton Kamen, M.D., Ph.D., chief medical officer for theLeukemia & Lymphoma Societyociety. In fact, researchers suggest that one-third of CT scans could be unnecessary. High doses of radiation can trigger leukemia, so make sure scans are not repeated if you see multiple doctors, and ask if another test, such as an ultrasound or MRI, could substitute.

The good news: The five-year survival rate for all people with leukemia has more than tripled in recent decades, from about 14 percent in the 1960s to about 65 percent today. “New advancements now help us determine who is a good candidate for a bone marrow transplant and who might respond better to other therapies,” says Kamen. “The result is more targeted treatment and better outcomes.”

Endometrial (Uterine) Cancer

Your Risk: 1 in 40. This is the fourth most common type of cancer in women—90 percent of cases occur in women over age 50. You’re more vulnerable if you’re toting extra weight: Obese women are two to three times as likely to develop the disease. “Fat acts like another gland, which increases the levels of estrogen and other hormones in your system. That stimulates the growth of abnormal tissues,” says Huerta.

Stay healthy: Mention any unusual bleeding. More than 80 percent of endometrial cancers are found in the earliest, most treatable stages because this symptom tends to send women promptly to their doctors. If you notice any vaginal bleeding after menopause or bleeding between your periods, or if you experience pelvic pain, especially during intercourse, tell your doctor immediately.

Know your family history: “The same genetic mutation that puts people at increased risk of colon cancer also ups their odds of getting endometrial cancer,” says Edward L. Trimble, MD, MPH, head of Gynecologic Cancer Therapeutics at the National Cancer Institute. If you have a parent or sibling with that disease, get screened yearly for endometrial cancer starting at 30.

Move more all day: In a recent report on more than 250,000 women, those who exercised several hours daily reduced their risk of endometrial cancer by up to 52 percent, probably because staying active reduces estrogen levels while helping you maintain a healthy weight. Exercise frequency mattered more than intensity—light housework, gardening, and walking are enough. Avoid iron: A Swedish study has found that taking iron supplements after menopause raises the risk of endometrial cancer by 70 percent. After age 50, the daily recommendation for iron drops from 18 mg per day to 8 mg, an amount easily obtained from food.

The good news: In the same study, calcium supplements halved endometrial cancer risk. (Researchers aren’t sure why, but eating high-calcium dairy products didn’t provide the same benefit.) Experts recommend that postmenopausal women consume up to 1,000 mg of calcium a day, and 1,200 mg after age 70.

Click to see Your Anti-Cancer Guide: -> prevention.com/cancer.

Sources: msn health & fitness

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Ailmemts & Remedies

Hypoglycemia

Definition:
Hypoglycemia is the clinical syndrome that results from low blood sugar. The symptoms of hypoglycemia can vary from person to person, as can the severity. Classically, hypoglycemia is diagnosed by a low blood sugar with symptoms that resolve when the sugar level returns to the normal range….CLICK & SEE

Risk Factor:
While patients who do not have any metabolic problems can complain of symptoms suggestive of low blood sugar, true hypoglycemia usually occurs in patients being treated for diabetes (type 1 and type 2). Patients with pre-diabetes who have insulin resistance can also have low sugars on occasion if their high circulating insulin levels are further challenged by a prolonged period of fasting. There are other rare causes for hypoglycemia, such as insulin producing tumors (insulinomas) and certain medications. These uncommon causes of hypoglycemia will not be discussed in this article, which will primarily focus on the hypoglycemia occurring with diabetes mellitus and its treatment.

Despite our advances in the treatment of diabetes, hypoglycemic episodes are often the limiting factor in achieving optimal blood sugar control. In large scale studies looking at tight control in both type 1 and type 2 diabetes, low blood sugars occurred more often in the patients who were managed most intensively. This is important for patients and physicians to recognize, especially as the goal for treating patients with diabetes become tighter blood sugar control.

Low Blood sugar is Also Bad:
The body needs fuel to work. One of its major fuel sources is sugars, which the body gets from what is consumed as either simple sugar or complex carbohydrates. For emergency situations (like prolonged fasting), the body stores a stash of sugar in the liver as glycogen. If this store is needed, the body goes through a biochemical process called gluco-neo-genesis (meaning to “make new sugar”) and converts these stores of glycogen to sugar. This backup process emphasizes that the fuel source of sugar is important (important enough for human beings to have developed an evolutionary system of storage to avoid a sugar drought).

Of all the organs in the body, the brain depends on sugar (which we are now going to refer to as glucose) almost exclusively. Rarely, if absolutely necessary, the brain will use ketones as a fuel source, but this is not preferred. The brain cannot make its own glucose and is 100% dependent on the rest of the body for its supply. If for some reason, the glucose level in the blood falls (or if the brain’s requirements increase and demands are not met) there can be effects on the function of the brain.

Our Body’s Natural Protection
:
When the circulating level of blood glucose falls, the brain actually senses the drop. The brain then sends out messages that trigger a series of events, including changes in hormone and nervous system responses that are aimed at increasing blood glucose levels. Insulin secretion decreases and hormones that promote higher blood glucose levels, such as glucagon, cortisol, growth hormone and epinephrine, all increase. As mentioned above, there is a store in the liver of glycogen that can be converted to glucose rapidly.

In addition to the biochemical processes that occur, the body starts to consciously alert the affected person that is needs food by causing the signs and symptoms of hypoglycemia discussed below.

Signs and symptoms:
Hypoglycemic symptoms and manifestations can be divided into those produced by the counterregulatory hormones (epinephrine/adrenaline and glucagon) triggered by the falling glucose, and the neuroglycopenic effects produced by the reduced brain sugar.

Adrenergic manifestations

*Shakiness, anxiety, nervousness, tremor

*Palpitations, tachycardia

*Sweating, feeling of warmth

*Pallor, coldness, clamminess

*Dilated pupils (mydriasis)

Feeling of numbness “pins and needles” (parasthaesia) in the fingers

Glucagon manifestations:

*Hunger, borborygmus

*Nausea, vomiting, abdominal discomfort

*Headache

Neuroglycopenic manifestations:

*Abnormal mentation, impaired judgement

*Nonspecific dysphoria, anxiety, moodiness, depression, crying

*Negativism, irritability, belligerence, combativeness, rage

*Personality change, emotional lability

*Fatigue, weakness, apathy, lethargy, daydreaming, sleep

*Confusion, amnesia, dizziness, delirium

*Staring, “glassy” look, blurred vision, double vision

*Automatic behavior, also known as automatism

*Difficulty speaking, slurred speech

*Ataxia, incoordination, sometimes mistaken for “drunkenness”

*Focal or general motor deficit, paralysis, hemiparesis

*Paresthesia, headache

*Stupor, coma, abnormal breathing

*Generalized or focal seizures

Not all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms, if symptoms even occur. Specific manifestations may vary by age and by severity of the hypoglycemia. In young children, vomiting can sometimes accompany morning hypoglycemia with ketosis. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. The symptoms of a single person may be similar from episode to episode, but are not necessarily so and may be influenced by the speed at which glucose levels are dropping, and previous incidence.

In newborns, hypoglycemia can produce irritability, jitters, myoclonic jerks, cyanosis, respiratory distress, apneic episodes, sweating, hypothermia, somnolence, hypotonia, refusal to feed, and seizures or “spells”. Hypoglycemia can resemble asphyxia, hypocalcemia, sepsis, or heart failure.

In both young and old patients, the brain may habituate to low glucose levels, with a reduction of noticeable symptoms despite neuroglycopenic impairment. In insulin-dependent diabetic patients this phenomenon is termed hypoglycemia unawareness and is a significant clinical problem when improved glycemic control is attempted. Another aspect of this phenomenon occurs in type I glycogenosis, when chronic hypoglycemia before diagnosis may be better tolerated than acute hypoglycemia after treatment is underway.

Nearly always, hypoglycemia severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain. Cases of death or permanent neurological damage occurring with a single episode have usually involved prolonged, untreated unconsciousness, interference with breathing, severe concurrent disease, or some other type of vulnerability. Nevertheless, brain damage or death has occasionally resulted from severe hypoglycemia.

Causes:-
Hundreds of conditions can cause hypoglycemia. Common causes by age are listed below. While many aspects of the medical history and physical examination may be informative, the two best guides to the cause of unexplained hypoglycemia are usually

1.The circumstances

2.A critical sample of blood obtained at the time of hypoglycemia, before it is reversed.

There are several ways to classify hypoglycemia. The following is a list of the more common causes and factors which may contribute to hypoglycemia grouped by age, followed by some causes that are relatively age-independent. See causes of hypoglycemia for a more complete list grouped by etiology.

Hypoglycemia in newborn infants:-

Hypoglycemia is a common problem in critically ill or extremely low birthweight infants. If not due to maternal hyperglycemia, in most cases it is multifactorial, transient and easily supported. In a minority of cases hypoglycemia turns out to be due to significant hyperinsulinism, hypopituitarism or an inborn error of metabolism and presents more of a management challenge.

*Transient neonatal hypoglycemia

*Prematurity, intrauterine growth retardation, perinatal asphyxia

*Maternal hyperglycemia due to diabetes or iatrogenic glucose administration

*Sepsis

*Prolonged fasting (e.g., due to inadequate breast milk or condition interfering with feeding)

*Congenital hypopituitarism

*Congenital hyperinsulinism, several types, both transient and persistent

*Inborn errors of carbohydrate metabolism such as glycogen storage disease

Hypoglycemia in young children:-

Single episodes of hypoglycemia may occur due to gastroenteritis or fasting, but recurrent episodes nearly always indicate either an inborn error of metabolism, congenital hypopituitarism, or congenital hyperinsulinism. A list of common causes:

*Prolonged fasting

*Diarrheal illness in young children, especially rotavirus gastroenteritis

*Idiopathic ketotic hypoglycemia

*Isolated growth hormone deficiency, hypopituitarism

*Insulin excess

*Hyperinsulinism due to several congenital disorders of insulin secretion

*Insulin injected for type 1 diabetes

*Hyperinsulin Hyperammonia syndrome (HIHA)due toGlutamate dehydrogenase 1gene.Can cause mental retardation and epilepsy in severe cases.

*Gastric dumping syndrome (after gastrointestinal surgery)

*Other congenital metabolic diseases; some of the common include

*Maple syrup urine disease and other organic acidurias

*Type 1 glycogen storage disease

*Type III glycogen storage disease. Can cause less severe hypoglycemia than type I

*Disorders of fatty acid oxidation

*Medium chain acylCoA dehydrogenase deficiency (MCAD)

*Familial Leucine sensitive hypoglycemia

*Accidental ingestions

*Sulfonylureas, propranolol and others

*Ethanol (mouthwash, “leftover morning-after-the-party drinks”)

Hypoglycemia in older children and young adults:-

By far, the most common cause of severe hypoglycemia in this age range is insulin injected for type 1 diabetes. Circumstances should provide clues fairly quickly for the new diseases causing severe hypoglycemia. All of the congenital metabolic defects, congenital forms of hyperinsulinism, and congenital hypopituitarism are likely to have already been diagnosed or are unlikely to start causing new hypoglycemia at this age. Body mass is large enough to make starvation hypoglycemia and idiopathic ketotic hypoglycemia quite uncommon. Recurrent mild hypoglycemia may fit a reactive hypoglycemia pattern, but this is also the peak age for idiopathic postprandial syndrome, and recurrent “spells” in this age group can be traced to orthostatic hypotension or hyperventilation as often as demonstrable hypoglycemia.

*Insulin-induced hypoglycemia

*Insulin injected for type 1 diabetes

*Factitious insulin injection (Munchausen syndrome)

*Insulin-secreting pancreatic tumor

*Reactive hypoglycemia and idiopathic postprandial syndrome

*Addison’s disease

*Sepsis

Hypoglycemia in older adults:-

The incidence of hypoglycemia due to complex drug interactions, especially involving oral hypoglycemic agents and insulin for diabetes rises with age. Though much rarer, the incidence of insulin-producing tumors also rises with advancing age. Most tumors causing hypoglycemia by mechanisms other than insulin excess occur in adults.

*Insulin-induced hypoglycemia

*Insulin injected for diabetes

*Factitious insulin injection (Munchausen syndrome)

*Excessive effects of oral diabetes drugs, beta-blockers, or drug interactions

*Insulin-secreting pancreatic tumor

*Alimentary (rapid jejunal emptying with exaggerated insulin response)

*After gastrectomy dumping syndrome or bowel bypass surgery or resection

*Reactive hypoglycemia and idiopathic postprandial syndrome

*Tumor hypoglycemia, Doege-Potter syndrome

*Acquired adrenal insufficiency

*Acquired hypopituitarism

*Immunopathologic hypoglycemia

Treatment:-
Management of hypoglycemia involves immediately raising the blood sugar to normal, determining the cause, and taking measures to hopefully prevent future episodes.

Reversing acute hypoglycemia:-
The blood glucose can be raised to normal within minutes by taking (or receiving) 10-20 grams of carbohydrate. It can be taken as food or drink if the person is conscious and able to swallow. This amount of carbohydrate is contained in about 3-4 ounces (100-120 ml) of orange, apple, or grape juice although fruit juices contain a higher proportion of fructose which is more slowly metabolized than pure dextrose, alternatively, about 4-5 ounces (120-150 ml) of regular (non-diet) soda may also work, as will about one slice of bread, about 4 crackers, or about 1 serving of most starchy foods. Starch is quickly digested to glucose (unless the person is taking acarbose), but adding fat or protein retards digestion. Symptoms should begin to improve within 5 minutes, though full recovery may take 10-20 minutes. Overfeeding does not speed recovery and if the person has diabetes will simply produce hyperglycemia afterwards.

If a person is suffering such severe effects of hypoglycemia that they cannot (due to combativeness) or should not (due to seizures or unconsciousness) be given anything by mouth, medical personnel such as EMTs and Paramedics, or in-hospital personnel can establish an IV and give intravenous Dextrose, concentrations varying depending on age (Infants are given 2cc/kg Dextrose 10%, Children Dextrose 25%, and Adults Dextrose 50%). Care must be taken in giving these solutions because they can be very necrotic if the IV is infiltrated. If an IV cannot be established, the patient can be given 1 to 2 milligrams of Glucagon in an intramuscular injection. More treatment information can be found in the article diabetic hypoglycemia.

One situation where starch may be less effective than glucose or sucrose is when a person is taking acarbose. Since acarbose and other alpha-glucosidase inhibitors prevents starch and other sugars from being broken down into monosaccharides that can be absorbed by the body, patients taking these medications should consume monosaccharide-containing foods such as glucose tablets, honey, or juice to reverse hypoglycemia.

Prevention:
The most effective means of preventing further episodes of hypoglycemia depends on the cause.

The risk of further episodes of diabetic hypoglycemia can often (but not always) be reduced by lowering the dose of insulin or other medications, or by more meticulous attention to blood sugar balance during unusual hours, higher levels of exercise, or alcohol intake.

Many of the inborn errors of metabolism require avoidance or shortening of fasting intervals, or extra carbohydrates. For the more severe disorders, such as type 1 glycogen storage disease, this may be supplied in the form of cornstarch every few hours or by continuous gastric infusion.

Several treatments are used for hyperinsulinemic hypoglycemia, depending on the exact form and severity. Some forms of congenital hyperinsulinism respond to diazoxide or octreotide. Surgical removal of the overactive part of the pancreas is curative with minimal risk when hyperinsulinism is focal or due to a benign insulin-producing tumor of the pancreas. When congenital hyperinsulinism is diffuse and refractory to medications, near-total pancreatectomy may be the treatment of last resort, but in this condition is less consistently effective and fraught with more complications.

Hypoglycemia due to hormone deficiencies such as hypopituitarism or adrenal insufficiency usually ceases when the appropriate hormone is replaced.

Hypoglycemia due to dumping syndrome and other post-surgical conditions is best dealt with by altering diet. Including fat and protein with carbohydrates may slow digestion and reduce early insulin secretion. Some forms of this respond to treatment with a glucosidase inhibitor, which slows starch digestion.

Reactive hypoglycemia with demonstrably low blood glucose levels is most often a predictable nuisance which can be avoided by consuming fat and protein with carbohydrates, by adding morning or afternoon snacks, and reducing alcohol intake.

Idiopathic postprandial syndrome without demonstrably low glucose levels at the time of symptoms can be more of a management challenge. Many people find improvement by changing eating patterns (smaller meals, avoiding excessive sugar, mixed meals rather than carbohydrates by themselves), reducing intake of stimulants such as caffeine, or by making lifestyle changes to reduce stress.

Herbal medication for Hypoglycemia:-
THE following HERBS as stated below can help to ease low blood sugar with symptoms that include lightheadedness, headache, irritability, depression, anxiety, cravings for sweets, confusion, night sweats, weakness in the legs and arms, swollen feet, insatiable hunger, eye pain, nervous tics, mental disturbances, insomnia, aggressiveness, hair-trigger temper.

Cinnamon bark extract, coral calcium with trace minerals, L-carnitine, bilberry extract, Mexican wild yam, dandelion root, milk thistle extract.

Quik Tip
: Cinnamon bark decreases insulin resistance and improves blood-sugar profiles better than most prescription drugs, USDA studies confirm.

Hypoglycemia as “folk” medicine:-
Hypoglycemia is also a term of contemporary folk medicine which refers to a recurrent state of symptoms of altered mood and subjective cognitive efficiency, sometimes accompanied by adrenergic symptoms, but not necessarily by measured low blood glucose. Symptoms are primarily those of altered mood, behavior, and mental efficiency. This condition is usually treated by dietary changes which range from simple to elaborate. Advising people on management of this condition is a significant “sub-industry” of alternative medicine. More information about this form of “hypoglycemia”, with far more elaborate dietary recommendations, is available on the internet and in health food stores. Most of these websites and books describe a conflation of reactive hypoglycemia and idiopathic postprandial syndrome but do not recognize a distinction. The value of most of their recommendations is – from a scientific perspective – unproved.

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.medicinenet.com/hypoglycemia/article.htm
http://en.wikipedia.org/wiki/Hypoglycemia
http://www.herbnews.org/hypoglycemiadone.htm

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Suppliments our body needs

Glucosamine

Definition:
Glucosamine (C6H13NO5) is an amino sugar and a prominent precursor in the biochemical synthesis of glycosylated proteins and lipids. A type of glucosamine forms chitin, which composes the exoskeletons of crustaceans and other arthropods, cell walls in fungi and many higher organisms. Glucosamine is one of the most abundant monosaccharides. It is produced commercially by the hydrolysis of crustacean exoskeletons or, less commonly and more expensive to the consumer, by fermentation of a grain such as corn or wheat. Glucosamine is commonly used as a treatment for osteoarthritis, although its acceptance as a medical therapy varies.

CLICK & SEE

Glucosamine is a compound found naturally in the body, made from glucose and the amino acid glutamine. Glucosamine is needed to produce glycosaminoglycan, a molecule used in the formation and repair of cartilage and other body tissues. Production of glucosamine slows with age.

Glucosamine is available as a nutritional supplement in health food stores and many drug stores. Glucosamine supplements are manufactured in a laboratory from chitin, a substance found in the shells of shrimp, crab, lobster, and other sea creatures. In additional to nutritional supplements, glucosamine is also used in sports drinks and in cosmetics.

Glucosamine is often combined with chondroitin sulfate, a molecule naturally present in cartilage. Chondroitin gives cartilage elasticity and is believed to prevent the destruction of cartilage by enzymes. Glucosamine is sometimes combined with methylsulfonylmethane, or MSM, in nutritional supplements.

Biochemistry:
Glucosamine was first identified in 1876 by Dr. Georg Ledderhose, but the stereochemistry was not fully defined until 1939 by the work of Walter Haworth.[1] D-Glucosamine is made naturally in the form of glucosamine-6-phosphate, and is the biochemical precursor of all nitrogen-containing sugars.   Specifically, glucosamine-6-phosphate is synthesized from fructose-6-phosphate and glutamine[3] as the first step of the hexosamine biosynthesis pathway.[4] The end-product of this pathway is UDP-N-acetylglucosamine (UDP-GlcNAc), which is then used for making glycosaminoglycans, proteoglycans, and glycolipids.

As the formation of glucosamine-6-phosphate is the first step for the synthesis of these products, glucosamine may be important in regulating their production. However, the way that the hexosamine biosynthesis pathway is actually regulated, and whether this could be involved in contributing to human disease, remains unclear.

Health effects:
Oral glucosamine is commonly used for the treatment of osteoarthritis. Since glucosamine is a precursor for glycosaminoglycans, and glycosaminoglycans are a major component of joint cartilage, supplemental glucosamine may help to rebuild cartilage and treat arthritis. Its use as a therapy for osteoarthritis appears safe, but there is conflicting evidence as to its effectiveness. A randomized, double-blind, placebo-controlled trial found glucosamine sulfate is no better than placebo in reducing the symptoms or progression of hip osteoarthritis.

There is promising evidence that glucosamine may reduce pain symptoms of knee osteoarthritis and possibly slow the progression of osteoarthritis. For example, a study published in the journal Archives of Internal Medicine examined people with osteoarthritis over three years. Researchers assessed pain and structural improvements seen on x-ray. They gave 202 people with mild to moderate osteoarthritis 1,500 mg of glucosamine sulfate a day or a placebo.

At the end of the study, researchers found that glucosamine slowed the progression of knee osteoarthritis compared to the placebo. People in the glucosamine group had a significant reduction in pain and stiffness. On x-ray, there was no average change or narrowing of joint spaces in the knees (a sign of deterioration) of the glucosamine group. In contrast, joint spaces of participants taking the placebo narrowed over the three years.

One of the largest studies on glucosamine for osteoarthritis was a 6-month study sponsored by the National Institutes of Health. Called GAIT, the study compared the effectiveness of glucosamine hydrochloride (HCL), chondroitin sulfate, a combination of glucosamine and chondroitin sulfate, the drug celecoxib (Celebrex), or a placebo in people with knee osteoarthritis.

Glucosamine or chondroitin alone or in combination didn’t reduce pain in the overall group, although people in the study with moderate-to-severe knee pain were more likely to respond to glucosamine.

One major drawback of the GAIT Trial was that glucosamine hydrochloride was used rather than the more widely used and researched glucosamine sulfate. A recent analysis of previous studies, including the GAIT Trial, concluded that glucosamine hydrochloride was not effective. The analysis also found that studies on glucosamine sulfate were too different from one another and were not as well-designed as they should be, so they could not properly draw a conclusion. More research is needed.

Still, health care providers often suggest a three month trial of glucosamine and discontinuing it if there is no improvement after three months. A typical dose for osteoarthritis is 1,500 mg of glucosamine sulfate each day.

Other Conditions
Other conditions for which glucosamine is used include rheumatoid arthritis, inflammatory bowel disease (Crohn’s disease and ulcerative colitis), chronic venous insufficiency, and skin conditions, although further evidence is needed.

Use:
A typical dosage of glucosamine salt is 1,500 mg per day. Glucosamine contains an amino group that is positively charged at physiological pH. The anion included in the salt may vary. Commonly sold forms of glucosamine are glucosamine sulphate and glucosamine hydrochloride. The amount of glucosamine present in 1500 mg of glucosamine salt will depend on which anion is present and whether additional salts are included in the manufacturer’s calculation. Glucosamine is often sold in combination with other supplements such as chondroitin sulfate and methylsulfonylmethane.

Glucosamine is a popular alternative medicine used by consumers for the treatment of osteoarthritis. Glucosamine is also extensively used in veterinary medicine as an unregulated but widely accepted supplement.

Bioavailability and pharmacokinetics:
Two recent studies confirm that glucosamine is bioavailable both systemically and at the site of action (the joint) after oral administration of crystalline glucosamine sulfate in osteoarthritis patients. Steady state glucosamine concentrations in plasma and synovial fluid were correlated and in line with those effective in selected in vitro studies

Clinical studies:
There have been multiple clinical trials of glucosamine as a medical therapy for osteoarthritis, but results have been conflicting. The evidence both for and against glucosamine’s efficacy has led to debate among physicians about whether to recommend glucosamine treatment to their patients.

Multiple clinical trials in the 1980s and 1990s, all sponsored by the European patent-holder, Rottapharm, demonstrated a benefit for glucosamine. However, these studies were of poor quality due to shortcomings in their methods, including small size, short duration, poor analysis of drop-outs, and unclear procedures for blinding. Rottapharm then sponsored two large (at least 100 patients per group), three-year-long, placebo-controlled clinical trials of the Rottapharm brand of glucosamine sulfate. These studies both demonstrated a clear benefit for glucosamine treatment. There was not only an improvement in symptoms but also an improvement in joint space narrowing on radiographs. This suggested that glucosamine, unlike pain relievers such as NSAIDs, can actually help prevent the destruction of cartilage that is the hallmark of osteoarthritis. On the other hand, several subsequent studies, independent of Rottapharm, but smaller and shorter, did not detect any benefit of glucosamine.

Due to these controversial results, some reviews and meta-analyses have evaluated the efficacy of glucosamine. Richy et al. performed a meta-analysis of randomized clinical trials in 2003 and found efficacy for glucosamine on VAS and WOMAC pain, Lequesne index and VAS mobility and good tolerability.

Recently, a review by Bruyere et al. about glucosamine and chondroitin sulfate for the treatment of knee and hip osteoarthritis concludes that both products act as valuable symptomatic therapies for osteoarthritis disease with some potential structure-modifying effects.

This situation led the National Institutes of Health to fund a large, multicenter clinical trial (the GAIT trial) studying reported pain in osteoarthritis of the knee, comparing groups treated with chondroitin sulfate, glucosamine, and the combination, as well as both placebo and celecoxib. The results of this 6-month trial found that patients taking glucosamine HCl, chondroitin sulfate, or a combination of the two had no statistically significant improvement in their symptoms compared to patients taking a placebo. The group of patients who took celecoxib did have a statistically significant improvement in their symptoms. These results suggest that glucosamine and chondroitin did not effectively relieve pain in the overall group of osteoarthritis patients, but it should be interpreted with caution because most patients presented only mild pain (thus a narrow margin to appraise pain improvement) and because of an unusual response to placebo in the trial (60%). However, exploratory analysis of a subgroup of patients suggested that the supplements taken together (glucosamine and chondroitin sulfate) may be significantly more effective than placebo (79.2% versus 54%; p = 0.002) and a 10% higher than the positive control, in patients with pain classified as moderate to severe (see testing hypotheses suggested by the data).

In an accompanying editorial, Dr. Marc Hochberg also noted that “It is disappointing that the GAIT investigators did not use glucosamine sulfate … since the results would then have provided important information that might have explained in part the heterogeneity in the studies reviewed by Towheed and colleagues” But this concern is not shared by pharmacologists at the PDR who state, “The counter anion of the glucosamine salt (i.e. chloride or sulfate) is unlikely to play any role in the action or pharmacokinetics of glucosamine”. Thus the question of glucosamine’s efficacy will not be resolved without further updates or trials.

In this respect, a 6-month double-blind, multicenter trial has been recently performed to assess the efficacy of glucosamine sulfate 1500 mg once daily compared to placebo and acetaminophen in patients with osteoarthritis of the knee (GUIDE study). The results showed that glucosamine sulfate improved the Lequesne algofunctional index significantly compared to placebo and the positive control. Secondary analyses, including the OARSI responder indices, were also significantly favorable for glucosamine sulfate.

A subsequent meta-analysis of randomized controlled trials, including the NIH trial by Clegg, concluded that hydrochloride is not effective and that there was too much heterogeneity among trials of glucosamine sulfate to draw a conclusion.[46] In response to these conclusions, Dr. J-Y Reginster in an accompanying editorial suggests that the authors failed to apply the principles of a sound systematic review to the meta-analysis, but instead put together different efficacy outcomes and trial designs by mixing 4-week studies with 3-year trials, intramuscular/intraarticular administrations with oral ones, and low-quality small studies reported in the early 1980s with high-quality studies reported in 2007.

However, currently OARSI (OsteoArthritis Research Society International) is recommending glucosamine as the second most effective treatment for moderate cases of osteoarthritis. Likewise, recent European League Against Rheumatism practice guidelines for knee osteoarthritis grants to glucosamine sulfate the highest level of evidence, 1A, and strength of the recommendation, A.

Safety:
Clinical studies have consistently reported that glucosamine appears safe. Since glucosamine is usually derived from shellfish, those allergic to shellfish may wish to avoid it. However, since glucosamine is derived from the shells of these animals while the allergen is within the flesh of the animals, it is probably safe even for those with shellfish allergy. Alternative sources using fungal fermentation of corn are available. Another concern has been that the extra glucosamine could contribute to diabetes by interfering with the normal regulation of the hexosamine biosynthesis pathway, but several investigations have found no evidence that this occurs. A review conducted by Anderson et al in 2005 summarizes the effects of glucosamine on glucose metabolism in in vitro studies, the effects of oral administration of large doses of glucosamine in animals and the effects of glucosamine supplementation with normal recommended dosages in humans, concluding that glucosamine does not cause glucose intolerance and has no documented effects on glucose metabolism. Other studies conducted in lean or obese subjects concluded that oral glucosamine at standard doses does not cause or significantly worsen insulin resistance or endothelial dysfunction.

The U.S. National Institutes of Health is currently conducting a study of supplemental glucosamine in obese patients, since this population may be particularly sensitive to any effects of glucosamine on insulin resistance.

In the United States, glucosamine is not approved by the Food and Drug Administration for medical use in humans. Since glucosamine is classified as a dietary supplement in the US, safety and formulation are solely the responsibility of the manufacturer; evidence of safety and efficacy is not required as long as it is not advertised as a treatment for a medical condition.

In Europe, glucosamine is approved as a medical drug and is sold in the form of glucosamine sulfate. In this case, evidence of safety and efficacy is required for the medical use of glucosamine and several guidelines have recommended its use as an effective and safe therapy for osteoarthritis. Actually, the Task Force of the European League Against Rheumatism (EULAR) committee recently granted glucosamine sulfate a level of toxicity of 5 in a 0-100 scale, and recent OARSI (OsteoArthritis Research Society International) guidelines for hip and knee osteoarthritis also confirm its excellent safety profile.

Most studies involving humans have found that short-term use of glucosamine is well-tolerated. Side effects may include drowsiness, headache, insomnia, and mild and temporary digestive complaints such as abdominal pain, poor appetite, nausea, heartburn, constipation, diarrhea, and vomiting. In rare human cases, the combination of glucosamine and chondroitin has been linked with temporarily elevated blood pressure and heart rate and palpitations.

Since glucosamine supplements may be made from shellfish, people with allergies to shellfish should avoid glucosamine unless it has been confirmed that it is from a non-shellfish source. The source of glucosamine is not required to be printed on the label, so it may require a phone call to the manufacturer.

There is some evidence suggesting that glucosamine, in doses used to treat osteoarthritis, may worsen blood sugar, insulin, and/or hemoglobin A1c (a test that measures how well blood sugar has been controlled during the previous three months) levels in people with diabetes or insulin resistance.

Theoretically, glucosamine may increase the risk of bleeding. People with bleeding disorders, those taking anti-clotting or anti-platelet medication, such as warfarin, clopidogrel, and Ticlid, or people taking supplements that may increase the risk of bleeding, such as garlic, ginkgo, vitamin E, or red clover, should not take glucosamine unless under the supervision of a healthcare provider.

The safety of glucosamine in pregnant or nursing women isn’t known.

Resources:
http://altmedicine.about.com/cs/herbsvitaminsek/a/Glucosamine.htm
http://en.wikipedia.org/wiki/Glucosamine

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Categories
Suppliments our body needs

Fucoxanthin

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Definition:Fucoxanthin is a carotenoid, with formula C42H58O6. It is found as an accessory pigment in the chloroplasts of brown algae and most other heterokonts, giving them a brown or olive-green color. Fucoxanthin absorbs light primarily in the blue-green to yellow-green part of the visible spectrum, peaking at around 510-525 nm by various estimates and absorbing significantly in the range of 450 to 540 nm. Some metabolic and nutritional studies carried at Hokkaido University indicate that fucoxanthin promotes fat burning within fat cells in white adipose tissue by increasing the expression of thermogeniIt is a type of carotenoid found naturally in edible brown seaweed such as wakame (Undaria pinnatifida) and hijiki (Hijikia fusiformis), which are used widely in Asian cuisine. Wakame is the seaweed used in miso soup….CLICK & SEE THE PICTURES

Fucoxanthin is also found in much smaller amounts in red seaweed (the kind typically used in Japanese sushi rolls) and green seaweed.

Both wakame and hijiki are available at Japanese specialty food stores, some health food stores and online. Although brown seaweed is the richest source of fucoxanthin, you would have to eat an unrealistic amount of it daily to get fucoxanthin levels close to those used in research studies.

Fucoxanthin is also available as a nutritional supplement in capsule form and can be found in some health food stores and online.

Medicinal Uses:

Weight Loss
Fucoxanthin is being explored for weight loss. So far, only animal studies have been done. Japanese researchers have found that fucoxanthin (isolated from wakame) promotes the loss of abdominal fat in obese mice and rats. Animals lost five to 10% of their body weight.

Although it’s not fully understood how fucoxanthin works, it appears to target a protein called UCP1 that increases the rate at which abdominal fat is burned. Abdominal fat, also called white adipose tissue, is the kind of fat that surrounds our organs and is linked to heart disease and diabetes. Fucoxanthin also appears to stimulate the production of DHA, one of the omega-3 fatty acids found in fatty fish such as salmon.

Although it’s promising and already a popular nutritional supplement, more research is needed to determine if fucoxanthin will work in the same way in humans. If it does prove to be effective, fucoxanthin could be developed into a diet pill for obesity.

You may click to see:->Brown Seaweed that may Help Fight Obesity

Diabetes
Fucoxanthin has also been found in animal studies to decrease insulin and blood glucose levels. Researchers hypothesize that fucoxanthin anti-diabetes effect may be because fucoxanthin appears to promote the formation of DHA (the omega-3 fatty acid found in fish oil). DHA is thought to increase insulin sensitivity, improve triglycerides and reduce LDL (“bad”) cholesterol.

Cancer
Preliminary research in test tubes suggests that fucoxanthin may have anti-tumor effects. No studies have looked at whether this holds true in humans or if taken orally. It’s far too early for fucoxanthin to be used as a complementary treatment for cancer.

Side Effects
Because there hasn’t been research on fucoxanthin in humans, the possible side effects aren’t known.

People shouldn’t consume large amounts of wakame or other types of seaweed as a source of fucoxanthin. Seaweed is rich in iodine and excessive consumption may result in iodine poisoning. High levels of iodine can interfere with the function of the thyroid gland. Also, consuming excess amounts of iodine-rich foods isn’t recommended if there is a known allergy or hypersensitivity to iodine.

Resources:
http://en.wikipedia.org/wiki/Fucoxanthin
http://altmedicine.about.com/od/herbsupplementguide/a/fucoxanthin.htm

Categories
Herbs & Plants Herbs & Plants (Spices)

Star Anise

Japanese star aniseImage via Wikipedia

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Botanical Name: Illicium verum
Kingdom: Plantae
Division: Magnoliophyta
Class: Magnoliopsida
Order: Austrobaileyales
Family: Illiciaceae/Magnoliaceae
Genus: Illicium
syn: I. anisatum
Other Names:-Anise Stars, Badain, Badiana, Chinese Anise
French: anis de la Chine, anise étoilé, badiane
German: Sternanis
Italian: anice stellato
Spanish: anis estrllado,badian
Chinese: ba chio, ba(ht) g(h)ok, bart gok, pa-chiao, pak kok, peh kah
India:Chakra Phool
Indonesian: bunga lawang

Habitat: Native to China and Vietnam, star anise is today grown almost exclusively in southern China, Indo-China, and Japan. It was first introduced into Europe in the seventeenth century.

Plant Description and Cultivation:
A small to medium evergreen tree of the magnolia family, reaching up to 8m (26ft). The leaves are lanceolate and the axillary flowers are yellow. The tree is propagated by seed and mainly cultivated in China and Japan for export and home markets. the fruits are harvested before they ripen, then sun dried.

..CLICK & SEE

Spice Description:
Star anise is the unusual fruit of a small oriental tree. It is, as the name suggests, star shaped, radiating between five and ten pointed boat-shaped sections, about eight on average. These hard sections are seed pods. Tough skinned and rust coloured, they measure up to 3cm (1-1/4”) long. The fruit is picked before it can ripen, and dried. The stars are available whole, or ground to a red-brown powder....CLICK & SEE
Bouquet: Powerful and liquorice-like, more pungent and stronger than anise.
Flavour: Evocative of a bitter aniseed, of which flavour star anise is a harsher version. Nervertheless, the use of star anise ensures an authentic touch in the preparation of certain Chinese dishes.

Star anise is a spice that closely resembles anise in flavor, obtained from the star-shaped pericarp of Illicium verum, a small native evergreen tree of southwest China. The star shaped fruits are harvested just before ripening. It is widely used in Chinese cuisine, in Indian cuisine where it is a major component of garam masala, and in Malay/Indonesian cuisine. It is widely grown for commercial use in China, India, and most other countries in Asia. Star anise is an ingredient of the traditional five-spice powder of Chinese cooking. It is also one of the ingredients used to make the broth for the Vietnamese noodle soup called ph?. It is used as a spice in preparation of Biryani in Andhra Pradesh, a south Indian State.

Medicinal Properties:
Like anise, star anise has carminative, stomachic, stimulant and diuretic properties. In the East it is used to combat colic and rheumatism. It is a common flavouring for medicinal teas, cough mixtures and pastilles.

Medicinal uses:
Star anise has been used in a tea as a remedy for colic and rheumatism, and the seeds are sometimes chewed after meals to aid digestion.

Shikimic acid, a primary feedstock used to create the anti-flu drug Tamiflu, is produced by most autotrophic organisms, but star anise is the industrial source. In 2005, there was a temporary shortage of star anise due to its use in making Tamiflu. Late in that year, a way was found of making shikimic acid artificially. A drug company named Roche now derives some of the raw material it needs from fermenting E. coli bacteria. There is no longer any shortage of star anise and it is readily available and is relatively cheap.

Star anise is grown in four provinces in China and harvested between March and May. The shikimic acid is extracted from the seeds in a ten-stage manufacturing process which takes a year. Reports say 90% of the harvest is already used by the Swiss pharmaceutical manufacturer Roche in making Tamiflu, but other reports say there is an abundance of the spice in the main regions – Fujian, Guangdong, Guangxi and Yunnan.

Japanese star anise (Illicium anisatum), a similar tree, is not edible because it is highly toxic; instead, it has been burned as incense in Japan. Cases of illness, including “serious neurological effects, such as seizures”, reported after using star anise tea may be a result of using this species. Japanese star anise contains anisatin, which causes severe inflammation of the kidneys, urinary tract and digestive organs.

Culinary Uses:
Star anise is used in the East as aniseed is in the West. Apart from its use in sweetmeats and confectionery, where sweeteners must be added, it contributes to meat and poultry dishes, combining especially well with pork and duck. In Chinese red cooking, where the ingredients are simmered for a lengthy period in dark soy sauce, star anise is nearly always added to beef and chicken dishes. Chinese stocks and soups very often contain the spice.. It flavours marbled eggs, a decorative Chinese hors d’oeuvre or snack. Mandarins with jaded palates chew the whole dried fruit habitually as a post-prandial digestant and breath sweetener – an oriental comfit. In the West, star anise is added in fruit compotes and jams, and in the manufacture of anise-flavoured liqueurs, the best known being anisette. It is an ingredient of the mixture known as “Chinese Five Spices”.

Star anise contains anethole, the same ingredient which gives the unrelated anise its flavor. Recently, star anise has come into use in the West as a less expensive substitute for anise in baking as well as in liquor production, most distinctively in the production of the liquor Galliano. It is also used in the production of Sambuca, pastis, and many types of absinthe.

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.theepicentre.com/Spices/staranis.html
http://en.wikipedia.org/wiki/Star_anise

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