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Avoid Crash Diets: Healthy Weight-Loss Tips

FitSugar — Thu, 10 Sep 2009 03:00:55 -0700

I read a very sad and unfortunate tale of an English bride-to-be's death after crash dieting. After eating only 530 calories a day for 11 weeks, the 34-year-old collapsed. Having weighed 244 pounds at the start of the controversial LighterLife diet, Samantha Clowe had lost 42 pounds when she collapsed and died of heart failure. Her family and fiancé are in my thoughts, and in light of this tragedy, I would like to review five rules for healthy and sustainable weight loss.

To lose weight you need to be in a caloric deficit, meaning you consume fewer calories than you are expending. Think of it like this: calories coming in need to be fewer than calories going out. It really is pretty simple.
To lose one pound a week you need to be in a caloric deficit of 3,500 calories. The best way to do this is to combine eating fewer calories and burning more calories - that means exercise! Cardio is great for burning calories. See these posts for ideas to freshen up your cardio routine.

Learn the other three tips when you continue reading.

True or False:

FitSugar — Thu, 16 Nov 2006 15:53:32 -0800

True or False: Crash diets (or eating almost nothing) are OK methods of weight loss as long as it's only for a few days.

Grab Bag: Are Rom-Coms Bad For You?

TresSugar — Fri, 23 Oct 2009 12:00:00 -0700

4 bad dating habits learned from rom-coms. - Your Tango
Help! My sister's fiance confessed he wants me. - Lemondrop
Beautiful women with not-so-beautiful men. - The Frisky
Are men hardwired to cheat? - Em & Lo
What might fix the WNBA. - Double X
Pageant mom puts 8-year-old daughter on a crash diet. - Jezebel
5 ways the crappy economy has ruined our dating lives. - Glamour

No-Carb Diets Could Crash Your Brain's Memory

FitSugar — Tue, 16 Dec 2008 03:30:00 -0800

As far as fad diets go, the low-carbohydrate train has enjoyed a prolonged ride when compared to its more trendy counterparts. Some dieters shun carbs because their bodies respond by shedding pounds, but new research shows they could also be sacrificing some very important brain power.

The brain converts carbohydrates to glucose for proper functionality, and severely restricting carb intake can limit our ability to remember. Nineteen women were put on either a very low-carb diet or the low-calorie diet recommended by the American Dietetic Association, and after just one week the low-carb dieters performed worse on memory-based tasks than the women following the ADA diet.

While low-carb participants consumed almost no carbohydrates during the first week, limited carbs were introduced during the second week and their memories showed improvement with the revised diet. The study's co-author Holly A. Taylor, PhD commented on the bottom line, saying, "Although this study only tracked dieting participants for three weeks, the data suggest that diets can affect more than just weight."

Have you noticed that some diets affect your brain's ability to function properly?

Source

Reality Check: Losing Baby Weight

FitSugar — Thu, 25 Jun 2009 09:57:28 -0700

Women get pregnant and gain weight. Then they have the baby and have to lose the weight. Celeb moms just seem to do so at an alarmingly quick rate. We read tales of Naomi Watts simply using breastfeeding to get back to her pre-baby weight in a matter of weeks, and Jessica Alba bouncing back in record time. This, however, is not the reality for most women.

European healthcare officials are trying to add some common sense to the conversation about losing the baby weight. For most women it takes three months to a year to lose the weight, and it is important to do so. While breastfeeding can help burn calories and help new moms shed pounds, many new mothers cannot lose weight because they are breastfeeding. The body holds on to excess fat to ensure the mom has enough energy/calories to produce milk for the baby. Common sense tells us it is easier to lose the baby weight if you don't gain excessive amounts while pregnant - there is no real need to eat for two. Since the vast majority of new moms are without a personal trainer, a personal chef, and a nanny - common elements of a celeb's life - losing the baby weight will take some time. Instead of embarking on a crash diet to drop pounds, it is best to eat a healthy and balanced diet, while increasing your fitness level at a reasonable rate. Slow and sustained weight loss is the best approach, and a new mom who is cutting too many calories is a cranky new mom.

10 Fit Rules to Live By

FitSugar — Mon, 20 Apr 2009 04:30:00 -0700

A couple of weeks ago, I decided to give myself a break and ask FitSugar readers: what's the best health or fitness advice you've ever heard? As always, I appreciated the thoughtful, thought-provoking, and often amusing responses; it's always great to remind ourselves why and how to live healthy. Here are my 10 favorite pieces of health and fitness advice from Fit readers:

No one has ever regretted working out. - Hippiecowgirl
Don't eat any food that your great grandma wouldn't have recognized. - Spectra
Consistency is key. - Lizkiernan
Work up a sweat and make it an activity you enjoy. - Gothamgal
Crash dieting and restrictive diets rarely work and are difficult to maintain. Make changes that you can see yourself keeping up for life. - Yaliyah

To see the other five, read more.

Eat a rainbow! Eat foods that are the colors of the rainbow every day. - Kate516
Get enough sleep. Without that, all your other good acts start off with a handicap. - Pixelhaze
Exercise is an investment, not a sacrifice. - Zuzanka
Eat when you're hungry, stop when you're content (not full). Food = energy. Fiber is awesome. - Lemuse20
Suck your stomach in when you're waiting in line. It tightens your abs and doesn't take up any time. - GenesisRocks

Source

Dos and Don'ts of Healthy Wedding Planning

FitSugar — Wed, 22 Apr 2009 08:00:00 -0700

Let's face it: planning a wedding is stressful. Depending on how big your wedding is, it could be one of the most stressful projects you've ever taken on. So amid all the excitement, it's important to keep yourself fit, healthy, centered, and sane. Here's what do to (and what not to do) when planning a wedding the fit and healthy way.

Do make a plan. It sounds basic, but start by planning out your timeline, then go down the list one by one. Otherwise, you'll easily feel overwhelmed.
Don't be shy about accepting help. People have gotten married many times before, so why start from scratch? Registry checklists, like our downloadable registry, will save you serious time. You'll also have people offering to help you left and right, so let them!
Do come up with a fitness plan. If part of your plan includes getting fit for the big day, map out a workout schedule - with the help of online programs or a trainer - to keep yourself on track.

For a few other ideas for how to stay sane while planning your wedding, read more.

Don't overdo it. Getting in shape shouldn't mean setting unrealistic goals that require crash-dieting and unsafe lifestyle changes. Losing a maximum of two pounds a week is considered reasonable.
Do make time for yourself. You'll be bombarded by people and questions right through the wedding day, so set aside some alone time for yoga, massages, walks - whatever.
Don't neglect your workouts. Make sure your exercise routine doesn't get lost in the shuffle. Put workouts on your calendar, alongside all your wedding appointments. If you want, recruit a special wedding workout buddy.
Do control your party-food intake. You're likely to attend some engagement and bachelorette parties before the big day, but if you're trying to stay slim, keep your indulging in check. Have a bite of something you're craving, then move on.

Any of you recent brides out there have anything to add? If so, share them in the comments!
Source

Gout

FitSugar — Wed, 08 Oct 2008 17:35:16 -0700

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Types of Gout:

There are two types of gout -- primary and secondary.

Primary gout: The cause is usually unknown. However, primary gout is likely the result of a combination of genetic, hormonal, and dietary factors.
Secondary gout: Secondary gout is caused by medications or medical conditions that cause an increase in the serum (blood) levels of uric acid.

Risk Factors:

Risk factors for gout include:

Advancing age
Male gender
Family history of the condition
Obesity
Use of certain drugs, including diuretics, aspirin, cyclosporine, or levodopa
Drinking a large amount of alcohol, particularly beer
Exposure to lead
Organ transplants
Thyroid problems

Symptoms of a Gout Attack:

Symptoms of a gout attack include:

Severe pain at and around the joint
- May feel like "crushing" or a dislocated bone
- Walking and the weight of bed sheets may be unbearable
- Usually takes 8 - 12 hours to develop
- Occurs late at night or early in the morning and may wake you up
Swelling that may extend beyond the joint
Red, shiny, tense skin over the affected area, which may peel after a few days
Chills and mild fever, loss of appetite, and feelings of ill health

Research News

A large study found that people with gout are at an increased risk of having metabolic syndrome. Metabolic syndrome is a collection of problems, such as abdominal obesity, high blood pressure, and low "good" cholesterol. This syndrome increases a person's risk of heart disease and diabetes.

Introduction

Gout is a painful and common type of arthritis. About 1 in 100 people develop gout. The condition is usually associated with a long-lasting, abnormally high amount of uric acid in the blood, called chronic hyperuricemia.

The rate of gout has increased in recent decades, not only in America but also in other developed countries. The increase is possibly due to dietary and lifestyle changes, greater use of medications that cause hyperuricemia, and aging populations. Gout is very uncommon in developing countries.

Click the icon to see an animation about gout.

Metabolism of Purines. The process leading to hyperuricemia and gout begins with the metabolism of purines, nitrogen-containing compounds that are important for energy. Purines can be divided into two types:

Endogenous purines are manufactured within human cells.
Exogenous purines are obtained from foods.

The process of breaking down purines results in the formation of uric acid in the body. Most mammals have an enzyme called uricase, which breaks down uric acid so it can be easily removed from the body. Because humans lack uricase, uric acid is not as easily removed, and can build up in body tissues.

Uric Acid and Hyperuricemia. Purines in the liver produce uric acid. The uric acid enters the bloodstream, and most of it eventually goes through the kidneys and is excreted in the urine. The remaining uric acid travels through the intestines, where bacteria help break it down.

Normally these actions keep the level of uric acid in the blood plasma (the liquid part of the blood) at a healthy level, which is below 6.8 mg/dL. But under certain circumstances, the body produces too much uric acid or removes too little. In either case, concentrations of uric acid increase in the blood. This condition is known as hyperuricemia.

If concentrations of uric acid reach 7 mg/dL and above, needlelike crystals of a salt called monosodium urate (MSU) form. As MSU crystals build up in the joints, they trigger inflammation and pain, the characteristic symptoms of gout.

Symptoms

The specific symptoms of gout depend on the stage of the disease. Gout is often divided into four stages:

Asymptomatic hyperuricemia
Acute gouty arthritis
Intercritical gout
Chronic tophaceous gout

Asymptomatic means there are no symptoms. Asymptomatic hyperuricemia is considered the first stage of gout. MSU levels slowly increase in the body. This stage lasts for an average of 30 years.

Note: Hyperuricemia does not inevitably lead to gout. In fact, less than 20% of cases develop the full-blown arthritic gout disease.

Acute gouty arthritis occurs when the first symptoms of gout appear. Sometimes the first signs of gout are brief twinges of pain (petit attacks) in an affected joint. These attacks can precede the actual full-blown condition by several years.

MSU crystals form at normal body temperature when the concentration of uric acid in the blood reaches 7 mg/dL. At lower temperatures, MSU crystals form at lower concentrations of uric acid. Since blood temperature falls the further blood gets from the heart, gout strikes the toes and fingers first.

Symptoms of acute gouty arthritis include:

Severe pain at and around the joint
- May feel like "crushing" or a dislocated bone
- Walking and the weight of bed sheets may be unbearable
- Usually takes 8 - 12 hours to develop
- Occurs late at night or early in the morning and may wake you up
Swelling that may extend beyond the joint
Red, shiny, tense skin over the affected area, which may peel after a few days
Chills and mild fever, loss of appetite, and feelings of ill health

Most often symptoms start in one joint.

Monoarticular Gout. Gout that occurs in one joint is called monoarticular gout. About 60% of all first-time monoarticular gout attacks in middle-aged adults occur in the big toe. This occurrence is known as podagra. Symptoms can also occur in other locations, such as the ankle or knee.

Polyarticular Gout. If more than one joint is affected, the condition is known as polyarticular gout. Multiple joints are affected in only 10 - 20% of first attacks. Older people are more likely to have polyarticular gout. The most frequently affected joints are the foot, ankle, knee, wrist, elbow, and hand. The pain usually occurs in joints on one side of the body and it is usually, although not always, in the lower legs and the feet. People with polyarticular gout are more likely to have a slower onset of pain and a longer delay between attacks. People with polyarticular gout are also more likely to experience low-grade fever, loss of appetite, and a general feeling of poor health.

An untreated attack will typically peak 24 - 48 hours after the first appearance of symptoms, and go away after 5 - 7 days. However, some attacks last only hours, while others persist as long as several weeks.

Intercritical gout is the term used to describe the periods between attacks. The first attack is usually followed by a complete remission of symptoms, but, if left untreated, gout nearly always returns. Over two-thirds of patients will have at least one further attack within 2 years of the first attack. By 10 years, over 90% of the patients are likely to have repeat attacks.

Chronic Tophaceous Gout and Tophi. After several years, persistent gout can develop into a condition called chronic tophaceous gout. This long-term condition often produces tophi, which are solid deposits of MSU crystals that form in the joints, cartilage, bones, and elsewhere in the body. In some cases, tophi break through the skin and appear as white or yellowish-white, chalky nodules that have been described as looking like crab eyes.

Click the icon to see an image of tophi gout.

Without treatment, tophi develop about 10 years after the initial onset of gout, although the occurence can range from 3 to 42 years. Tophi are more likely to appear early in the course of the disease in older people. In the elderly population, women appear to be at higher risk for tophi than men. Certain people, such as those who are receiving cyclosporine after a transplant, have a high risk of developing tophi.

Development of Chronic Pain. When gout remains untreated, the intercritical periods typically become shorter and shorter, and the attacks, although sometimes less intense, can last longer. Over the long term (about 10 - 20 years) gout becomes a chronic disorder characterized by constant low-grade pain and mild or acute inflammation. Gout may eventually affect several joints, including those that may have been free of symptoms at the first appearance of the disorder. In rare cases, the shoulders, hips, or spine are affected.

Location of Tophi. Tophi generally form in the following locations:

Curved ridge along the edge of the outer ear
Forearms
Elbow or knee
Hands or feet -- older patients, particularly women, are more likely to have gout in the small joints of the fingers.
Around the heart and spine (rare)

Tophi are generally painless. However, they can cause pain and stiffness in the affected joint. Eventually, they can also erode cartilage and bone, ultimately destroying the joint. Large tophi under the skin of the hands and feet can give rise to extreme deformities.

Uric Acid Nephrolithiasis (Kidney Stones). Persons who have kidney stones that formed from uric acid are more likely to have higher levels of uric acid in their blood than in their urine. This suggests that gout is responsible for this type of kidney stones. Uric acid stones and other forms of kidney stones are present in 10 - 25% of patients with primary gout, a rate of more than 1,000 times that of the general population. In gout caused by other conditions (called secondary gout), the reported rate reaches 42%.

Click the icon to see an image of nephrolithiasis.

Not all of the kidney stones in patients with gout are made of uric acid. Some are made from calcium oxalate, calcium phosphate, or substances combined with uric acid. Uric acid stones can also form when you do not have gout or hyperuricemia.

Chronic Uric Acid Interstitial Nephropathy. Chronic uric acid interstitial nephropathy occurs when crystals slowly form in the structures and tubes that carry fluid from the kidney. It is reversible and not likely to injure the kidneys.

Kidney Failure. Sudden overproduction of uric acid can occasionally block the kidneys and cause them to fail. This occurrence is very uncommon but can develop after any of the following:

Chemotherapy for leukemia or lymphoma
Severe heat stress from vigorous exercise
Epileptic seizures
Corticosteroid therapy for severe allergic reactions

Causes and Risk Factors

Gout is classified as either primary or secondary, depending on what causes the high levels of uric acid in the blood (hyperuricemia).

More than 99% of primary gout cases are referred to as idiopathic, meaning that the cause of the hyperuricemia cannot be determined. Primary gout is most likely the result of a combination of genetic, hormonal, and dietary factors. Secondary gout is caused by drug therapy or by medical conditions other than a metabolic disorder.

The following factors increase your risk for gout:

Advancing age
Male gender
Family history of the condition
Obesity
Use of certain drugs, including diuretics ("water pills"), aspirin, cyclosporine, or levodopa
Drinking a large amount of alcohol, particularly beer
Exposure to lead
Organ transplants
Thyroid problems
Other serious illness

Each risk factor is discussed in more detail below.

Middle-Aged Adults. Gout usually occurs in middle-aged men, peaking in the mid-40s. It is most often associated in this age group with obesity, high blood pressure, unhealthy cholesterol levels, and heavy alcohol use.

Elderly. Gout can also develop in older people, when it occurs equally in men and women. In this group, gout is most often associated with kidney problems and the use of diuretics. It is less often associated with alcohol use.

Children. Except for rare inherited genetic disorders that cause hyperuricemia, gout in children is rare.

Men. Men are significantly at higher risk for gout. In males, uric acid levels rise substantially at puberty. In about 5 - 8% of American men, levels exceed 7 mg/dL (indicating hyperuricemia). However, gout typically strikes after 20 - 40 years of persistent hyperuricemia, so men who develop it usually experience their first attack between the ages of 30 and 50.

Women. Before menopause, women have a significantly lower risk for gout than men, possibly because of the actions of estrogen. This female hormone appears to facilitate uric acid excretion by the kidneys. (Only about 15% of female gout cases occur before menopause.) After menopause the risk increases in women. At age 60 the incidence is equal in men and women, and after 80, gout occurs more often in women.

According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases, up to 18% of people with gout have a family history of the condition. Some people with a family history of gout have a defective protein (enzyme) that interferes with the way the body breaks down purines.

Researchers report a clear link between body weight and uric acid levels. In one Japanese study, overweight people had two to more than three times the rate of hyperuricemia as those who maintained a healthy weight. Children who are obese may have a higher risk for gout in adulthood.

Thiazide diuretics are "water pills" used to control hypertension. The drugs are strongly linked to the development of gout. In fact, 75% of patients who develop gout at an older age report the use of diuretics.

Several other medications can increase uric acid levels and raise your risk for gout. These include:

Aspirin -- low doses of aspirin reduce uric acid excretion and increase the chance for hyperuricemia. This may be a problem for older people who take baby aspirin (81 mg) to protect against heart disease.
Niacin (used to treat cholesterol problems)
Pyrazinamide (used to treat tuberculosis)

Drinking excessive amounts of alcohol can raise your risk of gout. Beer is the kind of alcohol most strongly linked with gout, followed by spirits. Moderate wine consumption does not appear to increase the risk of developing gout.

Alcohol use is highly associated with gout in younger adults. Binge drinking particularly increases uric acid levels. Alcohol appears to play less of a role among elderly patients, especially among women with gout.

Alcohol increases uric acid levels in the following three ways:

Providing an additional dietary source of purines (the compounds from which uric acid is formed)
Intensifying the body's production of uric acid
Interfering with the kidneys' ability to excrete uric acid

Chronic occupational exposure to lead is associated with build-up of uric acid and a high incidence of gout.

Kidney transplantation poses a high risk for renal insufficiency and gout. In addition, other transplantation procedures, such as heart and liver, increase the risk of gout. The procedure itself poses a risk of gout, as does the medication (cyclosporine) used to prevent rejection of the transplanted organ. Cyclosporine also interacts with indomethacin, a common gout treatment.

The kidneys are responsible for removing waste from the body, regulating electrolyte balance and blood pressure, and stimulating red blood cell production.

Treatment of several other conditions can cause significant elevations of uric acid in the blood, and therefore a gout attack. These conditions include:

Leukemia
Lymphoma
Psoriasis

Triggers

Triggers are events or conditions that can set off a gout attack. Certain risk factors, including a purine-rich diet, are also considered a trigger. Triggers include:

Joint injury
Overindulging in alcohol or purine-rich foods
Over-strenuous exercise
Severe illness or infection
Stress
Sudden weight loss
Surgery
Using certain drugs

Hot and humid weather may also be strongly associated with recurrent gout attacks. Such weather can cause sweating and, ultimately, dehydration, which has long been recognized as a potential trigger for gout attacks.

Drinking more water and fluids when it's warm outside could help persons with gout prevent future attacks.

Diagnosis

The first step in diagnosing the disease is to determine which joints are affected. A physical examination and medical history can help confirm or rule out gout. For example, gout is more likely if arthritis first appears in the big toe.

The speed of the onset of pain and swelling is also important. Symptoms that take days or weeks (rather than hours) to develop probably indicate a disorder other than gout.

Abnormal enlargements in joints that had been affected by previous injury or osteoarthritis are possible signs of gout. This is particularly significant in older women who take diuretics ("water pills").

A blood test is usually done to measure uric acid levels and detect hyperuricemia. A low level of uric acid in the blood makes a diagnosis of gout much less probable, and a very high level increases the likelihood of gout, especially if patient has symptoms of gout. Nevertheless, uric acid levels in the blood during an attack of gout can be within or below the normal range, and the presence of hyperuricemia does not necessarily mean someone has gout. However, most doctors feel that closer monitoring of blood uric acid levels in people with gout may help reduce gout flares.

Synovial fluid examination is the most accurate method for diagnosing gout. The synovial fluid is the lubricating liquid that fills the synovium (the membrane that surrounds a joint and creates a protective sac). The fluid cushions joints and supplies nutrients and oxygen to the cartilage surface that coats the bones. This exam also helps detect gout during intercritical periods.

The health care provider uses a needle attached to a syringe to draw out fluid from the affected joint. This is called aspiration. Local anesthesia is not used because it can reduce the effectiveness of the procedure. However, the procedure is usually only mildly uncomfortable. Afterwards, there can be some minor discomfort in the area where the needle was inserted, but it usually goes away quickly.

The fluid sample is sent to a laboratory for analysis. Testing can reveal the presence of monosodium urate (MSU) crystals, which will nearly always confirm a diagnosis of gout. The laboratory can also test the sample for infection.

The procedure itself can cause infection, though this occurs in less than 0.1% of patients. Aspiration sometimes eases the patient's symptoms by reducing swelling and pressure on the tissue surrounding the joint.

Synovial fluid analysis is a method to look at the fluid that cushions a joint. It is done to help diagnose and treat joint-related problems such as gout.

It is sometimes helpful to gauge the amount of uric acid found in a patient's urine, particularly if the patient is young and has pronounced hyperuricemia that might be related to a metabolic disorder. If uric acid in the urine exceeds a particular value, further tests for an enzyme defect or other identifiable cause of gout should be performed. Greater-than-normal amounts of uric acid in the urine also mean that the patient is more likely to develop uric acid kidney stones.

Typically, a 24-hour urine test is performed. The patient discards the first urination sample on the day of the test. Afterward all urine passed over the next 24 hours is collected into a special container, including the first urination on the morning of day two. The container is delivered to the patient's health care provider or sent directly to the laboratory.

The urine is collected during an intercritical period, after the patient has been placed on a purine-reduced diet. The patient is also asked to temporarily stop using alcohol and any medications that can interfere with the test. The patient should not change any of his or her usual eating or drinking patterns when performing this test.

Click the icon to see an image of a uric acid test.

X-Rays. For the most part, x-rays do not reveal any problems during the early stages of gout. Their usefulness lies in assessing the progress of the disorder in its chronic phase and identifying other health problems with symptoms similar to gout. Tophi can be seen on x-rays before they become apparent on physical examination.

Advanced Imaging Techniques. Advanced imaging techniques being investigated for identifying tophi include computed tomography (CT), magnetic resonance imaging (MRI), and Doppler ultrasonography.

As part of the diagnosis, other disorders that produce gout-like symptoms or cause hyperuricemia should be ruled out. In general, it is easy to distinguish acute gout that occurs in one joint from other arthritic conditions. The two disorders that may confuse this diagnosis are pseudogout and septic arthritis. Pseudogout is a condition most likely to be confused with gout.

Chronic gout can often resemble rheumatoid arthritis. Several other conditions may at some point in their course resemble gout.

Pseudogout (also called calcic gout and calcium pyrophosphate dihydrate deposition disease) is a common inflammatory arthritis among older adults. It is very similar to gout, but is caused by deposits of calcium pyrophosphate dihydrate crystals in and around the joints.

Although symptoms of pseudogout resemble gout in some ways, there are differences:

The first attack typically strikes the knee. Other joints commonly affected are the shoulders, wrists, and ankles. At least two-thirds of cases affect more than one joint during a first attack. Pseudogout may involve any joint, although the small joints in the fingers or toes are not commonly affected.
The symptoms of pseudogout also appear more slowly than those of gout, taking days rather than hours to develop.
Pseudogout is more likely to first develop in elderly people, particularly those with osteoarthritis. (It affects 10 - 15% of people over 65.)

Pseudogout is more likely to occur in the autumn while gout attacks are most common in the spring.

Conditions that are associated with a higher risk for pseudogout in elderly patients include underlying acute medical conditions, trauma, or surgery. Medical conditions associated with pseudogout include hypothyroidism, diabetes, gout, and osteoarthritis. Liver transplantation also may increase the risk.

There is no cure for pseudogout. It is a progressive disorder that can eventually destroy joints. Treatments for pseudogout are similar to those for gout and are aimed at relieving the pain and inflammation and reducing the frequency of attacks.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are effective for treating inflammation and pain from pseudogout.
For acute attacks in large joints, fluid aspiration alone or with corticosteroids may help.
Colchicine may be used for acute attacks.
Magnesium carbonate may help dissolve crystals, but existing hard deposits may remain.
Surgery may be required for joint replacement.

Rheumatoid Arthritis. Rheumatoid arthritis can distort the joints of the finger and cause inflammation and pain that may mimic gout. In older people, it is particularly difficult to distinguish chronic gout from rheumatoid arthritis. A proper diagnosis can be made with a detailed medical history, laboratory tests, and identification of MSU crystals.

Osteoarthritis. Gout can coincide and be confused with osteoarthritis in older people, particularly when it occurs in arthritic finger joints in women. In general, gout should be suspected if the joints in the fingertips are unusually enlarged.

Click the icon to see an image of osteoarthritis.

Infections. Joint infections can have features that resemble gout. A correct diagnosis is critical for appropriate treatment. For example, some cases of gout have been confused with infection after joint replacement. On the other hand, joint infection not associated with surgery might indicate sepsis, which is a widespread and potentially life-threatening bacterial infection that can cause inflamed joints, chills, and a spiking fever. The severity of the fever and a high white blood cell count in the joint fluid helps diagnose a septic infection, while urate crystals in the joint are a good indicator of gout.

Charcot Foot. Between 1 - 2.5% of people with diabetes have Charcot foot or Charcot joint (medically referred to as neuropathic arthropathy). This condition is caused by problems in the nerves in the feet. Early changes may resemble gout, with the foot becoming swollen, red, and warm. Recognition and treatment of this condition is very important. A seriously affected foot can become deformed. The bones may crack, splinter, and erode, and the joints may shift, change shape, and become unstable.

Bunions. A bunion is a foot deformity that usually occurs at the head of the first of five long bones (the metatarsal bones) that extend from the arch and connect to the toes, and may be confused with gout. The first metatarsal bone is the one that attaches to the big toe. A bunion begins to form when the big toe is forced in toward the rest of the toes, causing the head of the first metatarsal bone to jut out and rub against the side of the shoe. The underlying tissue becomes inflamed, and a painful bump forms. As this bony growth develops, the bunion is formed as the big toe is forced to grow at an increasing angle towards the rest of the toes.

Click the icon to see an illustrated series detailing bunion removal.


Disease	Specific Subtypes
Osteoarthritis
Infectious Arthritis	Lyme disease, septic arthritis, bacterial endocarditis, mycobacterial and fungal arthritis, viral arthritis, osteomyelitis
Postinfectious or Reactive Arthritis	Reiter syndrome (a disorder characterized by arthritis and inflammation in the eye and urinary tract), rheumatic fever, inflammatory bowel disease
Pseudogout
Rheumatic Autoimmune Diseases	Rheumatoid arthritis, systemic vasculitis, systemic lupus erythematosus, scleroderma, Still's disease (also called juvenile rheumatoid arthritis)
Fibromyalgia
Other Diseases	Chronic fatigue syndrome, hepatitis C, familial Mediterranean fever, cancers, AIDS, leukemia, bunions, Whipple's disease, dermatomyositis, Behcet's disease, Henoch-Schonlein purpura, Kawasaki's disease, erythema nodosum, erythema multiforme, pyoderma gangrenosum, pustular psoriasis

Treatment: Acute Gout Attack

Acute attacks of gout and long-term treatment of gout and hyperuricemia require different approaches. Treatment usually involves medication. After the first attack, some health care providers advise their patients to keep a supply of medications on hand so that self-medication can begin at the first sign of symptoms of a second acute attack. There are also specific treatments for conditions associated with gout, including uric acid nephropathy and uric acid nephrolithiasis.

Many patients do not require medications. During the period between gout attacks, patients are advised to avoid foods high in purines and to maintain a healthy weight. Patients should also avoid alcohol and reduce any stress.

Drug treatments for acute attacks of gout are aimed at relieving pain and reducing inflammation. They should be started as early as possible.

Medications used in the treatment of gout include:

NSAIDs (nonsteroidal anti-inflammatory drugs)
Colchicine
Corticosteroids

Powerful forms of nonsteroidal anti-inflammatory drugs (NSAIDs) are the drugs of choice for an acute attack in younger, healthy patients with no serious health problems, particularly problems that affect the kidneys, liver, or heart. Usually indomethacin is prescribed for 2 - 7 days.

There are dozens of NSAIDs available. Over-the-counter NSAIDs include:

Low-dose Ibuprofen (Motrin IB, Advil, Nuprin)
Naproxen (Aleve)
Ketoprofen (Actron, Orudis KT)

Prescription NSAIDs include:

Ibuprofen (Motrin)
Naproxen (Naprosyn, Anaprox)
Flurbiprofen (Ansaid)
Diclofenac (Voltaren)
Tolmetin (Tolectin)
Ketoprofen (Orudis, Oruvail)
Dexibuprofen (Seractil)
Indomethacin (Indocin)

Indomethacin (Indocin) is typically the first choice of treatment for patients who have no medical conditions that would interfere with its use. Usually 2 - 7 days of high-dose indomethacin is enough to treat a gout attack. The first dose of indomethacin usually begins to act against the pain and inflammation within 24 hours and often much sooner.

Ibuprofen, naproxen, sulindac, or NSAIDs are good alternatives, particularly for elderly patients who might experience confusion or bizarre sensations with indomethacin. (Aspirin is an NSAID, but is associated with a higher risk for gout and should be avoided.)

Regular use of even over-the-counter NSAIDs can cause certain health problems, such as:

Ulcers and gastrointestinal bleeding
Increased blood pressure -- people with hypertension, severe vascular disease, kidney, or liver problems and those taking diuretics must be closely monitored if they need to take NSAIDs.
Delayed emptying of the stomach, which could interfere with the actions of other drugs. The elderly are at special risk.
Dizziness
Tinnitus (ringing in the ear)
Headache
Skin rash
Depression
Confusion or bizarre sensation (in some higher-potency NSAIDs, notably indomethacin)
Kidney damage

NSAIDs can cause kidney problems, especially in the elderly and those with kidney disease. When caught early enough, these problems generally resolve if the drugs are stopped. Any sudden weight gain or swelling should be reported to a physician. Anyone with kidney disease should avoid these drugs.

Patients with diabetes who take hypoglycemics by mouth may need to adjust their medication dosage if they also take NSAIDs, because of possible harmful interactions between these classes of drugs.

Some studies reported that ibuprofen (but not other NSAIDs) may reduce the heart-protective effects of low-dose aspirin. Additional research is needed to confirm these findings.

Long-term use of NSAIDs is a common cause of ulcers. NSAID-related bleeding and stomach problems may be responsible for over 100,000 hospital admissions and over 15,000 deaths each year. Because there are usually no gastrointestinal symptoms from NSAIDs until bleeding begins, health care providers cannot predict which patients taking these drugs will develop bleeding.

Those at high risk for NSAID-related bleeding include the elderly, anyone with a history of an ulcer or gastrointestinal bleeding, patients with serious heart conditions, those who drink too much alcohol, and persons on certain medications, such anticoagulants (blood thinners), corticosteroids, or bisphosphonates (drugs used for osteoporosis).

Preventing NSAID-Related Ulcers. Switching to alternative pain relievers is the first step in preventing or healing ulcers caused by NSAIDs. If people cannot change drugs, they should use the lowest NSAID dose possible.

In addition, medications are available that may help prevent ulcers in people who need to take NSAIDs. Proton-pump inhibitors (PPIs) are the first drug of choice for preventing ulcers in high-risk individuals. They have been shown to reduce NSAID-ulcer rates by as much as 80% compared with no treatment. Types of these drugs include omeprazole (Prilosec), esomeprazole (Nexium), lansoprazole (Prevacid), rabeprazole (AcipHex ), and pantoprazole (Protonix). Prevacid is the first proton-pump inhibitor specifically approved for protecting against ulcers in chronic NSAID users.

Arthrotec is a combination of an ulcer-protective drug called misoprostol and the NSAID diclofenac. It too may reduce the risk for gastrointestinal bleeding.

Colchicine is a derivative of the autumn crocus (also called the meadow saffron). It has been used against gout attacks for centuries. It is highly effective, although it is no longer the first drug of choice because of its frequent, unpleasant, and sometimes very serious side effects.

Colchicine may be given to a healthy adult within 48 hours of an attack. It should not be used by elderly patients or those with kidney, liver, or bone marrow disorders. It can also affect fertility and should not be used during pregnancy. The drug can cause gastrointestinal side effects at high dose, including nausea, vomiting, diarrhea, and abdominal cramps. Low doses do not pose as high a risk for gastrointestinal symptoms, and can prevent further attacks, including attacks in patients who are starting anti-hyperuricemic therapies.

Colchicine may be taken by mouth or given by an intravenous line. Those who take it by mouth need doses every hour until either symptoms improve or side effects develop. Improvement should be seen by the tenth dose. It usually eliminates the pain of an acute attack within 48 hours. The intravenous route has some serious side effects, however, and poses an increased risk for injury to the kidney, liver, central nervous system, and bone marrow.

The antibiotic erythromycin, or H2 blockers such as famotidine (Pepcid AC), cimetidine (Tagamet), or ranitidine (Zantac) may intensify the gastrointestinal side effects of colchicine.

Warning Note: Overdose of colchicine can be dangerous, and there have even been reports of death. The drug may also suppress blood cell production and cause nerve and muscular injury in certain people, sometimes even in those not taking high doses.

Corticosteroids may be used in patients who cannot tolerate NSAIDs and they may be particularly beneficial for elderly patients. Injections into an affected joint provide effective relief for many patients, but this is not useful for patients who have multiple affected joints. Steroids taken by mouth may be used for patients who cannot take NSAIDs or colchicine and who have gout in more than one joint. Corticosteroids include triamcinolone and prednisone.

Treatment: Preventing Attacks

After an acute attack some patients remain at high risk for another attack for several weeks during the intercritical period. Such patients include those with kidney insufficiency or those with congestive heart failure who are on diuretics. Low doses of colchicine or NSAIDs may be used to during this period for prevention of another attack. They should be taken in low doses for 1 - 2 months after an attack, or for longer periods in patients who have experienced frequent attacks.

Antihyperuricemic medications reduce levels of uric acid in the body. The decision whether to use an antihyperuricemic medicine and at what point is not entirely clear. Some health care providers do not prescribe them if hyperuricemia is mild, or until a patient has had two gout attacks. Others prescribe them immediately after a single attack. Most of the time, antihyperuricemic therapy means taking a drug routinely throughout life, which many people find difficult.

Experts do not recommend treatment for hyperuricemia that causes no symptoms. Asymptomatic hyperuricemia often does not lead to gout or other health problems. In addition, the drugs used to treat it are expensive and carry certain risks. In unusual circumstances treatment may be justified, for example in patients with very high uric acid levels that threaten the kidney or those with a personal or strong family history of gout, kidney stones, or kidney damage.

Before treatment, some experts recommend a 24-hour urine collection sample in patients with frequent gout attacks to determine whether they are over-producers or under-excreters of uric acid. Also, before starting one of these drugs, any previous acute attack should be completely controlled and the joints should not be inflamed. Some health care providers prefer to wait about a month after an attack.

Low doses of NSAIDs or colchicine are used during several months after introducing anti-hyperuricemic therapies to prevent gout attacks. It should be noted that NSAIDs, particularly aspirin and similar drugs, reduce the effectiveness of uricosurics. These are drugs given to under-excreters of uric acid (see below). Patients taking uricosurics should avoid NSAIDs, if possible.

Long-term treatment of hyperuricemia may be recommended for people who have:

A risk for tophaceous gout
Had more than two or three acute attacks of gout in the past
Unusually severe attacks, or attacks that affect more than one joint
Joint damage from gout, as shown on x-rays
Hyperuricemia caused by an identifiable inborn metabolic deficiency

Uricosurics. These drugs prevent the kidney from reabsorbing uric acid, and therefore increase the amount excreted in the urine. They are appropriate when gout is caused by under-excretion of uric acid, which occurs in about 80% of gout cases. They are not used for patients with reduced kidney function or those with tophaceous gout. Uricosurics are usually the choice for preventing gout in the following patients:

Those under 60 years of age
Those with normal diets
Those who have normal kidney function
Those who have no risk of kidney stones

Uricosuric drug candidates should produce no more than 700 - 800 mg of uric acid in the urine over a 24-hour period.

Probenecid (Benemid, Probalan) and sulfinpyrazone (Anturane) are the standard uricosurics. A more potent uricosuric, benzbromarone, may work for people with severe tophaceous gout and kidney impairment when other drugs do not. In some studies, benzbromarone was equal to or even more effective than allopurinol, another type of antihyperuricemic drug. Because benzbromarone can cause liver failure in some patients, it is available in the U.S. only with special authorization. A uricosuric combined with allopurinol may be beneficial in some cases.

Probenecid is taken two to three times a day, and sulfinpyrazone begins at twice a day and increases to three or four times daily. The initial doses should be low and gradually increased. Probenecid combined with colchicine is more effective than probenecid alone, but everyone responds differently, so the dose should be carefully individualized.

The possible side effects of probenecid and sulfinpyrazone include skin rashes, gastrointestinal problems, anemia, and kidney stone formation. To help reduce acidity and the risk for kidney stones, patients should drink plenty of fluids (ideally water, not caffeinated beverages). Sodium bicarbonate supplemented by acetazolamide can also reduce acidity and the risk for stones.

NSAIDs, particularly aspirin, as well as other salicylate drugs, interfere with uricosuric drugs and reduce effectiveness. Patients who require minor pain relief should instead take acetaminophen (Tylenol). Uricosurics interact with many other drugs, and a patient should be sure to inform their health care provider of all medications they are taking.

People who take these drugs should have normal kidney function. This therapy may not be as beneficial in many elderly patients, who often have some kidney insufficiency.

Allopurinol (Lopurin, Zyloprim). Allopurinol blocks uric acid production. It is the drug most often used in long-term gout treatment for older patients and those who overproduce uric acid.

Allopurinol is taken by mouth once a day in doses of 100 - 600 mg, depending on the patient's response to treatment. When it is first used, allopurinol can trigger further attacks of gout. Therefore, during the first months (or longer) of therapy, the patient also takes an NSAID or colchicine to reduce that possibility.

Allopurinol has positive effects on "bad" cholesterol levels, so it may be better than other drugs for patients with both gout and coronary artery disease.

Side effects, which can be severe, include:

Rash
Diarrhea
Headache
Fever
Leukopenia (a reduction in the number of white blood cells)
Thrombocytopenia (a reduction in the number of platelets)
Cataracts

In rare cases, the rash can become severe and widespread enough to be life threatening (this condition is called toxic epidermal necrolysis, or TEN). Allergic individuals who experience only a mild rash may be able to build up their tolerance for the drug by undergoing a desensitization process.

Allopurinol interacts with certain other drugs, such as azathioprine.

Puricase (PEG-Uricase). This is an experimental drug that has been shown to rapidly reduce excess uric acid. If approved, it may help those who have failed other treatments.

It should be noted that many drugs used for gout can also precipitate acute gout symptoms and so should not be used until symptoms have subsided. The patient should then start treatment with small doses that gradually increase.

Hypertensive Agents. People with gout have a higher risk for high blood pressure. Some of the drugs used to treat hypertension, such as thiazide diuretics, can increase the risk for gout attacks. Newer agents, such as losartan (an angiotensin II receptor antagonist), and amlodipine (a calcium channel blocker), may have beneficial effects on both high blood pressure and gout.

Febuxostat. Febuxostat is the first drug to emerge in many decades as a potential new treatment for chronic gout. It may prove to be an alternative for patients who are allergic to allopurinol. The drug is awaiting approval from the U.S. Food and Drug Administration (FDA).

Other Treatments

Surgery. Large tophi that are draining, infected, or interfering with the movement of joints may need to be surgically removed. When infection is present, the procedure carries a high risk for complications. People most likely to have surgery also tend to have other medical conditions that might worsen their outlook. In one study, experts suggested that better preventive measures, such as the use of allopurinol, could reduce the need for surgery.

Several other surgical procedures are available for relieving pain and improving the function of affected joints. It is sometimes necessary to replace joints.

Hot and Cold Therapy. Rest and protecting the affected joint with a splint can also promote recovery. One study reported that applying ice packs for 30 minutes four times daily significantly reduced pain. However, a different study recommended applying warm water continuously and moving the joint. The theory behind this advice was that the pain in a gout attack is due to grinding from the crystals and that warmth would help dissolve the crystals and relieve pain.

Lifestyle Changes

Any activities that increase energy demands on the body also increase metabolism of purines, which produces uric acid. Avoiding stress and staying healthy are important for the prevention of attacks.

Because uric acid levels are only mildly affected by diet, dietary therapy does not play a large role in the prevention of gout. Still, people who have had an attack of gout may benefit from reducing their intake of purine-rich foods, particularly if they eat unusually large quantities of such foods.

While meat and certain types of seafood and shellfish do produce high levels of purines in the blood, research has suggested that not all purine-rich foods are associated with gout. Eating a moderate amount of purine-rich vegetables (spinach, cauliflower, mushrooms, legumes) does not appear to increase the risk of gout.

Dairy products, especially low-fat products (low-fat yogurt and skim milk), may actually protect against gout. Researchers have also found that taking 500 mg a day of vitamin C significantly reduces uric acid levels. They are investigating whether vitamin C can be used to prevent or treat gout.

Foods to Avoid:

Organ meats (liver, kidneys, sweetbreads)
Red meat (beef, pork, lamb)
Meat extracts (soup, broth, gravies)
Seafood (anchovies, sardines, herring, fish roe, canned tuna fish, shrimp, lobster, scallops, mussels)
Yeast products (beer and baked goods)

A supervised weight-loss program may be a very effective way to reduce uric acid levels in overweight patients. Crash dieting, on the other hand, is counterproductive because it can increase uric acid levels and may cause an acute attack.

Drinking plenty of water and other nonalcoholic beverages helps remove MSU crystals from the body.

Alcohol should be avoided, since it promotes purine metabolism and uric acid production. It also may reduce excretion of uric acid. Heavy drinking, especially binge drinking of beer or distilled spirits, should be avoided.

People with gout should also attempt to avoid activities that cause repetitive joint trauma, such as wearing tight shoes.

Travel is an example of an activity that increases the risk for gout. It not only increases stress, but eating and drinking patterns may change. Before traveling, patients should discuss preventive measures with their health care providers. The doctor may prescribe a prednisone tablet to be taken immediately at the first sign of a gout attack. In most cases, this stops the episode.

Complications

Properly treated gout rarely poses a long-term health threat, though it can be a cause of short-term pain and incapacity for thousands of Americans.

Left untreated, gout can develop into a painful and disabling chronic disorder. Persistent gout can destroy cartilage and bone, causing irreversible joint deformities and loss of motion. Survey results released in 2006 show that two-thirds of persons with gout consider the pain of attacks among the worst they've ever experienced. An estimated 75% of those surveyed said flare-ups made walking very difficult, and about 70% reported trouble putting on shoes or playing sports.

Tophi are firm chalky, gritty clumps of uric acid crystals that build up in tissue surrounding a joint. If gout is not treated, tophi can grow to the size of golf balls and can destroy bone and cartilage in the joints, similar to the process in rheumatoid arthritis. If they lodge in the spine, tophi can cause serious damage including compression, although this is very rare. In extreme cases, joint destruction results in complete disability.

Kidney Stones. Kidney stones occur in 10 - 40% of gout patients, and can occur at any time after the development of hyperuricemia. Although the stones are usually composed of uric acid, they may also be mixed with other materials.

Kidney stones result when urine becomes too concentrated, and substances in the urine crystallize to form stones. Symptoms occur when the stones begin to move down the ureter and cause intense pain. Kidney stones may form in the pelvis or calyces of the kidney or in the ureter.

Kidney Disease. About 25% of patients with chronic hyperuricemia develop progressive kidney disease, which sometimes ends in kidney failure. It should be noted, however, that many experts believe that chronic hyperuricemia is unlikely to be a common cause of kidney disease. In most cases, the kidney disease comes first and causes high concentrations of uric acid.

Gout is found in higher rates in people with high blood pressure, coronary artery disease, and heart failure. Hyperuricemia, in fact, has been associated with a higher risk of death from heart conditions. A large study published in 2007 found an association between gout and having the metabolic syndrome -- a collection of problems, such as abdominal obesity, high blood pressure, high triglycerides levels, and low "good" cholesterol levels. This syndrome increases a person's risk of heart disease and diabetes.

A study published in the August 2006 journal Arthritis & Rheumatism found that gout increases the risk of heart attacks in men with no previous history of heart problems. According to some studies, hyperuricemia may be associated with heart disease, but there is not enough data to confirm such an association.

Click the icon to see an image of coronary artery blockage.

The following are some conditions that are associated with long-term gout:

Cataracts
Dry eye syndrome
Complications in the lungs (in rare cases, uric acid crystals occur in the lungs)

Resources

www.niams.nih.gov -- National Institute of Arthritis and Musculoskeletal and Skin Diseases
www.rheumatology.org -- American College of Rheumatology
www.arthritis.org -- The Arthritis Foundation
www.gouteducation.org -- The Gout & Uric Acid Education Society

References

Choi HK, Ford ES, Li C, Curhan G. Prevalence of the metabolic syndrome in patients with gout: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2007;57(1):109-15.

Huang HY, Appel LJ, Choi MJ et al. The effects of vitamin C supplementation on serum concentrations of uric acid: results of a randomized controlled trial. Arthritis Rheum. 2005 Jun;52(6):1843-7.

Krishnan E, Baker JF, Furst DE, Schumacher HR. Gout and the risk of acute myocardial infarction. Arthritis Rheum. 2006 Aug;54(:2688-96.

Underwood M. Diagnosis and management of gout. BMJ. 2006;332(7553):1315-9.

Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65(10):1301-11.

Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65(10):1312-24.

Zhang YQ, Chaisson CE, Chen CA, McAlindon TE, Hunter DJ. High Humidity and High Temperature Increase the Risk of Recurrent Gout Attacks: The Online Case-crossover Gout Study. Presentation Number 707. American College of Rheumatology Annual Scientific Meeting, Washington, DC, November 2006.

Review Date:
1/21/2008
Reviewed By:
Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

A.D.A.M., Inc. is accredited by URAC, also known as the American Accreditation HealthCare Commission (www.urac.org). URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. A.D.A.M. is among the first to achieve this important distinction for online health information and services. Learn more about A.D.A.M.'s editorial policy, editorial process and privacy policy. A.D.A.M. is also a founding member of Hi-Ethics and subscribes to the principles of the Health on the Net Foundation (www.hon.ch).

A.D.A.M. Copyright

The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. © 1997-2009 A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.

adam.com

Anne Hathaway Drinks Thermo Bubbles to Boost Fat Burning

FitSugar — Tue, 10 Feb 2009 11:00:00 -0800

Hollywood is getting ready for the Oscars, and Us Weekly is making us privy to celebs' red-carpet secrets. Among their arsenal of tricks is trainer David Kirsch's Thermo Bubbles ($40 for 10 servings). Supposedly Anne Hathaway, among other actresses and models, partake in this herbal drink that claims to "melt away the fat naturally" along with boosting energy and metabolism levels.

Each 16-oz. serving contains 10 calories with no added sugar. Its ingredients are white tea, guarana (which makes the list of a prominent cardiologist's dangerous diet supplements), ginseng, and green tea. The energy boost probably comes from the caffeine in the green tea. Drinking this fizzy beverage, made from powder you add to water, is said to curb appetites, and the website claims Thermo Bubbles won't give you the jitters or make you crash like coffee or other energy drinks can.

To find out if this can help you lose weight read more.

I don't believe this is the magic pill to make fat melt away, and I am not a fan of appetite suppressants. Your body needs calories to burn in order to function. Kirsch recommends drinking his bubbly twice a day, making this an expensive habit - well over $50 a week. But what happens when you stop drinking it? Will your raging appetite return? The best way to lose weight is to exercise and limit your calorie intake under the amount of calories you're burning, without dipping under 1200 calories a day. Why not just drink some green tea, which is considerably cheaper and offers a bevy of health benefits? Or try these five foods to boost your metabolism.

Source

Restless legs syndrome and related disorders

FitSugar — Wed, 08 Oct 2008 17:35:14 -0700

In This Report

Highlights
Introduction
Causes
Risk Factors
Complications
Diagnosis
Treatment
Medications
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Treatment

The American Academy of Sleep Medicine recommends medications for restless legs syndrome (RLS) or periodic limb movement disorder (PLMD) only for persons who fulfill strict diagnostic criteria and experience too much daytime sleepiness as a result of these conditions. (Excessive daytime sleepiness results from nighttime sleeplessness due to RLS or PLMD symptoms).
The U.S. Food and Drug Administration (FDA) announced in March 2007 that the dopamine agonist drug pergolide (Permax) has been voluntarily withdrawn from the market. This drug can cause serious damage to the heart valves of patients who take it.
The FDA approved pramipexole (Mirapex) for use in moderate-to-severe restless legs syndrome (RLS) in November 2006.
Bupropion (Wellbutrin), a newer antidepressant, may also be helpful for RLS. Bupropion, a weak dopamine reuptake inhibitor, causes a slight increase in the availability of dopamine in the brain. It is not addictive and does not have the severe side effects of other RLS drugs, but more research is needed to determine its usefulness. It is not FDA approved for RLS.

Research

Results from a large study show that RLS is more common in children and teens than epilepsy and diabetes. The study also found that more than 70% of affected children had at least one biological parent with RLS.
Two recently-published studies found an abnormal gene on chromosome 6 makes some people susceptible to RLS and PLMD.
People with type 2 diabetes have higher rates of secondary RLS. Nerve pain (neuropathy) related to their diabetes cannot fully explain this increased rate in RLS.

Introduction

Restless legs syndrome (RLS) is an unsettling and poorly understood movement disorder affecting 3 - 15% of the general population. RLS can affect both children and adults. Although effective treatments are available, the condition often remains undiagnosed.

Symptoms of RLS. The core symptom of RLS is an irresistible urge to move the legs (medically known as akathisia). Some people describe this symptom as a sense of unease and weariness in the lower leg, which is aggravated by rest and relieved by movement. Specific characteristics of RLS include:

"Pulling, searing, drawing, tingling, bubbling, or crawling" beneath the skin, usually in the calf area, causing an irresistible urge to move the legs. These sensations can occur not only in the lower legs, but they can also affect the thighs, feet, and even the upper body. RLS-type symptoms may also occur in the arms. This may be the first symptom of RLS in some people.
About 80% of patients with RLS also experience semi-rhythmic movements called periodic limb movement disorder (PLMD).
Itching and pain, particularly aching pain, may be present.
Patients experience symptoms when they feel most relaxed and their legs are at rest. (Movement, however, brings relief.) Symptoms usually occur at night when lying down, or sometimes during the day while sitting.
Episodes of RLS usually develop between 10 p.m. and 4 a.m. Symptoms are often most severe shortly after midnight. They typically occur for 30 - 60 seconds, and they usually resolve by morning. If the condition becomes more severe, people may begin to have symptoms during the day. These symptoms are always worse at night, however.
At night, the unpleasant sensations and the resulting uncontrollable urge to move the legs can often disturb sleep. Ignoring the need to move the legs usually only builds up tension until they jerk uncontrollably. If patients experience symptoms during the day, they usually feel compelled to move their legs in order to relieve the symptoms, making it difficult to sit during air or car travel or through classes or meetings.

Late-onset and Early-onset Forms. There appear to be two forms of RLS, early-onset and late-onset. Each form may have different characteristics:

People with early-onset RLS (occurring in the teenage years or earlier) tend to have a family history of the disorder. They also usually have RLS without accompanying pain.
Those with late-onset RLS usually do not have a family history of RLS. Their condition is more likely the result of a problem with the nervous system, and symptoms may include pain in the lower legs.

The medical term for periodic limb movement disorder (PLMD) is nocturnal myoclonus. PLMD symptoms include:

Episodes that usually occur during the night, peaking near midnight, as they do in restless legs syndrome (RLS).
Leg muscles contract and jerk every 20 - 40 seconds during sleep. Such movements may last less than 1 second, or as long as 10 seconds.
Unlike RLS, contractions in PLMD usually do not wake patients. PLMD is distinct from the brief and sudden movements that occur just as people are falling asleep, jolting them awake.

Although 80% of RLS sufferers have PLMD, only about 30% of people with PLMD also have RLS. While treatments for the two conditions are similar, PLMD is a separate syndrome. PLMD is also very common in narcolepsy, a sleep disorder that causes people to fall asleep suddenly and uncontrollably.

Cramps that awaken people during sleep are very common, and they are not part of restless legs syndrome or periodic limb movement disorder. They can be very painful and may cause a person jump out of bed in the middle of the night. They typically affect a specific area of the calf or the sole of the foot.

Circadian Rhythm. In sleep studies, subjects spend about one-third of their time asleep, suggesting that most people need about 8 hours of sleep each day. However, individual adults differ in the amount of sleep they need to feel well rested. Infants may sleep as many as 16 hours a day.

The daily cycle of life, which includes sleeping and waking, is called a circadian rhythm (circadian means "about a day"), or the biological clock. Hundreds of bodily functions follow biologic clocks, but sleeping and waking comprise the most prominent circadian rhythm. The sleeping and waking cycle is about 24 hours long. If confined to windowless apartments, with no clocks or other time cues, sleeping and waking only as their bodies dictate, humans typically live on slightly longer than 24-hour cycles.

The circadian rhythm usually takes the following daily patterns:

Humans prefer daytime activity and nighttime rest.
A natural peak in sleepiness occurs at mid-day, the traditional siesta time.
Daily rhythms interact with other factors that may interfere or change individual patterns:
- The fraction-of-a-second-firing of nerve cells in the brain may be faster or slower in different individuals.
- The monthly menstrual cycle in women can shift the pattern.

Light signals coming through the eyes reset the circadian cycles each day, so changes in season, or changes in exposures to light and dark, can unsettle the pattern.

The Response in the Brain to Light Signals. The brain's response to light signals is an important key factor in sleep:

Light signals travel to a tiny cluster of nerves in the hypothalamus (in the center of the brain). This cluster is the body's master clock, which is called the supra chiasmatic nucleus (SCN). The SCN is named for its location, which is just above (supra) the optic chiasm, a major junction where nerves transmit information about light from the eyes.
The approach of dusk each day prompts the SCN to signal the nearby pineal gland (named so because it resembles a pinecone) to produce the hormone melatonin.
Researchers think that melatonin acts as the body's time-setting hormone. It also appears to trigger the need to sleep. The longer a person is in darkness, the longer the duration of melatonin secretion. Staying in bright light can decrease the secretion of melatonin.

Sleep consists of two distinct states that alternate in cycles, and reflect differing levels of brain nerve cell activity:

Non-Rapid Eye Movement Sleep. Non-rapid eye movement (NREM) sleep is also called quiet sleep. NREM is further subdivided into three stages of progression:

Stage 1: Light sleep
Stage 2: "True" sleep
Stage 3 to 4: Deep "slow-wave" or delta sleep

With each ascending stage, awakening becomes more difficult. It is not clear what governs NREM sleep in the brain. A balance between certain hormones, particularly growth and stress hormones, may be important for deep sleep.

Rapid Eye-Movement Sleep. Rapid eye-movement (REM) sleep is also called active sleep. Most vivid dreams occur in REM sleep. Brain activity in REM sleep is comparable to that in waking, but the muscles are virtually paralyzed, possibly preventing people from acting out their dreams. Except for vital organs like the lungs and heart, the only muscles not paralyzed during REM sleep are the eye muscles. REM sleep may be critical for learning and for day-to-day mood regulation. When people are sleep-deprived, their brains must work harder than when they are well rested.

The REM/NREM Cycle. The cycle between quiet and active sleep generally follows this pattern:

After about 90 minutes of NREM sleep, eyes move rapidly behind closed lids, giving rise to REM sleep.
As sleep progresses the NREM/REM cycle repeats.
With each cycle, NREM sleep becomes progressively lighter, and REM sleep becomes progressively longer, lasting from a few minutes early in sleep to perhaps an hour at the end of the sleep cycle.

The hypothalamus is a highly complex structure in the brain that regulates many important brain chemicals. Malfunction of this area of the brain may give rise to cluster headaches.

Causes

The main cause of restless legs syndrome (RLS) is unknown. Researchers are investigating neurologic (nervous system) problems that may arise either in the spinal cord or the brain. One current theory suggests that a deficiency in a brain chemical called dopamine causes restless legs syndrome.

RLS may often have a genetic basis, particularly in those who develop it before age 40. When the condition occurs in older adults, it is most likely due to a neurological problem.

The central nervous system is comprised of the brain and spinal cord. The peripheral nervous system includes all peripheral nerves.

People with restless legs syndrome (RLS) often have a family history of the disorder. Researchers have detected specific genetic locations or factors that might be responsible for this condition. Much of the research comes from studies of families with a strong history of RLS-related conditions. In 2005, researchers linked a location on chromosome 12 to RLS. They named this genetic marker RLS1. Locations on chromosomes 14 and 9 may also be associated with hereditary forms of RLS.

Dopamine and Neurologic Abnormalities in the Brain. Some research suggests that neurologic abnormalities involved with restless legs syndrome (RLS) and periodic limb movement disorder (PLMD) start in the brain. A variety of studies support the theory that an imbalance in neurotransmitters (chemical messengers in the brain), notably dopamine and serotonin, may play a part in RLS. Dopamine and serotonin cause numerous nerve impulses that affect muscle movement. The effect is similar to what happens in Parkinson's disease. Moreover, drugs that increase dopamine levels treat both disorders. However, Parkinson's disease itself does not seem to increase the risk for RLS. Nor does RLS early in life predispose to Parkinson's later on.

Neurologic Abnormalities in the Spine. Other research suggests that restless legs syndrome may be due to nerve impairment in the spinal cord. Researchers considered that such abnormalities were likely to start in nerve pathways in the lower spine. However, some patients with RLS have symptoms in the arms, indicating that the upper spine may also be involved.

Neuropathy. Some experts suggest that RLS, particularly if it occurs in older adults, may be a form of neuropathy, which is an abnormality in the nervous system outside the spine and brain. Nevertheless, there is no evidence of a causal relationship.

Iron deficiency, even at a level too mild to cause anemia, has been linked to restless legs syndrome (RLS) in some people. Studies suggest, in fact, that RLS in some people may be due to a problem with getting iron into cells that regulate dopamine in the brain. Some studies have reported RLS in 25 - 30% of people with low iron levels. The common connection between RLS and Parkinson's disease, in turn, may be not having enough iron in these patients.

The cause or causes of periodic limb movement disorder (PLMD) are not clear. Some research suggests that it may be due to abnormalities in the autonomic nervous system, which regulates the involuntary actions of the smooth muscles, heart, and glands.

Risk Factors

Restless legs syndrome (RLS) may affect 2.5 - 15% of the general population. It is more common in women than in men, and its frequency increases with age. The disorder affects an estimated 10 - 28% of adults older than age 65. In about 40% of patients, RLS begins in adolescence.

RLS may be more common than epilepsy and diabetes in children and teens. More than 70% of affected children in one study had at least one biological parent with RLS.

As many as two-thirds of people with restless legs syndrome (RLS) have a family history of the disorder. If so, RLS is more likely to occur before they turn 40. (A family history of RLS is less likely in people who develop it as older adults.) RLS is also more common in people from northern and western Europe, giving added support for a genetic basis for some cases.

Restless legs syndrome (RLS) and periodic leg movement disorder (PLMD) in children are strongly associated with inattention and hyperactivity. One study suggested that a quarter of children diagnosed with attention-deficit hyperactivity disorder (ADHD) also have RLS or PLMD, and this may actually contribute to inattentiveness and hyperactivity. The disorders have much in common, including poor sleep habits, twitching, and the need to get up suddenly and walk about frequently. Some evidence suggests that the link between the diseases may be a deficiency in the brain chemical dopamine.

About 20% of pregnant women report having restless legs syndrome (RLS). The condition usually goes away about a month after delivery. RLS in this population has been strongly associated with deficiencies in iron and the B vitamin folate.

Between 20 - 62% of people undergoing dialysis report restless legs syndrome. Symptoms often disappear after a kidney transplant.

Anxiety can cause restlessness and agitation at night. These symptoms can cause (or strongly resemble) restless legs syndrome.

The following medical conditions are also associated with restless legs syndrome (RLS), although the relationships are not clear. In some cases, these conditions may contribute to RLS, or they may have a common cause. In some cases, they may coexist due to other risk factors:

Osteoarthritis (degenerative joint disease). About 72% of patients with RLS also have osteoarthritis, a common type of arthritis affecting mostly older adults.
Varicose veins. Varicose veins occur in 14% of patients with RLS. Sclerotherapy treatments, in which doctors inject medications into affected veins, may relieve symptoms in such cases.
Obesity
Diabetes -- people with type 2 diabetes may have higher rates of secondary RLS. Nerve pain (neuropathy) related to their diabetes cannot fully explain this increased rate in RLS.
Hypertension
Hypothyroidism (a condition in which the thyroid gland does not make enough hormones)
Fibromyalgia (chronic pain of unknown cause)
Rheumatoid arthritis
Emphysema (a lung disease usually caused by smoking)
Chronic alcoholism
Sleep apnea (pauses in breathing during sleep) and snoring
Chronic headaches
Brain or spinal injuries

Many muscle and nerve disorders. Hereditary ataxia, a group of genetic diseases that affects the central nervous system and causes loss of motor control, is of particular interest. Researchers believe that hereditary ataxia may supply clues to the genetic causes of RLS.

Osteoarthritis is a chronic disease of the joint cartilage and bone, often thought to result from "wear and tear" on a joint, although there are other causes such as congenital defects, trauma, and metabolic disorders. Joints appear larger, are stiff and painful, and usually feel worse the more they are used throughout the day.

Click the icon to see an image of hypothyroidism.

Click the icon to see an image of fibromyalgia.

Click the icon to see an image of rheumatoid arthritis.

Click the icon to see an image of emphysema.

Several environmental and dietary factors can worsen or provoke restless legs syndrome (RLS):

Iron deficiencies. People who are deficient in iron are at risk for restless legs syndrome, even if they do not have anemia
Folic acid or magnesium deficiencies
Smoking
Alcohol abuse
Caffeine (coffee drinking is specifically associated with PLMD)
Stress
Fatigue
Prolonged exposure to cold

Drugs that worsen or provoke the condition include:

Antidepressants
Antipsychotic drugs
Anti-nausea drugs
Beta-blockers (a type of heart medication)
Antihistamines
Oral decongestants
Diuretics
Asthma drugs
Spinal anesthesia (anesthesia-induced restless legs syndrome typically disappears on its own within several months)

About 6% of the general population has periodic limb movement disorder (PLMD). Among the elderly, the prevalence increases to 25 - 58%. Studies suggest that PLMD may be especially common in elderly women. As with RLS, numerous conditions are associated with PLMD. They include sleep apnea, spinal cord injuries, stroke, narcolepsy, and diseases that destroy nerves or the brain over time. Certain medications, including some antidepressants and anti-seizure medications, may also contribute to PLMD.

Complications

Restless legs syndrome rarely results in any serious consequences. But in some cases, severe and persistent symptoms can cause considerable mental distress, chronic insomnia, and daytime sleepiness.

Sleep deprivation, and the daytime sleepiness that follows, is increasingly recognized as a cause of mood disruption and a contributor to industrial errors and motor vehicle crashes.

Effect on Daily Performance and Activities. Studies suggest that sleeplessness worsens many waking behaviors. These include:

Reduced concentration. Deep sleep deprivation appears to impair the brain's ability to process information.
Impaired task performance. Missing several hours of nightly sleep over the course of a week can negatively affect performance levels and mood. In fact, sleep deprivation can cause impaired performance levels comparable to those of intoxicated people.
Effect on learning. Whether sleeplessness significantly impairs learning is unclear. Some studies have reported problems in memorization, although others have found no differences in test scores between people with temporary sleep loss and those with full sleep.

In addition, since restless legs syndrome (RLS) is worse when resting, people with severe RLS may avoid daily activities that involve long periods of sitting, such as going to movies or traveling long distances.

Studies in Swedish working-aged men and women reported that those with restless legs syndrome (RLS) were more apt to be socially isolated, to have frequent daytime headaches or depression, and to complain of reduced libido or problems related to sleepiness.

RLS can contribute to insomnia. Insomnia itself can increase the activity of hormones and pathways in the brain that produce emotional problems. Even modest alterations in waking and sleeping patterns can have significant effects on a person's mood. Persistent insomnia may even predict the future development of mood disorders in some cases.

It is not clear if RLS is responsible for negative mood states or if anxiety or depression contributes to RLS. Anxiety can cause agitation and leg restlessness that resemble RLS, and depression and RLS symptoms also overlap. In addition, certain types of antidepressant drugs -- such as serotonin reuptake inhibitors -- can increase periodic limb movements during sleep.

Diagnosis

A diagnosis of restless legs syndrome or nocturnal leg cramps often relies solely on the patient's description of symptoms. In general, the recommended approach is first to take a sleep and personal history. The doctor may conduct an interview that includes the following questions:

How would you describe your sleep problem?
How long have you had this sleep problem?
How long does it take you to fall asleep?
How many times a week does the problem occur?
How restful is your sleep?
What are the leg problems like (cramps, twitching, crawling feelings)?
What is your sleep environment like? Noisy? Not dark enough?
What medications are you taking (including the use of antidepressants and self-medications -- such as herbs, alcohol, and over-the-counter or prescription drugs)?
Are you taking or withdrawing from stimulants, such as coffee or tobacco?
How much alcohol do you drink per day?
What stresses or emotional factors may be present in your life?
Have you experienced any significant life changes?
Do you snore or gasp during sleep? (This may be an indication of sleep apnea. Sleep apnea is a condition in which breathing stops for short periods many times during the night. It may worsen symptoms of restless legs syndrome or insomnia.)
If you have a bed partner, does he or she notice that you have jerking legs, interrupted breathing, or thrashing while you sleep?
Are you a shift worker?

Keeping a Record of Sleep. To help answer these questions, the patient may need to keep a sleep diary. Every day for 2 weeks, the patient should record all sleep-related information, including responses to questions listed above described on a daily basis. Recording sleep behavior using an extended-play audio or videotape can be very helpful in diagnosing sleep apnea.

A bed partner can help by adding their observations of the patient's sleep behavior.

Some high-risk patients may need to consult a sleep specialist or go to a sleep disorders center before their sleep problem can be diagnosed. At most centers, patients undergo an in-depth analysis, usually supervised by a team of consultants from various specialties, who can provide both physical and psychiatric evaluations. Centers should be accredited by the American Academy of Sleep Medicine.

Among the signs that may indicate a need for a sleep disorders center are:

Insomnia due to psychological disorders
Sleeping problems due to substance abuse
Snoring and sudden awakening with gasping for breath (possible sleep apnea)
Severe restless legs syndrome
Persistent daytime sleepiness
Sudden episodes of falling asleep during the day (possible narcolepsy)

Overnight polysomnography involves several tests to measure different functions during sleep. It is typically performed in a sleep center and may help rule out sleep apnea or confirm the effectiveness of restless legs syndrome (RLS) treatments.

The patient arrives about 2 hours before bedtime without having made any changes in daily habits. Polysomnography electronically monitors the patient as he or she passes, or fails to pass, through the various sleep stages. Polysomnography tracks the following:

Brain waves
Body movements
Breathing
Heart rate
Eye movements
Changes in breathing and blood levels of oxygen

Actigraphy uses a small wristwatch-like device (such as Actiwatch) to monitor sleep quality in people with suspected restless legs syndrome (RLS), periodic leg movement disorder (PLMD), insomnia, sleep apnea, and other sleep-related conditions. Patients can wear the device on their wrists or ankles. It measures and records muscle movements during sleep. For example, with PLMD, actigraphy can provide information on the total duration of movements, the number of occurrences, whether PLMD occurs simultaneously in both legs, and its effects on sleep.

Actigraphy is not as accurate as polygraphy because it cannot measure all the biological effects of sleep. It is more accurate than a sleep log, however, and very helpful for recording long periods of sleep.

The Epworth sleepiness scale uses a simple questionnaire to measure excessive sleepiness during eight situations.


Situation	Chance of Dosing
Sitting and reading	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Watching TV	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Sitting inactive in a public place	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Riding as a passenger in a car for an hour without a break	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Lying down to rest in the afternoon when circumstances permit	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Sitting and talking to someone	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Sitting quietly after a lunch without alcohol	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Sitting in a car while stopped for a few minutes in traffic	(Indicate a score of 0 to 3) 0 = no chance of dozing 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing
Score Results 1-6: Getting enough sleep. 4-8: Tends to be sleepy but is average. 9 and over: Very sleepy and suggestive of sleep-disordered breathing. Patient should seek medical advice.

Because of the high association between restless legs syndrome and iron deficiency, a test for low iron stores should be part of the diagnostic workup in restless legs syndrome (RLS). There are two steps in making this diagnosis:

The first step is to determine if a person is actually deficient in iron.
If iron stores are low, the second step is to diagnose the cause of the iron deficiencies, which will help determine treatment.

Determining if Iron Stores are Low: The following findings are important in determining that a person is iron deficient:

Blood cells viewed under the microscope are pale (hypochromic) and abnormally small (microcytic). They are also mostly uneven in shape. These findings suggest iron deficiency, but they can also appear in anemia resulting from chronic disease and in thalassemia.
Hemoglobin and iron levels are low. These findings further suggest iron deficiency, but they can also occur in cases of anemia due to chronic disease.
Ferritin levels are low. Ferritin is a protein that binds to iron, and low levels typically mean the patient does not have enough iron in their body. However, high levels of ferritin in the blood do not always mean a patient has enough iron. For example, pregnant women may have high ferritin levels even in their third trimester, yet still be iron deficient. Ferritin levels may also be normal, or even elevated, in patients with inflammation resulting from anemia due to chronic disease, even if these patients also so not have enough iron in their body.
A test that measures a factor called serum transferrin receptor (TfR) is proving to be very sensitive in identifying iron deficiency in some patients, including the elderly with chronic diseases and possibly pregnant women.

Determining Causes of Iron Deficiency. When iron deficiency anemia is diagnosed, the next step is to determine what causes the iron deficiency itself.

Dietary iron deficiency is most common in children and infants. It is rare in adults.
Heavy menstrual or abnormal uterine bleeding is usually the cause of iron deficiencies in young women. Increased need for iron during pregnancy is also a common cause of iron deficiency in pregnant women.
If doctors suspect internal bleeding as the cause of iron deficiency, they look first to the digestive tract as the possible source. A diagnosis in such cases can often be made if the patient has noticed blood in their stools, (the stool would be black and tarry or red-streaked). Often, however, bleeding may be present but not visible. In such cases, stool tests for this hidden (occult) blood are required. The patient may need additional tests to diagnose the cause of bleeding. One common test is endoscopy, in which a fiberoptic tube is used to look into the gastrointestinal tract. Doctors recommend it particularly when the source of bleeding is unclear.

If the patient's diet suggests low iron intake and doctors cannot find other causes of iron deficiency, they may recommend a month-long trial of iron supplements. If the patient fails to respond, they will need further evaluation.

Certain laboratory tests may be helpful in determining causes of restless legs syndrome (RLS) or conditions that rule it out. They include:

Blood glucose tests for diabetes
Tests for kidney problems
In certain cases, tests for thyroid hormone, magnesium, and folate levels

In addition to other sleep-related leg disorders, a number of other medical conditions may have features that resemble restless legs syndrome (RLS). The doctor will need to consider these disorders in making a diagnosis.

Peripheral Neuropathies. Peripheral neuropathies are nerve disorders in the hands or feet. Several conditions can cause these disorders, and they can produce pain, burning, tingling, or shooting sensations in the arms and legs. Diabetes is a very common cause of painful peripheral neuropathies. Other causes include alcoholism, rheumatoid arthritis, systemic lupus erythematosus, amyloidosis, HIV infection, kidney failure, and certain vitamin deficiencies. Symptoms of peripheral neuropathies may mimic RLS. However, unlike RLS, they are not usually associated with restlessness, movement does not relieve the discomfort, and they do not worsen at bedtime.

Deep Vein Thrombosis. Deep vein thrombosis (DVT) is a blood clot in a deep vein in the body, usually in the leg. It may cause pain, swelling, and aching in the leg where the clot has developed. It can occur in people with heart disease, with varicose veins, during pregnancy, in women from hormonal treatments, from injury to the leg, or from inactivity (such as after surgery or during long flights). In women, it can also result from hormonal treatments. Left untreated, DVT can be a very serious and even life-threatening condition.

This picture shows a red and swollen thigh and leg caused by a blood clot (thrombus) in the deep veins in the groin (iliofemoral veins), which prevents normal return of blood from the leg to the heart.

Intermittent Claudication and Peripheral Artery Disease. Peripheral artery disease (PAD) occurs when atherosclerosis (commonly called hardening of the arteries) affects the feet and legs. In such cases, blocked arteries reduce the flow of oxygen-rich blood to the legs or feet. Intermittent claudication is an important symptom of PAD and occurs in between one-third and one-half of these patients. The word claudication describes the pain that occurs in PAD patients when they exercise, particularly when they walk. In intermittent claudication, blood flows only enough to meet the needs of the person at rest. The result is leg pain during exercise, which disappears during rest.

Click the icon to see an image of peripheral artery disease.

Akathisia. Akathisia is a state of restlessness or agitation, and feelings of muscle quivering. A condition called hypotensive akathisia is caused by failure in the autonomic nervous system. Unlike RLS, it occurs at any time of the day and usually only when the patient is sitting -- not lying down. Drugs used to treat schizophrenia and other psychoses can cause akathisia, as can anti-nausea drugs. The condition also occurs when drugs to treat Parkinson's disease are withdrawn.

Painful Legs and Moving Toes Syndrome. A rare disorder affecting one or both legs, painful legs and moving toes syndrome is marked by a constant, deep, throbbing ache in the limbs and involuntary toe movements. The discomfort may be mild or severe. It gets worse with activity and usually stops during sleep. Usually, the cause is unknown, though it may arise from spinal injuries or herpes zoster infection. The condition is difficult to treat, although the drug baclofen, combined with either clonazepam or carbamazepine, has shown some success. Other treatments that may help include orthotics for the shoes and transcutaneous electrical nerve stimulation (TENS).

Meralgia Paresthetica. An uncommon nerve condition, meralgia paresthetica causes numbness, pain, tingling, or burning on the front and side of the thigh. It usually occurs on one side of the body, and the cause may be compression of the thigh nerve as it passes through the pelvis. It typically occurs in people aged 30 - 60 years, but it can affect people of all ages. It often goes away on its own.

Treatment

The first step in treating a patient who complains of sleeplessness and restless legs syndrome is to try to improve sleep and eliminate possible causes of restless legs syndrome (RLS). Doctors normally try to achieve these goals without the use of drugs, initially. A non-drug approach is a particularly important first step for elderly patients.

The doctor should first try to treat any underlying medical conditions that may be causing restless legs.
If medications may be causing RLS, the doctor should try to prescribe alternatives, if possible.

If the cause cannot be determined, it is best to first try better sleep habits and relaxation methods. These approaches may help, even if the patient needs drug therapy later on.

Some people report help or relief from restless legs syndrome (RLS) with the following behaviors or devices:

Hot baths or cold compresses help some patients.
Ergonomic measures -- for example, patients might find it useful to work at a high stool, where they can dangle their legs. In meetings or during air travel, it is helpful to have an aisle seat.
Changing sleep patterns -- some patients report that symptoms do not occur if they sleep late in the morning. Therefore, if feasible, patients can try changing sleep patterns.
Avoiding caffeine, alcohol, and nicotine also improves some cases of RLS.

Some patients recommend alternative treatments for RLS, such as acupuncture and massage. To date, however, there is not enough data on the effectiveness of these treatments.

Some people have reported benefits from:

Vitamin E (800 - 1,200 IU per day)
Calcium, magnesium, or potassium supplements
Folic acid supplements for people with folate deficiencies

Folate (folic acid) is necessary for the production of red blood cells and for the synthesis of DNA (which controls heredity and is used to guide the cell in its daily activities). Folic acid also helps with tissue growth and cell function. In addition, it helps to increase appetite when needed and stimulates the formation of digestive acids.

Because restless legs syndrome (RLS) is associated with iron insufficiency, people with the condition should get enough iron from their diet. [See In-Depth Report #57: Anemia.] Iron is found in foods either in the form of heme or non-heme iron:

Foods containing heme iron are the best for increasing or maintaining healthy iron levels. Such foods include (in decreasing order of iron-richness) clams, oysters, organ meats, beef, pork, poultry, and fish.
Non-heme iron is less well absorbed. About 60% of the iron in meat is non-heme (although meat itself helps absorb non-heme iron). Eggs, dairy products, and iron-containing vegetables (including dried beans and peas) have only the non-heme form. Other sources of non-heme iron include iron-fortified cereals, bread, and pasta products, dark green leafy vegetables (chard, spinach, mustard greens, kale), dried fruits, nuts, and seeds.

The Effects of Food on Iron Absorption. The absorption of non-heme iron often depends on the food balances in meals. The following are foods that enhance absorption of non-heme iron.

Meat and fish not only contain heme iron, the best form for maintaining stores, but they also help absorb non-heme iron.
Eating more vitamin C-rich foods can enhance absorption of non-heme iron during a single meal. In any case, vitamin C-rich foods are healthy. They include broccoli, cabbage, citrus fruits, melon, tomatoes, and strawberries. One orange or 6 ounces of orange juice can double the amount of iron your body absorbs from plant foods. (Taking vitamin C supplements does not appear to have any significant effect on how much iron your body stores.)
Foods containing riboflavin (vitamin B2) may help enhance the formation of hemoglobin from iron. Sources include liver, dried fortified cereals, and yogurt.

Certain nutrients impede the body's absorption of dietary iron. They include:

Polyphenols (found in tea, coffee, red wine, berries, and apples)
Phytates (found in foods such as seeds, dried beans, soy, and bran). Such foods are typically high in fiber. It is often believed that fiber itself impedes iron absorption, but researchers report that it has little or no effect.
Calcium. Calcium impairs the absorption of heme and non-heme iron. However, calcium intake must be quite high to cause any significant problems.

The Effects of Cooking Methods on Iron. Cooking methods can enhance the amount of iron in your body. Cooking in cast iron pans and skillets is a well-known way to increase the iron content of food. According to one study, boiling, steaming, or stir-frying in utensils composed of any material significantly increased the release of non-heme iron stored in vegetables.

Iron supplements can significantly reduce symptoms in people with restless legs syndrome (RLS) who are also iron deficient. Patients should use them only when dietary measures have failed. Iron supplements do not appear to be useful for RLS patients with normal or above normal iron levels.

Supplement Forms. To replace iron, the preferred forms of iron tablets are ferrous salts, usually ferrous sulfate (Feosol, Fer-In-Sol, Mol-Iron). Other forms include ferrous fumarate (Femiron, FerroSequels, Feostat, Fumerin, Hemocyte, Ircon), ferrous gluconate (Fergon, Ferralet, Simron), polysaccharide-iron complex (Niferex, Nu-Iron), and carbonyl iron (Elemental Iron, Feosol Caplet, Ferra-Cap). Specific brands and forms may have certain advantages. The following are some examples:

Prolonged-release ferrous sulfate (Slow Fe) may enhance iron absorption with fewer side effects than standard ferrous sulfate pills.
FerroSequels contains a stool softener, which helps prevent constipation.
Polysaccharide-iron complex has fewer side effects and equal absorption rates compared to ferrous salts. It is very expensive, however.
Carbonyl iron is composed of very fine tiny uniform spheres of iron powder and may prove to be less toxic than ferrous iron.
Coated or combination pills do not appear to offer any additional advantages and may hinder absorption of the iron.

Regimen. A reasonable approach for patients with RLS is to take 65 mg of iron (or 325 mg of ferrous sulfate) along with 100 mg of vitamin C on an empty stomach, 3 times a day.

IMPORTANT: As few as 3 adult iron tablets can poison, and even kill, children. This includes any form of iron pill. No one, not even adults, should take a double dose of iron if they miss one dose.

Tips for taking iron are:

For best absorption, take iron between meals. (Iron may cause stomach and intestinal disturbances, however. Some experts believe that you can take low doses of ferrous sulfate with food and avoid the side effects.)
Always drink a full 8 ounces of fluid with an iron pill.
Keep tablets in a cool place. Bathroom medicine cabinets may be too warm and humid, which may cause the pills to disintegrate.

Side Effects. Common side effects of iron supplements include the following:

Constipation and diarrhea -- these are rarely severe, although iron tablets can aggravate existing digestive problems such as ulcers and ulcerative colitis.
Nausea and vomiting may occur with high doses, but you can control this by taking smaller amounts. Switching to ferrous gluconate may help some people with severe digestive problems.
Black stools are normal when taking iron tablets. In fact, if they do not turn black, the tablets may not be working effectively. This tends to be a more common problem with coated or long-acting iron tablets.
If the stools are tarry looking as well as black, if they have red streaks, or if cramps, sharp pains, or soreness in the stomach occurs, bleeding in the digestive tract may be causing the iron deficiency, and the patient should call the doctor immediately.
Acute iron poisoning is rare in adults, but can be fatal in children who take adult-strength tablets.

Interactions With Other Drugs. Certain medications, including antacids, can reduce iron absorption.

Iron tablets may also reduce the effectiveness of other drugs, including:

Antibiotics: tetracycline, penicillamine, and ciprofloxacin
Anti-Parkinson's disease drugs: methyldopa, levodopa, and carbidopa

At least 2 hours should elapse between doses of these drugs and doses of iron supplements.

Supplementary Treatments. The following supplements may improve iron absorption:

Adding either ascorbic acid (vitamin C) or succinic acid to ferrous sulfate treatment will improve absorption of iron stores. Ascorbic acid added to iron treatment, however, may worsen some of the side effects. Succinic acid added to ferrous sulfate does not appear to increase side effects.
Some studies have found that the addition of zinc to iron supplements increases hemoglobin levels more than iron alone. Some evidence suggests that zinc affects a hormone called insulin-like growth factor-I (IGF-I), which plays a role in the regulation of red blood cell production.

Exercise earlier in the day may be one of the best ways to achieve healthy sleep. However, vigorous exercise and stimulation (including sexual activity) within 1 - 2 hours of bed time may worsen restless legs syndrome (RLS). A study found that people who walked briskly for 30 minutes, four times a week, improved minor sleep disturbances after 4 months. Regular, moderate exercise, healthful in any case, may help prevent RLS. Patients report that either bursts of excessive energy or long sedentary periods worsen symptoms.

Benign nocturnal leg cramps, sometimes known as a charley horse, are muscle spasms in the calf that can occur one or many times during the night. Cramping may also occur in the soles of the feet. They typically last from a few seconds to a few minutes. Some people experience them regularly, others only on isolated occurrences.

Causes of Nocturnal Leg Cramps. In most cases, the cause of nocturnal leg cramps remains unknown. Among the conditions that might cause leg cramps are:

Calcium and phosphorus imbalances, particularly during pregnancy
Low potassium or sodium (salt) levels
Overexertion, standing on concrete for long periods, or prolonged sitting (especially with the legs contorted)
Having structural disorders in the legs or feet (such as flat feet)
Medical causes of muscle cramping include hypothyroidism, Addison's disease, uremia, hypoglycemia, anemia, and certain medications. Various diseases that affect nerves and muscles, such as Parkinson's, cause leg cramps. Peripheral neuropathy, a complication of diabetes, can cause cramp-like pain, numbness, or tingling in the legs. Patients with kidney disease undergoing dialysis are also prone to leg cramps.

Individuals at Higher Risk for Nocturnal Leg Cramps. Nocturnal leg cramps occur at all ages but peak at different times. They are particularly common in adolescence, during pregnancy, and in older age, affecting up to 70% of adults over age 50 at some point.

Pregnant women and those taking diuretics are also at risk for leg cramps because of low calcium levels and an imbalance in calcium and phosphorus.

Consequences of Nocturnal Leg Cramps. Nocturnal leg cramps, like restless legs syndrome, rarely have any serious consequences. However, they can be extremely painful and long lasting. In some cases, severe and persistent symptoms can cause chronic insomnia and considerable mental distress.

Managing Nocturnal Leg Cramps. Once a cramp begins, straighten the leg, flex the foot upward toward the knee, or grab the toes and pull them toward the knee.

Walking or shaking the affected leg, then elevating it, may also help.

If soreness persists, a warm bath or shower or an ice pack may bring relief.

Lifestyle Tips for Preventing Nocturnal Leg Cramps. Nighttime leg cramps are generally treated with lifestyle changes.

Everyone with leg cramps should drink plenty of water (at least 6 - 8 glasses daily) to maintain adequate fluid levels.
Pregnant women and others who get legs cramps due to low calcium levels should reduce milk intake, because drinking milk does not correct the underlying imbalances in calcium and phosphorus. Instead, they should boost calcium levels by taking nonphosphate calcium supplements.
To prevent cramps from occurring, nightly stretching exercises may be the best preventive measure. Patients should stand about 30 inches from a wall and, keeping the heels flat on the floor, lean forward and slowly move the hands up the wall to achieve a comfortable stretch. A few minutes on a stationary bicycle at bedtime may also help.
While in bed, loose covers should be used to prevent the toes and feet from pointing, which causes calf muscles to contract and cramp. Propping the feet up higher than the torso may also help.
During the week, swimming and water exercises are a good way to keep muscles stretched, and wearing supportive footwear is also important.

Quinine. Quinine had been widely used to prevent leg cramping. The U.S. Food and Drug Administration (FDA) banned its sale over the counter because it reportedly caused some serious, although rare, side effects. These side effects include bleeding problems and heart irregularities. Other, less serious side effects include headaches, vision problems, and rash.

The FDA has since banned the marketing of most quinine drugs, cautioning against the off-label (non-approved) use of the drug to treat RLS. Only one form of the drug, Qualaquin, is approved for sale, for the treatment of some types of malaria. Pregnant women and those with liver problems should avoid quinine in any form.

Supplements. Some small studies indicate that the mineral magnesium, taken as magnesium citrate or magnesium lactate, may provide some benefit to people with leg cramps, including pregnant women.

In one small study, taking vitamin B complex was helpful. Other supplements tried for leg cramps include vitamin E, calcium, and potassium or sodium chloride, but these do not appear to be very effective. Sodium chloride (salt) may be helpful, but Western diets already contain too much sodium.

Medications

The American Academy of Sleep Medicine recommends medications for restless legs syndrome (RLS) or periodic limb movement disorder (PLMD) only for persons who fit strict diagnostic criteria, and who experience excessive daytime sleepiness as a result of these conditions. (Excessive daytime sleepiness results from nighttime sleeplessness due to RLS or PLMD symptoms). Little is known about the best way to treat RLS, but some experts suggest the following:

Over-the-counter pain relievers and possibly mineral and vitamin supplements (particularly folic acid in people who might be deficient) should be the first form of treatment.
People with RLS should have a test for iron deficiency. If they are iron deficient, they should start treatment with iron supplements.
Dopaminergic drugs (drugs that increase levels of dopamine) are the standard medicines for treating severe RLS, PLMD, or both.
Other drugs may be helpful if dopaminergic drugs fail, or for patients who have frequent -- but not nightly -- symptoms. These include opiates (pain relievers), benzodiazepines (sedative hypnotic drugs), or anticonvulsants. However, benzodiazepines and opiates can become habit forming and addictive.

Before taking stronger medications, people should try over-the-counter pain relievers, such as acetaminophen (Tylenol) or non-steroidal anti-inflammatory drugs (NSAIDs), which include ibuprofen (Advil, Motrin, Rufen), naproxen (Anaprox, Naprosyn, Aleve), and ketoprofen (Orudis KT, Aktron).

Although NSAIDs work well, long-term use can cause stomach problems, such as ulcers and bleeding, and possible heart problems. In April 2005, the Food and Drug Administration asked drug manufacturers of NSAIDs to include a warning label on their product that alerts users of an increased risk for heart-related problems and digestive tract bleeding.

Dopaminergic drugs increase the availability of the chemical messenger dopamine in the brain, and are the first-line treatment for severe restless legs syndrome (RLS) and periodic leg movement disorder (PLMD). These drugs significantly reduce the number of limb movements per hour, and improve the subjective quality of sleep. Patients with either condition who take these drugs have experienced up to 100% reduction in symptoms.

Dopaminergic drugs, however, can have severe side effects (they are ordinarily used for Parkinson's disease). They do not appear to be as helpful for RLS related to dialysis as they do for RLS from other causes.

Dopaminergic drugs include dopamine precursors and dopamine receptor agonists.

Dopamine Precursors. The dopamine precursor levodopa (L-dopa) was once a popular drug for severe RLS. The standard preparations (Sinemet, Atamet) combine levodopa with carbidopa, which improves the action of levodopa and reduces some of its side effects, particularly nausea. Levodopa can also be combined with benserazide (Madopar) with similar results, but Sinemet is almost always used in America. (Levodopa combinations are well tolerated and safe.)

Patients typically start with a very low dose taken 1 hour before bedtime. The dosage is increased until the patient finds relief. Patients sometimes need to take an extended form or to take it again during the night.

Levodopa acts fast, and the treatment is usually effective within the first few days of therapy. One study reported that a combination therapy of regular-release L-dopa plus sustained release L-dopa was effective in improving sleep.

Serious common side effects of L-dopa treatment (and, to lesser extent, of dopamine receptor agonists) are augmentation and rebound. Many studies report that augmentation (worsening of symptoms that occur earlier in the day) occurs in up to 70% of patients who take L-dopa. The risk is highest for patients who take daily doses, especially doses at high levels (greater than 200 mg/day). For this reason, patients should use L-dopa only intermittently (fewer than 3 times per week). The drug should be immediately discontinued if augmentation does occur. Following withdrawal from L-dopa, patients can switch to a dopamine receptor agonist.

The rebound effect causes increased leg movements at night or in the morning as the dose wears off, or as tolerance to the drug builds up.

Dopamine Receptor Agonists. Dopamine receptor agonists (also called dopamine agonists) mimic the effects of dopamine by acting on dopamine receptors in the brain. They are now generally preferred to L-dopa. Because they have fewer side effects than L-dopa, including rebound effect and augmentation, these drugs may be used on a daily basis. (Rebound effect is the worsening of symptoms over time; augmentation means the appearance of symptoms earlier in the day. About 30% of patients who take dopamine receptor agonists have reported augmentations symptoms. As the newer drugs are taken for longer periods and at higher doses, however, their augmentation rates may become closer to those of L-dopa.)

Dopamine agonists have been shown to relieve symptoms in 70 - 90% of patients. Dopamine agonists can be ergot-derived (such as cabergoline) or non-ergot derived (such as pramipexole and ropinirole). The newer non-ergotamine derivatives may induce fewer side effects than ergot-derived drugs. Studies on these medications report the following:

Ropinirole (Requip) is a non-ergotamine dopamine agonist. Approved in 2005, ropinirole is the first drug approved specifically for treatment of moderate-to-severe RLS (more than 15 RLS episodes a month). Side effects are generally mild but may include nausea, vomiting, drowsiness, and dizziness.
The Food and Drug Administration (FDA) approved pramipexole (Mirapex) for use in moderate-to-severe RLS in November 2006. However, patients may fall asleep, without warning, while taking this drug, even while performing activities such as driving.

Cabergoline (Dostinex) is also showing promise in clinical trials. In one study, cabergoline was used for RLS after levodopa had either failed or resulted in increased symptoms. Patients in the study reported relief or freedom from symptoms after 4 weeks of use. A 2006 study indicated that a single evening dose of cabergoline improved both day and nighttime limb movements, and sleep disturbances.The FDA announced in March 2007 that the dopamine agonist pergolide (Permax) was voluntarily withdrawn from the market. Studies confirmed that this drug could cause serious damage to the heart valves of patients who take it. These problems have not been reported with ropinirole or pramipexole, which are chemically different then pergolide.

Other Dopamine Agonists. Rotigotine is a unique dopamine agonist that is being developed in patch form for RLS. In May 2007, the FDA approved this patch for treatment of early Parkinson's disease. Other dopamine agonists that have shown some promise in small studies include alpha-dihydroergocryptine, or DHEC (Almirid), and piribedil (Trivastal).

Regimens. The effects of L-dopa are apparent in 15 - 30 minutes. Dopamine receptor agonists, meanwhile, take at least 2 hours to start working. Some doctors recommend regular use of dopamine receptor agonists for patients who experience nightly symptoms, and L-dopa for those whose symptoms occur only occasionally.

Side Effects. Common side effects of dopaminergic drugs vary but may include feeling faint or dizzy (especially when standing up), headaches, abnormal muscle movements, rapid heartbeat, insomnia, bloating, chest pain, and dry mouth. Nausea may be especially common. Adding the drug domperidone may help to relieve this side effect. In rare cases, dopaminergic drugs can cause hallucinations or lung disease.

Because these drugs may cause daytime drowsiness, patients should be extremely careful while driving or performing tasks that require concentration.

Long-term use of dopaminergic drugs can lead to loss of effectiveness (tolerance). Adding a drug called entacapone (Comtan) may prolong the duration of action of carbidopa-levodopa therapy (Sinemet), but it can cause nausea.

Rebound effect, augmentation, and tolerance can reduce the value of dopaminergic drugs in the treatment of RLS. Using the lowest dose possible can minimize these effects.

Withdrawal Symptoms. Patients who withdraw from these drugs typically experience very severe RLS symptoms for the first 2 days after stopping. RLS eventually returns to pre-treatment levels after about a week. The longer a patient uses these drugs, the worse their withdrawal symptoms.

Benzodiazepines, such as clonazepam (Klonopin), are known as sedative hypnotics. Doctors prescribe them for insomnia and anxiety. They may be helpful for some patients with restless legs syndrome (RLS) that disrupts sleep. Clonazepam may be particularly helpful for children with both periodic limb movement disorder and symptoms of attention deficit hyperactivity disorder. The medicine also may be helpful for patients with RLS who are undergoing dialysis.

Side Effects. Elderly people are more susceptible to side effects. They should usually start at half the dose prescribed for younger people, and should not take long-acting forms. Side effects may differ depending on whether the benzodiazepine is long-acting or short-acting.

The drugs may increase depression, a common condition in many people with insomnia.
Breathing problems may occur with overuse or in people with pre-existing respiratory illness.
Long-acting drugs have a very high rate of residual daytime drowsiness compared to others. They have been associated with a significantly increased risk for automobile accidents and falls in the elderly, particularly in the first week after taking them. Shorter-acting benzodiazepines do not appear to pose as high a risk.
There are reports of memory loss (so-called traveler's amnesia), sleepwalking, and odd mood states after taking triazolam (Halcion) and other short-acting benzodiazepines. These effects are rare and probably enhanced by alcohol.
Because benzodiazepines cross the placenta and enter breast milk, pregnant and nursing women should not use them. There are some reports of an association between the use of benzodiazepines in the first trimester of pregnancy and the development of cleft lip in newborns. Studies are conflicting at this point, but, due to other known side effects of benzodiazepines, pregnant women should not use these drugs, if possible.
In rare cases, overdoses have been fatal.

Interactions. Benzodiazepines are potentially dangerous when used in combination with alcohol. Some drugs, such as the ulcer medication cimetidine, can slow the breakdown of benzodiazepine.

Withdrawal Symptoms. Withdrawal symptoms usually occur after prolonged use and indicate dependence. They can last 1 - 3 weeks after stopping the drug and may include:

Gastrointestinal distress
Sweating
Disturbed heart rhythm
In severe cases, patients might hallucinate or experience seizures, even a week or more after they stop taking the drug.

Rebound Insomnia. Rebound insomnia, which often occurs after withdrawal, typically includes 1 - 2 nights of sleep disturbance, daytime sleepiness, and anxiety. The chances of rebound are higher with the short-acting benzodiazepines than with the longer-acting ones.

Narcotics are pain-relieving drugs that act on the central nervous system. They are sometimes prescribed for severe cases of restless legs syndrome (RLS). They may be a good choice if pain is a prominent feature. Some evidence also suggests that narcotics reduce the frequency of periodic leg movements.

There are two types of narcotics, both of which have been used for severe RLS:

Opiates (such as morphine and codeine) come from natural opium. Some patients report relief with the use of the opiate fentanyl (Duragesic), available in skin patch form. An implanted pump that uses morphine and an anesthetic called bupivacaine is showing promise for patients with severe RLS. The pump delivers the drugs to the fluid surrounding the spinal cord (cerebrospinal fluid).
Opioids are synthetic drugs. The most common example is oxycodone (Percodan, Percocet, Roxicodone, Oxycontin). Apomorphine is a morphine derivative. In one study, when injected under the skin at night, it reduced nocturnal discomfort and leg movements in some patients.

Although the use of narcotics for severe RLS is controversial, some studies have suggested that even when the treatments are long-term, they are rarely addictive for pain sufferers except among patients with a history of substance abuse.

The use of such drugs may be beneficial when included as part of a comprehensive pain management program. Such a program involves screening prospective patients for possible drug abuse, and regularly monitoring those who are taking narcotics. Doses should be adjusted as necessary to achieve an acceptable balance between pain relief and side effects. Patients on long-term opiate therapy should also be monitored periodically for sleep apnea, a condition that causes breathing to stop for short periods many times during the night. Sleep apnea may worsen symptoms of RLS, insomnia, and other complaints.

Tramadol. Tramadol (Ultram) is a pain reliever that has been used as an alternative to opioids. In one study, tramadol was very effective for RLS and produced few or no side effects. It has opioid-like properties, but is not as addictive. (However, there are reports of dependence and abuse with this drug as well.) Withdrawal after long-term use (longer than a year) can cause intense symptoms, including diarrhea, insomnia, and even restless legs syndrome itself.

Antiseizure drugs -- such as gabapentin (Neurontin), valproic acid (valproate, divalproex, Depakote, Depakene), and carbamazepine (Tegretol) -- relax blood vessels and are being tested for restless legs syndrome (RLS). Gabapentin, a newer antiseizure drug, is showing particular promise for mild-to-moderate RLS. One study reported that it improved RLS symptoms and sleep, particularly in patients who also experienced pain. It was also effective for periodic leg movement disorder. A new gabapentin product is in phase III clinical trials for the treatment of RLS. The new drug, known as XP13512, converts to gabapentin in the intestines, and therefore may reduce some of the side effects experienced by patients taking antiseizure medications.

Side Effects. All antiseizure drugs have potentially severe side effects. Therefore, patients should try these medications only after non-drug methods have failed. Side effects of many anti-seizure drugs include nausea, vomiting, heartburn, increased appetite with weight gain, hand tremors, irritability, and temporary hair thinning and hair loss (taking zinc and selenium supplements may help reduce this last effect). Some antiseizure drugs can also cause birth defects and, in rare cases, liver toxicity. Gabapentin may have fewer of these side effects than valproic acid or carbamazepine.

Antidepressants. Bupropion (Wellbutrin), a newer antidepressant, may be helpful for restless legs syndrome (RLS). Bupropion is a weak dopamine reuptake inhibitor -- it causes a slight increase in the availability of dopamine in the brain. The drug is not addictive and does not have the severe side effects of other RLS drugs, but more research is needed to determine if it is useful.

Clonidine. Clonidine (Catapres), a drug used for high blood pressure, is helpful for some patients and may be an appropriate choice for patients who have RLS accompanied by hypertension. It also may help patients with RLS who are undergoing hemodialysis.

Baclofen. The anti-spasm drug baclofen (Lioresal) appears to reduce intensity of RLS (although not frequency of movements).

Resources

www.aasmnet.org -- American Academy of Sleep Medicine
www.sleepfoundation.org -- National Sleep Foundation
www.ninds.nih.gov -- National Institute of Neurological Disorders and Stroke
www.nhlbi.nih.gov/about/ncsdr/ -- National Center on Sleep Disorders Research
www.rls.org -- Restless Legs Syndrome Foundation
www.wemove.org -- Worldwide Education and Awareness for Movement Disorders

References

Bogan RK, Fry JM, Schmidt MH, Carson SW, Ritchie SY. Ropinirole in the treatment of patients with restless legs syndrome: a US-based randomized, double-blind, placebo-controlled clinical trial. Mayo Clin Proc. 2006 Jan;81(1):17-27.

Claman DM; Redline S; Blackwell T, Ancoli-Israel S, Surovec S, Scott N, et al. Prevalence and correlates of periodic limb movements in older women. J Clin Sleep Med. 2006 Oct;2(4):438-445.

Merlino G, Fratticci L, Valente M, et al. Association of restless legs syndrome in type 2 diabetes: a case-control study. Sleep. 2007; 30(7): 866-71.

Oertel WH, Benes H, Bodenschatz R, Peglau I, Warmuth R, Happe S, et al. Efficacy of cabergoline in restless legs syndrome: a placebo-controlled study with polysomnography (CATOR). Neurology. 2006 Sep 26;67(6):1040-6.

Partinen M, Hirvonen K, Jama L, Alakuijala A, Hublin C, Tamminen I, et al. Efficacy and safety of pramipexole in idiopathic restless legs syndrome: a polysomnographic dose-finding study--the PRELUDE study. Sleep Med. 2006 Aug;7(5):407-17.

Picchietti D, Winkelman JW. Restless legs syndrome, periodic limb movements in sleep, and depression. Sleep. 2005 Jul 1;28(7):891-8.

Picchietti D. Restless legs syndrome: prevalence and impact in children and adolescents--the Peds REST study. Pediatrics. 2007; 120(2): 253-66.

Stefansson H, Rye DB, Hicks A, et al. A Genetic Risk Factor for Periodic Limb Movements in Sleep. N Engl J Med. 2007;357:639-47.

Winkelman JW, Sethi KD, Kushida CA, Becker PM, Koester J, Cappola JJ, et al. Efficacy and safety of pramipexole in restless legs syndrome. Neurology. 2006 Sep 26;67(6):1034-9.

Winkelmann J, Schormair B, Lichtner P, et al. Genome-wide association study of restless legs syndrome identifies common variants in three genomic regions. Nat Genet (in press). [cited in: Winkelmann J. Periodic Limb Movements in Sleep - Endophenotype for Restless Legs Syndrome? N Engl J Med. 2007; 357:703-05.]

Review Date:
10/22/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

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