Gout Triggers :Sleep Apnea

Can Gout be Triggered By Sleep Apnea? 

 Someone sent me this stunning article about a little known trigger of gout namely sleep Apnea.If you, like many others still battle painful gout attacks this (to me )revelation ,might just be the break through that you have been looking for.

 

  Curing Gout — My Personal Discovery

Guess what! I stumbled on a way to cure my gout! It happened when I cured my sleep apnea!

   (Note from Joe: I stumbled across this article while searching Google for sleep apnea information for a friend. I found it very interesting that this person cured his gout by curing his sleep apnea - using a very unique "home remedy" involving Wiffle balls, of all things!

 I thought I'd pass this along to you... I don't know who this person is that wrote it - he gave no name or reference or copyright information... but it certainly wouldn't hurt to try this remedy in hopes to cure your gout - because, like he says, you don't have to worry about what you eat, but only how you sleep). What’s The Connection? A gout attack is caused when uric acid reaches such high concentration in the blood that it precipitates as monosodium urate crystals which then become deposited in a joint, often causing severe and widespread pain and inflammation in that joint and the area surrounding it. Sleep apnea (literally, absence of breathing) in adults occurs when the tissues around the soft palate and the pharynx have become flabby usually due to age and/or obesity, so that they relax during sleep sufficiently to close off the air passage to the lungs. Usually, after many seconds of apnea the reduction of oxygen to the brain causes an unconscious response that jolts the sleeper to open the airway so that breathing is restored, at least until the next apnea episode occurs a short while later. Almost everyone who has sleep apnea is also a snorer, but not all snorers have sleep apnea. Sleep apnea in particular and sleep disorders in general have been recognized as problems by the medical profession only in the last few decades. Much more remains to be learned. So what could be the connection between sleep apnea and gout? I asked every physician I came in contact with that question, including my rheumatologist (joint disease specialist). All were clueless. But I trusted my own observation that my gout disappeared immediately and completely as a direct result of my sleep apnea cure. As of this writing I have been gout free for over sixteen months, except for one event, which I will describe later. Before my sleep apnea cure I would have gout attacks every few weeks, with varying degrees of severity, over a period of at least fifteen years. After realizing the connection between my gout and sleep apnea, and that no doctors recognized the connection, I began researching as much information as I could about these conditions. I was able to piece together information from articles in medical journals that confirm the connection. This information was first published around 1990, but nobody pieced it together until now. I sure wish that I had known about it years ago, so that my gout would have alerted me to resolve my sleep apnea before it led to any serious problems. For everyone else's benefit, I have included a list of references to those medical journal items at the end of this article, as well as one that I wrote recently to synopsize this information for doctors. In layman’s language, they describe how reduction of oxygen in the blood, which results from sleep apnea, has been shown to cause the cells in the body to begin to disintegrate and generate an excess of uric acid in the blood. Drinking alcohol has a similar effect on the cells, but it may be even more pronounced in causing gout by the fact that alcohol helps to induce sleep apnea. In some people, including me, the excess uric acid precipitates to cause a gout attack (and maybe uric acid kidney stones as well.) Other evidence that further corroborates their connection is that the typical (with some exceptions) profile of the person who first experiences either gout or sleep apnea is the same—MOM (middle-aged, overweight, male). Second, sleep apnea and gout are both far more common in women after menopause than before menopause. In addition, a large neck circumference is associated with both gout and sleep apnea. The most important piece of evidence, though, is that the onset of a gout attack commonly occurs when the gout sufferer is asleep. That was always my own experience as well. I don’t know how commonplace this connection is in other people. One other person has posted a web message at www.sleepnet.com/apnea81/messages/648.html about his gout disappearing when he resolved his obstructive sleep apnea (OSA). Former U.S. President Taft is known to have had gout and is now reputed to have had sleep apnea, because his own journals record him frequently falling asleep at meetings. But sleep apnea was not known in Taft’s time. Of the four acquaintances of mine who have been diagnosed with sleep apnea, none has ever had gout. (None of us is obese either, even though sleep apnea is much more common in obese people.) In fact, the percentage of people that have gout is much smaller than the percentage that have sleep apnea. Thus, it is clear to me that there is not a one-to-one correspondence between gout and sleep apnea or obesity. Yet to be determined is how high a percentage of gout sufferers also have sleep apnea, and vice versa. Some gout sufferers test high for uric acid in their blood. My tests were always normal, and maybe that is a factor that distinguishes those with the sleep apnea connection from those with a different underlying cause for their gout. Medical science needs to conduct some epidemiological studies to answer these questions. How I Discovered My Sleep Apnea My discovery of sleep apnea occurred because of an astute physician who was treating me in the hospital for another ailment, and he knew that sleep apnea was implicated in that ailment. In the presence of my wife, he asked if I snore. Before I could respond, she jumped in quickly with a passionate and animated description of my snoring. Then the doctor turned his questioning to her, and he paid as much attention to me as he did to the furniture. He next asked her if it ever seems like I stop breathing in my sleep, and she replied affirmatively. I am extremely grateful that my wife was there to answer that question. I knew that I had been accused of snoring, and I begrudgingly accepted that as fact. I thought I knew what sleep apnea was, but if anyone were to ask me if I had it, I would have said no. My limited knowledge of sleep apnea was that people who had it would nod off during the day, and even fall asleep while driving. Since I didn’t have those symptoms, I thought that I didn’t have sleep apnea. I now know that a person can have sleep apnea without those symptoms. This physician arranged a consultation for me with a pulmonologist (lungs)/sleep specialist who had me tested overnight with a monitoring device called a pulse oximeter. This machine had a cable attached to a sensor that slips over a finger, and illuminates it like ET’s finger. It is not uncomfortable to be connected to it. It measures both the pulse rate and the blood’s oxygen saturation percentage. The machine that was attached to me was able to print out a reading every few minutes on a thermal paper tape so that my overnight readings were recorded for examination in the morning. The first sign of a possible sleep apnea problem is to see if overnight the oxygen saturation level ever dips below 90%. Mine dipped down to 80%. I was recommended to have further, more extensive testing as an outpatient in the hospital’s sleep lab. But to me the problem was clear, and worrisome. How I Cured My Sleep Apnea At the sleep lab I was attached to many types of sensors all over my head and body to monitor many things overnight, including sleep apnea. I found out in that test that my blood oxygen saturation level had dipped as low as 88%. It was still below the 90% target, but I wondered why it was so much higher than the 80% measured in the hospital. In my investigation of sleep apnea, I learned that an effective remedy for some people is to avoid sleeping on one’s back, since in that position the airway is more likely to become closed. It just so happened that when I went to the sleep lab I was engaged in a bout with sciatica that was more painful when I slept on my back, so I tried not to sleep that way. Previously in the hospital, however, I didn’t have the sciatica pain, and I purposely slept on my back to avoid disturbing my IV drip. While I was in the hospital I had a gout attack. I subsequently learned that gout sufferers are more likely to have an attack in the hospital than at home. I now know why. There are established methods to allow sleep apneacs to avoid sleeping on their backs. One method is to insert a tennis ball in a sock and pin the sock to the back of one’s pajama tops. The idea of this method is to arouse the sleeper by the ball’s discomfort if he ever turns over onto his back. Since I don’t like to wear pajama tops, I cut two slits in a tennis ball through which I slipped an elastic belt. When I went to bed I buckled the belt around my torso with the ball in the back. In order to test the effectiveness of my method, I rented a tape-printout pulse oximeter from a medical supply company for $50 (not covered by my health insurance) to use for several nights in my own bed. With the ball, my lowest reading was 94%. I tested without the ball one night and found several times when my percentage dropped to 87%, even though I tried to sleep lying always on my side. During subsequent use of my belt and tennis ball method, I found that I would occasionally awaken lying on my back with the ball pushed aside. I upgraded my method to straddle my spine using the belt with two tennis balls, one of which I jokingly labeled "Venus" and the second of which I labeled "Serena". Since then I introduced a second upgrade by replacing the tennis balls by Wiffle® perforated plastic softballs*. Compared to the slitted tennis balls, the Wiffle® balls are larger, less compressible, lighter weight, come with the slits built into them, and dry faster after washing. The one time that I suffered a gout attack with the balls in place, I awakened to find my neck turned so that my body was lying on its side and my head on its back, my wife was complaining about my excessively loud snoring, and my foot was screaming with the searing pain of gout. I know that avoiding sleeping on one’s back is not sufficient to prevent apnea for many sleep apneacs. There are other methods that are much less user friendly, such as a pressurized CPAP mask or even surgery. The ball method is the simplest and most user-friendly one that I know, and I could demonstrate its effectiveness for me by my own testing. And I continue to demonstrate its effectiveness by remaining cured of gout. In order to mitigate my gout, my physicians had advised me to avoid eating foods with high purine content. Following that advice produced at best minimal benefit for me. The foods that I used to avoid, I now eat with relish, and I have had no gout attacks. What matters is not how I eat, but how I sleep. Epilogue It is now more than 18 months after I first cured my sleep apnea by using the ball method to keep me from sleeping on my back. For the past four weeks I have tried sleeping without a net, so to speak, to see if I had trained myself well enough to stay off my back without the balls. It worked - no gout. I just rented a pulse oximeter again for four nights to see if the numbers were good. They're great! Recommendation If you suffer from gout, check with your doctor about getting tested for sleep apnea. If your doctor needs convincing, provide him or her with the list of references below. Based on my own doctor's new results from screening his gout patients for sleep apnea, it appears that almost everyone with gout also has sleep apnea. While overcoming your gout is important to achieve, overcoming your sleep apnea is even more important because sleep apnea can have life-threatening consequences over the long term, such as high blood pressure, heart arrhythmia, heart attack, stroke, diabetes, and even sudden death, as happened with former football great Reggie White. Overcoming your sleep apnea not only will stop your gout, but it also will greatly reduce your risk of future development of these life-threatening diseases. Heed the alarm that your gout is screaming at you! *WIFFLE is a registered trademark owned by The Wiffle Ball, Inc., Shelton, CT, and is used with the written permission of that company. 

 

 References [1] Abrams B. Gout Is an Indicator of Sleep Apnea, Journal SLEEP Feb 2005;28(2):275. [2] Grum CM. Cells in Crisis: Cellular Bioenergenics and Inadequate Oxygenation in the Intensive Care Unit, Chest 1992;102(2):329-30. [3] Hasday JD, Grum CM. Nocturnal Increase of Urinary Uric Acid:Creatine Ratio: a Biological Correlate of Sleep-Associated Hypoxemia, American Review of Respiratory Diseases 1987;135:534-38. [4] McKeon, JL.,et al “Urinary Uric Acid with Obstructive Sleep Apnea,” American Review of Respiratory Diseases 142 (1), 1990, pp. 8-13. [5] Sahebjani, H., “Changes in Urinary Uric Acid Excretion in Obstructive Sleep Apnea Before and After Therapy with Nasal Continuous Positive Airway Pressure,” Chest 113(6), 1998, pp. 1604-1608. [6] Saito, H., et al, “Tissue Hypoxia in Sleep Apnea Syndrome as Assessed by Uric Acid and Adenosine,” Chest 121 (55), November 1, 2002, pp. 1686-1694. [7] Schafer, H., et al, “Body Fat Distribution, Serum Leptin, and Cardiovascular Risk Factors in Men with Obstructive Sleep Apnea (Clinical Investigations),” Chest, Sept. 2002, pp. 829-839. [8] Silverberg, DS., et al, “Treating Obstructive Sleep Apnea Improves Essential Hypertension and Quality of Life,” American Family Physician, Jan. 15, 2002, pp. 229-240. [9] Brown, LK., “A Waist Is a Terrible Thing to Mind: Central Obesity, the Metabolic Syndrome, and Sleep Apnea Hypopnea Syndrome (editorial),” Chest, Sept. 2002, pp. 774-778. [10] Khokhar, N., “Hyperuricemia and Gout in Secondary Polycythemia Due to Chronic Obstructive Pulmonary Disease,” Journal of Rheumatology 7(1), Jan.-Feb. 1980, pp.114-116. [11] Khokhar, N., “Gouty Arthritis in Chronic Obstructive Pulmonary Disease,” Archives of Internal Medicine 142(4), Apr. 1982,  

Gout Triggers: Food.

Foods That Trigger Gout:

If you only knew which foods triggered another painful gout attack you could avoid them!
There is a whole list of foods that are "purine rich foods". Some are obvious no -no's and other might surprise you.

Foods That Trigger Gout.

Foods that trigger gout include:

Shellfish like mussels,prawns,crayfish.
Fish : sardines,anchovies,herring, mackerel.
Mushrooms,
Meat gravies and broths,
Peanuts,
Asparagus,
White flour,
Sugar products, 
Caffeine
Dried beans and Lentils,
Cakes and Pies,
Spinach,
Yeast Products,
Alcohol,
Organ Meats:kidney , liver.
 Meat!Avoid all meat including poultry.

8 Gout-Causing Foods - Health.com If you're prone to gout, the foods you eat, and don't eat, play a key role in keeping your joints pain-free. Here are eight foods to avoid. www.health.com/health/gallery/0,,20448674,00.html

Get to Know Your Gout Triggers If you know you have gout, you should try to stay away from these gout triggers. Foods -- Foods that are high in a substance called purines can raise the uric acid ... arthritis.webmd.com/features/gout-triggers

Foods that Cause Gout - Buzzle Jan 10, 2013 ... Gout is a type of arthritis characterized by joint inflammation and pain, arising due to an excess of uric acid in blood and synovial fluid. www.buzzle.com/articles/foods-that-cause-gout.html

What are Some Foods That Cause Gout? Jan 1, 2013 ... Most of the foods that cause gout contain a lot of purine. This includes most red meat, fatty white meats, whole milk, and even... www.wisegeek.org/what-are-some-foods-that-cause-gout.htm

Foods That Trigger Gout | LIVESTRONG.COM Mar 28, 2011 ... Foods That Trigger Gout. Gout is a form of arthritis that is caused by a chemical called uric acid. Under normal circumstances, uric acid gets ... www.livestrong.com/article/28218-foods-trigger-gout/

 

Gout Triggers:Obesity

 Obesity As A Gout Trigger:

If you are reading this post you are most likely looking for a cure for your gout.There is a correlation between obesity and gout! The chances of being obese and having gout are very high ,as you will read in the following articles that I found.Gout and obesity go hand in hand.
Why? The answer is simple : Obesity is an condition of extreme acidity in the body,therefore increasing the uric acid levels and aggravating and even causing gout .Gout in the obese person can be extremely painful because of the added weight, the pain experienced feels as if they are walking on glass!

Gout and obesity go hand in hand.

Here are the articles that I found :

Gout and Obesity Someone with obesity is four times as likely to develop gout. gouteducation.org/patient/living-with-gout/gout-and-obesity/

Obesity: A Major Risk Factor For Gout | Obesity Mar 16, 2009 ... Among the many risk factors of gout such as lifestyle factors, sex, age etc. people who are obese are at high risk of getting gout. obesity.ygoy.com/2009/.../obesity-a-major-risk-factor-for-gou...

More Americans developing gout; obesity blamed | Reuters Aug 31, 2011 ... NEW YORK (Reuters Health) - A growing number of Americans are being diagnosed with the painful form of arthritis known as gout -- thanks in ... www.reuters.com/.../us-gout-obesity-idUSTRE77U5BG20110...

Recent Developments in Diet and Gout: The Impact of Obesity on Gout A review on recent developments on diet and gout and their implications for clinical practice, including how we advise patients on appropriate diets and ... www.medscape.com/viewarticle/524766_2

Obesity and Gout - Arthritis If you're looking to prevent gout, learn about the connection between obesity and gout and how your diet, food choices and exercise can play a part in ... www.arthritistoday.org/conditions/gout/.../obesity-and-gout.ph...

Herbs For Gout Treatment

Usually when someone reaches the stage that they are looking at herbs for gout treatment, they have explored all the other avenues to relieve gout pain!

Devil's Claw :
  If you are looking at long term relief of gout pain"Devil's Claw"is definitely one of the herbs that I can recommend. It relieves pain and is anti inflammatory.Devil's claw contains chemicals that stimulate circulation and carry away inflammatory chemicals from the affected areas.
To relieve gout pain enteric coated capsules have to be taken. there is a specific waythat you must take it: An hour before meals ! The reason for this is that the pain relieving chemicals are activated by intestinal bacteria.For that reason it is also less effective after a bout of antibiotic treatment. The effect of the antibiotics can last up to 2 weeks.

Contra indications: Devil's Claw relaxes arterial tension  and thus lowers blood pressure.This can reduce the force of the heartbeat and slow the pulse.Therefor it should be avoided by people with congestive heart failure.Do not use devil's Claw if you have  an ulcer or you are pregnant or breast feeding.

 Celery Seed And Stalks:
I found this  site that describes how to use the various celery seed products:

Source: http://www.umm.edu/altmed/articles/celery-seed-000231.htm#ixzz2IhvKhuBt
Follow us: @UMMC on Twitter | MedCenter on Facebook

Celery seed oil capsules or tablets: 1 - 2 capsules or tablets 3 times a day, as directed by your health care provider.

Celery seed extract: 1/4 to 1/2 tsp 3 times a day, or as directed by your health care provider. Always take with plenty of juice or with water at mealtime, unless instructed otherwise.

Whole celery seeds: Prepare a tea by pouring one cup boiling water over one teaspoon (1 - 3 g) of freshly crushed seeds. Steep for 10 - 20 minutes before straining and drinking. Drink 3 times a day.

The Celery plant:

The celery plant itself is very useful to combat the symptoms of gout.The Phtalides found in celery are the miracle workers.The substance 3nB (3-n-Butylpthalide is the factor in celery that gives celery its distinctive smell and taste (Phthalides are also found in lovage and walnuts).But why does it work?
 Like the flavonoid anthocyanidins that is found in cherries, 3nB  inhibits xanthine oxidase.This enzyme is involved in  the production of uric acid in the liver. Celery also contains the flavonoids luteolin and apigenin.These flavanoids have anti inflammatory abilities . Luteolin and apigenin also plays a role in pain relief.
 The alkalizing mineral potassium is also found in celery. 100 Grams of raw celery contains a wopping  260 mg of potassium.The more alkaline the body the less gout pain will be experienced.



Celery Seed Conquers Gout Pain - The People's Pharmacy®
Sep 21, 2009 ... Q. I began taking celery seed extract capsules six months ago for gout. Within a day, all foot pain was gone. A blood test six weeks later showed ...
www.peoplespharmacy.com/.../celery-seed-conquers-gout-pai...

 Celery Works Great for Inflammation, Gout, Cancer, and High Blood ...
Sep 10, 2008 ... (NaturalNews) A nutrient found in celery has been shown highly effective against inflammation and cancer. Luteolin is a bioflavonoid also ...
www.naturalnews.com/024135_cancer_celery_inflammation.h...

 Gout Natural Remedies - Celery Seeds - YouTube
http://www.cure-gout-now.com/vid/4 Things to take to ease gout symptoms - Part 1 Celery Seeds.
www.youtube.com/watch?v=FKQiuseSaZ0


As you can see from the above resources, celery is a very popular gout treatment.
Please take the time to read them and also watch the video!

Some More" Herbs For Gout Treatment "Resources:

Herbs: gout treatment, uric acid crystals, local health food store Jun 27, 2005 ... Gout if left untreated (conventionally or naturally) can lead to kidney ... If you would like information on natural and herbal remedies for human ... en.allexperts.com/q/Herbs-720/gout-treatment.htm

Herbs For Gout Herbal Remedies Natural Home Herbal Remedies ... Herbal gout remedies concentrate detoxification to reduce levels of uric acid, while relieving the ... Herbal Treatments for Gout ... www.anniesremedy.com/chart_remedy.php?tag=gout

Herbs and Herbal Supplements for Natural Gout Treatment Herbs for natural gout treatment focus on underlying causes of gout; which holistic practitioners often view as a lifestyle illness. Any herbal remedy for gout ... www.herbal-supplement-resource.com/natural-gout-treatment....

Gout Herbal Remedies - Alleviate gout symptoms naturally Dec 30, 2010 ... In his book "Jude's Herbal Home Remedies," Jude Todd recommends drinking black currant leaf herbal tea as a natural gout treatment. www.naturalnews.com/030866_herbal_remedies_gout.html

Gout Remedy Choices - Alternative - Natural - Herbal - Home ... Information on natural gout remedy choices. Info on alternative gout treatment options. Information on the various herbs and herbal remedy choices for gout. arthritis.about.com/.../Gout_Remedy_Alternative_Natural_Her...   Cured My Gout With Herbs - 5 Gout Herbal Remedies Jun 21, 2009 ... I recently was reading one of the hundreds of emails I get in my inbox and the subject said, "I cured my gout with herbs." I was immediately ... ezinearticles.com/?I-Cured-My-Gout-With-Herbs...

Natural Remedies For Gout

Natural Remedies For Gout.

 

 

 There is a huge move from medical solutions ,to natural remedies.The reasons being:   any drugs taken will have side effects.Drugs are a short term solution to the problem. Natural  Gout Remedies offer just that:lifestyle changes with no side effects!  

 The natural remedies for gout usually include the following lifestyle changes:

The use of cherries in alleviating gout . The use of this natural remedy for gout can be found from a study as far back as 1950 .When 12 patients consumed about a pound of cherries daily,it was found that their uric acid levels dropped back to normal.Their pain levels dropped with it and their movement without pain improved with it.

Drinking a lot of water helps the body remove uric acid from the bloodstream.

A natural remedy for an  acute attack of gout may involve bed rest.

Immobilization of the affected part and local application of a heat pad and cold compresses.

  A low purine diet.  A diet that excludes organ meat like liver and  kidney.Cutting out the following: alcohol,poultry, fish, rich pastries, and fried foods. To promote uric acid clearance by the kidneys, individuals with gout will usually be encouraged to drink water with lemon added.

Here are some very useful resources for finding more natural remedies for gout:

Five Steps to Natural Gout Treatment Put a stop to the excruciating pain of a gout attack by understanding its real cause. Learn these ... articles.mercola.com/.../five-steps-to-overcoming-gout-naturall...

3 Easy To Use Home Remedies For Gout | Gout Revolution Diet
A great resource providing 3 easy to implement home remedies for gout plus the truth about how best to utilize gout home remedies in your attempt to reduce ...
goutrevolution.com/3-home-remedies-for-gout/
 Discovery Health "Home Remedies for Gout"
Learn about natural home remedies that can keep away gout, a painful affliction caused by the buildup of uric acid in the blood.
health.howstuffworks.com/home-remedies-for-gout.htm

 Natural Treatment of Gout - Dr. Weil
Find more articles and information on the treatment of gout from Dr. Andrew Weil, your trusted health advisor.
www.drweil.com/drw/u/ART00368/Gout.html

Gout Natural Cures That Work - 5 Easy Steps - YouTube
http://www.goutremoval.com The only way to truly be gout free is to completely eliminate the ...
www.youtube.com/watch?v=i1EZT8fMTUw

Related articles

• Gout Remedy Report Reviews. Does Gout Remedy Report Really Work?
• Home Remedies for Gout - 12 Natural Solutions
• Gout Diet Ideas

Cherries For Gout

Cherries For Gout.

Cherries for gout  is a natural remedy that is suggested for all gout sufferers.The reason why cherries is such a successful aid for gout pain relief ,is that it neutralizes the gout forming substances. Cherry juice is used all over Europe as a bona fide treatment for gout.The cherries are rich in anthocyanidin which lower and or normalize uric acid levels.It is  generally acccepted that cherries also contain anti inflammatory compounds.Cherries can be consumed either fresh or frozen.225 Grams of cherries per day will prevent gout attacks.Cherry extracts or tablets will work just as well when cherries are not in season.To make the cherry consumption more interesting try these juice recipes:

Cherry Juice for Gout

Juice 1 apple
8 oz of prunes
and 8 oz of cherries
Consume 3 times a day.

Vegetables that lower uric acid levels can also be added to the cherries. Here is a potent  gout fighter:

8 oz of cherries
Half an English cucumber
3 sticks of celery
Make fresh bathes 3 times a day and drink!

Cherries and apples also make a palatable gout  remedy.

Juice 8 oz of cherries
and 2 apples. Drink  fresh juices as soon as possible for the best effect.


Here are also other Cherries for Gout articles that I found :

Cherries And Gout - The GoutWife'sadinwhich lower uric acid levels. View Cherries and gout - there has been and proanthocy a lot of debate about them lately. Does eating cherries cure your gout - or is it all a bunch of old wives tales? The connection ... www.squidoo.com/cherriesandgout

Cherries May Cut Gout Pain - ABC News Sep 28, 2012 ... A Boston University study found eating up to a cup and a half of cherries within 48 hours of a gout attack lowers recurrence by 35 percent. abcnews.go.com/Health/cherries-cut-gout-pain/story?id...

Can Eating Cherries Prevent Gout Attacks? - Forbes Nov 30, 2012 ... Cherries (Photo credit: sk8geek) Based on a recent study in the Journal Arthritis & Rheumatism, patients with gout were less likely to ... www.forbes.com/.../can-eating-cherries-prevent-gout-attacks/

Cherries For Gout Review Oct 8, 2012 ... Cherries For Gout Review shows you the benefits of cherries and cherry products like cherry concentrate, cherry extract and cherry juice in ... cherriesforgout.com/

Cherries May Cut Risk of Gout Flare-ups Nov 11, 2010 ... People with gout may potentially cut in half their risk of recurrent attacks by eating about 20 cherries a day, preliminary research suggests. arthritis.webmd.com/.../cherries-may-cut-risk-of-gout-flare-up...

Related articles

• Can eating cherries prevent gout attacks?
• Cherries' anti-inflammatory action helps prevent gout

Gouty Arthritis Teatment.

English: Severe gout complicated by tophi (exudate is uric acid crystals) (Photo credit: Wikipedia)

 Gouty Arthritis.

 I must say I was quite disappointed when it turned out that gouty arthritis is exactly  the same  painful condition as just plain old gout.As for the treatment of "gouty arthritis" Who to better  define and recommend treatment for  this painful condition that plagues 1 in 7 of the world population, than Wikipedia? Read the very informative article that follows:

 

 

 Gout

From Wikipedia, the free encyclopedia

Jump to: navigation, search

"Podagra" redirects here. For the moth genus, see Podagra (moth).

Gout
Classification and external resources
Gout, a 1799 caricature by James Gillray
ICD-10	M10
ICD-9	274.00 274.1 274.8 274.9
OMIM	138900 300323
DiseasesDB	29031
MedlinePlus	000422
eMedicine	emerg/221 med/924 med/1112 oph/506 orthoped/124 radio/313
MeSH	D006073

Gout (also known as podagra when it involves the big toe)^[1] is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis—a red, tender, hot, swollen joint. The metatarsal-phalangeal joint at the base of the big toe is the most commonly affected (approximately 50% of cases). However, it may also present as tophi, kidney stones, or urate nephropathy. It is caused by elevated levels of uric acid in the blood. The uric acid crystallizes, and the crystals deposit in joints, tendons, and surrounding tissues.
Clinical diagnosis is confirmed by seeing the characteristic crystals in joint fluid. Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, or colchicine improves symptoms. Once the acute attack subsides, levels of uric acid are usually lowered via lifestyle changes, and in those with frequent attacks, allopurinol or probenecid provide long-term prevention.
Gout has increased in frequency in recent decades, affecting about 1–2% of the Western population at some point in their lives. The increase is believed due to increasing risk factors in the population, such as metabolic syndrome, longer life expectancy and changes in diet. Gout was historically known as "the disease of kings" or "rich man's disease".

Contents 1 Signs and symptoms 2 Cause 2.1 Lifestyle 2.2 Genetics 2.3 Medical conditions 2.4 Medication 3 Pathophysiology 4 Diagnosis 4.1 Synovial fluid 4.2 Blood tests 4.3 Differential diagnosis 5 Prevention 6 Treatment 6.1 NSAIDs 6.2 Colchicine 6.3 Steroids 6.4 Pegloticase 6.5 Prophylaxis 7 Prognosis 8 Epidemiology 9 History 10 In other animals 11 Research 12 References 13 External links

Signs and symptoms

Gout presenting in the metatarsal-phalangeal joint of the big toe: Note the slight redness of the skin overlying the joint.

Gout can present in a number of ways, although the most usual is a recurrent attack of acute inflammatory arthritis (a red, tender, hot, swollen joint).^[2] The metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for half of cases.^[3] Other joints, such as the heels, knees, wrists and fingers, may also be affected.^[3] Joint pain usually begins over 2–4 hours and during the night.^[3] The reason for onset at night is due to the lower body temperature then.^[1] Other symptoms may rarely occur along with the joint pain, including fatigue and a high fever.^[1][3]
Long-standing elevated uric acid levels (hyperuricemia) may result in other symptomatology, including hard, painless deposits of uric acid crystals known as tophi. Extensive tophi may lead to chronic arthritis due to bone erosion.^[4] Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent urate nephropathy.^[5]

Cause

Hyperuricemia is the underlying cause of gout. This can occur for a number of reasons, including diet, genetic predisposition, or underexcretion of urate, the salts of uric acid.^[2] Renal underexcretion of uric acid is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%.^[6] About 10% of people with hyperuricemia develop gout at some point in their lifetimes.^[7] The risk, however, varies depending on the degree of hyperuricemia. When levels are between 415 and 530 μmol/l (7 and 8.9 mg/dl), the risk is 0.5% per year, while in those with a level greater than 535 μmol/l (9 mg/dL), the risk is 4.5% per year.^[1]

Lifestyle

Dietary causes account for about 12% of gout,^[2] and include a strong association with the consumption of alcohol, fructose-sweetened drinks, meat, and seafood.^[4][8] Other triggers include physical trauma and surgery.^[6] Recent studies have found dietary factors once believed associated are, in fact, not, including the intake of purine-rich vegetables (e.g., beans, peas, lentils, and spinach) and total protein.^[9][10] The consumption of coffee, vitamin C and dairy products, as well as physical fitness, appear to decrease the risk.^[11][12][13] This is believed partly due to their effect in reducing insulin resistance.^[13]

Genetics

The occurrence of gout is partly genetic, contributing to about 60% of variability in uric acid level.^[6] Three genes called SLC2A9, SLC22A12 and ABCG2 have been found to commonly be associated with gout, and variations in them can approximately double the risk.^[14][15] Loss of function mutations in SLC2A9 and SLC22A12 cause hereditary hypouricaemia by reducing urate absorption and unopposed urate secretion.^[15] A few rare genetic disorders, including familial juvenile hyperuricemic nephropathy, medullary cystic kidney disease, phosphoribosylpyrophosphate synthetase superactivity, and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch-Nyhan syndrome, are complicated by gout.^[6]

Medical conditions

Gout frequently occurs in combination with other medical problems. Metabolic syndrome, a combination of abdominal obesity, hypertension, insulin resistance and abnormal lipid levels, occurs in nearly 75% of cases.^[3] Other conditions commonly complicated by gout include: polycythemia, lead poisoning, renal failure, hemolytic anemia, psoriasis, and solid organ transplants.^[6][16] A body mass index greater than or equal to 35 increases a male's risk of gout threefold.^[10] Chronic lead exposure and lead-contaminated alcohol are risk factors for gout due to the harmful effect of lead on kidney function.^[17] Lesch-Nyhan syndrome is often associated with gouty arthritis.

Medication

Diuretics have been associated with attacks of gout. However, a low dose of hydrochlorothiazide does not seem to increase the risk.^[18] Other medicines that have been associated include niacin and aspirin (acetylsalicylic acid).^[4] The immunosuppressive drugs ciclosporin and tacrolimus are also associated with gout,^[6] the former particularly when used in combination with hydrochlorothiazide.^[19]

Pathophysiology

Structure of uric acid (keto form) (Photo credit: Wikipedia)

Uric acid

Gout is a disorder of purine metabolism,^[6] and occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating in joints, on tendons, and in the surrounding tissues.^[4] These crystals then trigger a local immune-mediated inflammatory reaction,^[4] with one of the key proteins in the inflammatory cascade being interleukin 1β.^[6] An evolutionary loss of uricase, which breaks down uric acid, in humans and higher primates has made this condition common.^[6]
The triggers for precipitation of uric acid are not well understood. While it may crystallize at normal levels, it is more likely to do so as levels increase.^[4][20] Other factors believed important in triggering an acute episode of arthritis include cool temperatures, rapid changes in uric acid levels, acidosis,^[21][22] articular hydration, and extracellular matrix proteins, such as proteoglycans, collagens, and chondroitin sulfate.^[6] The increased precipitation at low temperatures partly explains why the joints in the feet are most commonly affected.^[2] Rapid changes in uric acid may occur due to a number of factors, including trauma, surgery, chemotherapy, diuretics, and stopping or starting allopurinol.^[1] Calcium channel blockers and losartan are associated with a lower risk of gout as compared to other medications for hypertension. ^[23]

Diagnosis

Gout on X-rays of a left foot: The typical location is the big toe joint. Note also the soft tissue swelling at the lateral border of the foot.

Spiked rods of uric acid crystals from a synovial fluid sample photographed under a microscope with polarized light. Formation of uric acid crystals in the joints is associated with gout.

Gout may be diagnosed and treated without further investigations in someone with hyperuricemia and the classic podagra. Synovial fluid analysis should be done, however, if the diagnosis is in doubt.^[1] X-rays, while useful for identifying chronic gout, have little utility in acute attacks.^[6]

Synovial fluid

A definitive diagnosis of gout is based upon the identification of monosodium urate crystals in synovial fluid or a tophus.^[3] All synovial fluid samples obtained from undiagnosed inflamed joints should be examined for these crystals.^[6] Under polarized light microscopy, they have a needle-like morphology and strong negative birefringence. This test is difficult to perform, and often requires a trained observer.^[24] The fluid must also be examined relatively quickly after aspiration, as temperature and pH affect their solubility.^[6]

Blood tests

Hyperuricemia is a classic feature of gout, but it occurs nearly half of the time without hyperuricemia, and most people with raised uric acid levels never develop gout.^[3][25] Thus, the diagnostic utility of measuring uric acid level is limited.^[3] Hyperuricemia is defined as a plasma urate level greater than 420 μmol/l (7.0 mg/dl) in males and 360 μmol/l (6.0 mg/dl) in females.^[26] Other blood tests commonly performed are white blood cell count, electrolytes, renal function, and erythrocyte sedimentation rate (ESR). However, both the white blood cells and ESR may be elevated due to gout in the absence of infection.^[27][28] A white blood cell count as high as 40.0×10⁹/l (40,000/mm³) has been documented.^[1]

Differential diagnosis

The most important differential diagnosis in gout is septic arthritis.^[3][6] This should be considered in those with signs of infection or those who do not improve with treatment.^[3] To help with diagnosis, a synovial fluid Gram stain and culture may be performed.^[3] Other conditions that look similar include pseudogout and rheumatoid arthritis.^[3] Gouty tophi, in particular when not located in a joint, can be mistaken for basal cell carcinoma,^[29] or other neoplasms.^[30]

Prevention

Both lifestyle changes and medications can decrease uric acid levels. Dietary and lifestyle choices that are effective include reducing intake of food such as meat and seafood, consuming adequate vitamin C, limiting alcohol and fructose consumption, and avoiding obesity.^[2] A low-calorie diet in obese men decreased uric acid levels by 100 µmol/l (1.7 mg/dl).^[18] Vitamin C intake of 1,500 mg per day decreases the risk of gout by 45%.^[31] Coffee, but not tea, consumption is associated with a lower risk of gout.^[32] Gout may be secondary to sleep apnea via the release of purines from oxygen-starved cells. Treatment of apnea can lessen the occurrence of attacks.^[33]

Treatment

The initial aim of treatment is to settle the symptoms of an acute attack.^[34] Repeated attacks can be prevented by different drugs used to reduce the serum uric acid levels.^[34] Ice applied for 20 to 30 minutes several times a day decreases pain.^[2][35] Options for acute treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine and steroids,^[2] while options for prevention include allopurinol, febuxostat and probenecid. Lowering uric acid levels can cure the disease.^[6] Treatment of comorbidities is also important.^[6]

NSAIDs

NSAIDs are the usual first-line treatment for gout, and no specific agent is significantly more or less effective than any other.^[2] Improvement may be seen within four hours, and treatment is recommended for one to two weeks.^[2][6] They are not recommended, however, in those with certain other health problems, such as gastrointestinal bleeding, renal failure, or heart failure.^[36] While indomethacin has historically been the most commonly used NSAID, an alternative, such as ibuprofen, may be preferred due to its better side effect profile in the absence of superior effectiveness.^[18] For those at risk of gastric side effects from NSAIDs, an additional proton pump inhibitor may be given.^[37]

Colchicine

Colchicine is an alternative for those unable to tolerate NSAIDs.^[2] Its side effects (primarily gastrointestinal upset) limit its usage.^[38] Gastrointestinal upset, however, depends on the dose, and the risk can be decreased by using smaller yet still effective doses.^[18] Colchicine may interact with other commonly prescribed drugs, such as atorvastatin and erythromycin, among others.^[38]

Steroids

Glucocorticoids have been found as effective as NSAIDs^[39] and may be used if contraindications exist for NSAIDs.^[2] They also lead to improvement when injected into the joint; a joint infection must be excluded, however, as steroids worsens this condition.^[2]

Pegloticase

Pegloticase (Krystexxa) was approved in the USA to treat gout in 2010.^[40] It is an option for the 3% of people who are intolerant to other medications.^[40] Pegloticase is administered as an intravenous infusion every two weeks,^[40] and has been found to reduce uric acid levels in this population.^[41]

Prophylaxis

A number of medications are useful for preventing further episodes of gout, including xanthine oxidase inhibitor (including allopurinol and febuxostat) and uricosurics (including probenecid and sulfinpyrazone). They are not usually commenced until one to two weeks after an acute attack has resolved, due to theoretical concerns of worsening the attack,^[2] and are often used in combination with either an NSAID or colchicine for the first three to six months.^[6] They are not recommended until a person has had two attacks of gout,^[2] unless destructive joint changes, tophi, or urate nephropathy exist,^[5] as medications have not been found cost effective until this point.^[2] Urate-lowering measures should be increased until serum uric acid levels are below 300–360 µmol/l (5.0-6.0 mg/dl), and are continued indefinitely.^[2][6] If these medications are being used chronically at the time of an attack, discontinueation is recommended.^[3] If levels cannot be brought below 6.0 mg/dl and there are recurrent attacks, this is deemed treatment failure or refractory gout.^[42] Overall, probenecid appears less effective than allopurinol.^[2]
Uricosuric medications are typically preferred if undersecretion of uric acid, as indicated by a 24-hour collection of urine results in a uric acid amount of less than 800 mg, is found.^[43] They are, however, not recommended if a person has a history of kidney stones.^[43] In a 24-hour urine excretion of more than 800 mg, which indicates overproduction, a xanthine oxidase inhibitor is preferred.^[43]
Xanthine oxidase inhibitors (including allopurinol and febuxostat) block uric acid production, and long-term therapy is safe and well tolerated, and can be used in people with renal impairment or urate stones, although allopurinol has caused hypersensitivity in a small number of individuals.^[2] In such cases, the alternative drug, febuxostat, has been recommended.^[44]

Prognosis

Without treatment, an acute attack of gout usually resolves in five to seven days. However, 60% of people have a second attack within one year.^[1] Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and renal and cardiovascular disease, thus are at increased risk of death.^[6][45] This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.^[45]
Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless tophi.^[6] These tophi occur in 30% of those who are untreated for five years, often in the helix of the ear, over the olecranon processes, or on the Achilles tendons.^[6] With aggressive treatment, they may dissolve. Kidney stones also frequently complicate gout, affecting between 10 and 40% of people, and occur due to low urine pH promoting the precipitation of uric acid.^[6] Other forms of chronic renal dysfunction may occur.^[6]

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  Nodules of the finger and helix of the ear representing gouty tophi
  
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  Tophus of the knee
  
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  Tophus of the toe, and over the external malleolus
  
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  Gout complicated by ruptured tophi (exudate tested positive for uric acid crystals)
  

Epidemiology

Gout affects around 1–2% of the Western population at some point in their lifetimes, and is becoming more common.^[2][6] Rates of gout have approximately doubled between 1990 and 2010.^[4] This rise is believed due to increasing life expectancy, changes in diet, and an increase in diseases associated with gout, such as metabolic syndrome and high blood pressure.^[10] A number of factors have been found to influence rates of gout, including age, race, and the season of the year. In men over the age of 30 and women over the age of 50, prevalence is 2%.^[36]
In the United States, gout is twice as likely in African American males as it is in European Americans.^[46] Rates are high among the peoples of the Pacific Islands and the Māori of New Zealand, but rare in Australian aborigines, despite a higher mean concentration of serum uric acid in the latter group.^[47] It has become common in China, Polynesia, and urban sub-Saharan Africa.^[6] Some studies have found attacks of gout occur more frequently in the spring. This has been attributed to seasonal changes in diet, alcohol consumption, physical activity, and temperature.^[48]

History

Antonie van Leeuwenhoek described the microscopic appearance of uric acid crystals in 1679.^[49]

The word "gout" was initially used by Randolphus of Bocking, around 1200 AD. It is derived from the Latin word gutta, meaning "a drop" (of liquid).^[49] According to the Oxford English Dictionary, this is derived from humorism and "the notion of the 'dropping' of a morbid material from the blood in and around the joints".^[50]
Gout has, however, been known since antiquity. Historically, it has been referred to as "the king of diseases and the disease of kings"^[6][51] or "rich man's disease".^[52] The first documentation of the disease is from Egypt in 2,600 BC in a description of arthritis of the big toe. The Greek physician Hippocrates around 400 BC commented on it in his Aphorisms, noting its absence in eunuchs and premenopausal women.^[49][53] Aulus Cornelius Celsus (30 AD) described the linkage with alcohol, later onset in women, and associated kidney problems:

Again thick urine, the sediment from which is white, indicates that pain and disease are to be apprehended in the region of joints or viscera... Joint troubles in the hands and feet are very frequent and persistent, such as occur in cases of podagra and cheiragra. These seldom attack eunuchs or boys before coition with a woman, or women except those in whom the menses have become suppressed... some have obtained lifelong security by refraining from wine, mead and venery.^[54]

In 1683, Thomas Sydenham, an English physician, described its occurrence in the early hours of the morning, and its predilection for older males:

Gouty patients are, generally, either old men, or men who have so worn themselves out in youth as to have brought on a premature old age—of such dissolute habits none being more common than the premature and excessive indulgence in venery, and the like exhausting passions. The victim goes to bed and sleeps in good health. About two o'clock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle or instep. The pain is like that of a dislocation, and yet parts feel as if cold water were poured over them. Then follows chills and shivers, and a little fever... The night is passed in torture, sleeplessness, turning the part affected, and perpetual change of posture; the tossing about of body being as incessant as the pain of the tortured joint, and being worse as the fit comes on.^[55]

The Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of urate crystals in 1679.^[49] In 1848, English physician Alfred Baring Garrod realized this excess uric acid in the blood was the cause of gout.^[56]

In other animals

Gout is rare in most other animals due to their ability to produce uricase, which breaks down uric acid.^[57] Humans and other great apes do not have this ability, thus gout is common.^[1][57] The Tyrannosaurus rex specimen known as "Sue", however, is believed to have suffered from gout.^[58]

Research

A number of new medications are under study for treating gout, including anakinra, canakinumab, and rilonacept.^[59] A recombinant uricase enzyme (rasburicase) is available; its use, however, is limited, as it triggers an autoimmune response. Less antigenic versions are in development.^[1]

 

For references please visit the wikipedia site at http://en.wikipedia.org/wiki/Gout.

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I also found this article that gives another perspective on "Gouty Arthritis":

Painful gouty arthritis is caused by uric-acid-crystal deposits in joint tissue. ... Gouty arthritis attacks can be precipitated by dehydration, injury, fever, heavy eating ...
www.medicinenet.com/gout/article.htm