I'm beginning to wonder if there's anything this plant can't do.... 
Cannabinoids, Positive Results for Gout
Arthropathy (Gout)
A disturbance of uric-acid metabolism occurring chiefly in males, characterized by painful inflammation of the joints, especially of the feet and hands.
Gout (also known as podagra when it involves the big toe) 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. However, it may also present itself as tophi, kidney stones, or urate nephropathy. It is caused by elevated levels of uric acid in the blood which crystallize and are deposited in joints, tendons, and surrounding tissues.
Diagnosis is confirmed clinically by the visualization of the characteristic crystals in joint fluid. Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, or colchicine, and most importantly medical marijuana improves symptoms. Once the acute attack has subsided, levels of uric acid are usually lowered via lifestyle changes.
Gout has increased in frequency in recent decades affecting approximately one to two percent of the Western population at some point in their lives. The increase is believed to be 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".
Signs and symptoms
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). T he metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for half of cases. Other joints, such as the heels, knees, wrists and fingers, may also be affected. Joint pain usually begins over 2–4 hours and during the night. The reason for onset at night is due to the lower body temperature then. Other symptoms that may occur along with the joint pain include fatigue and a high fever.
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. Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent urate nephropathy.
Cause
Hyperuricemia is the underlying cause of gout. This can occur for a number of reasons, including diet, genetic predisposition, or under excretion of urate, the salts of uric acid. Renal under excretion of uric acid is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%. About 10% of people with hyperuricemia develop gout at some point in their lifetimes. The risk, however, varies depending on the degree of hyperuricemia.
Lifestyle
Dietary causes account for about 12% of gout, and include a strong association with the consumption of alcohol, fructose-sweetened drinks, meat, and seafood. Other triggers include physical trauma and surgery. Recent studies have found dietary factors once believed to be associated are in fact not, including the intake of purine-rich vegetables and total protein. The consumption of coffee, vitamin C and dairy products as well as physical fitness appear to decrease the risk. This is believed to be partly due to their effect in reducing insulin resistance.
Genetics
The occurrence of gout is genetic, contributing to about 60% of variability in uric acid level. A few rare genetic disorders, including familial juvenile hyperuricemic nephropathy, medullary cystic kidney disease, phosphoribosylpyrophosphate synthetase super activity, and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch-Nyhan syndrome, are complicated by gout.
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. Other conditions which are commonly complicated by gout include:polycythemia, lead poisoning, renal failure, hemolytic anemia, psoriasis, and solid organ transplants. A body mass index greater than or equal to 35 increases a male's risk of gout threefold. Chronic lead exposure and lead-contaminated alcohol are risk factors for gout due to the harmful effect of lead on kidney function. Lesch-Nyhan syndrome is often associated with gouty arthritis.
Prognosis
Without treatment, an acute attack of gout will usually resolve in 5 to 7 days. However, 60% of people will have a second attack within one year. Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and renal and cardiovascular disease and thus at increased risk of death. This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.
Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless tophi. 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. 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. Other forms of chronic renal dysfunction may occur.
Epidemiology
Gout affects around 1–2% of the Western population at some point in their lifetimes, and is becoming more common. Rates of gout have approximately doubled between 1990 and 2010. This rise is believed to be due to increasing life expectancy, changes in diet, and an increase in diseases associated with gout, such as metabolic syndrome and high blood pressure. 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%.
In the United States, gout is twice as likely in African American males as it is in European Americans. Rates are high among the peoples of the Pacific Islands and the Maori of New Zealand, but rare in Australian aborigines, despite a higher mean concentration of serum uric acid in the latter group. I t has become common in China, Polynesia, and urban sub-Saharan Africa. 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.
Medication
Diuretics have been associated with attacks of gout. However, a low dose of hydrochlorothiazide does not seem to increase the risk. Other medicines that have been associated include niacin and aspirin (acetylsalicylic acid). Cyclosporine is also associated with gout, particularly when used in combination with hydrochlorothiazide, as are the immuno-suppressive drugs ciclosporin and tacrolimus.
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. A low-calorie diet in obese men decreased uric acid levels. Vitamin C intake of 1,500 mg per day decreases the risk of gout by 45% compared to 250 mg per day. Coffee, but not tea, consumption is associated with a lower risk of gout. 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.
Treatment
The initial aim of treatment is to settle the symptoms of an acute attack. Different drugs used to reduce the serum uric acid levels can prevent repeated attacks. Ice applied for 20 to 30 minutes several times a day decreases pain. Options for acute treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine and steroids, while options for prevention include allopurinol, febuxostat and probenecid. Lowering uric acid levels can cure the disease. Treatment of co morbidities is also important.
NSAIDs
NSAIDs are the usual first-line treatment for gout, and no specific agent is significantly more or less effective than any other is. Improvement may be seen within 4 hours, and treatment is recommended for 1–2 weeks. They are not recommended, however in those with certain other health problems, such as gastrointestinal bleeding, renal failure, or heart failure. 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. For those at risk of gastric side effects from NSAIDs, an additional proton pump inhibitor may be given.
Colchicine
Colchicine is an alternative for those unable to tolerate NSAIDs. Its side effects (primarily gastrointestinal upset) limit its usage. Gastrointestinal upset, however, depends on the dose, and the risk can be decreased by using smaller yet still effective doses. Colchicine may interact with other commonly prescribed drugs, such as atorvastatin and erythromycin, among others.
Steroids
Glucocorticoids have been found to be as effective as NSAIDs and may be used if contraindications exist for NSAIDs. They also lead to improvement when injected into the joint; the risk of a joint infection must be excluded, however, as they worsen this condition.
Pegloticase
Pegloticase (Krystexxa) was approved in the USA to treat gout in 2010. It will be an option for the 3% of people who are not adequately treated with other medications due to their association with severe allergic reactions. Pegloticase is administered as an intravenous infusion every two weeks. As of March 2010, however, no double blind, placebo controlled trials have been completed.
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, and are often used in combination with either an NSAID or colchicine for the first 3–6 months. They are not recommended until a person has suffered two attacks of gout, unless destructive joint changes, tophi, or urate nephropathy exist, as it is not until this point that medications have been found to be cost effective. Urate-lowering measures should be increased until serum uric acid levels are below (5.0-6.0 mg/dL) and are continued indefinitely. If these medications are being used chronically at the time of an attack, it is recommended they be continued.
As a rule of thumb, uricosuric drugs are preferred if there is under secretion of uric acid, in turn indicated if a 24-hour collection of urine results in a uric acid amount of less than 800mg. They are, however, contraindicated if the person has a history of renal stones. In contrast, a 24-hour urine excretion of more than 800mg indicates overproduction, and xanthine oxidase inhibitors are preferred. Overall, probenecid appears to be less effective than allopurinol.
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. I n such cases, the alternative drug febuxostat have been recommended.
The Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of urate crystals in 1679. In 1848 English physician, Alfred Baring Garrod realized that this excess uric acid in the blood was the cause of gout.
Gout is a disorder of purine metabolism, an nd occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating in joints, on tendons, and in the surrounding tissues. These crystals then trigger a local immune-mediated inflammatory reaction with one of the key proteins in the inflammatory cascade being interleukin 1β. An evolutionary loss of uricase, which breaks down uric acid, in humans and higher primates is what has made this condition so common.
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. Other factors believed to be important in triggering an acute episode of arthritis include cool temperatures, rapid changes in uric acid levels, acidosis, articular hydration, and extracellular matrix proteins, such as proteoglycans, collagens, and chondroitin sulfate. The increased precipitation at low temperatures partly explains why the joints in the feet are most commonly affected. Rapid changes in uric acid may occur due to a number of factors, including trauma, surgery, chemotherapy, diuretics, and stopping or starting allopurinol.
Gout is rare in most other animals due to their ability to produce uricase, which breaks down uric acid. Humans and other great apes have lost this ability, and thus gout is common. The Tyrannosaurus rex specimen known as "Sue", however, is believed to have suffered from gout.
Benefits of Marijuana
One of marijuana’s oldest recorded uses is relieving swelling and inflammation. Currently, modern scientists are exploring a network of cannabinoid receptor sites located throughout the body. This new understandings of cannabinoid research clearly supports the historical references on treating inflammation with marijuana. Different cannabinoids founds naturally in marijuana have different benefits for arthritis sufferers. Tetrahydroconnabinol (THC) is beneficial as a pain reliever. Cannabichromene (CBC) and cannabidiol (CBD) have been shown in clinical studies to have valuable anti-inflammatory properties.
Condition Description
Arthritis literally means "joint inflammation". It consists of more than 100 different conditions. The common symptoms for all these conditions are joint and musculoskeletal pain, which is why they are all considered forms of “arthritis'. Often the pain associated with arthritis is a result of inflammation of the joint lining. Inflammation is the body's natural response to injury. The warning signs that inflammation presents are redness, swelling, heat and pain. When a joint becomes inflamed, it can prevent the normal use of the joint and therefore it can cause the loss of function of joint.
Gout is one of the most painful forms of arthritis. Gout is caused when crystals of uric acid form in the connective tissue and/or joint spaces
Cont. for Research credits....
Cannabinoids, Positive Results for Gout
Arthropathy (Gout)
A disturbance of uric-acid metabolism occurring chiefly in males, characterized by painful inflammation of the joints, especially of the feet and hands.
Gout (also known as podagra when it involves the big toe) 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. However, it may also present itself as tophi, kidney stones, or urate nephropathy. It is caused by elevated levels of uric acid in the blood which crystallize and are deposited in joints, tendons, and surrounding tissues.
Diagnosis is confirmed clinically by the visualization of the characteristic crystals in joint fluid. Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, or colchicine, and most importantly medical marijuana improves symptoms. Once the acute attack has subsided, levels of uric acid are usually lowered via lifestyle changes.
Gout has increased in frequency in recent decades affecting approximately one to two percent of the Western population at some point in their lives. The increase is believed to be 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".
Signs and symptoms
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). T he metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for half of cases. Other joints, such as the heels, knees, wrists and fingers, may also be affected. Joint pain usually begins over 2–4 hours and during the night. The reason for onset at night is due to the lower body temperature then. Other symptoms that may occur along with the joint pain include fatigue and a high fever.
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. Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent urate nephropathy.
Cause
Hyperuricemia is the underlying cause of gout. This can occur for a number of reasons, including diet, genetic predisposition, or under excretion of urate, the salts of uric acid. Renal under excretion of uric acid is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%. About 10% of people with hyperuricemia develop gout at some point in their lifetimes. The risk, however, varies depending on the degree of hyperuricemia.
Lifestyle
Dietary causes account for about 12% of gout, and include a strong association with the consumption of alcohol, fructose-sweetened drinks, meat, and seafood. Other triggers include physical trauma and surgery. Recent studies have found dietary factors once believed to be associated are in fact not, including the intake of purine-rich vegetables and total protein. The consumption of coffee, vitamin C and dairy products as well as physical fitness appear to decrease the risk. This is believed to be partly due to their effect in reducing insulin resistance.
Genetics
The occurrence of gout is genetic, contributing to about 60% of variability in uric acid level. A few rare genetic disorders, including familial juvenile hyperuricemic nephropathy, medullary cystic kidney disease, phosphoribosylpyrophosphate synthetase super activity, and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch-Nyhan syndrome, are complicated by gout.
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. Other conditions which are commonly complicated by gout include:polycythemia, lead poisoning, renal failure, hemolytic anemia, psoriasis, and solid organ transplants. A body mass index greater than or equal to 35 increases a male's risk of gout threefold. Chronic lead exposure and lead-contaminated alcohol are risk factors for gout due to the harmful effect of lead on kidney function. Lesch-Nyhan syndrome is often associated with gouty arthritis.
Prognosis
Without treatment, an acute attack of gout will usually resolve in 5 to 7 days. However, 60% of people will have a second attack within one year. Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and renal and cardiovascular disease and thus at increased risk of death. This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.
Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless tophi. 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. 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. Other forms of chronic renal dysfunction may occur.
Epidemiology
Gout affects around 1–2% of the Western population at some point in their lifetimes, and is becoming more common. Rates of gout have approximately doubled between 1990 and 2010. This rise is believed to be due to increasing life expectancy, changes in diet, and an increase in diseases associated with gout, such as metabolic syndrome and high blood pressure. 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%.
In the United States, gout is twice as likely in African American males as it is in European Americans. Rates are high among the peoples of the Pacific Islands and the Maori of New Zealand, but rare in Australian aborigines, despite a higher mean concentration of serum uric acid in the latter group. I t has become common in China, Polynesia, and urban sub-Saharan Africa. 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.
Medication
Diuretics have been associated with attacks of gout. However, a low dose of hydrochlorothiazide does not seem to increase the risk. Other medicines that have been associated include niacin and aspirin (acetylsalicylic acid). Cyclosporine is also associated with gout, particularly when used in combination with hydrochlorothiazide, as are the immuno-suppressive drugs ciclosporin and tacrolimus.
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. A low-calorie diet in obese men decreased uric acid levels. Vitamin C intake of 1,500 mg per day decreases the risk of gout by 45% compared to 250 mg per day. Coffee, but not tea, consumption is associated with a lower risk of gout. 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.
Treatment
The initial aim of treatment is to settle the symptoms of an acute attack. Different drugs used to reduce the serum uric acid levels can prevent repeated attacks. Ice applied for 20 to 30 minutes several times a day decreases pain. Options for acute treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine and steroids, while options for prevention include allopurinol, febuxostat and probenecid. Lowering uric acid levels can cure the disease. Treatment of co morbidities is also important.
NSAIDs
NSAIDs are the usual first-line treatment for gout, and no specific agent is significantly more or less effective than any other is. Improvement may be seen within 4 hours, and treatment is recommended for 1–2 weeks. They are not recommended, however in those with certain other health problems, such as gastrointestinal bleeding, renal failure, or heart failure. 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. For those at risk of gastric side effects from NSAIDs, an additional proton pump inhibitor may be given.
Colchicine
Colchicine is an alternative for those unable to tolerate NSAIDs. Its side effects (primarily gastrointestinal upset) limit its usage. Gastrointestinal upset, however, depends on the dose, and the risk can be decreased by using smaller yet still effective doses. Colchicine may interact with other commonly prescribed drugs, such as atorvastatin and erythromycin, among others.
Steroids
Glucocorticoids have been found to be as effective as NSAIDs and may be used if contraindications exist for NSAIDs. They also lead to improvement when injected into the joint; the risk of a joint infection must be excluded, however, as they worsen this condition.
Pegloticase
Pegloticase (Krystexxa) was approved in the USA to treat gout in 2010. It will be an option for the 3% of people who are not adequately treated with other medications due to their association with severe allergic reactions. Pegloticase is administered as an intravenous infusion every two weeks. As of March 2010, however, no double blind, placebo controlled trials have been completed.
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, and are often used in combination with either an NSAID or colchicine for the first 3–6 months. They are not recommended until a person has suffered two attacks of gout, unless destructive joint changes, tophi, or urate nephropathy exist, as it is not until this point that medications have been found to be cost effective. Urate-lowering measures should be increased until serum uric acid levels are below (5.0-6.0 mg/dL) and are continued indefinitely. If these medications are being used chronically at the time of an attack, it is recommended they be continued.
As a rule of thumb, uricosuric drugs are preferred if there is under secretion of uric acid, in turn indicated if a 24-hour collection of urine results in a uric acid amount of less than 800mg. They are, however, contraindicated if the person has a history of renal stones. In contrast, a 24-hour urine excretion of more than 800mg indicates overproduction, and xanthine oxidase inhibitors are preferred. Overall, probenecid appears to be less effective than allopurinol.
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. I n such cases, the alternative drug febuxostat have been recommended.
The Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of urate crystals in 1679. In 1848 English physician, Alfred Baring Garrod realized that this excess uric acid in the blood was the cause of gout.
Gout is a disorder of purine metabolism, an nd occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating in joints, on tendons, and in the surrounding tissues. These crystals then trigger a local immune-mediated inflammatory reaction with one of the key proteins in the inflammatory cascade being interleukin 1β. An evolutionary loss of uricase, which breaks down uric acid, in humans and higher primates is what has made this condition so common.
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. Other factors believed to be important in triggering an acute episode of arthritis include cool temperatures, rapid changes in uric acid levels, acidosis, articular hydration, and extracellular matrix proteins, such as proteoglycans, collagens, and chondroitin sulfate. The increased precipitation at low temperatures partly explains why the joints in the feet are most commonly affected. Rapid changes in uric acid may occur due to a number of factors, including trauma, surgery, chemotherapy, diuretics, and stopping or starting allopurinol.
Gout is rare in most other animals due to their ability to produce uricase, which breaks down uric acid. Humans and other great apes have lost this ability, and thus gout is common. The Tyrannosaurus rex specimen known as "Sue", however, is believed to have suffered from gout.
Benefits of Marijuana
One of marijuana’s oldest recorded uses is relieving swelling and inflammation. Currently, modern scientists are exploring a network of cannabinoid receptor sites located throughout the body. This new understandings of cannabinoid research clearly supports the historical references on treating inflammation with marijuana. Different cannabinoids founds naturally in marijuana have different benefits for arthritis sufferers. Tetrahydroconnabinol (THC) is beneficial as a pain reliever. Cannabichromene (CBC) and cannabidiol (CBD) have been shown in clinical studies to have valuable anti-inflammatory properties.
Condition Description
Arthritis literally means "joint inflammation". It consists of more than 100 different conditions. The common symptoms for all these conditions are joint and musculoskeletal pain, which is why they are all considered forms of “arthritis'. Often the pain associated with arthritis is a result of inflammation of the joint lining. Inflammation is the body's natural response to injury. The warning signs that inflammation presents are redness, swelling, heat and pain. When a joint becomes inflamed, it can prevent the normal use of the joint and therefore it can cause the loss of function of joint.
Gout is one of the most painful forms of arthritis. Gout is caused when crystals of uric acid form in the connective tissue and/or joint spaces
Cont. for Research credits....
