The main problem that RLS sufferers face when they visit their doctor for a diagnosis, is that the doctor is joined at the hip with the pharmaceutical industry, and all of its products.
They're even given incentives by the Drug Companies to push their products.
There are a few doctors moving toward a more natural practice, but they are few and far between.
If a scientist happens to run a few tests one day on some poor mouse and discovers that inflammation is at the core of Restless Legs Syndrome, doctors are not going to start prescribing curcumin or ginger root to their RLS patients.
Doctors prescribe drugs. That's what they're trained to do. If the issue is inflammation, what they will prescribe to you is a Nonsteroidal anti-inflammatory drug (NSAID).
The problem is, NSAIDs usually feature powerful side effects that don't allow the patient to stay on them too long.
Here's an excerpt from an article about Restless Legs Syndrome from the The NY Times website.
The key words in the above summary are "NSAIDs worked well."
So, that tells us something. It's a clue. It tells us the MAYBE inflammation is the problem. However, the profound side effects that NSAIDs create eliminate them an option as a long lasting remedy for RLS.
This is where the herbs and supplements come in. They're just as effective and feature no dangerous side effects.
Here is an exerpt from an article about the dangerous side effects of NSAIDs.
It's your choice on whether or not to avoid the unpleasantness. It's simply a case of changing one's attitude towards herbs and supplements. Again, scientific studies have proven that they're just as effective in the healing of inflammation.
The rest of this page features an overview of NSAIDs and more about the potential side effects.
Nonsteroidal anti-inflammatory drugs, usually abbreviated to NSAIDs or NAIDs, are drugs with analgesic, antipyretic (fever-reducing) and, in higher doses, with anti-inflammatory effects (reducing inflammation). The term "nonsteroidal" is used to distinguish these drugs from steroids, which (among a broad range of other effects) have a similar eicosanoid-depressing, anti-inflammatory action. As analgesics, NSAIDs are unusual in that they are non-narcotic.
NSAIDs are sometimes also referred to as nonsteroidal anti-inflammatory agents/analgesics (NSAIAs) or nonsteroidal anti-inflammatory medicines (NSAIMs). The most prominent members of this group of drugs are aspirin, ibuprofen, and naproxen partly because they are available over-the-counter in many areas.110
NSAIDs are associated with several side effects. The frequency of side effects varies among NSAIDs. The most common side effects are nausea, vomiting, diarrhea, constipation, decreased appetite, rash, dizziness, headache, and drowsiness. NSAIDs may also cause fluid retention, leading to edema (observable swelling from fluid accumulation in body tissues). The most serious side effects are kidney failure, liver failure, ulcers and prolonged bleeding after an injury or surgery.
NSAIDs also decrease the ability of the blood to clot and therefore increase bleeding. When used with other drugs that also increase bleeding [for example, warfarin (Coumadin)], there is an increased likelihood of serious bleeding or complications of bleeding. Therefore, individuals who are taking drugs that reduce the ability of blood to clot should avoid prolonged use of NSAIDs.
Nonsteroidal antiinflammatory drugs also may increase blood pressure in patients with hypertension (high blood pressure) and therefore antagonize the action of drugs that are used to treat hypertension.108
Most NSAIDs penetrate poorly into the central nervous system (CNS). However, the COX enzymes are expressed constitutively in some areas of the CNS, meaning that even limited penetration may cause adverse effects such as somnolence and dizziness.
In very rare cases, ibuprofen can cause aseptic meningitis.
As with other drugs, allergies to NSAIDs might exist. While many allergies are specific to one NSAID, up to 1 in 5 people may have unpredictable cross-reactive allergic responses to other NSAIDs as well.110
The main ADRs (adverse drug reactions) associated with use of NSAIDs relate to direct and indirect irritation of the gastrointestinal tract (GIT). NSAIDs cause a dual insult on the GIT: the acidic molecules directly irritate the gastric mucosa, and inhibition of COX-1 reduces the levels of protective prostaglandins. Inhibition of prostaglandin synthesis in the GI tract causes increased gastric acid secretion, diminished bicarbonate secretion, diminished mucous secretion and diminished trophic effects on epithelial mucosa.
Common gastrointestinal ADRs include:
* Gastric ulceration/bleeding
Risk of ulceration increases with duration of therapy, and with higher doses. In attempting to minimise GI ADRs, it is prudent to use the lowest effective dose for the shortest period of time, a practice which studies show is not often followed. Recent studies show that over 50% of patients taking NSAIDs have sustained damage to their small intestine.111
There are also some differences in the propensity of individual agents to cause gastrointestinal ADRs. Indomethacin, ketoprofen and piroxicam appear to have the highest prevalence of gastric ADRs, while ibuprofen (lower doses) and Diclofenac appear to have lower rates.
Certain NSAIDs, such as aspirin, have been marketed in enteric-coated formulations which are claimed to reduce the incidence of gastrointestinal ADRs. Similarly, there is a belief that rectal formulations may reduce gastrointestinal ADRs. However, in consideration of the mechanism of such ADRs and indeed in clinical practice, these formulations have not been shown to have a reduced risk of GI ulceration.109
Commonly, gastrointestinal adverse effects can be reduced through suppressing acid production, by concomitant use of a proton pump inhibitor, e.g. omeprazole, esomeprazole; or the prostaglandin analogue misoprostol. Misoprostol is itself associated with a high incidence of gastrointestinal ADRs (diarrhea). While these techniques may be effective, they prove to be expensive for maintenance therapy.110
A recent meta-analysis of all trials comparing NSAIDs found an 80% increase in the risk of myocardial infarction with both newer COX-2 antagonists and high dose traditional anti-inflammatories compared with placebo.112
NSAIDs aside from (low-dose) aspirin are associated with a doubled risk of symptomatic heart failure in patients without a history of cardiac disease. In patients with such a history, however, use of NSAIDs (aside from low-dose aspirin) was associated with more than 10-fold increase in heart failure. If this link is found to be causal, NSAIDs are estimated to be responsible for up to 20 percent of hospital admissions for congestive heart failure.113
NSAIDs are also associated with a relatively high incidence of renal adverse drug reactions (ADRs). The mechanism of these renal ADRs is due to changes in renal haemodynamics (blood flow), ordinarily mediated by prostaglandins, which are affected by NSAIDs. Prostaglandins normally cause vasodilation of the afferent arterioles of the glomeruli. This helps maintain normal glomerular perfusion and glomerular filtration rate (GFR), an indicator of renal function. This is particularly important in renal failure where the kidney is trying to maintain renal perfusion pressure by elevated angiotensin II levels. At these elevated levels, angiotensin II also constricts the afferent ateriole into the glomerulus in addition to the efferent arteriole one it normally constricts. Prostaglandins serve to dilate the afferent arteriole; by blocking this prostaglandin-mediated effect, particularly in renal failure, NSAIDs cause unopposed constriction of the afferent arteriole and decreased renal perfusion pressure. Horses are particularly prone to these adverse affects compared to other domestic animal species.
Common ADRs associated with altered renal function include: 109
* Salt and fluid retention
* Hypertension (high blood pressure)
These agents may also cause renal impairment, especially in combination with other nephrotoxic agents. Renal failure is especially a risk if the patient is also concomitantly taking an ACE inhibitor and a diuretic - the so-called "triple whammy" effect.114
In rarer instances NSAIDs may also cause more severe renal conditions:109
* Interstitial nephritis
* Nephrotic syndrome
* Acute renal failure
* Acute tubular necrosis
NSAIDs in combination with excessive use of phenacetin and/or paracetamol may lead to analgesic nephropathy.115
Photosensitivity is a commonly overlooked adverse effect of many of the NSAIDs.116 It is somewhat ironic that these anti-inflammatory agents may themselves produce inflammation in combination with exposure to sunlight. The 2-arylpropionic acids have proven to be the most likely to produce photosensitivity reactions, but other NSAIDs have also been implicated including piroxicam, diclofenac and benzydamine.
Benoxaprofen, since withdrawn due to its hepatotoxicity, was the most photoactive NSAID observed. The mechanism of photosensitivity, responsible for the high photoactivity of the 2-arylpropionic acids, is the ready decarboxylation of the carboxylic acid moiety. The specific absorbance characteristics of the different chromophoric 2-aryl substituents, affects the decarboxylation mechanism. While ibuprofen is somewhat of an exception, having weak absorption, it has been reported to be a weak ph.110
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