I've been dealing with rheumatoid arthritis for over 10 years, my specialist says that activity really helps, between bike riding and Enbrel, my issues (ankles, wrists, hands, some knees) are under control.
Spin as fast as possible, and don't do any work - less resistance, the better, along with more movement, the better.
Take time to warm up before starting out.
I think my condition is not classified as artritis yet but i will probably end up with that. I'll see another orthopedist on Monday to see the latest status. Today i felt a small locking on my right knee. There is no pain now though. Maybe the mixture of ginger, turmeric and cherry stem helped to alleviate the inflammation.
In addition we should not overlook the use of topical anti-inflammatory drugs like Voltaren for arthritis. The dosage of such drugs is necessarily low compared to a systemic absorption of NSAIDs taken enterally or parenterally. Similarly the side effects of such drugs should be reduced compared to effective doses of systemically absorbed NSAIDs. The topical NSAIDs are very inconvenient, but they can be very attractive to those who cannot safely take NSAIDs by mouth.
Argue with Lancet-these folks will tell you the risk level.
The new study, published in The Lancet, found that high doses of not only coxibs but also older-generation NSAIDs like ibuprofen (Advil) or diclofenac (Voltaren) were associated with heart disease risk.
"For every 1,000 individuals with a moderate risk of heart disease allocated to one year of treatment with high-dose diclofenac or ibuprofen, about three would experience an avoidable heart attack of which one would be fatal," said a press statement accompanying the study.
"In addition, all NSAIDs double the risk of heart failure and produce a 2-4 times increased risk of serious upper gastrointestinal complications such as bleeding ulcers," said the statement.
A high dose of diclofenac is indicated as 150 milligrammes per day and of ibuprofen about 2,400 milligrams per day.
"High doses are generally doses available only with a prescription," said Griffin.
Read more: http://www.nydailynews.com/life-styl...#ixzz2ooMBzisy
The OTC folks beat back the suggested labeling change-MI risks- so I was wrong suggesting you would find it on the label-my mistake.
However-what i said-not one bit biased- "just the facts" according to our Limey friends.
Oh-I never said NSAID shouldn't be used-I use them- use home made pepper cream also.
My comment was in response to surgeonstone's blanket condemnation of opiates for "arthritic pain"
The conclusion of the study is that non-aspirin NSAIDs should not be used with the expectation if protection from serious cardiac episodes, but no mention is made of avoiding them due to their causation of such episodes.
As I said the decision whether or not to use NSAIDs and which one to use is complex and personal, but blanket avoidance isn't automatically indicated. I don't think we are that so far apart. I just feel that many people who could be helped on balance by NSAID therapy are improperly frightened away from it by the sensational press the subject has received.
Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trials
Coxib and traditional NSAID Trialists' (CNT) Collaboration†
The vascular and gastrointestinal effects of non-steroidal anti-inflammatory drugs (NSAIDs), including selective COX-2 inhibitors (coxibs) and traditional non-steroidal anti-inflammatory drugs (tNSAIDs), are not well characterised, particularly in patients at increased risk of vascular disease. We aimed to provide such information through meta-analyses of randomised trials.
We undertook meta-analyses of 280 trials of NSAIDs versus placebo (124 513 participants, 68 342 person-years) and 474 trials of one NSAID versus another NSAID (229 296 participants, 165 456 person-years). The main outcomes were major vascular events (non-fatal myocardial infarction, non-fatal stroke, or vascular death); major coronary events (non-fatal myocardial infarction or coronary death); stroke; mortality; heart failure; and upper gastrointestinal complications (perforation, obstruction, or bleed).
Major vascular events were increased by about a third by a coxib (rate ratio [RR] 1·37, 95% CI 1·14—1·66; p=0·0009) or diclofenac (1·41, 1·12—1·78; p=0·0036), chiefly due to an increase in major coronary events (coxibs 1·76, 1·31—2·37; p=0·0001; diclofenac 1·70, 1·19—2·41; p=0·0032). Ibuprofen also significantly increased major coronary events (2·22, 1·10—4·48; p=0·0253), but not major vascular events (1·44, 0·89—2·33). Compared with placebo, of 1000 patients allocated to a coxib or diclofenac for a year, three more had major vascular events, one of which was fatal. Naproxen did not significantly increase major vascular events (0·93, 0·69—1·27). Vascular death was increased significantly by coxibs (1·58, 99% CI 1·00—2·49; p=0·0103) and diclofenac (1·65, 0·95—2·85, p=0·0187), non-significantly by ibuprofen (1·90, 0·56—6·41; p=0·17), but not by naproxen (1·08, 0·48—2·47, p=0·80). The proportional effects on major vascular events were independent of baseline characteristics, including vascular risk. Heart failure risk was roughly doubled by all NSAIDs. All NSAID regimens increased upper gastrointestinal complications (coxibs 1·81, 1·17—2·81, p=0·0070; diclofenac 1·89, 1·16—3·09, p=0·0106; ibuprofen 3·97, 2·22—7·10, p<0·0001; and naproxen 4·22, 2·71—6·56, p<0·0001).
The vascular risks of high-dose diclofenac, and possibly ibuprofen, are comparable to coxibs, whereas high-dose naproxen is associated with less vascular risk than other NSAIDs. Although NSAIDs increase vascular and gastrointestinal risks, the size of these risks can be predicted, which could help guide clinical decision making.
ME AGAIN- my whole point was objecting to a blanket condemnation of opiates for osteoarthritis- USA medicine swings back and forth-20-30 year cycles-on that point-
Opiates keep making comebacks because the alternatives-have problems-
I take naproxen for joint pain-works great.Sure as hell wouldn't take ANY of the rest.
This study was HIGH DOSE.
A low dose of ibuprofen would be maybe 800mg/d this study was 2400mg- a max dose would be 3200/d
Was the earlier study with "all doses"?
There is almost always a dose effect on "side effects" (except allergies)-take more have more problems-take less fewer problems.
Topically??- probably ZERO detectable MI or stomach risk.
Blood levels are sooooo low-no problems-
Yeah I wouldn't worry one bit about topical application.
Oh-slight aside-indications that various NSAID cause problems with some ACE inhibitors for HBP-making them less effective
and some indications they can decrease kidney function with chronic use.
I think the other good news regarding the topical NSAID application is you can continue an aspirin regimen along with the non-aspirin NSAID without either unduly stressing the GI tract or losing any of the protective effect. I am just assuming that, but it makes sense if the systemic absorption of the topical NSAID is really so low.
Relative to taking it by mouth-topical absorption of most drugs-minimal.
Takes "lots of doing" and lots of time and high lipid solubility to get various estrogen preps properly absorbed-probably only 2-3% of estrogen in various patches is absorbed-and that takes 4 days-high lipid solubility-perfect contact
Now "some" of your topical NSAID gets absorbed-but blood levels would be much much lower than oral-probably can find a study showing just that-bet peak blood level 1/100 to 1/10,000 peak level of oral dose-
Yes-I take lisinopril also- cheap safe effective hard to beat- maybe it makes my nose run-but no cough
And good evidence that NSAID decrease renal artery flow-transient of course-(pretty sure I have noticed that I get up less at night(63yo) when I take a naproxen in the late evening-anecdote of course,but...)
The speculation is the decreased renal artery blood flow-triggers increase in BP(maybe pulse too) and that-along with the "not aspirin effect(sorta opposite effect) on platelet adhesion" is the WHY of the increased MI risk from NSAID
I'm in River Ridge now-between harahan and kenner -lived off Tulane then on State street near the river then off Claiborne near Broadway -moved to River Ridge 25 years ago
I'm almost exactly one mile from the river-
makes rides nice-ride down to levee-climb levee 15 times-ride home
Nice day today-a bit miserable yesterday.Did you ride today?
Now the saints-hmmmm- never an optimist when it comes to the saints-but these saints sure aren't "the old saints"
With regards to NSAID use I agree with the Lancet entirely. There are side effects and one must, with the help of a doc, do some risk assessment. is the risk of a fatal heart attack less or more than the risk of a fatal pulmonary embolism secondary to a DVT post op hip replacement. For me, I have no history of heart disease in the family, no history of hypertension nor a history of elevated lipids. I thus rationalize the use and risk of NSAID's as being reasonable for now. Were I suffering from hypertension, were I at a significant familial risk of MI, I might very well reduce or avoid the NSAID's and go for reparative surgery earlier.
It's all a risk relevant crap shoot and you can never know for sure the outcome...... except for one of the topics discussed above. And that is that repeated opiate use for chronic pain will cause addiction and is, IMHO, malpractice.
Now there are some situations where even that state can't be avoided, the patient with severe RA that can't move, that can't get surgery, that quite literally has no other options. In that situation even the "malpractice" option may be needed but all concerned need to completely understand the path they are embarking on.
An interesting side note, we in America comprise 4.28% of the worlds population and consume 70 percent of the worlds narcotics.
I thought aspirin is supposed to reduce the risk of heart attacks?
surgeonstone, thanks that is a very helpful treatment of the issue. Appreciated.