The article points out that Clinton had a few advantages from the outset that Bush didn't have: 1) an economy that was beginning to run at optimum as he took office, and 2) an end to the Cold War that allowed him to reduce military spending even as it gave Fed Chairman Alan Greenspan the confidence to reduce interest rates.

Democrats have been attempting to demonize the economy under Bush for several years now.  It isn't true now.  It never was true.

Bush vs. Clinton: The Economic Verdict

April 18, 2007 03:49 PM ET | Permanent Link

Capital Commerce hosted a compelling, no-holds-barred economics debate last week between financial pros and blogging greats Donald Luskin and Barry Ritholtz, which had the one downside of not letting me address the controversy that flared up over which economy has been superior–the Bush economy or the Clinton economy.

First, some context. When Bill Clinton became president in 1993, he was dealt the greatest hand since Phil Jackson became coach of the Chicago Bulls with probable future hall-of-famers Michael Jordan and Scottie Pippen already on the team. The U.S. economy was already expanding, and the disintegration of the Soviet Union seemingly meant that defense spending could come down–which encouraged Federal Reserve Chairman Alan Greenspan to cut interest rates. Then Clinton got a Republican Congress in 1995 that was also eager to bring the budget into balance.

By contrast, Bush inherited an expansion that was on its last legs, and then he had to raise defense spending to deal with the biggest attack on America in its history–of course, neither Bush nor Congress has shown a whole lot of interest in controlling nondefense spending. Now, one way to statistically compare the two economic records is by looking at the Bush expansion vs. the Clinton expansion. And 21 quarters into each, the economy has grown 16.6 percent under Bush vs. 19.9 percent under Clinton–advantage No. 42. And the unemployment rate 22 quarters into each expansion–jobs numbers come out more frequently – show that the current unemployment rate is 4.4 percent vs. 4.5 percent under Clinton. Slight edge to No. 43. Now, when you add in–or subtract out–the effects of the stock market (for Clinton) and housing bubbles (for Bush) and where each president began, I think this ends up as a "pick 'em" situation at this point. Here is what White House spokesman Tony Fratto told the Washington Examiner last week:

"This is a much stronger expansion in a lot of ways. It's much deeper and more measured ... If you go back to this point in the Clinton expansion, they would have loved to have seen the numbers that we have right now. ... On the unemployment rate, we're a full percentage point below where they were at the same point in the expansion–60 or 61 months in. They would have loved to have been at 4.4 percent. They were still up in the mid-5s, which is huge, when you think about it."

OK, let's use Fratto's methodology. I checked the employment data from the U.S. Bureau of Labor Statistics and found that 60 months into the Clinton expansion, the unemployment rate was 4.7 percent vs. 4.5 percent for Bush. The last time the jobless rate was as high as 5.3 percent under Clinton was January 1997, 49 months into the Clinton expansion. Fratto and I went back and forth on the numbers and how to best date the expansions, but his bottom line–via E-mail–is this:

"The Clinton administration clearly benefited from an expansion that began well before the election and well before they ever passed a single piece of economic legislation. This administration was clearly hurt by being greeted with a recession and the implosion of the technology bubble – well before we ever passed any part of our economic policy."

But my bottom line is that neither Clinton nor Bush was or has been a game changer. (My friend Larry Kudlow has a great post on this topic here.) FDR was a game changer. Reagan was a game changer. I think to be a game changer today you have to 1) revamp America's social insurance program for the 21st-century challenges of globalization and changing demographics, and 2) reform America's creaky and complex tax system to better allow the nation to innovate and compete. Still waiting on those.

I wrote an article titled "How to Demagogue the Economy."  The facts of the matter are that the United States has the strongest and most competitive economy in the world, and that the media have a documented history of viewing the economy through rose-colored glasses during Democratic administrations, but an unrelentingly critical scowl during Republican administrations.

If Barack Obama is elected President, the same numbers that were portrayed as terrible will suddenly be portrayed as good.

I want people to vote according to their consciences and their worldviews, even if my "side" loses as a result.  What I most assuredly don't want is for people to be tricked into voting for a media-created narrative that simply isn't true.

*...But as I am writing it now, I've modified it significantly so as to blend better with current thought, and also to incorporate recent concepts when relevant...*

As I explained in Playing the Victim, one of my co-workers was suffering from acute depression, and asked for advice. The solution I gave her was *obviously* to stop "playing the victim", and accept responsibility for her life - thus empowering herself and providing the psychological leverage needed to deal with the other issues, and begin progressing with life again. Although this solution is logically valid, I've become to realize more and more how much truth cannot be logically justified -so, for lack of better feelings, I should  "be more considerate of her feelings"- for lack of better phrasing - So this depression needs to be handled more gradually, using "gentler" methods :P

Due to the ever-constant chaos already eminent in her life, dealing with it logically would be impossible, because logic has already become irrelevant. I assured her that I would see what I could do in finding a [irony alert!] more *reasonable* solution, and fortunately, I think I've found one. Well, from the looks of things the *best* solution is a work-in-progress, but at the very least it's something to work off of. Of course the solution has nothing to do with drugs. I was medicated for several years in the past, and although I definitely had, and *have* the illnesses I was diagnosed with, I found I did far better without them. Come to think of it, the several different medications I was given did little more than sedate me. As far as I can tell, that was about it. Don't ask why, I have know clue :P

As I mentioned in that same post ("Playing the Victim") I was able to deal with my psychological issues best (by an overwhelming margin) without medication; if anything the medication just made things worse. So although I cannot speak for anyone else, From my person experiences I would definitely recommend against the ingestion of psychological drugs of any kind. Treatment is frequently contrasted with "Cure", being only a temporary/partial solution (i.e. to minimize symptoms)- Cures are permanent.

I think the fact that medication only minimizes symptoms is particularly interesting- after all, "Symptoms" are the proof that the body/mind/etc. is fighting against the disease/etc. If the symptoms disappear, that doesn't mean the person is better. In fact, if the disease/etc. still exist despite symptoms, that should be considered a bad thing, since the immune system is essentially being suppressed, allowing the disease freely roam, resulting in far worse [in this case] mental health. Well, that's just speculation on my part, but such an opinion is also implied in "I Never Promised you Roses". In the cases of depression, the "cure" might well be to deal with the problem as described in "Playing the Victim"- however, for now, a temporary solution [*treatment*] should suffice.

Among many-- more minor illnesses, I have Bipolar- previously known as "manic-depressive" disorder. The previous name is much more descriptive, but I guess they're trying to be more politically correct :P I regularly go through cycles- between depressive and more manic states; I maintain a more "normal" demeanor in-between. The upside and downside of Bipolar is the same: the cycles are predictable. That is- I only get depressed or manic "when I'm supposed to"- this makes cycles very predictable, and I can schedule accordingly, since it works like clockwork. But of course, no one likes getting depressed-- well, I'm sure plenty of people like getting manic though :P Then again, I don't ever get anxious (for certain reasons that I'll cover in later posts) so I don't have to deal with that part of the manic cycle...but for whatever its worth, that's the downside.

A while ago I realized that I could completely thwart the depression cycles (although the manic isn't so bad) by making a habit of automatically rejecting the logical validity of all negative thoughts. Although I did not realize it then, I had already been doing such a thing for a few years now. But I have also realized that, in accordance with balance, to disregard any emotion logically, I had to lose my emotions; this is because to logically get rid of emotions, one must believe any previous emotions to never have existed- this is necessary because emotions are the backbone of passion and desire- no decision can follow through without one's emotions backing it.

Getting back to habits though, as I detailed in [insert post], it's possible to force oneself to change the perception of anything you want, even if it is the exact opposite of the original and natural perception. In that experiment, as I was walking in the freezing cold (of last winter, to be exact) I decided to imagine the pain as being pleasure, and concentrated on the cold being a good thing, setting aside all "common sense" in favor of this perception. The result was a bit surprising- by concentrating the pain completely went away- it was very exciting seeing how perceptions can be manipulated this way.

The only thing lacking with this is that one must concentrate to experience the conversion. That's where habits come in. The purpose of habits is to keep of memory of thing that are done often, and usually require a degree of concentration. It is an adaptation that allows us to perform tasks better the more that we do it, because those things we've already concentrated on a lot are stored in our "cache", which frees up our "memory" to focus on the finer details, or other tasks. Although perhaps I'm a bit partial due to my hobbies, I think that the human brain is strikingly similar to the computer- or, even more likely, the other way around.

As a result of these habits, I have not felt depressed for a few years now.

*Note "felt"- "depression can mean more than one thing; "felt" meaning that I have not had any sad or depressing thoughts for a while. In retrospect BTW this is not a good thing- to accomplish this required "unbreacheable" psychological walls to be put up, resulting in an almost completely nonchalant perspective towards everything; the root meaning of depression ("to slow down"/ "fall" / "be undone" /etc) is still true even now- the depression just does not include the emotional components (i.e. sadness/melancholy/etc.)*

There was one brief period a while back (see Self-Awareness post ) but that only last half an hour. I was thrust into a terrible depression, due to not being able to prepare a decent resume (I had no work experience at the time). But, seeing that I needed it to get done, I forcibly moved myself forward, and was able to pull off what had appeared to be impossible, thus effectively ending that "episode". Recalling this incident has also played a key role in determining another, more "reasonable" solution to my coworker's problem.

All of "today" (*see top*), as expected, I experienced the usual wave of depression. Well, I say depressed, but (as explained above) the only symptom I still experience is a complete lack of motivation to do anything productive. On these days I might normally do nothing but watch anime- and in WCS even lack the motivation to play games. But even when I have such days, going to work is not a problem. Actually, on these days going to work is actually more of a vacation, anyway. Much of the reason for this is explained in Opportunity- that is, working each day with the awareness that half my pay is not in the salary, but in the opportunity to work. As I've discovered over time, the reason why working can be so fulfilling- is because of expectations- knowing that our coworkers and supervisors expect us to do the job well, and fullfilling those expectations, fills us with a wonderful sense of pride. The way I see it, this is "running away from ourselves"- here's why:

Who we are- that which we perceive ourselves to be, and also who and that which we perceive others to be, is dependent on memory, which also means that we can only see ourselves and other people as we were in the past. That is because we are contantly changing and growing, clarifying and building upon who we are every second, although the changes may not be noticed for years. Because of that, the person we perceive ourselves to be, is actually the past, and is not entirely accurate. The irony (and amusement) of this, is that we are able to change in the first place for this same reason. See, to move forward and grow, we must leave our past behind us, which I believe is a necessity due to balance. Interestingly enough, it is also a central theme for reincarnation. So "running away" from ourself in essence means "leaving behind the past" to move towards a better future. So perhaps a more optimistic phrasing would be "running to" (although that would totally kill the visual)

Since I am a restless individual, lacking in patience (although I have aquired a significant patience these past few months, in recognition of the need) I first dealt with my lack of motivation by being confrontational (i.e. a complete ass) with my roommates. Thinking about it now, that initial approach is strikingly similar to Linkin Park's song "Breaking the Habit". From what I can tell, this journey I'm going through has an extremely close likeness that the journey that Linkin Park depicts in their music, so I often listen to the words of their songs for guidance. As the contributers (of that song) in Linkin Park did though, I realized that there were better ways of dealing with it, that I needed to 'break the habit'.

So I started settling down, and played games with them instead. Here I realized another way of self-treating depression. Summing it all up, a person's psychological health is primarily dependent on one factor- pride. This is why it's important to not play the victim- depression is caused by insecurity. The opposite of insecurity is self-control. Taking control of a situation is an active way of alleviating insecurity (and thus depression), but it's likely that in most cases of depression, the person's state-of-mind renders them incapable of taking the initiative- thus a passive response is necessary. By playing games with my roommates that I knew I would win, and by following through with that expectation, I am able to alleviate my insecurity in a passive manner. That is, it required no initiative, because they already wanted to play- I only had to say "yes". Thus, one of the best ways to alleviate depression passively, without initiative, is to put oneself in an environment where we will succeed, and have the expectations of others to drive and support that success.

With both the resume incident and the days that I played games to relieve depression, the key factor is power. In one way or another, empowering oneself plays a vital role in allowing us to move on. To put in another way, the most efficient way to get over depression is to "pet your ego" by showing off your strengths to others. Pride is, after all, one of our greatest needs as humans, making this a reliable "quick fix" for depression

Gym class for me means changing, listening to the "coach" (although he's really not a coach) mumble through whatever we're doing that day (the more he talks the more stupid he looks, yet he keeps on talking) and then i stand around with my freinds for the whole period.  sometimes when we play football we just walk around on the field.  i mean, you'd think we sound like losers, the gym class nerds, but we're not alone.

i'm a senior in high school so i've completed three years of (actual) gym class.  i can't honestly say i've sweet once.  i've come back in soaking wet, because according to the teacher, a little rain never hurt anybody.  i guess according to the gym teacher there's no such thing as chafing. 

not only do they make us go to gym class, but my school makes it a graduation requirment!   they try to pass of that excuse for a class as something useful, like i'm getting something out of it.  like learning the rules of football is so important that i can't graduate without it.

people laugh at the ones who fail gym.  "how can you fail gym?" obviously it istn' hard, based on what i've already written, but the truth is, your grade depends on your willingness to bring, and change into, gym clothes.  if you forget to bring them five times, you fail.  you have to take gym in the summer.  so first they tell us that gym is a graduation requirment, pretending that we get something usefull out of it, but then they say, really the only thing you have to do in gym is change into a pair of shorts.  seems a little hypicrytical to me.

the sad thing is, when budget cuts come around, the first programs to get cut are music, drama, art, bassically anything that requires creative thinking.  because running around a track is more important.  put the crayons away, turn your brain off, practice hard ss oyou can become a professionaly athlete and earn millions and millions of dollars that you don't deserve. (sure, you agree they shouldn't get paid so much, but you don't turn them off.  i told my dad i'd boycott professional sports because i don't agree with the amount they get paid, he said, "yeah me neither"  obviously not, mr. 'i have to watch my game every sunday and if you annoy me i'll ground you for a year,' yeah, you agree with me.)

Gym is hurtful to a lot of people too.  the fat ones.  the ones who have to take off they're baggy clothes to tell the whole world they're a few pounds over weight.  i guarentee gym is not helping them lose those pounds.  it's just making them feel bad about them, it lowers their self esteem. 

i just hate it so much that not only is gym such a joke, but it's a joke that's a graduation requirment, while creative thinking classes are thrown out.  they're implying that physical activity is more important than engaging your mind.  that if your over wieght, it's a problem you have to fix or you'll lose out.  "stop engaging your mind and rund around the track, because if you're fat, you're worthless."  and that is why i refuse to take any gym class, gym teacher, or athletic program seriously.

and i WON'T watch professional sports.

Rheumatoid arthritis (RA) is a common disease that affects about 1% of the population worldwide. Women are affected almost 3 times as often as men. The prevalence increases with advancing age, and 4% to 6% of the white population older than 65 years may have RA. Although the cause is unknown, evidence suggests an association between severe RA and HLA, particularly to alleles coding for a shared epitope on the HLA-DRB1 molecule.

Major features of active disease include symmetrical polyarthritis with joint swelling and tenderness and morning stiffness lasting for an hour or longer. Subcutaneous nodules, presence of rheumatoid factor (in about 80% of patients with RA), and radio graphically evident erosions or juxta-articular osteoporosis in or adjacent to the involved joints are further characteristics of RA.

The onset and clinical course of RA are variable. Gradual onset is most common. About 20% of patients will have a monocyclic course, which will abate within 2 years, whereas the rest will have a polycyclic or progressive course.¹ The long-term prognosis of patients with abrupt onset of disease is similar to that for patients with gradual onset of disease.²

Rheumatoid arthritis is one of the most common causes of disability. After 12 years of disease, more than 80% of patients with RA are partially disabled, and 16% are completely disabled.³ Life expectancy is shortened by an average of 7 years in men and 3 years in women, an outcome equivalent to the increased mortality of patients with Hodgkin disease, diabetes, and stroke.⁴ Factors contributing to the poor prognosis include the presence of extra-articular disease and infections, as well as complications of treatment such as gastrointestinal (GI) toxic effects of nonsteroidal anti-inflammatory drugs (NSAIDs).

MANAGEMENT PRINCIPLES

The goals of therapy for RA are to alleviate pain, control inflammation, preserve the ability of the patient to function in activities of daily living and work, and prevent joint destruction. Appropriate and timely therapeutic intervention after accurate diagnosis diminishes not only the symptoms but also the progress of RA. The primary care physician has a crucial role in this process by early recognition of the symptoms of RA, leading to its diagnosis and use of the resources necessary to establish a successful treatment program to achieve these goals, and by participating in the ongoing management of the patient with RA.Early in the course of RA, education on the disease and vocational, lifestyle, and family counseling must be provided. Patients are best served by a multidisciplinary team that includes a rheumatologist and other specially trained medical personnel, including nurses and occupational and physical therapists skilled and knowledgeable about RA. Physical modalities such as joint protection, orthotics and other adaptive devices, and exercises improve the symptoms, function, and well-being of the patient. Adequate rest reduces the fatigue associated with active RA, and resting the involved joints lessens the symptoms of inflammation.

THERAPY

Nonsteroidal anti-inflammatory drugs reduce inflammation and help relieve pain but seldom completely eliminate signs and symptoms of active arthritis. They inhibit 1 or both types of cyclooxygenase (COX). Cyclooxygenase-1 is constitutively expressed in the GI mucosa, kidneys, platelets, and vascular endothelium. Cyclooxygenase-2 is functionally expressed and promotes the elaboration of prostaglandins in inflamed tissues.

Selective blockage of COX-2 may lead to an improved safety profile for these agents. Celecoxib and rofecoxib are the first such agents available in the United States that selectively block COX-2. Rofecoxib is withdrawn from the market due proven increase in cardiac risk.  Of importance, the efficacy of these COX-2 inhibitors does not differ substantially from that of conventional NSAIDs. Their putative advantage is principally because of a reduced rate of adverse events, especially upper GI bleeding.⁵ Cyclooxygenase-2 inhibitors should be considered in patients at high risk of GI bleeding, including those older than 65 years and those with a previous history of GI bleeding. Despite advantages, these drugs may be associated with important adverse reactions, including allergy and fluid retention, and like other NSAIDs should be used with caution in patients with renal insufficiency.

Glucocorticoids are the most potent suppressors of inflammation and may be needed to control severe polyarticular disease until disease-modifying antirheumatic drugs (DMARDs) have been added and become effective. At that point, the glucocorticoids should be tapered and discontinued. Glucocorticoids should not be used alone in the management of RA. Oral prednisone or an equivalent is given in dosages typically ranging between 2 and 15 mg/d, often in divided doses (eg, 2 mg twice a day). A split-dosing regimen is frequently necessary because the anti-inflammatory effect is relatively short. It is preferable, but often not possible, to avoid long-term glucocorticoid therapy in patients with RA because of the well-appreciated adverse effects of these drugs. Systemic extra-articular manifestations such as rheumatoid vasculitis may require treatment with initial prednisone dosages of 40 to 60 mg/d, tapering according to response.⁶ Intra-articular injection of glucocorticoids is an effective means for reducing pain and inflammation in individual recalcitrant joints.

Disease-modifying antirheumatic drug therapy is associated with reduced morbidity and mortality in patients with RA.⁷ It should be used when the diagnosis of RA has been established and before erosive change appears. Disease-modifying antirheumatic drugs are usually given with NSAIDs and glucocorticoids, if needed. The DMARDs currently in use are listed in Table 1. The mechanism of action of most of these agents is diverse and to a variable extent overlapping. For many of the agents, the mechanism of action is defined incompletely, whereas for some, including the new class of tumor necrosis factor (TNF) blockers, it is better understood.

For patients with mild disease, hydroxychloroquine is often the first drug of choice because of ease of use and its favorable toxicity profile. Retinopathy due to hydroxychloroquine rarely develops when appropriate dosages are used. The onset of antirheumatic disease activity occurs in about 3 to 4 months in almost 50% of patients, although 6 months may be needed for the full benefit to be realized. For patients with moderately active or severe newly diagnosed disease, methotrexate or sometimes sulfasalazine is a preferred initial choice. In patients with continuing active established disease, methotrexate may be used in combination with other agents including hydroxychloroquine, sulfasalazine, or both or cyclosporine, azathioprine, and the more recently available DMARDs.⁹

For patients with acute and severe disease, a combination of DMARDs, prednisone, and an NSAID may be initiated; the dose of prednisone should be tapered during the ensuing weeks to months as disease control improves.

Because of its favorable efficacy and toxicity profile, methotrexate is regarded by many rheumatologists as the anchor therapy for RA. The initial dosage is usually 7.5 to 10.0 mg/wk, titrated upward to an average dosage of 12.5 to 15.0 mg/wk, although dosages of 20 to 30 mg/wk (if tolerated) may be necessary to realize this drug’s therapeutic potential before the response is deemed “inadequate.” Methotrexate may be given in tablet or liquid form; the liquid form is substantially less expensive than tablets, and injection may be associated with less stomatitis and GI upset. Appropriately managed, methotrexate can be used effectively for long periods to control RA. Although generally well tolerated, methotrexate can cause GI upset and hepatotoxicity including liver fibrosis and cirrhosis. Concomitant alcohol use is an important risk factor for methotrexate-related hepatotoxicity, and thus alcohol should not be used by patients taking this drug. Methotrexate can also cause a syndrome of pulmonary hypersensitivity manifested by dyspnea, cough, and fever and should not be used in patients with hepatic or renal insufficiency or severe lung disease. Supplemental folate (usually 1 mg/d) seems to reduce the occurrence of other adverse effects, including stomatitis, hair thinning, and bone marrow suppression. In patients taking methotrexate, physicians should avoid prescribing antifolate drugs such as sulfamethoxazole for sinusitis or cystitis, which may precipitate pancytopenia.

Use of DMARDs has substantially improved disease control and the long-term outlook for patients with RA. Their use may be associated with a lower incidence of extra-articular disease manifestations such as systemic vasculitis. In a series of more than 3000 patients monitored for up to 20 years, patients who had received DMARD therapy had a 30% reduction in long-term disability and improvement in survival compared with patients who had received NSAIDs alone.⁷ Despite these successes, major challenges exist. For example, DMARDs are becoming more accepted among practicing physicians and their patients¹⁰ however, adverse effects or failure of the drug to produce long-term disease control often leads to a change in DMARD treatment.

To improve disease control, therapies that contain combinations of DMARDs are often used. About 50% of patients with RA treated by rheumatologists are prescribed combination therapies with either 2 or 3 DMARDs. The combination of methotrexate, hydroxychloroquine, and sulfasalazine is among the most popular regimens. Methotrexate is often combined with other DMARDs including cyclosporine, but many other combinations of DMARDs have also been used.

In addition to hydroxychloroquine and methotrexate, other traditional DMARDs include penicillamine, gold, and sulfasalazine. Sulfasalazine was among the first drugs to be developed for the treatment of RA and may be chosen as the initial DMARD for patients with no allergy to sulfa, rather than hydroxychloroquine or methotrexate. The use of gold or penicillamine is seldom recommended because of the limited efficacy and the pronounced incidence of adverse effects associated with these drugs.

Three to 6 months may be needed before agents such as gold, hydroxychloroquine, and even sulfasalazine are effective. If the response is inadequate after 6 months of treatment, a second DMARD should be added or the DMARD regimen should be changed.

In the past year, 3 new DMARDs, etanercept, infliximab, and leflunomide, have been approved for the treatment of patients with RA.^11,12 Etanercept and infliximab are TNF-α antagonists that have powerful anti-inflammatory effects in patients with RA. Tumor necrosis factor is a potent inflammatory cytokine expressed in increased amounts in the serum and synovial fluid of patients with RA. It promotes the release of other proinflammatory cytokines, particularly interleukin (IL) 1, IL-6, and IL-8 and stimulates protease production. Etanercept consists of fusion monoclonal antibody composed of 2 identical chains of recombinant human TNF-α receptor fused with the Fc portion of human IgG1. In vitro it binds to soluble TNF. About 70% of patients receiving subcutaneous etanercept at dosages of 25 mg twice a week have substantial improvement in the extent of joint inflammation, often within 1 to 2 weeks after initiation of therapy. This improvement can be enhanced by combination with methotrexate. Adverse effects of etanercept are influenza-like symptoms and reactions at the injection site, which usually abate after the first few injections. The efficacy of infliximab, a recombinant TNF receptor fusion protein, seems to be roughly equivalent to that of etanercept. Infliximab is given intravenously once every 8 weeks, a regimen that may be more convenient for some patients. Potential long-term risks of these TNF-α antagonists have not been established. Infliximab may be associated with development of autoantibodies such as antinuclear antibodies. To date, neither drug has an increased risk of malignancy, autoimmune disease, or infection, issues that are the subject of ongoing postmarketing surveillance. The cost of these drugs is about $10,000 to $12,000 a year, generally higher for etanercept than infliximab. The available TNF-α antagonists should be considered in patients with recalcitrant disease not controlled by methotrexate.

Leflunomide is a pyrimidine synthesis inhibitor with clinical efficacy generally equivalent to methotrexate.¹³ Adverse effects reported include rash, alopecia, allergy, weight loss, thrombocytopenia, and diarrhea. Diarrhea often occurs early in the course of treatment and may abate, but discontinuation of the drug is necessary when the diarrhea cannot be ameliorated with dose reduction or concomitant use of antidiarrheal agents.

Serious extra-articular disease manifestations including vasculitis, scleritis, and recalcitrant serositis generally require systemic glucocorticoids and may necessitate the use of immunosuppressive agents such as cyclophosphamide. In my opinion, the only indication for cyclophosphamide in the treatment of RA is severe extra-articular disease, especially vasculitis.

Of importance, the decision about the use and aggressiveness of DMARD therapy should not be based solely on the presence or absence of the rheumatoid factor. Early in the course of RA, the rheumatoid factor may be absent, whereas in patients with established poly articular arthritis, absence of the rheumatoid factor is not invariably associated with mild disease and good disease outcome. Treatment must be tailored to the disease manifestations and needs of the individual patient. Consultation with a rheumatologist is helpful for patients who are pregnant or considering pregnancy because many antirheumatic drugs have severe fetal toxic effects including teratogenicity. Management suggestions for several clinical scenarios involving patients with RA are listed in Table 2.

When the symptoms of RA are well controlled, the glucocorticoids should be tapered, and the NSAIDs may also be tapered or used as needed. As a generalization, DMARD therapy should be continued indefinitely; however, if the patient does well and has no signs of active disease for at least 1 year, DMARD therapy could be carefully tapered. With combination DMARD therapy, one of the DMARDs could be tapered if the patient has been in remission for at least 6 months. Methotrexate can be considered as an “anchor” therapy and generally continue this drug for the longest period. Of note, less than 5% of patients with bona fide seropositive RA remain in long-term disease-free remission.

Rheumatoid arthritis is a serious disease. Follow-up early in the course of disease and in patients with poorly controlled disease should be every 2 to 6 weeks. Patients with well-controlled disease may be seen every 3 to 6 months. The primary care physician has an important role in the management of RA and can effectively guide and monitor routine therapy, with periodic consultation by a rheumatologist as needed. Assessment of disease activity and treatment efficacy is enhanced substantially with serial use of standard outcome measures, including duration of morning stiffness, severity of fatigue, presence and degree of joint pain and stiffness including joint counts, global and disease-specific health assessment instruments such as the modified Health Assessment Questionnaire, erythrocyte sedimentation rate, and radiographs of involved joints.

Appropriate medical care for patients with RA includes immunization and prompt treatment of infections. Patients with RA have a high risk of infections even if they are not taking DMARDs but particularly when they are taking immunosuppressive drugs. Several medications used to manage RA, including NSAIDs, cyclosporine, and glucocorticoids, may cause or exacerbate hypertension. Rheumatoid arthritis is associated with an increased incidence of pulmonary disease, and patients who smoke have an especially high rate of lung disease. In patients at high risk of GI bleeding, including elderly women and those with a previous history of GI bleeding, prophylaxis is achieved with agents such as proton pump inhibitors and misoprostol. As a general principle, use of NSAIDs should be avoided when possible and certainly discontinued when symptoms diminish. Virtually all patients with RA have or develop osteoporosis as a complication of the disease or its treatment. Adequate intake of calcium (1200-1500 mg/d) and vitamin D (400 IU/d) is important. In all patients receiving long-term corticosteroid therapy, including men, an antiresportive agent such as bisphosphonates or calcitonin should be considered. In postmenopausal women, estrogen replacement therapy or agents such as raloxifene may be considered. Finally, mouth and eye moisturization is necessary for patients with sicca complex symptoms.

Understanding the relationship of disease susceptibility and severity with genetic factors may provide an avenue for individualized treatment of patients with RA in the future. It may be possible to treat patients lacking genetic markers of severe disease with milder agents, while those with markers of severe disease may be treated more aggressively. More than 80 drugs are currently being developed for treatment of RA; thus, further advances in the management of the disease are forthcoming.

Questions About Treatment of RA

1. Which one of the following would be an acceptable therapeutic program for a patient with early mild RA?

1. Hydroxychloroquine with an NSAID
2. Hydroxychloroquine, methotrexate, and an NSAID
3. Methotrexate and prednisone at 5 to 15 mg/d
4. Etanercept and prednisone
5. Leflunomide and sulfasalazine

2. Which one of the following regimens would be appropriate for a patient with RA and new-onset systemic vasculitis?

1. Azathioprine, hydroxychloroquine, and prednisone at 10 to 15 mg/d
2. Prednisone, 20 mg/d, and methotrexate, 25 mg/wk
3. Prednisone, 40 to 60 mg/d, and cyclophosphamide
4. Cyclosporine and prednisone at 20 to 30 mg/d
5. Prednisone, 40 to 60 mg/d, and immunoabsorption column treatment

3. Which one of the following situations is not a relative contraindication to the use of etanercept?

1. Patient with history of tuberculosis exposure
2. Patient with history of lymphoma
3. Patient with active chronic infection
4. Patient with newly diagnosed RA
5. Patient with established RA receiving hydroxychloroquine and methotrexate

4. Which one of the following statements about the clinical course of RA is false?

1. The median life expectancy of patients with RA is the same as that for the general population
2. Most patients with RA have some disability after 12 years of disease
3. Predictors of poor outcome in patients with RA include the extent of radiographic erosions, female sex, and functional class
4. Patients in whom the rheumatoid factor is present have a worse prognosis than those with seronegative disease
5. Disease-free remission is unusual

5. Which one of the following statements about COX is true?

1. Cyclooxygenase-1 is constitutively expressed in the gastric mucosa, kidney, and platelets
2. Use of the currently available selective COX-2 inhibitors is safe in patients with renal failure
3. Currently available selective COX-2 inhibitors have been proved in multiple clinical trials to be safe in patients who are taking warfarin
4. Cyclooxygenase-1 is functionally expressed and promotes the elaboration of prostaglandins important in the inflammatory cascade
5. Selective COX-2 inhibitors are not associated with risk of GI bleeding Correct answers: 1. a, 2. c, 3. e, 4. a, 5. a

REFERENCES

1. Masi AT. Articular patterns in the early course of rheumatoid arthritis. Am J Med. 1983;75(suppl 6A):16-26.
2. Jacoby RK, Jayson MI, Cosh JA. Onset, early stages, and prognosis of rheumatoid arthritis. BMJ. 1973;2:96-100.
3. Sherrer YS, Bloch BA, Mitchell DM, Young DY, Fries JF. The development of disability in rheumatoid arthritis. Arthritis Rheum. 1986;29:494-500.
4. Mitchell DM, Spitz PW, Young DY, Bloch BA, McShane DJ, Fries JF. Survival, prognosis, and causes of death in rheumatoid arthritis. Arthritis Rheum. 1986;29:706-714.
5. Wolf MM, Lichtenstein DR, Singh G. Gastrointestinal toxicity of nonsteroidal antiinflammatory drugs. N Engl J Med. 1999;340:1888-1899.
6. Matteson EL, Conn DL. Extraarticular manifestations of rheumatoid arthritis. In: Weisman MH, Weinblatt ME, eds. Treatment of the Rheumatic Diseases. Philadelphia, Pa: WB Saunders Co; 1995:52-67.
7. Fries JF, Williams CA, Morfeld D, Singh G, Sibley J. Reduction in long-term disability in patients with rheumatoid arthritis by disease-modifying antirheumatic drug-based treatment strategies. Arthritis Rheum. 1996;39:616-622.
8. American College of Rheumatology Ad Hoc Committee on Clinical Guidelines. Guidelines for monitoring drug therapy in rheumatoid arthritis. Arthritis Rheum. 1996;39:723-731.
9. Borigini MJ, Paulus HE. Rheumatoid arthritis. In: Weisman MH, Weinblatt ME, eds. Treatment of the Rheumatic Diseases. Philadelphia, Pa: WB Saunders Co; 1995:31-51.
10. Ward MM, Fries JF. Trends in antirheumatic medication used among patients with rheumatoid arthritis, 1981-1996. J Rheumatol. 1998;25:408-416.
11. Weinblatt ME, Kremer JM, Bankhurst AD, et al. A trial of etanercept, a recombinant tumor necrosis factor recepton:Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate. N Engl J Med. 1999;340:253-259.
12. Moreland LW, Baumgartner SW, Schiff MH, et al. Treatment of rheumatoid arthritis with a recombinant human tumor necrosis factor receptor (p75)-Fc fusion protein. N Engl J Med. 1997;337:141-147.
13. Mladenovic V, Domljan Z, Rozman D, et al. Safety and effectiveness of leflunomide in the treatment of patients with active rheumatoid arthritis. Arthritis Rheum. 1995;38:1595-1603.

The area where I live, and I am referring to about a 150 mile radius, I have noticed the leaves changing colors.  Oh so pretty ~ Just dazzling with the reds, yellows, and hues of brown ~ heck ~ in some areas where trees are left because the local government was forced to leave parks, they have tours.

Something interesting has happened over the last three years ~ The mighty Oak Trees in some of these areas ~ the leaves are not changing colors at all; the leaves are just falling.  Strange isn't?  Even when there are drought conditions, the leaves have always changed colors before falling.  And on an Oak Tree no less ~ where the roots of these trees run deep into the ground and search out the water. 

I wonder just how bad the polluants and toxins are in the air and what the hell is in the ground water now ~~ or maybe it is another example of how the climate is changing ~~

What are the first signs??  Remember not all deserts were deserts.

She is still my best friend and always will be.  She is positive, gives her time to me (knowing I need it so much right now).  She is creative, funny, different, kind, beautiful inside and out, smart, contains more wisdom than she knows and has a strong faith in God.  We are different but so much alike in ways too.  I can identify with her. I am blessed and I wanted to give this testimate for her.  She deserves all the beauty life has to offer.  She is my best friend always and forever, until the end. 

(I am praying for a move closer to her. Then we can live out some of our dreams together...we'll see :) )

Low-and-behold, after accidentally revealing details in a cartoon, Google has today confirmed that a Gbrowser will be launched tomorrow and named Google Chrome.

On the surface, we designed a browser window that is streamlined and simple. To most people, it isn’t the browser that matters. It’s only a tool to run the important stuff — the pages, sites and applications that make up the web. Like the classic Google homepage, Google Chrome is clean and fast. It gets out of your way and gets you where you want to go.

Under the hood, we were able to build the foundation of a browser that runs today’s complex web applications much better. By keeping each tab in an isolated “sandbox”, we were able to prevent one tab from crashing another and provide improved protection from rogue sites. We improved speed and responsiveness across the board. We also built a more powerful JavaScript engine, V8, to power the next generation of web applications that aren’t even possible in today’s browsers.

Windows users can access the beta tomorrow (Tuesday) and we’ll have all the details right here.

Today, I celebrate 25 amazing years of life! I thought this would be an appropriate time to reflect on 25 simple things that make my life sweet. Ya know? Sometimes, we just need to stop and take the time to "smell the flowers." It's the little, everyday things that make life sweet. Here's just 25 of mine.

Enjoy!

1. Friendship with my Creator
2. My husbands arms around me
3. Olivia & Jackson's kisses
4. Worship
5. Quite time alone
6. Books
7. Writing
8. The piano keys beneath my fingers
9. Freedom
10. My church
11. Starbucks & PCJ
12. Technology & the WWW
13. The smell of Anthony (I know, wierd) but I like it.
14. Being free in Christ
15. Blogging
16. Sand, sun, & salt air
17. Music
18. Friends
19. Time with my family
20. Mocha Shakes & White Chocolate Mochas. Mmmmmmmmmm!
21. A good tube of lipgloss
22. Jackson's little toes
23. Olivia's hilarious phrases and imagination
24. A clean house
25. A great pair of jeans!....Never, and I repeat, NEVER underestimate the power of a great pair of jeans!

See how we've been celebrating so far by clicking here!

The bad news? Those games won't be done for another two to three years apparently.

"We have never neglected our core gamers. We still have developers working on popular core gaming franchises but we need longer to complete these games, approximately two to three years," the company told the October issue of Edge (via EG).

"These games are not ready to launch in early 2009 but are being worked on by all development teams."

"If there is any perception that Nintendo is ignoring the core gamers, it's a misunderstanding and we really want to get rid of that misunderstanding by any means," said company president Satoru Iwata in an interview last month.

Complaints that Nintendo have been ignoring fans of the company rose again after E3 when the company failed to announce and future Zelda games.

What do you think of the Wii and Nintendo's appeal to the hardcore and casual audiences? Let us know what you think in the forums.

 Check it out here...........

Yep!

We've been a couple for 7 years now!

I love you dude!

I love you. xo

I love you. xo