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It’s been three weeks since I had an anterior cervical discectomy and fusion (ACDF) surgery on vertebrae C5-C7. I outlined the procedure in an earlier post. Immediately upon coming out of surgery I could feel a positive difference in arm and shoulder pain – the site of most of the symptoms from herniated discs and bone spurs which pressed on my spinal cord and nerve roots which extend into the shoulders and arms. There have been times since surgery when I’ve experienced some finger tingling, arm pain, and shoulder spasms but that is to be expected as the surgery site recovers and the overall trend has been positive.

During ACDF surgery the neck vertebrae are expanded back to their normal distance apart after the herniated disc collapses. The disc replacement, in my case a plastic cage seeded with my own bone tissue, returns the space back to normal. I could tell things were stretched out as the muscles in my neck were tight and painful immediately following surgery. This subsided after a week or so and I can feel that these muscles are loosened up. Maybe I grew taller in the process!

neck scarIt looks like I got into a knife fight and lost (see picture) – but you should see the other guy (well, he got paid a lot of money). It’s pretty amazing that they can perform such a dramatic surgery through so small an incision. The surgeons rely on microscopes for parts of the procedure. There were no external stitches or staples in an effort to minimize the scar. It is in a rather conspicuous place. But like with similar incisions from other surgeries, I suspect that the scar will diminish over time.

Physical activities remain restricted. You are instructed not to lift anything over 5-10 pounds. This is the hardest restriction to follow as I find myself wanting to engage in regular activities around the house. I have to constantly catch myself and ask for help. Walking is highly recommended from the beginning and I’ve been doing about 1 mile each day. Since no longer taking narcotic pain meds, and getting some movement back in the neck, I did drive a short distance to the grocery store this week. Long drives are probably out for some time until more muscle strength is regained.

Rheumatoid arthritis symptoms flared after the surgery with increased joint pain and stiffness. Fatigue also increased but that could be from the recovery process. Flaring is to be expected given the stress put on my body from the anesthesia and surgery. Taking NSAIDs or steroids to help is not possible as they negatively impact the bone fusion process.

A follow-up appointment with the surgeon is in three weeks at which time they will take an x-ray to make sure the hardware remains in place and to check on the status of the bone fusion. It will be interesting to see the titanium hardware! The vertebrae can take 3-12 months to fully fuse.

At this early point, I am glad that I had the surgery. But time will tell if symptoms will continue to improve.

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In my last post, I briefly discussed how various metabolic systems are involved with RA and how something called Metabolic Syndrome is more common in RA patients and is implicated in increased risk for cardiovascular disease. A recent article written by Spanish researchers (Amaro, et al., 2013) provides an excellent overview of the connection between metabolic syndrome and rheumatoid arthritis. They stated that metabolic syndrome is characterized by high blood glucose, low HDL cholesterol, high triglycerides, obesity, and hypertension. Up to 39% of RA patients display symptoms of metabolic syndrome placing them at greater risk for cardiovascular diseases. They noted that something called insulin resistance is connected with RA, increased inflammation, cardiovascular disease, and type II diabetes. According to the U.S. National Institutes of Health,

“Insulin resistance is a condition in which the body produces insulin but does not use it effectively. When people have insulin resistance, glucose builds up in the blood instead of being absorbed by the cells, leading to type 2 diabetes or prediabetes.”

A review of research conducted by European rheumatologic researchers (Amaro, et al., 2011) connected insulin resistance to RA. They revealed that insulin resistance was more common in RA patients with higher inflammatory blood markers (c-reactive protein, ESR) and disease activity measured by the DAS28. In addition to helping curb joint destruction, these researchers also noted that the use of biologics that impact inflammatory cytokines, primarily the TNF inhibitors (e.g. Humira and Remicade), may benefit those with insulin resistance. For RA patients on TNF inhibitor treatment, improvements were seen in the insulin resistance in multiple studies over the past few years. In summarizing the topic, Amaro, et al, concluded,

“The role of chronic inflammation is becoming more and more important in the development of atherosclerosis. Likewise, the latter seems increasingly important as a determinant of mortality in patients with RA. In light of the observations, there seems to be ample evidence supporting a relationship between insulin resistance, inflammation and RA, as is also the case in other chronic diseases. In addition, such insulin resistance plays an initial role in vascular damage and appears to be (along with other mechanisms such as endothelial dysfunction, cellular adhesion, etc.) a link between inflammation and atherosclerosis. For all these reasons, rheumatologists should know insulin resistance better, become familiar with its concepts, learn how to measure it, relate it to other disease parameters and consider it as a another systemic manifestation of patients with RA.”

If you have RA, it is a good idea to pay attention to metabolic systems since you are at an increased risk for insulin resistance, increased inflammation, and cardiovascular disease. Below are some strategies that will likely benefit all RA patients.

  • Speak to your rheumatologist about this topic.
  • Get your lipids checked out. Traditional cholesterol tests do not provide enough detailed information. It is important to know LDL levels (“bad” cholesterol), HDL levels (“good” cholesterol), triglycerides, and insulin resistance. There are newer tests like the nuclear magnetic resonance (NMR) lipoprofile test which provides detailed information about the number and type of LDL particles. It also calculates an insulin resistance score. Ask your doctor to order this test. It’s not that expensive and most insurance companies cover it.
  • Watch your diet in terms of refined sugars and starches which rapidly increase blood glucose levels, cause insulin levels to spike, and add stored fat to the midsection. Such a diet increases the chances of developing insulin resistance. This is especially true for RA patients given the inflammatory connections. It is proposed that balancing low fat proteins with whole grain carbohydrates and small amounts of quality fats is the best diet for those with metabolic syndrome (see The Insulin Resistance Diet book by doctor and registered dietician Hart and Grossman for an excellent overview). In general, a low carb diet is suggested to lower levels of inflammation (see Forsythe, et al., 2008).
  • Exercise if possible. You don’t need to be a long distance runner or champion body builder. It is believed that muscle resistance exercise is better for insulin resistance as it burns excess glucose in the bloodstream (see this article).

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Although not publicly well known, scientists and doctors have known for sometime that rheumatoid arthritis is linked to an increased risk for cardiovascular disease (CVD) including heart attack and stroke. The first person I knew with RA some 20 years ago succumbed to heart problems at the age of 62. When I was informed of his death by his family, they immediately attributed his heart problems to the RA.

My doctors have been tracking some of the variables typically connected with CVD including blood pressure, lipids, and insulin. This came about when a sharp increase in these markers were noted while I was taking Actemra infusions (a listed side effect of Actemra). Even though I’m not on Actemra anymore, we continue to track these variables as the increase may be attributed to active RA.

According to a study at the Mayo Clinic, traditional forms of documenting CVD risk don’t necessarily apply to RA patients, particularly those who are seropositive for rheumatoid factor (RF). Traditional predictors of CVD are helpful with RA patients but not sufficient as in general populations. Systemic inflammation inherent in rheumatoid arthritis may play a role in the increased CVD risk (see this review). Some researchers have called for the development of specific CVD predictors for RA patients as a special population with unique characteristics.

My rheumatologist recently mentioned something called “metabolic syndrome” and it’s relationship to RA. Metabolic syndrome involves a set of interconnected risk factors which are related to cardiovascular disease and diabetes (see this excellent overview from the U.S. National Institutes of Health). All of these complex biochemical processes are connected and involve metabolism of food for energy, sugar processing, insulin, insulin resistance, fat/lipids including cholesterols and triglycerides, liver health, food types, excess weight, exercise, and systemic inflammatory responses. Whenever one of the interconnected systems gets out of normal parameters, a cascade of problems may occur which may impact cardiovascular health. In a study published in 2013, it was found that 18-49% of RA patients also had metabolic syndrome which was significantly higher than general populations. These researchers also found that RA patients with higher inflammatory blood markers and those who used corticosteroids were more likely to show signs of metabolic syndrome. Anti-inflammatory treatments for RA including DMARDS and many of the biologicals like anti-TNFs may impact the biochemical pathways involved in metabolism (see this recent study).

Cardiovascular risk is one extra-articular manifestation of RA that can have serious and fatal consequences. All RA patients and their doctors should be aware of the risk factors, closely monitor CVD related factors, and treat as needed. Ultimately, control of RA and it’s underlying systemic inflammation should help lower CVD risk.

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491px-Muscle_posteriorSeveral recent observations caused me to wonder about the impact of RA on muscles. In the almost five years since being diagnosed with RA, I’ve seen a steady decrease of muscle strength coupled with an increase in periodic pain and aching in muscle tissue. I’ve thought that the aching could be caused by either overuse (comparatively speaking) or by biomechanical processes since the muscles are attached to RA-damaged joints via tendons. I can feel myself getting weaker as time goes on. In fact, muscle strength in RA patients can be reduced by up to 75% of normal (see this study from 1992). During a follow-up visit about one of my ankle surgeries a few years back, the orthopedic surgeon noted in my chart that my calf muscles were getting atrophied. I no longer have the strength to open jars, dig a hole, or even maintain extended use of a muscle on a given task. I began to wonder about the impact of rheumatoid arthritis on muscles.

While muscles haven’t been a primary research target, there have been a few studies about muscles and RA. As far back as 1951, researchers found that inflammation of arteries in muscle tissue was observed in RA patients. In a study of 350 RA patients in Spain, weakness, muscle atrophy, and muscle inflammation were commonly observed in those suffering from RA. A detailed research study by Helliwell and Jackson published in 1994 documented RA’s impact on muscle tissue. They concluded, “Although there is significant muscle wasting in RA, it is likely that reduction in strength is also attributable to joint deformity and pain leading to inhibition of grip directly and, indirectly, by arthrogenous muscle inhibition. Doubts remain about the quality of muscle in RA”. Arthrogenous refers to “starting from a joint”. In 1993, Young produced a model demonstrating the connection between joint damage and muscles.

In addition to biomechanical problems, it is entirely plausible that biochemical processes involved with RA may negatively impact muscle tissue. According to some researchers, RA related cytokines including IL-1 and TNF are involved with breaking down the protein in muscles. According to Rall, et al (1996), “Adults with RA have increased whole-body protein breakdown, which correlates with growth hormone, glucagon, and TNFα production.” They concluded…”And although progressive resistance training led to improved strength and functional status in patients with RA and in controls, we saw no changes in protein metabolism or hormone levels as a result of the training intervention among any of the groups of subjects.” In other words, muscle breakdown continued even in midst of exercise. This mirrors a study by a group from Finland who noted that exercise helped RA patients’ muscle strength but not bone density. In 1974, a group of researchers from Sweden noticed changes in the muscle tissue of RA patients. They stated, “It is emphasized that the type II atrophy must be the result of a more complex mechanism than simple ‘disuse’.”

My suspicions about the biochemical impact and connectedness to RA impacted joints are both confirmed in the research literature. The question then remains as to what may be done to stop or reverse the impact of RA on muscles. Some argue that RA patients should engage in regular exercise in order to maintain muscle tone (see Mayo Clinic, NCHPAD). In a 2003 review of research studies on the impact of exercise on RA patients, it was found that most studies demonstrated that exercise positively impacted muscle strength without negatively impacting pain or daily activities. These results are interesting to me personally because every time I try to engage in exercise or strenuous activity, I feel worse and daily activities are limited (see recent post). Regarding exercise, many experts now recommend, “If you can, you should; if you can’t, you shouldn’t.” (Dr. Borogini Health Central RA website).

The evidence is clear – rheumatoid arthritis does impact muscle tissue. But more research is needed to identify the specific causes and to develop long term solutions. Of course, a bona fide cure for RA would do the trick. Fortunately, there are still researchers seeking answers as attested to by the fact that funding is being provided to study muscles in RA patients (see recent grant award in the UK).

Creative Commons Photo Credit – Public Domain: http://commons.wikimedia.org/wiki/File:Muscle_posterior.png

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The last four days have been a grand time of celebrating our oldest son’s college graduation. It’s been a whirlwind of events including his senior engineering project presentation, three formal ceremonies of various sizes and durations, dinners, and a large party hosted at our house. This meant much physical activity around the yard and house the principal of which was 10 hours of smoking five large pork shoulders for 50 people (it was tasty and you should check out the website http://www.amazingribs.com/).

Tired_brown_bear_050701_01Going into this set of events, a nagging thought persisted…”I’m going to pay for this later.” Sure enough, by Sunday evening I could barely walk, my fingers were swollen and throbbing in pain, and sheer exhaustion washed over my body causing me to collapse. I knew that going to work Monday morning would not be possible.

Many argue that movement and exercise is critical medicine for arthritic joints stating that it relieves pain and stiffness (see these websites – Mayo Clinic, NCHPAD). In addition to potential positive impact on joints and muscles, exercise is obviously important for other reasons include cardiovascular and mental health. But my experience over the years has been that exercise and movement causes rebound pain and stiffness. Yet, I know that I’m missing out on the benefits of exercise.

It’s interesting to read some of the recommendations from medical websites. From WedMD…“Regular exercise can actually reduce overall pain from rheumatoid arthritis.” In my experience with RA, exercise always causes more pain. There are many times when I’ve had to stop movement because the pain got worse. WebMD also makes this statement, “Regular exercise improves functional ability and lets you do more for yourself.” This may be true for some but the functional ability of my ankles and Achilles tendons actually got worse after exercising. The tendons tore at a quicker rate and my orthopedic surgeon and physical therapist both recommended that I avoid any activity that puts stress on the tendons.

Can exercise actually be contraindicated for RA? Kelly Young at RA Warrior has an excellent series of posts about this topic. She concludes, “If you can, you should; if you can’t, you shouldn’t.” At the Health Central RA website, Dr. Borogini wrote a balanced article about the topic and makes an excellent suggestion which is in alignment with Kelly Young’s statement, Rest More When RA Is Active, Exercise More When It Is Not. The Johns Hopkins Arthritis Center website makes a great observation about movement and RA.

Acutely, resting of involved joints can assist with pain management and decrease the inflammation of the involved joint. However, the potential side effects of inactivity include decrease range of motion, loss of strength, altered joint-loading response, and decrease aerobic capacity.

This leaves those with active disease in a real quandary.

The conclusion that must be drawn from the recent set of weekend experiences is that my RA is not under control and I should probably avoid strenuous physical activity. But of course, I already knew that going into the weekend. The difficulty lies in the fact that life must go on and I was not about to miss this once-in-a-lifetime celebration. I just have to be ready to pay the consequences afterwards.

Creative Commons Photo Credit: http://commons.wikimedia.org/wiki/File:Tired_brown_bear_050701_01.JPG

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Gardening has been a favorite outdoor activity for years. This love of the ground and raising plants began in 6th grade when I dug up a spot in our yard and planted a vegetable garden. Tomatoes grew like weeds and the joy that came with watching and nurturing plants sank deep in my psyche like tap roots.

As a twenty something high school teacher, summers were spent operating a small landscaping business. I had a truck and hired several high school students as laborers. We would plant shrubs and trees, build retaining walls, and haul bulk items like top soil, rock, and mulch. During this phase of life, I also regularly ran 20-30 miles per week and participated in 5Ks periodically. I never felt better!

527053415_e5df73b495Every home we lived in over the years would get hours of loving care in terms of landscaping and gardening. Redoing lawns, building greenhouses, planting flowers, edging and mulching planting beds, planting trees and shrubs, and building fences (see photo) were just a part of life.

Thirty years later and living with rheumatoid arthritis has dramatically changed these activities. This fact was recently evident when my wife started edging a planter bed and digging up sod in order to plant new flowers photoand lay mulch. In the past, I would’ve been in the thick of this kind of work. She began the digging knowing that I couldn’t help. We were delighted when our wonderful neighbor came over and started helping edge and pulling up sod. Instead of just passively standing by watching someone else do the work, I decided to work on bonsai gardening. The kind of work needed to maintain bonsai – pruning, watering, etc. – is doable given the impact of RA on my joints and energy levels. My dwarf Cedar of Lebanon and Western Red Cedar bonsai seem to be doing very well (see photo).

I can no longer dig sod or haul mulch, but I can still get my hands dirty and nurture plants – just on a much smaller scale!

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450px-Walking_ManThe other day I walked into the kitchen and my wife laughingly said to me, “You’re walking like Frankenstein”. I laughed back because I knew that I was like the “living dead” for many reasons but mostly because of changes in my joints. I have bursitis in both hips which radiates pain down the thigh and in the buttocks (I got two cortisone shots recently and they did nothing – but that’s another story), cartilage damage in both knees, and three surgeries on my ankles. Add to that, I could barely get out of bed and walk around this morning due to sharp pain in the same area of the right ankle that’s had two surgeries. I’ve felt that pain before which was from erosion in the heel bone causing spurs to dig into the Achilles tendon. Yep, I was walking stiffly and probably looked like a monster from a movie.

It’s a natural tendency to make adjustments due to pain or joints that aren’t working as designed. Joint changes from rheumatoid arthritis seem to be inevitable As bone and soft tissues are attacked, damaged, and eroded, the joints can no longer work as they should. Fortunately, disease modifying medications can slow down the damaging biochemical processes. In spite of being on medications, changes are still affecting my movement and activity.

When the term arthritis is mentioned, the first thing that comes to most people’s mind is probably bone damage. With the more common osteoarthritis (OA), there may be damaged cartilage causing bone to rub together. But with rheumatoid arthritis (RA), the immune system attacks the body’s own tissue. The capsule surrounding the joint, called the synovium, becomes enlarged due to an increase of immune cells. Eventually an overproduction of bone eroding cells and enzymes begins to erode bone tissue and soft tissues.[i] The soft tissues that hold the joint together including tendons, ligaments, and cartilage are also damaged.[ii] [iii] When all of these tissues become affected, the entire skeletal structure designed for movement cannot work properly. Add to that stiffness caused by RA, and the result is walking like Frankenstein!

My joints used for walking are changing and the effects are becoming noticeable not just to me, but to those around me. Add to that the fact that any hope for strenuous physical activity is pretty much gone for now. My daughter wants to go snow skiing but the best I could do is drive her there and sit in the lodge drinking cocoa. The hope is that treatments can keep the process at bay long enough so I can avoid more surgeries and using assistive devices just to carry out that common, everyday task we take for granted – walking.

Photo Credit: By Stefan Eggert (User:Berreu) (Own work) [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC-BY-SA-3.0 (http://creativecommons.org/licenses/by-sa/3.0/)], via Wikimedia Commons

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