Healing or just feeling better?

When I finally go into histologic remission, I will throw a party... that day will be worth celebrating.  So what do I mean by histologic remission?  I mean that I would like to have biopsy-confirmed results showing my gut has been healed by the motley collection of pills and injections that I find myself currently taking for Crohn's.  There are several types of medications that are prescribed to treat Crohn's disease (therapy options range from corticosteriods to so-called "antimetabolites"* to new biologic therapies*... and even antibiotics*), and they range in their efficacy and mechanisms of action.

In my personal experience thus far, I haven't found the right medication(s) to significantly impact the colonoscopic or pathologic results in my gut, but there has been one medication in particular that has improved my more quality-of-life-type symptoms (e.g. fevers and malaise)... prednisone.  At this point, I have heard a few gastroenterologists say that cortiosteroids (prednisone is one particular example of this class of medications) make Crohn's patients feel better, but don't actually get them better.  What this means is that while steroids are good at suppressing systemic (whole body) inflammation, they are potentially less good at actually healing the mucosa (lining) of the gut.  So even though the quality of life of a Crohn's patient on corticosteroids might be significantly improved, if that same patient were to get several gut biopsies, there might still be extensive evidence of active disease.

Pathologic features of Crohn's

In order to make a diagnosis of Crohn's disease, usually some kind of endoscopic examination will need to be done.  This can be in the form of a colonoscopy or upper endoscopy, and often both.  During that exam, if the gross pathology (evidence of the disease that can be seen with the naked eye or, in this case, camera) is suggestive of inflammation, the gastroenterologist can take a few biopsy specimens for further analysis under a microscope.  A gut with Crohn's disease will have some key features if examined under magnification... the microscopic architectural features will be disorganized and high levels of certain inflammatory cells will be present (Geboes and Dalle. 2002).  The inflammatory features on biopsy can sometimes be telltale for Crohn's (this situation will often include "granulomatous" inflammation), but in many cases the inflammatory process in the bowel can be non-specific and, thus, not itself diagnostic.

So, the ultimate goal for a Crohn's patient would be to achieve remission of the disease from an endoscopic and histologic standpoint... although symptomatic remission is what is most commonly achieved and, in a sense, is most important.  If a repeat colonoscopy is done when symptoms are under control, confirmation of gut healing by pathologic examination would be the best way to show that disease activity is absent or very low... and that the medications have done their job.

Prednisone & the power to heal?

Published studies seem to show poor colonic mucosal healing with corticosteroid use in patients with Crohn's disease (Landi et al. 1992., Oliason et al. 1990.).  Landi and colleagues gave high-dose prednisolone (the dose was 1 mg/kg/day, and prednisolone is an active corticosteroid that is essentially what prednisone gets converted into inside your body) to 147 patients with acute attacks of colonic or ileocolonic Crohn's disease.  After 5 weeks, they found that 136 of these patients had achieved clinical remission, but 96 still had lesions on endoscopy.  The study by Oliason and colleages was much smaller, having only 8 patients with ileal Crohn's disease... thus, I will consider these results as more of a case study than a controlled trial.  With 20-30 mg/kg/day doses of prednisolone for 6-9 weeks, the patients had significant improvement in activity indices, but essentially no improvement in ileal inflammation.  However, there was one study that showed rectal biopsy normalization in patients taking a combination of prednisolone and sulphasalazine; although the results with prednisolone on its own were less striking (Schmitz-Moorman et al. 1988.).  This study suggested there was a good relationship between Crohn's Disease Activity Index score and histologic improvement in their subjects.  Taken together, it seems that symptomatic relief with corticosteroid medications is much greater than the impact that steroids have on gut pathology.

Prednisone: commentary on the benefits and risks

My husband and I actually got into a heated debate about this topic, so I am going to try to summarize both of our viewpoints on this subject (while hopefully not completely botching his opinion).  I want to leave my commentary for this post open to different viewpoints on this subject.

First the setup to the debate: While short courses of corticosteroids can be fine, long-term corticosteroid use is considered relatively dangerous.  These drugs have a whole host fairly common, and fairly unpleasant, side effects, including weight gain, insomnia, bone loss, muscle loss, diabetes, and on and on.  I currently have a bit of a moon face from the several months of prednisone.

My opinion: Given all of the side effects, my opinion is that there must be some perceived health benefit of corticosteroids, beyond their ability to improve the quality of life for Crohn's patients, in order for them to be so widely prescribed for therapy.  This benefit need not be a real benefit of actually suppressing the overactive, damaging inflammation in the gut, but could just be a perceived benefit by  clinicians... i.e. because it is a known powerful immunosuppressive, it should, theoretically, impact the course of Crohn's disease.  My point is not to say that quality of life issues aren't important or shouldn't be treated... very much the contrary.  I know better than most how difficult it is to just go about normal life when running a fever or to the bathroom 10x per day.  My argument is simply that corticosteroid should be used sparingly if they do not impact the course of the inflammatory bowel disease.  The risks seem to outweigh the benefits of just making me "feel good".

I would analogize the situation to the use of opioid medications for pain.  My perception (which may or may not be true) is that physicians have a bias toward underusing opiates to relieve pain. Clearly, this is because there are certainly dangerous side effects of these medications.  But in addition, I think that the fact that opioids just relieve pain... and don't do anything to fix the underlying problem... is another reason why they may be cautiously prescribed.  Here there is a clear dissociation: a drug that can improve quality of life in a patient with chronic pain, but doesn't do anything to treat the underlying pain mechanism.  In my opinion, the cost-benefit calculus is shifted toward greater cost in this situation, where the benefit is one that only impacts quality of life for a risky medication.

Opiates are actually a great category of drug to talk about because an interesting counterpoint to the use of opiates for pain, is the use of opiates for diarrhea.  The notable medication here is loperamide (i.e. Imodium), which is the same type of medication as an opiate used to treat pain... with the important caveat that it doesn't cross the blood-brain barrier (thus, no pain relief or risk of addiction).  Similarly to opiates for pain, loperamide treats the symptoms of diarrhea, without healing the underlying cause of the diarrhea.  However, in this situation, the medication (generally) carries minimal risk of adverse effects, so it is used quite widely.  The cost-benefit analysis is heavily weighted toward the benefit of symptom relief, even if it will not impact the course of the illness.

My husband's opinion: I think he basically puts more weight on the improvement of quality-of-life-type symptoms, and, thus, his analysis of the costs versus benefits of prednisone (having seen my personal short-term response to it) is more favorable toward the benefits.  Even if there is no mucosal healing that occurs, because it eliminates fevers and improves general wellbeing, short-term use is fine (don't know the tipping point when short term ends and long term begins though).  Btw, he also thinks that opiates are under prescribed to treat pain... with which I do agree.

*The (very) basic run-down of Crohn's drugs (other than corticosteroids):

Antibiotics: Probably most everyone has been at least one, if not several, of these for various bacterial infections, so I don't need to be too detailed... but these medications either slow down the growth of or kill bacteria.  In Crohn's, antibiotics such as flagyl or ciprofloxacin are sometimes prescribed with the idea that if you change the bacterial balance in the colon, it could help slow the inflammatory response.

Antimetabolites: Generally speaking, antimetabolites are medications that inhibit the use of a chemical in normal metabolism.  For Crohn's disease, these medications include azathoprine, 6-mercaptopurine, and methotrexate and are drugs that impact the production of lymphocytes (white blood cells) in the bone marrow... the idea being if you have less lymphocytes around, they can't do as much damage to the GI tract.

Biologic therapies: These medications are the newer frontier of therapy for Crohn's disease.  Biologics are components that are synthesized by biologic processes instead of a chemical ones, but this descriptor really says nothing about what the drugs do.  Most of the current biologic therapies used for Crohn's are designed to bind to and inhibit TNF-alpha, a molecule that seems to be a be a bad actor in overaggressive inflammation.  Trials for different kinds of biologic therapies are currently underway though.

Bibliography:

Geboes and Dalle. 2002. Influence of treatment on morphological features of mucosal inflammation. Gut 50(Suppl III):iii37-iii42.

Landi et al. 1992. Endoscopic monitoring of Crohn's disease treatment: a prospective, randomized clinical trial. The Groupe d'Etudes Therapeutiques des Affections Inflammatoires Digestives. Gastroenterology 102:1647-1653.

Oliason et al. 1990. Glucocorticoid treatment in ileal Crohn's disease: relief of symptoms but not of endoscopically viewed inflammation. Gut 31:325-328.

Schmitz-Moorman et al. 1988. Relationships between drug regime and histology of rectal mucosa in CD. Pathology - Research and Practice 183:30–34. 

Team Challenge Progress: Week of 9.16 to 9.22

Thank you to my supporters during the past week... now several weeks into the Team Challenge program, things are still going strong!  Because of your generous donations, I am very close to the $2,000 fundraising mark for The Crohn's & Colitis Foundation of America.  Check out my status bar on my donation page.  Can't wait to run those 13.1 miles for you all!

This week's donor honor roll:

• Jenny Enright
• Marge Holzem
• Marv Holzem
• Alexandra Lingle
• B. K. Holzem Enterprises

Training/Crohn's progress:

I have started my training program this past week (see my last post for the whole schedule), and while I did not adhere to things perfectly, I have started working on my speed and endurance.  I did do some fartlek work and did my tempo, speed-building run mid-week.  As expected, going back up on prednisone has helped quench some of the pain in my right knee... making running more comfortable in that respect.

With regard to the Crohn's, my GI system has not really improved since this "flare" got going.  It is pretty frustrating to know that things were sort of in control a couple of weeks ago, and then they just sporadically snapped back out of hand.  So now, my gastroenterologist and I have reached the point in my treatment where it its time to test my response to a medication that we have been avoiding up to this point... methotrexate.  For those of you who don't know, methotrexate is an immunosuppressant drug that tends not to be first-line therapy for Crohn's in women of child-bearing years.  Methotrexate is a pregnancy category X medication, which means that this drug should not be used during pregnancy because it is a known teratogen (i.e. can cause developmental defects for the fetus).  Taking this drug does not prohibit me from ever getting pregnant... this drug would just need to be stopped before that can happen.  Am I worried about taking this medication?  Sure, I would have rather avoided it.  But research shows that having active Crohn's during pregnancy is one of the worst things for the developing fetus, so it's not like I could get pregnant until this disease gets under control anyway.  I need to be well first, and then worry other things in life later.  I will always keep running no matter what is going on (I do slow up if I need to)... running through it all keeps me feeling in control of something!

Team Challenge Progress: Weeks of 9.2 to 9.15

The training plan

So, I have made a regimen to get myself ready for the 13.1-mile haul.  My goals, in order of importance, for this Vegas race will be to 1) just finish... maybe with an at least slightly better time than I had for my first half marathon... 2) run the whole race, and 3) get a decent time.  I'm not exactly aiming to win the race... but I am hoping to survive better than my first half marathon attempt (an experience which I have recounted on my donation page).  At least I know what issues I am up against this time, which should help.

I made a training plan for myself from this week on out to race day.  It is somewhat based off of Hal Higdon's intermediate half marathon training program, but it does have several adjustments based on life events scheduled between now and December 2... and some alterations based on my personal exercise preferences.  Given that I have been running consistently for a couple of years now, I have incorporated some shorter speed work into the plan.  It would be nice to actually get a little bit faster, but it is only goal priority #3.

Here is the whole schedule:

So you may be wondering about the meaning of some of my training terms, so I will explain.

Crosstrain: Some kind of cardiovascular exercise that is not running... in order to mix up the training routine and to help prevent injuries.  Examples would be elliptical training, swimming, kickboxing, etc.

Fartlek: In addition to being a funny word to say, fartlek basically means "speed play" in Swedish.  It is  a type of workout that mixes continuous and interval training to stress both the aerobic and anaerobic (i.e. with and without oxygen) systems.  I will basically do several shorter runs (on the order of 400 meters) that are a mixture of sprints and easy runs.

Kickboxing: Basically my preference for crosstraining.  These are cardiovascular workouts that incorporate kicking and punching moves based off of the martial arts Muay Thai kickboxing and Karate, as well as some Western-style boxing.  I go to a gym in St. Louis called The Boxing Gym.

Pace: These runs are supposed to be done at the pace at which I intend to run the half marathon... I guess somewhere around a 9-minute mile.

Tempo: This is a continuous run with a speed buildup in the middle.  For this kind of run, I will start easy for the first 1/3, buildup to about a 10-K pace in the middle 1/3, and then return to an easy pace toward the end.

Strength: Maybe this is obvious, but I mean strength training... or weight bearing exercise.  I probably will do some push-ups, free-weights, and maybe some additional weight machine work at the gym.

Training & Crohn's progress:

I am sad to say that the past couple of weeks have been frustrating... weaning off of the steroids didn't quite work, and I started to flare.  I finally feel like I understand what a Crohn's "flare" is.  Basically I started to have fevers early last week, without clear additional symptoms, but then had worsening GI issues later in the week.  My interpretation of the flare is basically that the immune system starts getting overactive, but the damage resulting from that activity takes a few more days to develop.  Needless to say, this hasn't made training easy.  In addition, I have continued to have a bit of right knee pain.  I am pretty convinced that my knee just has some irritation and inflammation, and nothing more serious (I had my husband perform a bit of a physical exam from our med school training... and he couldn't provoke any pain), but I don't want to overdo my workouts on a painful joint.  So lately I have been mixing running and crosstraining... just doing what I can based on the degree of pain.  I am still managing to workout 5-6 days/week, but I think I will only log about 20 miles of running for this week.

Getting back to the Crohn's flare issue though, my doctor has told me to go back up on the steroids (prednisone) to the previous dosage that was working for me (20 mg/day, which thankfully is still a relatively low therapeutic dose).  As a bonus, the side benefit of the steroids will likely be some suppression of the inflammation in my knee joint as well.  My GI doc has also added the antibiotics flagyl and ciprofloxacin, so I will probably do a post in the near future about the scientific evidence on the use of antibiotics for Crohn's therapy.  These drugs are all on top of a background of Crohn's maintenance therapy with Humira + azathioprine.  So, yes, if you were counting, I am currently taking five medications for the same illness.  It seems pretty clear to me that the available therapies for Crohn's disease treatment are inadequate if a patient needs five different drugs simultaneously.  Also, while I do need to take these medicines to alleviate the damage of my immune system on my intestines (and body... it's also important to remember that systemic inflammation is bad for your whole system), a couple of the drugs I am taking have dangerous side effects, and should not be used for long periods of time.  Thus, we need more effective and specific medications to treat Crohn's... we need more research!

NSAIDs & Crohn's: Part I

The setup

On the day of my diagnosis, the gastroenterologist I was seeing at the time told me that I should totally avoid nonsteroidal anti-inflammatory drugs* (NSAIDs).  She mentioned that this class of medications was not safe for Crohn's patients because they could cause the disease to flare.  Acetominophen (which you probably know as the active ingredient in Tylenol), though, was considered a safe alternative therapy for general aches and pains.  I imagine many Crohn's patients were given similar recommendations by their GI physicians at or around the time of diagnosis.

In many regards, it seems plausible that NSAIDs could cause trouble for Crohn's patients.  NSAIDs definitely cause other GI problems, including stomach ulcers and colitis (remember colitis is the general term for colonic inflammation... but it can be inflammation due to anything, not necessarily inflammatory bowel disease), and there is a clear mechanism by which NSAIDs act to screw up the GI mucosal barrier (i.e. the protective lining of the GI tract).  But what gives... just because a doctor says its true doesn't make it true... the scientific data need to support the claim.  Thus, I have set out to investigate the research on NSAID use and Crohn's disease.  And this week I am in luck (or maybe not), because there are a plethora of publications on this topic... so much so that I might have to make this a two-post series.  I want to ensure that I look at enough published science so as to not be biased in my presentation.

An aside... evidence-based living

In my blog post from a week ago, I brought up the concept of evidence-based medicine (EBM) as the ultimate standard for clincal practice.  In this post I am going to mention another concept that I made up based off of EBM... evidence-based living (EBL)... basically, trying to make personal decisions for my own health based on strong scientific research.

Now, this is somewhat of an impossible goal... to live one's life in accordance with scientific evidence.  Everyone has their biases and quirks (including and especially me), and there is simply too much scientific literature out there to keep track of it all.  But, if I know that the scientific data support or refute some sort of behavior, I try my best not to ignore those results.  For example, I don't take a multivitamin anymore, because studies have generally shown either no benefit, or in some cases, even detrimental effects of their use (Dolara et al. 2012).  Also, new evidence from the Women's Health Initiative* that calcium supplementation may do more harm than good has prompted me to stop taking so much Viactiv (Jackson et al. 2011)... but these data are from older individuals and other published results disagree with this study.  A Swiss clinical trial actually showed that the risk of fractures was reduced in healthy individuals with calcium supplementation (Bischoff-Ferrari et al. 2008).  This latter study, and the maintained hope for the potential benefits of vitamin D (and the fact that the caramel flavor is actually quite tasty... not the chocolate, which tastes like chalk), have kept me taking the occasional Viactiv chew.  (An important note... I would like to be clear that these studies for multivitamin and calcium supplementation are specifically for supplementation on top of a normal diet.  Clearly, vitamins and minerals are important when consumed in foods as part of a healthy diet.  The major question with these research trials is whether or not there is added benefit to taking vitamins and minerals as pure-ish compounds in amounts above what is in the normal diet).  So, getting back to NSAIDs, my EBL intention is to make my personal decision about NSAID use based on the scientific evidence on the matter.

So how did this whole story about NSAIDs and Crohn's get started anyway?

Some of the first possible links between NSAID use and Crohn's exacerbations came in the form of case studies* stating that four individuals taking NSAID had their IBD flare up (Kaufmann and Taubin. 1987.).  In addition to only being putative associations, in my opinion, several of the first supposed cases of NSAID use and Crohn's exacerbations are pretty weak.  One patient had a diagnosis of Crohn's and was supposedly in remission for three years, when on one fateful day he was given the NSAID indomethacin for sciatica.  Twenty-four hours later he developed bloody diarrhea, and then had a flexible sigmoidoscopy that revealed 60 cm of uniform colitis.  Really, indomethacin was the cause of this guy's exacerbation?  With 60 cm of uniform inflammation, isn't it more likely that he had active Crohn's disease that had been going for a long time?  It seems possible to me that he maybe had some increased GI bleeding due to the indomethacin (NSAIDs are also well-known inhibitors of blood clotting... this is why "baby" aspirin is prescribed for the prevention of cardiovascular disease), but it seems unlikely that this single dose of medication played any role in his significant inflammation.  Thus, I would generally say interpret case "studies" with a grain of salt; they shouldn't result in significant shifts in clinical practice recommendations, but may point out the need for controlled studies on the subject.

For what it's worth, there were a couple other case reports from the 1980s suggesting an association between exacerbations of ulcerative colitis (the other major form of IBD) and NSAIDs (Rampton et al. 1981., Rampton et al. 1983.)... neither of the others discuss Crohn's disease.  Just want to mention that this sort of questionable association from my previous paragraph wasn't the only case report mention linking NSAIDs and IBD.

The other side of the NSAID coin (or pill)

Given that NSAIDs are part anti-inflammatory, it also seems conceivable that they could be beneficial in Crohn's disease.  Crohn's disease is over-activation of the immune system (see my previous blog post for a more detailed explanation on the mechanisms of Crohn's), and if NSAIDs could suppress this inflammation, then they could inhibit disease activity.  Unfortunately, the immune system is not quite so straightforward--there are many arms of it, and inhibiting one side could shift the balance too much toward the other, etc.  Also, NSAIDs have a lot of effects other than just being anti-inflammatory.  But, the potential benefit for NSAIDs in IBD was at least considered in some earlier publications (Campieri et al. 1980., Rask-Madsen et al. 1990.).  In the end, though, NSAIDs don't work as Crohn's treatment and are not indicated for IBD therapy.

NSAIDs and Crohn's incidence

There are a few studies that have looked at the relationship between NSAID use and the development of inflammatory bowel disease (IBD).  One cohort study* showed that there was a small (and I mean small) increase in the incidence (number of new cases in the population) of Crohn's disease and ulcerative colitis in women who were frequent NSAID users (Ananthakrishnan et al. 2012.)...  fyi, the authors of this study defined frequent use as greater than 15 days per month.  Now, this does not prove any sort of causal link between NSAID use and IBD.  To borrow an analogy from Stephen Dubner, author of Freakonomics, just because a lot of people carry umbrellas on a rainy day does not mean umbrellas caused it to rain.  Similarly, high NSAID use does not necessarily cause IBD.  An alternative explanation might be that women with IBD experience more pain from their disease, and, therefore, take more NSAIDs.  Also, this study showed no association between low NSAID use and IBD.

To be continued...

Due to the depth of this topic, it does seem deserving of more attention and justice than I can humanly summarize in a single blog post.  Thus, next week I will continue this subject with the scientific data on NSAIDs and Crohn's flares and on the potential differences between COX-1 and COX-2 inhibitors (and any other important NSAID-related matters I find in the meantime).  I will also weigh in on my own EBL decision about the use of NSAIDs.  So please check back next weekend for more!

Bibliography:

Ananthakrishnan et al. (2012) Asprin, nonsteroidal anti-inflammatory drug use, and risk for Crohn's disease ulcerative colitis: a cohort study. Annals of Internal Medicine 156:350-359.

Bischoff-Ferrari et al. (2008) Effect of calcium supplementation on fracture risk: a double-blind randomized controlled trial. American Journal of Clinical Nutrition 87:1945-51.

Bjamason et al. (1988) Clinicopathological features of nonsteroidal antiinflammatory drug-induced small intestinal strictures. Gastroenterology 94:1070-1074.

Dolara et al. (2012) Antioxidant vitamins and mineral supplementation, life span expansion and cancer incidence: a critical commentary. European Journal of Nutrition Jun 9 [Epub ahead of print].

Jackson et al. (2011) Calcium plus vitamin D supplementation has limited effects on femoral geometric strength in older postmenopausal women: the Women's Health Initiative. Calcified Tissue International 88:198-208.

Kauffman et al. (1987) Nonsteroidal anti-inflammatory drugs activate quiescent inflammatory bowel disease. Annals of Internal Medicine 107:513-516.

Rampton et al. (1981) Relapse of ulcerative proctocolitis during treatment with NSAID. Postgraduate Medical Journal 57:297-299.

Rampton et al. (1983) Analgesic ingestion and other factors preceding relapse in ulcerative colitis. Gut 24: 187-189.

*Some more specific terminology explanations:

Case study: The more preferable term to refer to a case study might actually be "case report" because "study" is sort of a misnomer, at least in terms of how these reports are used in the biomedical literature, in my opinion.  Case reports are basically descriptive or explanatory articles (i.e. published papers) on a single or small group of patients that have an interesting/unusual/rare medical issue.  They enable physicians to share patient cases that might have greater relevance or may establish a potential interesting disease association (e.g. NSAIDs and Crohn's)... but this putative association will need to be investigated in larger, controlled studies.

Cohort study: This is a particular type of research study in which a large group of people without a particular disease are followed over time to see if they develop the disease.  Then, basically, the researchers go back to see what kind of risk factors (e.g. smoking, dietary habits, etc.) might be present in those individuals who developed the disease of interest.  These studies are purely correlational... they do not prove that the risk factor caused the disease.

Nonsteroidal anti-inflammatory drugs (NSAIDs): This is a class of medications that provide analgesic (pain relieving), anti-pyretic (fever reducing), and, at high doses, anti-inflammatory effects.  Many of these medicines are available over the counter, and, chances are, most of you have taken them at some point in your lives.  Common examples are aspirin, ibuprofen, and naproxen.  The "NS" or "nonsteroidal" part of NSAIDs distinguishes these drugs from the steroid class of anti-inflammatory medications... steroids being a common class of anti-inflammatory drugs prescribed for a host of autoimmune diseases, including Crohn's disease.  NSAIDs are the most prescribed of the anti-rheumatic drugs (i.e. drugs prescribed for arthritis), which suggests that they are very efficacious as anti-inflammatory analgesics (Takeuchi et al. 2006.).

Women's Health Initiative (WHI): The WHI is a program started by the NIH (see previous post for information about the NIH) in order to investigate the major health problems in older women.  Some of the major WHI study topics include cardiovascular disease, osteoporosis, and cancer.

Team Challenge Progress: Week of 8.26 to 9.1

Happy Labor Day weekend and a big thank you to all of my Team Challenge donors from this past week!  With your help, we will make an impact on the future of Crohn's disease research and awareness.  I am > 60% of the way to reaching my fundraising goal.  Please check out my progress bar on my donation page.

This week's donor honor roll (in order by surname):

• Eva Glasser
• John Glasser
• Anne Klemens
• Chrissy Klemens
• Lee Klemens
• Florence Kozak
• Barb Peasall
• Jennifer Swenson
• David Van Essen
• Isabel Van Essen
• Ned Zeljkovich

There were several extremely generous donations this week, so thank you all for your support!  I would give a special word of appreciation to Lee & Anne Klemens, David & Isabel Van Essen, and Eva & John Glasser for being my top donors of the week!

Training Progress

I took things a bit easier this week because I've had a couple knee aches.  But I still managed to log 29 miles for the week.  I will probably take the holiday weekend as an opportunity to rest up a bit, but it is time for me to put my half marathon training schedule together.  Expect to see that posted next week!

Symptom wise, things have continued to be stable for the past week, so I am feeling pretty good about my current treatment regimen.  Things seem like they are finally falling into place.