Reflections on Turning 50

Earlier this year, I reached one of those dreaded milestones. I turned 50 years old.

Five decades. Half a century. Wow.

When you turn 30, you’re jokingly referred to as “over the hill.” But it’s only joking.

At 40, the joking has a hollow ring. You have the uncomfortable feeling that you've probably lived half your life already. The sense of a midlife crisis can become intense.

Then, there’s 50. All of a sudden, you qualify for your first AARP card. And the minor aches and pains you felt before can become lingering, even chronic issues if you’re not careful.

I’ve thought a lot about age and healing, especially after an orthopedist in Hong Kong cheerily told me about five years ago, after I described my knee pain symptoms, that I was over 40, my body was just going to go downhill, and I should accept that.

Fortunately, I didn’t accept that. I was convinced that there wasn’t some “ability to heal” switch that toggled to the off position when I reached a certain age. And, sure enough, after much perseverance, I managed to get better.

That’s not to suggest though that I believe in the saying “Age is just a number.” A realist has to concede age does indeed matter. Senescence is a real phenomenon. Older muscles, for example, don’t recover from hard exercise as quickly and are more prone to injury.

But that doesn’t mean age is a defining number. People can forestall and mitigate the effects of aging -- and it’s not that hard to do.

Vigorous exercise is a good way to slow the advance of the calendar. But, as you get older, it’s good to get smarter about how you exercise.

For example, in the weightroom, I warm up by doing 50 repetitions of an easy weight that’s one-half to one-quarter of the maximum I lift. When I bike in cold weather, besides warming up, I take care to keep my knees comfortable (unlike some cyclists I go out with, who wear jackets and arm warmers while leaving their knees bare!)

Also I’m more careful about taking part in impact sports or activities that involve a lot of jumping or running. It’s not that I can’t do them; it’s just I try to do them smarter (in my younger days, playing softball, I sometimes made leaping catches where I landed on my head -- these days, I’d let the ball drop :)).

So if your knees are bad, and not getting better, don’t blame your age. Blame your weight. Blame your job. Blame the fact that you don’t have a recovery plan, or if you do, it’s not the right one or you’re not following it closely enough.

Because age doesn’t matter nearly as much as others will tell you it does. Trust me here. This is something I happen to know firsthand.

Do You Train for Work?

I remember mentioning this concept to a colleague once. We were talking about our tiring 10-hour-a-day desk jobs. So I said that I “trained for work.” He gave me a sideways smirk, as if to say, “Yeah right. Like there’s a workout routine designed for someone who sits like a rock in a chair all day.”

But I was actually serious.

It’s not that you have to train to be able to do nothing but wiggle your fingers over a keyboard. It’s that you have to train to counteract the deleterious effects of doing nothing, for such long periods, but wiggling your fingers over a keyboard.

Sitting can be poisonous for our bodies, which were designed for movement. Doug Kelsey at Sports Center in Austin once wrote that an old teacher said something to the effect that sitting does for your spine what putting a plastic bag over your head does for your breathing.

So I actually do train for work. Every workday morning I do this “bird dog” exercise for three and a half minutes, to keep my back muscles strong. I also do this “rock ‘n roll” exercise (another great recommendation by Kelsey) for five minutes, for my neck, which is a little crackly and has given me minor problems in the past.

What about my knees?

Actually, what I do for my knees probably benefits my neck and back too. First, on the way to work, I walk a good three-quarters of a mile to my subway stop (bypassing two closer stops, just so I can get in some beneficial movement). During daily snack breaks (Bloomberg has lots of free food on the premises), I eat while slowly strolling the floor. And at lunch, after a quick, light meal, I head for the exits and walk the streets for a good 10 or 15 minutes.

So, in sum: I move as much as possible during work breaks, to try to negate the effect of all the toxic sitting. And early in the morning, I do various exercises to help prepare me to withstand all that sitting without discomfort.

Our bodies need movement. Our 21st-century jobs often don’t accommodate that need so well. So a little special effort is required to keep all our body parts running smoothly.

What Causes Patellofemoral Pain Syndrome and Chondromalacia, Part II

Last week I shared a “unified theory of chronic knee pain” -- basically, that bad cartilage was involved much of the time.

Let me be clear what we’re talking about: diffuse, achy pain generally. There are other, more specific pains when a doctor pokes something and you go “ouch.” Different structures are probably involved there (e.g., I wouldn’t consider “patellar tendinitis” to be PFPS -- I could be wrong here -- because patellar tendinitis diagnoses a clear, identifiable problem).

Now what are some objections to this “unified theory”?

An MRI shows that my cartilage is fine but I have knee pain! So how can the source of pain be the cartilage?

Remember, a typical MRI takes a picture that is imperfect. (Two wood-frame houses may look identical in a photograph, but if the beams of one have been hollowed out by termites, they will not perform the same structurally.)

Initial cartilage damage associated with chondromalacia starts deep within the tissue -- and so, it appears, would not be detectable by a standard MRI.

In chondromalacia of the patella, the initial lesion is a change in the ground substance and collagen fibers at the deep levels of the cartilage. It is a disorder of the deep layers of the cartilage that involves the surface layer only late in its development. (Weinstein, Stuart L. and Buckwalter, Joseph A., eds. Turek’s Orthopaedics: Principles and Their Application.)

Some people with cartilage lesions have no pain, and others with lesions have pain -- if that’s the case, how can bad cartilage be to blame?

Partly the answer appears to be that thin cartilage becomes a problem at some point, despite a knee pain sufferer having a number of initially non-painful lesions:

A recent study proved that one can have as much as Grade III wearing without pain. So, pain is variable. The source of chondromalacia pain is not the articular cartilage itself, but the thinning of it, which transfers loads onto the underlying subchondral bone, which is pain-sensitive. (UCSF School of Medicine, Physical Therapy and Rehabilitation, on patellofemoral pain)

Another important thing to consider here, it seems, is the quality of the remaining cartilage. Recall that chondromalacia literally is an abnormal softening of cartilage. It may have minor wear and be soft (and hurt more), or may have more wear but be fairly stiff (in a good way) and resilient (and hurt less).

Still, if you have a lot of deep lesions, chances are good you have more pain than someone with less damage.

The severity of cartilage lesions detected at arthroscopy highly correlates with incident pain (Aaron, Roy K. and Ciombor, Deborah M. “Pain in Osteoarthritis.” Medicine and Health Rhode Island, July 2004) 

How can damaged cartilage cause pain if the tissue has no nerves?

The key thing to remember here: the source of the pain sensation isn’t the cartilage itself.

Because there are no nerves in cartilage itself, the pain must emanate from subchondral bone, which is experiencing deficient conduction of stress through mechanically inadequate cartilage. ... Fibrillation of articular cartilage usually follows fissuring with progression to ulceration in some cases. When fibrillation progresses to a larger area of the patella, bone may begin to experience abnormal pressure increases or irritation from flaps of cartilage that are placed under pressure. (Fulkerson, John Pryor. Disorders of the Patellofemoral Joint.)

Or, here are some other ways bad cartilage triggers pain sensations:

The articular cartilage is not sensitive to stimulation, but ... the adjacent synovium is the primary pain source [fragments of cartilage can migrate through the synovial fluid to the synovium, irritating it]. The subchondral bone ... is another likely source of pain from excessive load on an unprotected bone surface. Finally, the resulting effusion [swelling] caused by articular breakdown may itself be a source of pain. (Johnson, Donald H. and Pedowitz, Robert A., eds. Practical Orthopaedic Sports Medicine and Arthroscopy)

And as for inflammation:

... Cartilage debris and sulfated polysaccharides liberated from cartilage breakdown have been shown to be inflammatory in joints and to stimulate the release of proinflammatory cytokines. (Aaron, Roy K. et al. “Pain in Osteoarthritis.” Medicine and Health Rhode Island, July 2004)

Then, if you happen to believe that where there’s smoke there’s fire, well, osteoarthritis and cartilage damage go hand in hand:

This loss or damage of articular cartilage is an early finding in osteoarthritis. Chondromacia patella is thus an arthritis involvement of the patella. (MDGuidelines, entry on patella chondromalacia)

But there are other things going on inside bad knees. How can you blame poor cartilage for everything? For example:

The association of bone marrow edema with pain in osteoarthritis of the knee has recently been emphasized. Bone marrow edema was found in 78% of patients with pain compared to 30% of patients without knee pain. The presence of bone marrow edema is associated with progression of cartilage degradation. (Aaron, Roy K. et al. “Pain in Osteoarthritis.” Medicine and Health Rhode Island, July 2004)

Here’s where a careful person has to admit, “Yeah, there's plenty going on that we don’t fully comprehend.”

But consider for a moment swelling of the bone marrow. The first matter to ponder: Does this contribute to cartilage degeneration or is this caused by cartilage degeneration? To me, the latter sounds more plausible. Still, let’s posit the former: that the bone marrow swelling is responsible for cartilage damage -- or that a third, even larger unknown force causes both the cartilage degeneration and the bone marrow swelling.

Okay then, where does that leave us, in terms of finding a path toward healing?

If your main problem is bone marrow swelling (or intraosseous hypertension, or focal osteonecrosis, or bone marrow lesions), then it seems you’d want a more bone-oriented treatment regimen. Now, I am way out on a limb here (I’ve done very little reading on this subject), but bone resembles cartilage a lot more than muscle. So I would think a gentle, joint-friendly program of high-repetition movement would be a smarter way to go than a “strengthen your quads” approach.

So even if the “unified theory” is wrong -- even if cartilage isn’t involved in much of all chronic knee pain -- I think the same activities that would strengthen and help repair this tissue would probably also benefit the joint overall.

What Causes Patellofemoral Pain Syndrome and Chondromalacia?

I got this question recently.

It’s a good one because, unfortunately, the answers aren’t easy. But they are important to seek out. As I mention in Saving My Knees, my first law of healing is:

Before devising a plan to heal, you need to know what’s wrong and what’s causing it to be wrong.

So let’s start with what causes patellofemoral pain syndrome (often abbreviated “PFPS”).

Ah, that’s easy! It’s psst ... psst ... psst.

Seriously: there are two ways to answer this question.

One is that no one knows what causes it. No one knows because no one can know. There is no such thing as PFPS. PFPS is an overly broad, useless pseudo diagnosis that, when translated to its constituent parts from the bewildering medical terminology, means:

You have knee pain (of unknown origin).

An analogy: Your elbow hurts. You see me, a learned doctor, and I say, in tones most grave and dignified, that you have “humeroulnar pain syndrome.” You leave my office, distraught, then do some research, and find out that I’ve told you:

You have elbow pain (of unknown origin).

Not too helpful, huh? Same with PFPS.

The second answer is a bit more sophisticated. PFPS does mean “knee pain,” but it does align with a certain set of symptoms (difficulty sitting and walking up and down stairs, for example). So what’s the most likely cause of that symptom set?

In a moment, I’ll offer an, um, “unified theory of chronic knee pain.”

But first, let’s look at chondromalacia in the knee joint. What is that? It’s an abnormal softening of cartilage. That literal definition is rather abstract though. More commonly, it can be thought of as “a condition in which the cartilage ... becomes worn from age or is damaged from injury.”

Now there's one more thing to introduce at this point: patellofemoral pain syndrome and chondromalacia are often used interchangeably. They are NOT the same thing, but the fact that this confusion exists is very interesting. It suggests that one (chondromalacia) may have something to do with the other (PFPS).

Which brings me to a unified theory of chronic knee pain.

Cartilage problems are involved in much of this kind of pain. So bad cartilage would be implicated in many cases of PFPS. What causes bad cartilage, or chondromalacia, in the first place? I doubt there’s a simple answer. It could be anything from an injury to overuse to obesity -- whatever causes wear or damage to the tissue.

Next week: Objections to the unified theory. A response to each objection. Finally, even if bad cartilage isn’t causing your knee pain, why it may not matter in terms of what you need to do to get better.

A Few Words About Hurricane Sandy (And What It Meant for My Knees)

For anyone living in the New York City area, there’s been only one story this week: Hurricane Sandy.

The weekend before the storm, I said to an acquaintance, “I’m worried less about the wind than the possible flooding.” I had seen water gushing from the ceiling of subway tunnels during no more than a heavy thunderstorm.

Sure enough, the big story turned out to be disruptions related to the incredible storm surge (not that the downed trees were minor -- strolling around my neighborhood post-Sandy, I counted 10 trees within an hour that had either fallen across the road or had crushed a car or smashed into a house).

Manhattan, as I’m sure most are aware, is an island. Those of us who live in the outer boroughs (such as Queens, where my family has an apartment) board long silver subway trains and are magically whisked through the bedrock, and under the East River, to arrive at our workplaces in the heart of the city.

Monday morning, there was no magic. The tunnels under the river had been overwhelmed by a wall of water and closed indefinitely. Whereas I usually walk three-quarters of a mile to a subway stop (not the nearest one either -- I just like to walk a little) and choose from E, F, M, and V trains, suddenly I had no choices.

Monday and Tuesday I worked at home. Wednesday, however, I had to get to work to lay out the weekly publication that I edit. I had no other option. My company was providing a bus shuttle, but it wasn’t conveniently located, so I thought:

What the heck.

I had for a while pondered what it would be like to walk to work. Make no mistake: it’s a serious walk to my office building in Manhattan from the east end of Forest Hills, where I live. Door to door, the distance is 8.4 miles, according to a Google estimate of the route.

So I set out at 6:42 a.m., into the pre-dawn, as the city was just rustling into life. I went most of the way down Queens Boulevard, then turned onto a street that took me (and lots of other New Yorkers, on bicycle and foot) over the Queensboro Bridge. By the way, on the bridge there were no slackers: everyone kept a brisk pace.

At 9:02 I walked through the doors of Bloomberg’s offices at 731 Lexington Avenue. At the end of the workday, I wound up walking back (I did the return leg in 2 hours and 18 minutes, 2 minutes faster, because I was motivated due to some of the neighborhoods I had to walk through ;))

So that’s 16.8 miles (actually probably 17, because I took a wrong detour on the way back and, on the way in, took the wrong approach to the bridge and had to double back a little).

The good news: I had a little sore spot on the back of my left heel, but my knees did just fine. That, I figure, is because I have spent the last three years strengthening them with 60 miles of vigorous cycling each Saturday, powering over the small hills of western Long Island.

I can remember a day, that seems not so long ago, when I lived in Hong Kong and was trying to heal my bad joints and would force myself to stop walking on trips after about 3,000 steps. I would make myself sit down and go no further because I knew I had to be very, very patient to restore my knees to good health.

Walking 17,000 steps in the morning -- and then 17,000 more in the evening -- would have been unthinkable. But that’s the nice thing about beating knee pain. Your knees get stronger. They no longer tell you what to do. You tell them what to do.

And that’s a great freedom, because it allows you to do something a bit offbeat and crazy -- like walk 8.4 miles to work when there’s no public transportation.

(By the way, for anyone thinking, “That’s dumb -- why didn’t you just take a taxi?”, the roads were clogged and a co-worker who did hire a car into work got stuck in traffic and ended up getting out and walking at the end -- and he arrived half an hour later than I did going the entire way on foot!)

Beating Knee Pain: Do You Have a Plan?

A while ago, while working out at the gym, I heard a canned announcement over the PA system designed to sell the services of the on-site trainers.

“Do you have a plan to get fit?” a pleasant voice asked.

At the time, it struck me as deeply ironic.

We accept the need for a plan to build muscle strength and improve cardiovascular fitness. But that’s child’s play compared with managing knee pain, with an eye toward actually getting better. If the former requires a half-page plan, the latter demands something like three pages of detailed notes.

Yet how many knee pain sufferers are there who just muddle along, day to day, and never try to plot a path toward healing?

Broadly, what should go into a plan for beating knee pain?

I think it helps to start with a realistic appraisal of your condition. And be willing to be humbled. You may want to start out walking three miles a day; your knees may quickly tell you that they can only do half that much comfortably.  

Also, of course, you have to decide what your regimen will consist of, day to day, in terms of walking/cycling/swimming/other joint-friendly activities, and how much of each.

Not too hard so far -- rather like designing a workout program in fact. Here’s where it gets tough. You need to be able to adjust on the fly, and play medical detective.

Example: You wake up one morning during week five and your bad knee is really stiff. Oh no! What do you do? You have to be able to ease off for a few days -- or even a few weeks, if needed. Also you need to try to figure out what may have caused the stiffness, so you can avoid doing that again.

So you want to keep some kind of knee journal, to make sure your plan is working and help guide you in revising your plan as your knee gets stronger (yay!) -- and also help you figure out what went wrong when your knee gets worse (ugh!).

To beat knee pain, I’m convinced you need a thorough, though flexible, plan. It may sound challenging. But the rewards are great if you succeed!

Yet More Proof Your Doctor Isn’t Infallible

One of the first criticisms I got about Saving My Knees went like this:

“This is a lousy book. All he does is complain about how all his doctors and physical therapists are wrong and I can’t tell if he got better anyway.”

(By the way, if anyone else is similarly puzzled on that last point, I can unequivocally state that yes, I got a whole lot better. My knees are fine today.)

Read between the lines, and the reviewer appears to be annoyed that I have the temerity to suggest there’s something wrong with the expert advice I was given on treating knee pain.

Why such a harsh reaction?

I think among certain people there is a reflexive, total deference to the opinions of “experts,” even though what is accepted as truth by one generation of experts may be soundly rejected by the next. (History is full of examples; in Saving My Knees I mention the once widespread medical practice of bloodletting to cure a host of ailments, which has been debunked as nonsense.)

Today I’m going to show you that your doctor is very much human -- and not an infallible expert at all -- with a bit of math. It’s taken from Fooled by Randomness by Nassim Taleb, who himself has borrowed the anecdote from Randomness by Deborah Bennett.

Medical doctors were given this problem to solve:

A test of a disease presents a rate of 5% false positives. The disease strikes 1/1,000 of the population. People are tested at random, regardless of whether they have the disease. A patient’s test is positive. What is the probability of the patient being stricken with the disease.

(If you want to try to figure it out yourself, go ahead. I start to disclose the solution immediately below.)

Most doctors -- more than four out of five -- got this wrong. They answered 95% because they focused solely on the accuracy rate. But the question being asked isn’t, “How accurate is the test?” The question, stated more fully, is “What’s the probability the patient has a somewhat rare disease if a test that’s wrong 5% of the time says he does?” And the answer to that question is very different: less than 2%.

Taleb explains how he arrives at that figure:

Assume no false negatives. Consider that out of 1,000 patients who are administered the test, one will be expected to be afflicted with the disease. Out of a population of the remaining 999 healthy patients, the test will identify about 50 with the disease (it is 95% accurate). The correct answer should be that the probability of being afflicted with the disease for someone selected at random who presented a positive test is the following ratio: number of afflicted persons/number of true and false positives. Here, 1 in 51.

Got that? The difference between the right answer and the most commonly mistaken one is very significant. It’s the difference between “you almost surely have the disease” and “you almost surely don’t have the disease.”

Wow.

There are a few points worth making here. The less interesting one, to me, is that doctors often can be mistaken.

The point that I find more interesting (and empowering) is that you don’t have to be a medical school graduate and a practicing physician to analyze information about medical conditions (claims, studies, empirical evidence) and come to conclusions that, in some cases, may be superior to those held by so-called experts.

What’s more, when it comes to your bad knees, you do know more than your doctor on one very important subject: how your knees behave (what they like and don’t like, what causes pain, etc.)

So if a doctor says, “Ah, your knees will never get better” (which is what I was wrongly told), remember: doctors can be wrong -- very wrong.

After all, four out of five missed the correct answer to a basic statistics problem. :)

Extra credit: Did you notice Taleb's approach to solving the problem? Out of a population of 1,000, he removed the person who has the disease (remember, it strikes 1 out of 1,000 people), then calculated that 5% of the remaining 999 were false positives (49.95). So the chance of having the disease is 1/50.95 or 1.9627%.

Alternatively, you could apply the 5% rate of false positives to the population of 1,000, resulting in 50 people who wrongly test positive for the disease, then add the one person who actually has it. So the chance of having the disease this way is exactly 1/51 or 1.9608% -- a bit different.

So, given the information as laid out in the problem, which answer is correct, and why?

Note: The difference in the results from the two approaches is trivial, so you may think it hardly matters which one is correct. While that's true for this example, it wouldn't be for another, say where 30% of the population has some disease and the test has a rate of say 20% false positives.