In this recent blog post, I discussed how my recovery after stem cell transplant has been much faster than average, and there are probably many reasons why that might be.  No doubt the fact that my donor’s genetic markers matched my own perfectly—well, the genetic markers that hospitals check were a perfect match, anyway.  There are literally hundreds of minor proteins that immune systems use to determine if cells are self or not. But maybe many of those were matched more than average, just by chance.  I know I’m not out of the woods just yet, but there are some other possible reasons for my rapid recovery so far.

Greg and I are fortunate that he rarely needs to go to an office.  Greg is a computer programmer, web designer and database manager; he has to work in an office about five days a year, and he goes to work-related retreats and conferences a couple of weeks a year. Otherwise, he’s at home.  As a result, his exposure to infectious agents that in me might cause life-threatening illness is extremely limited.  Most people don’t enjoy this situation, and so I’m sure the average person undergoing stem cell transplantation is exposed to many more infections than I have been.

But Greg and I have been extremely diligent as well.  We’ve taken extreme measures to guard against infection.  We’ve not allowed anyone in our house.  All food, gifts, and mail is wiped down completely with bacteria- and virus-killing chemicals. (Yes, these are nasty . . . and that’s the point: Kill or be killed.)  We got a high-end HEPA filter used in hospitals and endorsed by the American Lung Association.  And these measures are all in addition to the regular extreme rules about cleaning, washing clothes, washing dishes, and such.  And of course, I was a virtual hermit the entire time (with a couple of approved exceptions, when we walked in the park with friends).

Maybe all of this was overkill, or neurotic, or unnecessary.  I know our lead nurse thought so; she promoted much more lax precautions.  We didn’t buy what she was selling, however.  Neither did my physician.^‡ And even if my physician had agreed that these extra steps were a waste of time,  I would’ve ignored him.  If ever there was a time for overkill, I’d say this has been that time.  When it’s time for my nurse’s stem cell transplant, she can be just as lax as she wants.

I have also been exacting in my drug schedule, and Greg has helped a lot with that.  And we’ve learned about the drugs I’m taking so we can play a role in my care.  That has been very important; on three separate occasions, my physician has prescribed a drug, and the wrong dose.  This has happened every single time I have undergone cancer therapy (and I’ve had a lot of cancer therapy).  They screw up the dose, and we’re the ones who suffer.  I learned this lesson during my days of AIDS activism:  Watch the physician’s every move and challenge when necessary; physicians are the top of the hospital’s class hierarchy, and no one else can challenge their actions (a stupid, archaic system that harms only one person: the patient).

Maybe our extreme safety measures had nothing to do with my unusually rapid recovery after the transplant.  Maybe my insistence that the nurses gown, and wash their hands in addition to using ethanol gel, and use sterile technique in all their dealings (especially when accessing my chest port) played no role in my acquiring no nosocomial infections, but I’ll bet it did.  The items on this list of things I insisted of my nurses are all things they normally never do, and I had to fight to get them to do them (as I always do).  I rarely see nurses wash their hands, and when I’ve asked them to do so, they say the ethanol gel is enough.  But of course nurses rarely use enough gel (research shows you have to use a lot), and the ethanol has to evaporate entirely (leaving dry hands) in order to kill microorganisms, and nurses rarely wait for this.  And of course, washing hands plus using ethanol gel would be better than either precaution alone.  Even the infectious disease physician on my team said these measures, including sterile port access, were not important, despite solid evidence to the contrary.  In arguing with me, that same infectious disease physician repeatedly said that the infection rate in the cancer infusion bay was “acceptable.” That rate, by the bye, is three percent for blood infection; I wonder how many people have to get sick with blood infections before he’d consider the rate unacceptable? Four percent?  Five?

In any event, I’d be willing to bet that all these things Greg and I have done—keeping away from people, wiping down all the groceries, learning about my disease, and demanding excellence from the hospital staff and physicians—surely all of these have had a huge impact on my health.  I’m sure some luck was involved, too.  So some of the cards were dealt to us by chance, but we dealt some of the cards, stacking the deck in our own favor.

^‡It might seem weird that a physician and the main nurse working on a team together would not be on the same page about therapies, or how to reduce risk of infection, or whatever.  It certainly is unfortunate, but in my experience it’s not uncommon at all.   It’s surprisingly common for the members of a single team to have differing views about your care, and the members of that team don’t bother to coalesce their views into a single message.  The only sense I can make of this is that the egos involved are so unbridled that none of them are willing to budge.  Of course, this leaves the patient confused and often unable to make an informed decision.  And it’s cruel.  It’s especially cruel to the patients who cannot, for whatever reason, advocate for themselves.   I see no evidence that physicians’ very high view of themselves will change anytime soon.  And this single factor alone is one of the best of the many reasons why hospitals should have formally organized patient advocacy departments that are facilitating and conducting real patient advocacy, and not just walking patients through insurance paperwork (which is what most of them do now).

My good friend, Johanna Wilson, recently posted a comment to my last blog.  I find it so compelling that I’ve deleted the comment and reproduced it here in its entirety.  It is honest, humble (perhaps a bit too self-deprecating, though), and I think quite representative of the way people with cancer feel—and a strong denunciation of the popular view of how we feel.  This deserves front-and-center attention:

I’m with Ms. Ehrenreich in many of her objections to our society’s popular perspective of cancer.  Most of the “cancer people” I’ve spoken with don’t like the term “survivor.”  In my childish frame of reference, I survived chemo, not necessarily cancer. (It was the cancer that failed to survive the chemo!)  It seems to me that survivors are people who withstand a terrific onslaught because of something they did to promote their survival.  If you live through a catastrophic event as a passive observer, you just got lucky.

I also jump on the bandwagon of folks who object to the militarization of commentary on cancer: “battle,” “struggle,” “war.”  I don’t remember any battles or war.  I just remember treatment.  Likewise, terms like “brave” and “determined” didn’t apply to me.  All I did was have treatment.  My medical team and my caregiver put forth all the effort.  I just “took it.”  I certainly never wondered why more hadn’t been done in cancer research (speaking of Ms. Ehrenreich on that last point there).  I felt lucky to live in a society that could provide treatment, and I was lucky to be able to access it. (I know you share that appreciation.)

I may lack an important personality trait that promotes the survival of the species, but I just never felt any anger or sadness about having cancer. (A feeling of loss of control right there at the first, but that passed.)  Fortunately, I never wondered, “Why me?” (I’m always tempted to ask, “Who would you nominate as your replacement, then?”)  The cancer didn’t pick me. I may have actually contributed to its development with some lifestyle choices:  Poor diet, lack of exercise, stressful response to work, etc.  No one to blame except possibly myself.

What I did experience in my own cancer journey was an outpouring of friendship and caring, including the way out of the way side trip you and Greg took to visit me!  I am confirmed in the absolute knowledge that hair and boobs and fingernails are so overrated. (Well, fingernails and toenails are nice, but they’re not part of my identity.) For a brief time, my concerns were bigger than the petty irritations of daily life. (I’ve forgotten most of that lesson. Marty says I’ll have to repeat the exercise.)  Mind you, I’m quite aware that my journey and treatment pale in comparison with yours, but for me, it was a difficult time, but not a negative time. It just was . . . only bigger.  I’m not sure it’s any more appropriate to react emotionally to cancer than it is to an “angry sea” or a “merciless desert sun.”

That’s my story and I’m stickin’ to it! Let the games begin!

From a recent episode of the fantastic series, Glee (quote from the character Shelby Corcoran, played by the even more fantastic Idina Menzel):

I wanna a look so optimistic, it could cure cancer.

More evidence that Ehrenreich’s thesis is correct.  People!  That ain’t it.

Greg and I moved back to our home in Vermont today.  Now, instead of weekly visits to the hospital in Boston, we’ll only have monthly visits.  This would’ve come much earlier had it not been for the (likely) false diagnosis of CMV and the myelosuppressive therapy that ensued, which may well have been key to my contracting the C. difficile that knocked me down so far.  But despite all of this, I’m now doing quite well and feeling very strong.

Last Tuesday during my last weekly visit, I was in the room where nurses take vital signs, and a woman was sitting next to me. She was wearing a mask and gloves, and when this sort of thing happens—when two transplant patients are sitting next to each other—there’s this strange E.T.-and-Elliot thing that goes on; we just want to talk to each other.  Or in my case: I can tell they’d like to connect with me, and I usually resist this, being a curmudgeon and all.  But on Tuesday, the woman sitting next to me just jumped right in.  She started asking me questions about my progress since transplant.  I was in a pretty good mood that day, but had this happened on practically any other day, I’d probably have perceived this as rude prying.  On this day, I saw it as tolerable prying, so we had a chat.  During our discussion, she asked me how far along I was since transplant.  I told her just over two months; she was quite surprised.  She went on to say that she was six months out, and that I looked so good she thought I might be nine or more months since transplant, but certainly ahead of her.

I was pretty surprised by this reaction, and it made me realize that I just didn’t have any frame of reference for how well I’m recovering relative to the average patient.  I’ve always thought that I’ve been doing pretty well, but I’ve never really known.  So I asked my physician what he thought.  He said emphatically that I was doing much, much better than most in terms of recovery, energy level, activity level, and such.  In fact, except for the uncontrollable neuropathy and my problems with the treatment for that (more on that later), I don’t have many complaints.  I’m more energetic now than I’ve been in ten years, and my red blood cell count is still rather low, but rising steadily, so more energy is yet to come.

So, despite my setbacks—the main one being the serious blow I took from the C. difficile—I seem to have rebounded and my health status has more than “caught up.”  My blood cell counts look great for my stage, and my physician has actually started tapering my immunosuppressives, a month or two early.  That means my lymphocytes will come on board earlier (but still many months away), which means protection from viruses.  But this could also mean that Graft Versus Host Disease (GVHD) is going to hit soon.  But GVHD also means Graft Versus Lymphoma effect:  All my cells are me, including any remaining cancer cells that are almost certainly floating around.  If—or rather, when my new immune system recognizes that it’s in a body of foreign cells and initiates an attack on my whole body, that attack will be on any remaining cancer cells too.  In fact, because this attack is mediated by T-lymphocytes—and those cells normally communicate with B-cells when they initiate an immune response—this means that when GVHD does hit, those T-cells will preferentially seek out B-cells during their attack on my body.  As I have B-cell lymphoma, those lingering cancerous B-cells will very likely come into contact with those T-cells that are seeking to fight off my cells.  When this happens, the T-cells will recognize that my B-cells are foreign too, and some of those T-cells can kill my cancer cells on the spot (so-called, Cytotoxic T-cells).

So, GVHD is kind of a mixed bag.  But one thing is certain from the empirical literature: Long-term survivors of stem cell transplants have mild-to-chronic GVHD.  These people are far less likely to relapse, and people who have no GVHD are far more likely to relapse.  So even though I’m over some serious infection hurdles, and even though the majority of death risk is clustered in the first three months post-transplant, I’m about to start facing the next challenges.

But I’m happy to be healthy, at least for now.  And Greg and I are both very glad to be home.  But I think we will both miss our deluxe apartment in the sky-hi-hi.  And just for memento, here are some photos of the view we’ve lived with for the last 75 days:

The Prudential Building (tallest), and a couple of others that no one cares about.

Christian Science weirdos. Despite being cuh-ray-zee, their buildings are "truly beautiful to behold," including this lovely library.

More Christian "Scientists," with their absolutely lovely buildings (all the buildings in view are CS buildings in the famed "Church Park.") The shadow cast is from our sixties-built, 1984-style 12-story building (not run by the Christian Scientists . . . as far as we know).

A reader’s email:

Five hours!  Few of us healthy folks do that … at least not often enough! As we learned in desert survival school, if something CAN grow, something WILL. And that is the history of our planet.  More things grow than die.  In the midst of cancer treatment, it’s a tonic to know that.

So glad you got out amongst the living!   When you’re living “in the valley of the shadow of death”, you need to bask in the light whenever possible.

I might quibble with the assertion that “more things live than die.”  After all, every living thing dies, and 99% of all species that have ever arisen have gone extinct.  And even if the reader’s assertion were true, while such a rule would apply to “me” (the original “me,” that is) and my new stem cells, it would also apply to my cancer with equal force.  Cancer is life too, and it is struggling to live, just the same as the “me” that does not include the cancer—a majority of “me,” the original “me,” the un-mutated “me,” but not quite all of me.

But the central message of the email is clear:  I have reason for hope.  And despite my usually squinty-eyed, suspicious, sardonic predilection, I agree.  And I am glad to be among the living.

A good friend recently pointed out his surprise at my use of the word communist in this post, given my political leanings. He’s right; that wasn’t the right word. What I meant was totalitarian.  I do think that the cells in our body are locked in a kind of communism, but the negative aspect I was pointing out isn’t necessarily linked to that.  Obviously, communism has lead to totalitarianism often, but I hope it’s clear from my blogs that hyper-individuality in the midst of society has its serious costs as well. We’ve seen the cost of extreme individuality in the stock market (no surprise, from a historical perspective; it’s all right there in Marx), and we see its costs in cancer.

The experiment of America, of Federalism, is partly about grappling with these seemingly incongruous interests. The Founders tried to find a solution, and the Transcendentalists tried to find a solution. But so did the Bolsheviks. And so does Polistes, and so does Dictyostelium, and so do all living things.  For social creatures, negotiating the individual and the group is an everlasting struggle of life.

This conflict plays out in our bodies as well, at times.  That was the only message I intended.

I feel amazing.

I am so energetic, I can barely contain it.  Anyone who has spoken to me on the phone lately can attest.  For the last two weeks, my energy and strength has been rising every day, and now I feel better than I’ve felt in years.  In early 2007, I was in a brief remission, and I felt wonderful, like I’d felt years before—before the fatigue set it, which happened three full years before my diagnosis in 2006.  I now feel as good as I did during my remission, which can only be good news.

Reasons for my quick recovery are many: Being able to eat, no more diarrhea, and, most recently, the cessation of a particularly nasty treatment.  That treatment, with the drug ganciclovir, is for infection with CMV, cytomegalovirus, the a virus that in healthy people causes mononucleosis^‡.  I was taking this drug probably because of a hospital error.  In order to explain, a brief digression into biology is required. (Regular readers shouldn’t be much surprised.)

CMV is one of the most commonly transmitted viruses on the earth.  The probability of contracting CMV rises with every year over one’s lifetime, and virtually everyone has it by middle age.  Despite this, I luckily tested negative in my pre-transplant blood tests.  Even more luckily, my donor was also negative.  This was great news, as CMV can cause blindness, serious lung problems, meningitis, and death in immunosuppressed people—facts that I remember all too well from my AIDS activism days in the late ’80s and early ’90s.  My early blood tests found no antibodies for CMV, and a highly sensitive test for CMV’s DNA, called PCR (for polymerase chain reaction), also showed negative initially.  However, three weeks into my transplant, a weekly PCR test was positive.  This was somewhat odd.

CMV is a herpes virus, and like all herpes viruses (including the virus that causes chickenpox [Herpes zoster]; Epstein-Barr virus; and of course, Herpes simplex I and II), CMV can hide inside cells that it infects, inserting itself into our cellular DNA.  When this is the case, a DNA test of blood might well be negative.  So if the CMV became active later, a previously negative PCR could become positive.  That part wasn’t the odd piece.  The odd part was my antibody negativity.

Antibodies are those amazing, disease-specific chemicals that our body produces in response to invasion by viral infections.  For every virus that infects us, we have a different antibody (well, almost).  But I was antibody negative for CMV, and that was the weird piece.  If I had been infected before, and the CMV had become quiescent, and then reactivated three weeks after my transplant, I would’ve been antibody positive the whole time.  But despite my suspicions of the apparently discordant blood tests, the positive PCR meant action had to be taken, and fast.  Because of the great risk of CMV infection, my physician rightly put me on ganciclovir immediately.

The great thing about ganciclovir is that it is very successful in defeating CMV.  I remember when ganciclovir came to market; it was a revolution for people with AIDS.  Prior to ganciclovir, having AIDS often meant the loss of sight, or worse.  And nothing could be done to stop CMV.  Ganciclovir changed all that.  But the bad news about ganciclovir is that it suppresses the production of blood cells, especially white blood cells.  After I began taking the ganciclovir, all of the components of my blood—my platelets, red blood cells, and white blood cells all crashed.  After an unusually fast and strong engraftment of my donor’s stem cells, which resulted in my having normal or near-normal blood counts for the first time in years, I was back to square one, and continuing to take the drug kept me there.  And to boot, after this blood cell crash, I contracted that awful C. difficile infection. Administration of ganciclovir has a known association with infections like C. difficile.  I had to be treated for the apparent CMV infection, but the treatment made me fragile.

Two weeks ago, my DNA test for CMV was negative, as it had been every time after the first test.  I asked my physician why I would not have anti-CMV antibodies if I had CMV (again, antibodies are always produced when we’re exposed to an infection, and we keep them forever).  After some discussion, my physician agreed that this was odd, and hypothesized that perhaps I’d acquired the CMV infection from one of my many pre- and post-transplant blood transfusions.  But that didn’t explain everything, and I left that meeting unconvinced.

Over the next week I puzzled over all my clinical data.  Why was I antibody negative?  Maybe it was because my immune system was so shot that it couldn’t produce any antibodies.  That is very likely true, but even so, I should still have residual (and easily detectable) antibodies from before the transplant, as they remain in the blood months after they are created.  Considering the DNA tests, I wondered how the ganciclovir could have eradicated the infection so quickly; I’d started taking the drug on a Thursday evening, and by the following Tuesday morning all evidence of the viral DNA was gone.  Ganciclovir is a good drug, but that good?  I asked about this the following week (last week).  My physician—who is remarkable in being open to discussion and input—considered my concerns and took a third look at the data, treating them all together.  The negative antibody test, the lone positive PCR result, and the rapid PCR negativity that never reversed—they just didn’t add up.  After this, my physician concluded that the first CMV test may well have been a false negative positive (this can happen with PCR, because this DNA test is extremely sensitive, and in labs where these tests are run routinely [like mine], contamination can be a serious problem).  As a result, we decided to stop the ganciclovir.  My blood cells, in theory, should begin to rise again.

So, yesterday when Greg and I went to the hospital for my weekly appointment, we were a bit disappointed that my blood cells had not rebounded more.  My hematocrit (one measure of red blood cells) was a bit higher, my white blood cells had gained 500 cells per squared cm (up from ~1,100), but my platelets were down from 80,000 to 50, 000 (both well below normal)—a mixed result.

But given how amazing I feel, I wasn’t too worried about this.  I did ask about the possibility of graft failure—a topic I’ll take up a bit later—but looking at the data on the proportion of “my” blood cells that are truly mine verses from my doner, everything looked excellent.

Stem cell transplant is an unlikely business.  Juggling all the variables—the risk of infection, the risk of Graft Versus Host Disease, the many drugs, the side effects of those drugs—managing all these can all be . . . well . . . at times impossible for both the physician and patient.  This procedure is truly at the bleeding edge of our knowledge, and much of what goes on, and why certain aspects of the therapy work or don’t, is yet unknown. When in a situation like this, in my experience two factors are indispensable: patient self-advocacy, and physician finesse.  Having cut my teeth on AIDS activism, I have no problem telling physicians that this is my body, and we must work together, as co-equal partners, to manage my illness, treatments, and recovery.  My current physician agrees, unusually, and we cooperate to achieve our common goal.  That cooperation is a big part of why I’m so energetic and healthy today.

And it’s good to feel great for the first time in a long time.

^‡UPDATE:  See this post.

I do.

Being from Louisiana, and now living just south of the arctic circle, I need the sun.   But I can’t be out in it.   Sunlight can stimulate my immune system (particularly the immune-boosting helper T-cells), which will lead to that conflict I wrote about in the last post, known as Graft Versus Host Disease in medical circles.   Unlike the case of an organ transplant—where there is risk of Host (the person’s immune system) Versus Graft (the transplanted organ) Disease—Graft Versus Host Disease (GVHD) is the reverse, sort of.   In this case, my new immune system (the graft) attacks my entire body (the host). Scary, eh?

Even scarier, if GVHD happens, the risk of relapse is much lower in my cancer.   So ideally, GVHD will happen a bit, but not too much.   Walking that tightrope is up to my oncologist, and he says he can do it. Again . . . scary.   But if all goes well, GVHD won’t happen for many months, during which the immunosuppressive drugs I’m on are slowly removed.

But direct sunlight could counteract the effect of the immunosuppressives, awaking my sleeping, new immune system.   For now, I’m something of a vampire, coming out of my lair only at dusk, making sure to avoid direct sunlight.   So because of all this, a good friend of ours, Karole Moe, who is an amazing artist and who just happens to live in Boston, dropped off some sunlight for us:

A Pollock-esque joy.  Bright rays fill the foreground, and dusky wisps fade into the background. Few things make me genuinely happy these days.   This does every day.

An interesting article appeared in the NY Times a couple of days ago. I have my doubts about the general appeal of a rap performance about evolutionary biology, but maybe it’s great. Who knows? You can investigate Baba Brinkman’s “The Rap Guide to Evolution” for yourself here and here.

Of particular interest, the article highlights one part of the show:

Dictyostelium is notorious, in some circles, for its strange life-style. Usually, an individual Dictyostelium lives alone as a single cell. But when food is scarce, the single cells come together and form a being known as “the slug”; this crawls off in search of better conditions. When it finds them, the slug develops into a stalked fruiting body, and releases spores. But here’s the mystery: not all members of the slug get to make spores — and thereby contribute to the next generation — so why do they cooperate?

Dictyostelium is an incredibly interesting group of organisms. A genus of usually solitary, single-celled amoebae, members of the group are also facultatively social. Individual Dictyostelium cells spend most of their life on the forest floor, eating bacteria. When bacteria become scarce, and the amoeba cells start to starve, they release chemical pulses that draw individual cells together. Once together, the cells form a mound of cells, all piled on top of each other. And then something amazing happens, the mound starts to crawl (yes, crawl) as one unit, across the forest floor. This slug is now, by any reasonable definition, a multicellular individual.

A beautiful image of a Dictyostelium discoideum slugs (bottom) and stalks with spore masses on top. Photo credit: Owen Gilbert

But that’s not the end of this startling story. After crawling away a bit (and by the bye, these slugs are visible and you can watch them crawl), cells at the leading edge organize themselves into a stalk, a pillar, via which the lagging cells in the slug will eventually ascend. The stalk cells die, and the other cells crawl up the stalk and become a mass of sporulating cells, leaving clonal offspring that might disperse from the impoverished environment more easily because of the (slight) height. (Well, in fact, this particular sequence is not universal. Some species of Dictyostelium do it differently, but the ultimate product, the formation of a slug and stalked spore body, is the same).

The comparison to wasp workers and queens is clear enough, but the comparison to our bodies is even clearer. Dictyostelium is a group with sterile worker cells and reproductive cells, and the group is composed of genetically identical cells ( . . . well, sometimes). We are a group of cells with sterile workers cells (our soma, all of our tissues and body parts) and reproductive cells (our germ, egg and sperm). The only difference (and it’s a big one, admittedly) is that our worker cell caste has differentiated into many subcastes—different sterile cell types and tissues composed of sterile cells—just like the workers of highly social wasps.

So Dictyostelium is sort of like Polistes: it has cycles of solitary and social, and it bridges the gap between completely selfish and altruist. (In fact, some of the most important work on Dictyostelium comes from the lab of two former(-ish) social wasp researchers). Given this, the next time someone tells you there are no transitionary intermediates that reveal major shifts in evolution, you can point them to Dictyostelium.

So the question: Why do Dictyostelium cells seemingly willingly, suicidally sacrifice themselves, forgo reproduction, and form the structure (the tissue) that is the stalk? The same question applies to worker wasps, and the cells in your finger. The beginings of the answer were provided by Darwin, but the mathematical framework wasn’t worked out for just over a century later, by über-famous social wasp researcher Bill Hamilton. Hamilton’s insight was as simple as it was brilliant.

It goes like this. Imagine an individual I will call the actor. The actor has two reproductive choices: She can reproduce directly by having her own offspring (thus leaving her genes and heritable tendencies, including her tendency to reproduce directly), or she can reproduce indirectly by assisting relatives have enough additional offspring such that they compensate for our actor’s sacrifice in direct reproduction. This works because relatives share genes. So, for example, our actor (let’s assume she’s a human now) could have one child, or help a sister have two additional children (over the children her sister would normally have absent our actor’s help). Because our actor and her sister share genes by descent, in each case, the same amount of genes are left by the our actor. If the actor has one child, she leaves half of her genes to the next generation. If the actor helps her sister have two additional offspring—because she’s related to her full sister by half, and thus related to her nieces and nephews by one quarter—then our actor leaves two times one quarter of her genes, or half, the same as if our actor had one child directly.

Some individuals in populations will have heritable tendencies for direct reproduction (the selfish tendency). Others (due to natural variation) will have heritable tendencies for indirect reproduction (essentially, helping, or being a worker, an altruist). Whichever individuals actually reproduce more, leaving more copies of their genes—including their heritable tendencies for either selfish direct reproduction or altruist indirect reproduction . . . whichever tendency happens to leave the most genes to the next generation will become more common, generation after generation. The other tendency will wane. Either tendency could be more successful, and this can change depending on other external, environmental factors. But whatever the context, if being a sterile helper results in more genes’ being shuttled into the next generation, that tendency will evolve. And the same goes for the tendency for direct reproduction. Neither tendency is universally better. Natural selection decides.

In Dictyostelium, this calculus is simplified, because the cells are (often) all clones of one another, so if one cell reproduces directly or by helping a clone reproduce, the reproductive success to each cell is the same. In this context, conflict-free cooperation can much more easily evolve. Of course, I’ve already pointed out in previous blogs that mutation can strike, and change the behavior of a cell, just like in our bodies. When this happens, the happy harmony is disrupted, and the cheater cell might corrupt the system by reproducing wildly, or otherwise refusing to engage the social contract. This happens in Dictyostelium, just as it does in us. All social systems have cheaters, cancer.

The harmony of Dictyostelium can also be disrupted when slugs are composed of genetically different cells, or even (sometimes) different species. When this happens, cells don’t easily sacrifice themselves and become stalk tissue. It’s easy to see why that behavior might not be favored by natural selection. In this context, becoming a sterile worker might mean very little or no indirect reproduction (for example, if the spores are all distant relatives of the stalk cell). If sterility and helping leave no genes indirectly, the behavior washes away over generations. The only tendencies that are left are the selfish: In a mixed group, fight for direct reproduction or perish. So, this generates great conflict, and individual cells in the slug try to position themselves such that they will be in the spore mass.

Because of this kind of conflict, it was long ago predicted that members of social groups should be able to recognize close relatives. Since that prediction—a prediction that derives directly from the mathematical evolutionary framework I describe above—many social creatures have been shown to recognize kin. You might think this kind of conflict (from genetically distinct cells) has little bearing on humans, but it’s exactly the kind of conflict that stem cell transplants can generate. The potential for that conflict is playing itself out in me now. My new cells have kin recognition abilities, and if they aren’t tricked into thinking my body is kin, a significant conflict may erupt.

So now, I’m like a mixed colony of Dictyostelium. Having hopefully exterminated the mutant cheater cancer cells, I now face yet another other social conflict. As time passes, the probability of that conflict rises.

I’ve received a somewhat strong response to my last post, which is great. Keep the comments and email coming. Regarding that post, many have questioned my final comment about sympathy for my cancer. To be sure, I chose that word to be provocative, but I do have sympathy for all life that is marked for extermination (in this case, by my hand). I have sympathy for the forest that is clear-cut, and I have sympathy for the cattle that we grow to kill and eat. Of course these organisms are not trying to kill me, so naturally my sympathy is greater for them. But I don’t think my cancer is trying to kill me either.

Natural selection dictates that those that are more adept at doing whatever allows them to leave more offspring will be more common in future generations. If their reproductive advantage is heritable, then the traits that allowed them to be more numerous will also be more and more common in the population over time. Imagining, again, that our bodies are a colony of cells, or a nest of wasps, or a school of fish, or whatever, then it’s easy to see why slowly reproducing individuals or individuals that don’t reproduce at all will become less and less numerous over time relative to a rapidly reproducing member of the same group. I thought I’d made clear the restricted sense in which I invoked that term, sympathy.

Looking back, perhaps I could’ve been clearer, but that’s the nature of blogging. The arguments are made mostly extemporaneously, a kind of stream of consciousness. The entire work is presented piecemeal, across days, and new entries sometimes only make sense in light of previous posts. Plus my chief editor is on permanent leave. (Actually, Greg helps a lot with editing.) So I will clarify (or retort) a bit. I don’t mean to criticize any who have responded. (We normally live in Vermont, where I think criticism of what others have said is illegal). I’m just reasserting clarifying my view for the enjoyable dialogue.

When I first read some of the objections, the situation reminded me of a conversation I once had with a Physician’s Assistant who was at the time coring a hole in my ileum for bone marrow. During that delightful visit, we had a chat. At one point, I made some comment along the lines of what I’ve been saying here: The cancer cells are just doing their thing, trying to stay alive, like any creature. Stunned, he looked at me at asserted, “But cancer is bad.” I thought about his short sentence for a long time, and given the context of our conversation, he could only have meant one thing: Cancer is morally bad. Now, don’t get me wrong. He wasn’t suggesting that I had cancer because of my moral failings or past-life no-nos (although I’m amazed at how many do believe such things, and will actually tell me about it to my face). He meant that the cancer itself was evil. You know, just like how wolves are evil for eating cute bunnies.

I now get it that some of you thought that I had written the wrong word, intending instead to say empathy. The substance of the post shows my empathy for my cancer, certainly. I just wanted to express something else for the life that I am desperately trying to kill. That life is not evil; I just find myself in conflict with it.

Obviously, I hate (and I mean that word, too) that I have cancer. I often say (usually to poke fun at the bright-siders) that the only thing I’ve learned from cancer is that I don’t want to have it. I want each and every cell destroyed. Why else would I have endured four years of off-and-on therapy, with the last two years’ mostly futile treatments being virtually continuous. Just because I know the cancer cells are not trying to kill me does not mean I will relent in trying, by any means necessary, to kill them. Self-preservation trumps sympathy.

I invite dissent and alternate perspectives. I’m not doing this just to get my ideas out there; I hope to learn something from this blogging experience too. But I did say what I meant. Just because I have some sympathy for my cancer doesn’t mean I want to help it or keep it as a pet. Who didn’t have sympathy and cry for Ol’ Yeller? But that diseased, frothing mongrel still had to die.