why Vermont is right for us

Elana posted this story on Facebook, but for anyone who doesn’t follow us there, I’d like to repost the following funny story told by Christopher Kimball of Cook’s Illustrated:

My favorite Vermont story is about the city kid and the toad. A youngster comes up to Vermont for a couple of weeks one summer and, as he is walking down a dirt road, spies a large green toad. He soon starts to poke it with a stick. A local boy happens by and says, “Quit poking that toad!” The city kid shoots back, “Well, he’s my toad, ain’t he?” The country boy responds, “Nope. Here in Vermont, he’s his own toad.”

And I guess if anything in the world sums up our parenting philosophy, it’s that — “He’s his own toad.” We happened upon him, and we’re grateful to have done so. But he’s his own toad, and we have no right to poke him with a stick. The analogy isn’t perfect, of course, because he depends on us for certain things, including cues about how to act in the world. But in the main, we’d like to treat him like he’s on his way to being a guy with autonomy, someone who makes his own choices about things, knows how to reason his way through a problem, and can make cogent and persuasive arguments in favor of a course of action.

This is not some hippie bullshit, either. Well, maybe it is — but it’s hippie bullshit backed up by science. To wit:

Adolescents who held their own in family discussions were better at standing up to peer influences to use drugs or consume alcohol. The best protected of the group were the teens who persuaded their mothers with reasoned arguments, rather than with pressure, whining, or insults, when talking about topics like grades, money, household rules, and friends.

Let him be his own toad at home, and he’ll have the tools to be his own toad among his peers.


(I should state candidly that I do not live up to this parenting standard, and sometimes I yell at him or rudely make him do things, because I’m easily frustrated, and because the number of hours I have to spend investigating spots on the sidewalk is limited. But this is what we’re shooting for.)

i’m mike d and i’m back from the dead

Hello, Internet! Sorry we’ve been away for so long — I was concentrating very hard on my first semester of law school. But I’ve missed talking to you.

Here is a little snapshot of us as we are now:

  • Until a few minutes ago we had seaweed under our couch. I don’t know why I try to delude myself into thinking that, when I turn over the couch to retrieve his many, many missing toys and books, there won’t be food under there. But I always think, “Well, nobody eats under there — how would food get there?” But it does. Crackers, fried banana chips, a segment of tangerine… and dried seaweed.
  • Our bear is talking now — pretty much non-stop. He even talks in his sleep. Last night he asked aloud, without waking up, “What is that book doing??” Then he fell silent again.
  • Books are actually a big preoccupation. He really likes to read. The most commonly uttered sentence in our house is “Daddy, read-it Frances book!” The “it” particle at the end of some verbs seems to be a remnant from his first rudimentary attempts to understand English grammar
  • His speech tends to be very precise and clipped. Each word gets its due. E.g., “Don’t. Like. Chicken. Only. Sausage.”
  • He’s now three feet tall. This means that (a) he grew six inches in his second year — the normal range is two to five — and (b) he can now reach things that we put up on the highest counter. I don’t like this. He should stay short until he’s less likely to pull shit down and break it. So far we’ve been pretty successful at keeping him out of the kitchen, but I feel like it’s a siege, and sooner or later he’s going to invent Greek fire.
  • He’s old enough to memorize our instructions, but not old enough to act on them. So he will dutifully recite, “Don’t. Pour. Water. Out.” as he pours a glass of water onto the floor.
  • We are in good health. We have stopped eating very much in the way of bread, pasta, or potatoes, about which more in another post — but I have lost twenty pounds since the summer. I biked to school most of the semester, Elana is on Week One of the Couch To 5K program, and the kid works out by destroying everything we own and climbing up to stand on the table. (While saying cheerfully, “Don’t. Stand. On. Table.”)
  • I am freaking out about my grades. They will be out in January. I feel pretty good about Crim Law, but I really have no idea how I did on the other two, except after each of them I thought of at least one mistake.
  • H. frequently describes things as “nice.” Out of the blue he will look at our couch and say, “Nice couch!” And I’m always like, “Thank you! We feel it’s understated, but elegantly modern.”
  • He’s developed quite a sense of humor, and if he makes you laugh, he’s always eager to confirm with you that something was a “Funny joke?”
  • Elana finished her contract right before I started school, and she is now working on some pretty cool projects with various interesting parties around town. I will let her tell you more about that as she sees fit.
  • This means that we are both working kind of full-time now, and H. therefore goes to daycare. We were worried that this would not go well, but as it turns out, day care may be just the thing for a kid his age — he really seems to enjoy the running around, and I think it’s good that he talks to grown-ups who aren’t us. But it does seem to be a job for him, and at the end of the day he’s often wired and cranky.
  • Having a kid who reads is a funny thing — you really figure out quickly which kids’ books are written by people who know what they’re doing. Russell Hoban (pour some out for the dead homie) and Dr. Seuss are at the pinnacle of achievement in the form, Sandra Boynton follows not far behind, and then there are many, many lesser writers — some of whom are quite well-known. The interesting thing is that the kids seem to know which ones are good, too — H. loves Frances so much he can actually recite sentences from the books. (You know… short sentence without any prepositions. But still!) But every now and then he’s really entranced by something like Richard Scarry. I don’t get Richard Scarry. What’s with the weird, sexually-charged relationship between Miss Honey and Bruno? It’s this timid romance between two middle-aged people in a small town; very Winesburg, Ohio. Also, are Lowly Worm’s parents Calvinists? Why is he named that? If your last name is already “Worm,” do you really want to compound the problem for your poor son, just to teach him humility? (True story, though: Elana has an ancestor named Fear-Not Frink. That seems like it must have been a very comforting name.)

All right — that’s probably enough for now. We will try to update occasionally over the holidays, but I except this blog will fall dormant again when the new semester starts. Love to all.

the word became flesh and dwelt among us

The most interesting thing that’s been happening recently, in our toddler’s world, is that he turned some kind of corner regarding spoken language. In May I posted a list of signs he knew — it was about forty words. Since then he made the jump from mostly signing to mostly speaking, and now his spoken vocabulary is somewhere north of 75 words. We know this because his daycare providers have been tracking new words, and they’re keeping a running list in chalk on the wall.

Anyway, here are some developments of note:

  • He likes to do everything for himself, including feeding himself, drinking, walking up and down stairs, and operating the TV remotes. If you “forget” this preference of his, he will cheerfully remind you by shouting “Self! Self!”
  • I’m pretty sure he thinks his name is “you.” This isn’t too surprising, if you think about it — whenever we see a mirror, or a photo of him, of course we always say, “That’s you!” So now when he sees a mirror or a picture of himself, he points and shouts “Yooou!”
  • He’s getting pretty comfortable with two- and three-word sentences. For example, he was poking Elana the other day, and she warned him to be careful near her eye. He giggled delightedly, “Eye… poke… mama! Hahaha!”
  • He can identify written words, at least in the sense that if you show him a page and say, “Where are the words?” he can usually point to them.
  • Finally, he seems to use language to help him think through some of the moral lessons we dimly hope he’s learning. For instance, after a morning of out-of-control whacking that ended with me hiding his little wooden Thor-hammer, he sat next to me and pointed at my knee and said “Whack knee… noooooo….”
  • UPDATE: Forgot to mention — he’s also decided that “it” is some kind of suffix or language particle that goes with all verbs. And for the most part, he’s correct. When he says “want-it,” “have-it,” “like-it,” etc., that’s perfectly understandable English, even though it’s based on a formula that has the “wrong” underlying logic.

everything’s coming up videos

So I don’t really have time right now to write about science or even to record any clever observations about the nature of parenting. But here are some videos of our little fellow, for the grandparents, aunts, and other curious parties.


Here he is when Gram and Grandpa and Auntie were visiting:


Here he is climbing a rope ladder:


Here he and his mom play “Wipeout,” a game they invented on the spot.


Here he reads to you. Then he asks to see the video.


Here he uses the word “lap.”


Finally, here he plays the piano with this feet. It’s pretty great. He looks very serious about getting the notes right.

a brief and unscientific update on language

Since I last wrote about Henry’s language development, there’s been a ton more. My friend John commented a couple of months ago that his son had all of a sudden started picking up about a word a day, and this now seems like an accurate description of what’s going on with Henry. He’s learned, in the past few weeks, food, water, turtle, pool, wall, meat, hot, high-chair, bowl, hat, down, tea, oatmeal, towel, and, uh, cowpig, which is the name we’ve given to a certain stuffed animal of indeterminate species. Not all of these are enunciated perfectly, of course — oatmeal is rather charmingly said “Emile,” for example. But generally, if you were looking for the mythical “language explosion” point in his development, this is probably it.

And man is it awful. I mean, really. Over the course of the year I’ve been at home with him, Henry and I had developed a pretty good routine and a pretty good working relationship. Up to a few weeks ago, he would generally content himself with little physical projects during the day — moving things around the living room, climbing onto the windowsills, and so on. My job was to feed him, diaper, him and rescue him when he got stuck. But now he’s mastered physical movement, I guess, and the new obsession is talking. All. The. Time.

This creates two problems. First, his desire to express things rapidly outstrips his ability, and so he gets frustrated easily. It’s a constant chore to divine what he’s trying to tell you, and if you don’t get it quickly enough he throws himself on the floor and moans piteously, “Noooooooooooooooo!”

Second, I don’t want to talk all the time. I’m blogging! I’m reading the news! I’m disagreeing with some guy on the A.V. Club about the relative merits of Hello Nasty in the Beastie Boys canon!

This is hard to deal with. Without any exaggeration, I can say that the language explosion has made me like my kid less. There’s no need to comment on this — I’m aware that the problem is mine, not his.

But it’s funny that you think, when your kid is a newborn and won’t sleep for more than an hour-and-a-half at a time, “Oh, this is the hard part. I am really making sacrifices now.” And then you figure out sleep and feeding and you sort of expect that it’s all going to be smooth sailing from here on out, and for a while, it really is. From six months to about 18 months, this kid just gets better and better. He becomes charming and sweet; he smiles and laughs; he learns to walk and feed himself. At 18 months, you’re kind of like, “Oh, man — this kid is like some great combination of a best pal and a dog.”

And then two months later, he’s moody and easily frustrated and wants to talk all the time, and you realize he’s actually some horrible combination of unemployed roommate and ill-tempered parrot.

Also, a friend dealing with his own fatherly frustrations once told me, “Everyone complains about the terrible twos, but really, it just gets worse every year after that.” So… looking forward to that.

On the other hand, I think his kid was five at the time, and the coments in this thread at Ask Moxie are full of testimony that around five it gets better. Sort of….

I definitely thought 3 was the pinnacle of PITA behavior. Two was a breeze for me (relatively speaking).

For example:
Mom: You may have/do X or Y.
2 yo child: [chooses X or Y]
3 yo child: NO! I WANT Z!

(Of course now, at 5 1/2 and 7, I get: You told me on Thursday, June 22, 2009 that if the planets were aligned with mercury in retrograde, Z would be on the table as long as I was wearing long sleeves and said please. You promised, Mom.)


Toddlersaurus

Our kid is 20 months old (I guess he’s about 18 months, adjusted for his gestational age). He is both pretty cool – sweet and funny and learning words at a rapid pace – and INCREDIBLY HARD TO COPE WITH.

Pick me up! Put me down! Let me operate that power saw!

For instance, he is easily able to remove our current outlet covers (we have impossible-to-remove ones on order), and the other day Seth sprang from his seat and started shouting NO. NO. SERIOUSLY. NO. and I looked over to see that Henry had somehow found my keys, removed the covers on the outlet near the door, and was just about to insert the keys into the interesting slots. Totally ignoring our terrified outburst, he turned to us and grinned proudly and said “Keys?”

Everything is like that. Yesterday we were hanging out with some of Seth’s new law buddies, and there was another mom there with a similarly-aged kid. And I started to feel… like I was a hovering, overprotective parent. Because the other toddler roamed freely and didn’t really get into trouble of any kind! And we have now moved to student family housing, which is mostly set up to be kid friendly, and is entirely fenced. So as I sat with the other mom and chatted, I tried to suppress my instinct to chase Henry around. But when he disappeared around a building, with the other lady’s kid right behind him, it was TOO MUCH and I ran after him. Only to discover that he had stretched onto his tiptoes and figured out how to open the gate to the street and was about to lead the other toddler to FREEDOM! and ADVENTURE!!! (He was out of my line of sight for three or four seconds.)

When Seth starts law school, our bear is going to start going to daycare so I can still work. At first I was really ambivalent about this – he has only ever been home with a parent, and he’s still so little, and blah blah blah blah blah blah. Now I literally cannot wait. I’m going to throw him at the lovely couple who run the daycare and run away, cackling. GOOD LUCK SUCKAS!!!

I just this morning spotted this It Gets Better: Toddler Edition post on Ask Moxie and whispered OH THANK GOD as I scrolled through it.

science gone wrong, pt 2: am i having a heart attack?

I went to see a cardiologist recently.

If you’re the kind of person who can’t read all the way to the end without knowing, don’t worry: I’m fine.

But here’s the story.


When you walk into an urgent care facility and say that you have been have chest pain and shortness of breath all weekend, everybody who works there stops what they’re doing and looks up in alarm. “Urgent care” is pretty much the opposite of what it sounds like — they’re mostly set up for things like colds and sprained ankles; i.e., things that are basically going to get better on their own. They don’t really want you bringing your five-day-old heart attack through the door.

But the PA at the urgent care did her best, giving me a thorough examination, an EKG, and a chest X-ray. Everything looked okay (really — check out the pics after this paragraph), so she told me to be sure to visit my doctor right away. Which assumed that I had some sort of primary care doctor, but I told her not to worry, I would go back for a second visit to the guy I saw once to get some migraine medication.

My, um, primary care physician looked at the EKG and the X-ray and asked me some questions and then said it could be any number of things, probably nothing serious, but he wanted me to see a cardiologist (or, as we shall later see, “cardiologist”), and he had the front desk set up a referral. Under most insurance plans, you have to get a referral from a primary care physician to see a specialist, because obviously his half-assed guess that you probably don’t have heart disease but maybe ought to see someone just to be safe is much better than your half-assed guess of same.

At this point in the story, I want to point out that my wife had already been suggesting for a while that it might be acid reflux, which also causes chest pain and tightness of breath and, as an explanatory hypothesis, has the added benefit of being something other than vanishingly unlikely in a healthy 37-year-old man. PCP was also willing to consider reflux and recommended Prilosec. More on this later.


The first thing you see when you open the door to the cardiologist’s office is this cabinet full of dietary supplements for sale:

I didn’t realize that’s what it was, at first, because that’s such an unexpected thing to see in a doctor’s office that I think my brain just filtered it out. Instead of thinking about that, I checked in, sat down, and started flipping through a magazine.

It was early in the morning, so the TV was off. But a member of the staff soon rectified that, and after a few minutes I could no longer concentrate on my magazine over the insistent trumpeting of an ad for some kind of weight loss scheme called “Ideal Protein.” (It claims to “give your pancreas a rest.” And everybody likes rest!) I was mildly irritated by this, but I assumed that the video was some sort of freebie given out by a rep and thoughtlessly put on a loop by a staff member who wrongly assumed that any TV must be better than no TV.

But after I was called back to the exam room I began to notice that ads for “Ideal Protein” were everywhere. Of course, almost all doctors’ offices these days have those “Lower Back Inflammation? Find Out More” pamphlet-holders that always end up being sponsored by the makers of Lumbaleve, an anti-inflammatory for lower backs. But this wasn’t just that. This was… well… straight-up advertising. Weirdest of all, to my mind, was the “Certificate of Excellence” next to the check-in desk proclaiming her virtues as an Ideal Protein “Consultant.” Huh.

A nurse took my blood pressure. It was a little high (130s/80s), but after consulting with the doctor she took it again. I concentrated on relaxing (playing this Sheila Chandra song in my head), and my BP came back down to a perfectly normal 120/80. Satisfied, she left me alone with the Ideal Protein posters.

When the doctor finally came in for the exam, you may be unsurprised to learn, she seemed relatively uninterested in my symptoms, but was terrifically interested in my weight. She literally came into the room convinced I was overweight and demanded to know my “ideal weight,” and when I said I had no idea what that would mean, she clarified, “What did you weigh when you graduated high school?”

I’m not going to catalog the ways that’s a stupid, stupid standard.

Anyway, after deciding I was a big fat fatty, she turned me over to a technician for a “stress test,” aka power-walking while a guy tries to take your blood pressure. I did the stress test with no trouble, but the tech noted that while my diastolic BP held rock-steady at around 80, my systolic did rise to 170 by the end of the test. He felt this was a little high, but said cheerfully, “That’s minor. That’s not a big deal at all.”

I was then ushered into the doctor’s private office, where, after a while, she came to talk to me about my results. The good news, she told me, was that my heart was fine. The bad news? My blood pressure was too high during the stress test. Probably because (well, you’re a smart reader, I think you know where this is going) I was horribly, hideously fat. “There are two ways we can handle this,” she said. “One is that I can give you anti-hypertensive drugs. The other is very difficult, and not everybody can do it. You’ll have to lose about thirty pounds, at least twenty, and restrict your salt to less than 2,000 mg per day, stop smoking, cut back on alcohol, start an exercise program. Okay?”

So, uh… what was causing my chest pain? “I don’t know,” she said, sounding like that was the least interesting thing anyone could choose to discuss right now.

“Well,” I said, feeling my blood pressure rise for fat-unrelated reasons, “I’m not taking drugs. Come on. And to be honest, I have a hard time taking you seriously about losing weight when you sell weight-loss products out of your office.” I pointed at another small poster on her desk.

“Oh,” she said, “but that’s just one of the products we sell. You know, I was just talking to another patient about detoxifying his body using nothing but green plants….”

“Okay,” I said. “Anything else?”

“No,” she said, but she sort of looked like I had farted. I got up to leave. She followed me down the hall to the desk. “Do you want to do any kind of follow-up?” she asked.

“No,” I said. Because my mother raised me better than to say “You have to be fucking kidding.”


Was she right? Do I have high blood pressure? Do I need to stop eating salt and stop drinking the booze and most of all stop being such a huge fatwad?

I don’t know. But I’m sure as shit not taking her word for it.

This is the thing: being a doctor is probably the closest thing we have anymore to an actual sacred profession. Medical expertise vests you with perhaps the greatest personal authority one person can reasonably expect to have over another in a secular society. If anyone can explain the mysteries of being human and assuage our deepest fears — about life and death, about the validity of our personal choices, about whether our children are going to grow up okay — it’s doctors. Or at least medical scientists, on whose behalf doctors are presumably speaking to the layperson. A doctor is a kind of priest for science — he reads the arcane texts (JAMA, BMJ, Heart) and interprets them for the masses.

Any whiff of corruption that attaches itself to a doctor’s credibility, therefore, is extremely disturbing to the patient. When a person comes into a cardiologist’s office, he’s already frightened and bracing for the worst. He needs an honest diagnosis, one uninflected by either the doctor’s personal hangups (about fat, for instance) or any commercial interest in the cure.

This is why the AMA’s Code of Ethics strongly recommends that doctors minimize even the appearance of a conflict of interest:

In-office sale of health-related products by physicians presents a financial conflict of interest, risks placing undue pressure on the patient, and threatens to erode patient trust and undermine the primary obligation of physicians to serve the interests of their patients before their own….

Because of the risk of patient exploitation and the potential to demean the profession of medicine, physicians who choose to sell health-related products from their offices must take steps to minimize their financial conflicts of interest….

Physicians should not participate in exclusive distributorships of health-related products which are available only through physicians’ offices.

Maybe the cardiologist was 100% right about everything she said. But how can I trust her judgement? Why should I take her advice? The problem with conducting your practice the way she does is that you send patients scrambling back to their own meager resources in trying to separate science from bullshit.


Here, then, are the answers my meager resources have been able to uncover about my medical situation. No help from my cardiologist, sadly.

Do I Have Hypertension?

Maybe. We still have a blood pressure cuff from when Elana was recovering from eclampsia. I’ve been monitoring my BP in a kind of haphazard way since seeing the cardiologist. Systolic fluctuates between the high 110s and the 130s; diastolic between 75 and 85. That’s not great. It’s ranging between normal and what’s known as “pre-hypertensive” — actual hypertension being defined as greater than 140/90. It’s something I’m keeping an eye on.

But what about the specific claim that my 170/80 max during exercise was excessive and indicative of a hypertension problem so severe I needed to either go on medication or give up my Caligulan excesses? This looks like bullshit to me. I’ve googled and PubMeded any number of combinations of “blood pressure” and “exercise” and “stress test” and “hypertension” and “treadmill” over the past several weeks, and every source I can find that actually addresses the subject seems to think that a BP of 170/80 during moderately strenuous exercise is actually right about smack in the middle of the normal range. Reasonably non-crackpot-ish lay sources are here, here, and here. For those who would like something toothier, here’s a chart I pulled from a study in Stroke about the correlation between high BP during an exercise stress test and risk of stroke. The center line shows the mean response for a sample of “1026 men without clinical coronary heart disease, antihypertensive medication, or prior stroke at baseline.” (The X-axis is number of minutes exercising — on a bicycle rather than a treadmill, it should be noted, though I doubt that’s significant here.)

Or consider Figure 1 (page 4) in this study of BP during exercise (PDF) from the journal Hypertension. The 50th percentile BP at 50% Heart Rate Reserve in this sample of 1033 men “free from cardiovascular disease and with normal ECG results” was, in fact… 170/80. (Heart Rate Reserve is defined as Maximum Heart Rate minus Resting Heart Rate; I calculated mine to be right around 100 BPM, a number I greatly exceeded during the stress test.)

I call bullshit on this one. I’m actually apparently healthier when exercising than when sitting still.

Do I Need To Cut Salt?

I’m going to skip alcohol and tobacco, because I don’t drink or smoke. The fact that the cardiologist told me to cut alcohol without bothering to ask whether I drink, or how much, was one of the things that made me feel she wasn’t really paying much attention to me as an individual patient, though.

So, salt — ARE IT DANGEROUS????!!!!1!!??

This turns out to be a complicated question. Some things seem certain: in studies, lower salt intake is statistically associated with reduced risk of hypertension, and conversely, people with hypertension seem to eat more salt than normotensive people. (At least in Canada.) And in this admittedly very small study, patients with “resistant hypertension,” i.e., hypertension not ameliorated by up to three anti-hypertensive medications at a time, reduced their BP by an impressive 22.7/9.1 mmHg by drastically reducing salt. (If you had a BP of, say, 150/95, that would be enough to bring you down from “hypertension” to “pre-hypertension” or “high normal.”)

On the other hand, it’s possible to overstate the value of salt reduction. This 2004 meta-analysis of 28 studies found that

“In individuals with elevated blood pressure the median reduction in 24-h urinary sodium excretion was 78 mmol (4.6 g/day of salt), the mean reduction in systolic blood pressure was -4.97 mmHg (95%CI:-5.76 to -4.18), and the mean reduction in diastolic blood pressure was -2.74 mmHg (95% CI:-3.22 to -2.26).”

The authors of the study describe this finding (well, meta-finding) as “significant,” which in a statistical, population-wide sense is probably true. But note that that effect is for people who already have elevated blood pressure. For people with normal blood pressure, the effect of a similar drop in sodium reduction is only -2.03/0.99 mmHg.

What explains the difference? It turns out there is a population of people who are described as “salt-sensitive,” meaning their blood pressure rises by 10 mmHg or more after a load of sodium, while some other people are “salt-resistant,” meaning that ingesting a bunch of salt hardly moves the needle for them. Studies have found that as many as 50% of people with hypertension (73% for African-Americans), and 26% of normotensive people, are salt-sensitive. So if you have hypertension, you’re more likely to be salt-sensitive, and the Scammy Cardiologist’s advice is relatively sound — reducing salt has at least a 50/50 chance of having a positive effect on your blood pressure.

But that advice should come with some caveats. First, there are dissenters from the public health recommendations suggesting that everyone reduce sodium. In May Belgian researchers claimed to have found an inverse relationship between salt consumption and deaths from cardiovascular disease in a study of 2,856 patients followed over 7 years. They also found that sodium consumption was not correlated with new incidence of hypertension and with only a very mild rise in systolic BP (1.71 mm Hg) and no rise in diastolic at all. Based on these findings, the authors felt they could not support the common public health line that almost everyone should reduce sodium intake to below 1500 mg/day.

The primary author of the study, Jan Staessen, said in an interview with JAMA that one reason a low-sodium diet might be associated with negative outcomes is that it could trigger sodium-conserving mechanisms in the body, which, he says, are “known to have a negative influence on cardiovascular outcomes.”

It’s important not to read too much into a single study, and this study has been criticized for studying a relatively young population (average age was about 39) with a low risk of cardiovascular events to begin with. But Dr. Staessen has a point — there is certainly a level below which you’ve lowered people’s sodium levels too much, and that level could easily be higher in salt-resistant people than in salt-sensitive people.

Unfortunately, much of the practice of medicine is about playing the numbers rather than understanding the individual patient. So if a patient presents with hypertension (or pre-hypertension), a doctor will recommend many of the things Scammy Cardiologist recommended: stop smoking, cut drinking, lose weight, cut salt, get more exercise. Each of those recommendations has been shown, at a population level, to be likely to result in lowered blood pressure. So why not have the patient try them all? The problem with this, of course, is that if the patient actually does them all, you have no way of knowing which recommendation did the trick, and which ones were superfluous. And meanwhile there are, potentially, poorly-understood risks to each of these interventions for at least some patients. Moreover, lifestyle modifications are hard for most people to maintain over the long haul, and the more modifications, the harder the regimen will be to sustain.

Where does this leave us with sodium? Well, after seeing Scammy Cardiologist, I began keeping a food diary and tracking my blood pressure to see if I could find evidence of salt sensitivity in myself. Unfortunately, as I quickly realized, attempting to implement the other advice at the same time (dieting, increasing exercise) added potential confounding factors. Ideally after a doctor sees a patient with less-than-emergency-level high blood pressure for the first time, she should have that person change nothing about their routine except salt intake for a month or two, and see if that lowers blood pressure by itself. If it does, that would form a solid basis for concluding that the patient is salt-sensitive. If they’re not, then the doctor could move on to other tests, figuring out the source of this particular patient’s hypertension.

Of course, this is a time-consuming method that requires a lot of ongoing care and monitoring, which is expensive and hard to do. But it would be the approach of a scientist.

The other caveat about sodium is that salt-sensitivity doesn’t happen in a vacuum — the body’s response to salt is dependent on other factors in the body. One is insulin resistance, which we’ll talk more about in part 3 of this series, but which we should for now note is highly diet-dependent, meaning that the foods you eat can, themselves, have an effect on how salt-sensitive you are. Another may be exercise, which at least one study found can reduce salt-sensitivity.

So have I reduced my salt intake? Some days. When we cook from scratch at home, it’s often not hard to do. But sometimes we end up eating out, and sometimes I really want to eat sausage and bacon and feta cheese. All dusted with kosher salt and topped with sea-salt caramels. What can I say? I’d like to eat less salt… but you’re kind of fighting evolution there. Salt is delicious!

Ahem. Back to the science.

Should I Exercise More?

Sure! Why not? Exercise makes you feel good, and it makes your body stronger and more able to do hard work. I give Scammy Cardiologist a pass on this one. As a guy with an officially-okay ticker, I’ve embarked on a plan of running longer distances more often. Plus I’ve been skimming this hilarious blog, Fat Chicks Running, written by ladies who run half-marathons. Since I’d like to run a half-marathon myself someday, I find this girl’s wall of medals very inspiring.

Oh, but will it fix hypertension? The Mayo Clinic seems to think so, for mild cases:

Becoming more active can lower your systolic blood pressure — the top number in a blood pressure reading — by an average of 5 to 10 millimeters of mercury (mm Hg). That’s as good as some blood pressure medications.

Between you and me, that makes “some blood pressure medications” sound like bullshit. 5mm Hg? That’s a measurement error. But, to be serious, the journal Nature cautions that

Even though it is well established that moderate exercise lowers blood pressure in most hypertensives, about a quarter do not respond to exercise training. In particular, patients with ‘nondipping’ hypertension (ie, hypertensive patients with <10% reduction in average nighttime blood pressure compared to average daytime blood pressure — thought to reflect a greater blood pressure 'load') have been suggested to be nonresponders to exercise training.

But they also note that

The beneficial effect of regular exercise in hypertension is not limited to reduction of blood pressure only. It has also been shown to reduce left ventricular hypertrophy, improve exercise capacity and quality of life. When combined with dietary alterations, regular exercise causes reduction of oxidative stress, increases nitric oxide availability and improves the overall metabolic profile.

So, fuck it. Exercise! Final question:

Am I A Big Fat Fatty Who Needs To Lose Weight Right Away?

No.

I’m 75″ and about 220 lbs, and if you saw me “overweight” would not be the word that leapt to mind. “Overweight” is a medical category based on BMI, or “body mass index,” which is notoriously difficult to correlate with actual health, or even build, on an individual basis. I could cite you some studies, but instead, here is a hilarious Flickr user group called “Illustrated BMI Categories”. It’s full of pictures of people whose appearance is often comically out-of-sync with their supposed BMI category. E.g.,

Jessica is "overweight" -- and a triathlete.

There’s also been substantial research in recent years suggesting that, for example, merely being in the “overweight” category results in no higher rate of death than being “normal”, while being “underweight” does carry a higher risk of death. Or that when economic and behavioral risk factors are controlled for,

Compared to those in the “normal” weight category, neither overweight nor obesity was significantly associated with the risk of mortality. Among adults age 55 and older at baseline, the risk of mortality was actually reduced for those were overweight (hazard rate ratio = 0.83) and those who were obese (hazard rate ratio = 0.68), controlling for other health risk behaviors and health status.

That’s right old people — pack on the pounds! It’s good for you!

(The same study also found that “Having a low level of physical activity was a significant risk factor for mortality (hazard rate ratio = 1.58).” Tick up another notch for exercise.)

But we keep getting off track — what about hypertension? Well, other studies, including this one from 1999, seem to find that exercise and diet modification work to reduce blood pressure independently of weight loss. And liposuction, for example, does not appear to reduce blood pressure in the absence of lifestyle changes.

This may be because, even to the extent that fat is associated with disease, the arrow of causality may point in the other direction — i.e., disease causes people to gain weight. Paul Campos of the University of Colorado writes that when public health officials claim that fat causes disease, they’re treading uncertain ground:

With the exception of osteoarthritis, where increased body mass contributes to wear on joints, and a few cancers where oestrogen originating in adipose tissue may contribute, causal links between body fat and disease remain hypothetical. It is quite possible, and even likely, that higher than average body fat is merely an expression of underlying metabolic processes that themselves may be the sources of the pathologies in question. For example, much evidence suggests that insulin resistance is a product of an underlying metabolic syndrome that also predisposes persons to higher adiposity because compensatory insulin secretion promotes fat storage. Modern molecular genetics confirms the thrifty gene hypothesis that mutations favouring fat storage and survival of famine also confer risk of diabetes. Thus, obesity may be an early symptom of diabetes rather than its underlying cause.

I hope to get into this a little more in part 3 of “Science Gone Wrong,” but for now let’s say this — weight loss is not necessarily a good in itself, and if dieting causes “weight cycling” or “yo-yoing,” it may actually do substantially more harm than just remaining a little tubby. (More reading on the subject here.)

Conclusion Time!

To review:

- My blood pressure is probably somewhat too high at rest, but there’s really nothing all that alarming about my blood pressure during exercise.

- There’s a good chance reducing salt would help, but it would take some fairly careful testing to figure out if that’s true. Also, cheese is delicious, so good luck, salt-reduction proponents!

- Exercise — it’s fun and reduces mortality and morbidity. Does it help with hypertension? A bit. And particularly if your hypertension is at all stress-related. As My Sister The Doctor explains,

All the adrenaline and steroids that your body releases when you’re under stress are designed to help you fight sabre-toothed tigers. If you only do battle by typing on your laptop, those hormones will just bounce around in your body and drive up your BP. You need to simulate fighting off (or outrunning) a sabre-toothed tiger several times a week, to manage the physical effects of your stress.

- Finally, don’t stress about being fat too much. Instead, ask yourself if there are underlying health concerns (like diabetes) that might be causing you to get fat. If there aren’t, go for a short jog and don’t worry about it.


If you are very attentive, you may be asking, “But wait — weren’t you sick at the beginning of this?” Yes. I was. Pretty sure it was reflux — store-brand Prilosec really seems to have helped. I’ll be going to a doctor this week to check in, but really, score one for my wife, who sussed it early on.

science break! everybody play ball!

I hope to write more in the “Science Gone Wrong” series by the end of the week — i.e., after we move to our new apartment. Until then, please enjoy these videos of a small bear playing with his new ball and his new dump truck.

science gone wrong, pt 1: are vaccines really causing higher infant mortality rates?

This study, purporting to show that greater numbers of vaccines in the first year of life are associated with greater risk of infant mortality, came across my radar recently. I thought I’d take a moment to look at it in part of a series of posts on the emotionally fraught relationship between science and our everyday lives. This post is the one that has the most to do with parenting; the ones that follow will be more about a health scare I had recently and some of the changes it’s wrought on our life.


Neil Miller and Gary Goldman claim to have found a correlation, on a population scale, between the number of vaccines children receive in the first year of life in a given country and that country’s infant mortality rate. (Full text of the paper in PDF here.) Their work is riddled with conceptual and procedural problems, and of course whenever someone asserts a correlation without establishing a concrete causal mechanism, we should be skeptical. (Using the phrase “synergistic toxicity” over and over again does not count as establishing a causal mechanism.) But since this kind of “research” frequently gets turned into news items that get circulated among worried parents trying to make good decisions for their kids, I thought I’d delve into it a little bit, leaning gently on a couple of excellent analyses from David Gorski at Science-Based Medicine and Catherina at Just The Vax.

A summary of the problems addressed by Catherina and Dr. Gorski:

1. The paper is inconsistent in its definition of a “dose.” Catherina lays it out neatly:

[T]he way Miller and Goldman are counting vaccines is completely arbitrary and riddled with mistakes.

Arbitrary: they count number of vaccines in US bins (DTaP is one, hib is separate) and non-specific designations (some “polio” is still given as OPV in Singapore), rather than antigens. If they did that, Japan, still giving the live bacterial vaccine BCG, would immediately go to the top of the list. That wouldn’t fit the agenda, of course. But if you go by “shot” rather than by antigen, why are DTaP, IPV, hepB and hib counted as 4 shots for example in Austria, when they are given as Infanrix hexa, in one syringe?

Mistakes: The German childhood vaccination schedule recommends DTaP, hib, IPV AND hepB, as well as PCV at 2, 3 and 4 months, putting them squarely into the 21 – 23 bin. The fourth round of shots is recommended at 11 to 14 months, and MenC, MMR and Varicella are recommended with a lower age limit of 11 months, too, which means that a number of German kids will fall into the highest bin, at least as long as you count the Miller/Goldman way.

(If you’re bored and want to check their work, here are the vaccine schedules from Europe that Miller and Goldman claim to have relied on. They cite UNICEF’s website as their source for non-European countries, although, since they don’t provide a URL for a specific page on the site, I’ve been unable to find that data.)

The definition of a “dose” is critically important here. If you want to entertain the hypothesis that vaccines are in some way “toxic” because of, for example, preservatives or other foreign material, then the number of antigens matters less than the number of shots or vials. On the other hand, if you want to say that the antigens are the toxic substance, then as Catherina points out you have to account for different levels of antigens in different types of vaccines for the same diseases. Miller and Goldman’s vague and confusing approach does little to tease out or account for these differences.

2. Countries don’t all count dead infants the same way. Dr. Gorski quotes Bernardine Healy, former director of the NIH:

[I]t’s shaky ground to compare U.S. infant mortality with reports from other countries. The United States counts all births as live if they show any sign of life, regardless of prematurity or size. This includes what many other countries report as stillbirths. In Austria and Germany, fetal weight must be at least 500 grams (1 pound) to count as a live birth; in other parts of Europe, such as Switzerland, the fetus must be at least 30 centimeters (12 inches) long. In Belgium and France, births at less than 26 weeks of pregnancy are registered as lifeless. And some countries don’t reliably register babies who die within the first 24 hours of birth. Thus, the United States is sure to report higher infant mortality rates. For this very reason, the Organization for Economic Cooperation and Development, which collects the European numbers, warns of head-to-head comparisons by country.

Miller and Goldman claim to have accounted for these differences and quote a CDC paper which says that “[I]t appears unlikely that differences in reporting are the primary explanation for the United States’ relatively low international ranking.” Of course, this statement in itself is quite vague, giving no idea what percentage of the difference in rankings the reporting problem plays. But it also begs the question, “What is the primary explanation?” The same CDC paper gives a perfectly reasonable answer, to which we shall return later.

In the meantime, this paper commissioned by the Congressional Budget Office on the subject of America’s seemingly awful infant mortality stats provides more detail on the difficulties of accurately comparing IMRs:

In countries where physicians are more aggressive about attempting to resuscitate very premature newborns — of which the United States is probably the leading example — extremely small neonates are more likely to be classified as live births than in countries with less aggressive resuscitation policies. Thus, for example, if little attempt is made to resuscitate newborns weighing less than 500 grams (1 pound, 2 ounces), these births may be classified as fetal deaths and not be included in either the live birth or the infant mortality statistics. By contrast, when attempts are made to resuscitate the tiniest newborns, they are more likely to be classified as live births, although most will subsequently die and then be included in the infant mortality statistics.

(We’ll get back to this idea of aggressive treatment in the final section.)

3. Miller and Goldman selected data from a single year, 2009. But why? Surely an analysis over multiple years, or multiple decades, would be more useful. We could be more certain that the IMRs in 2009 weren’t some sort of statistical fluke. And we could watch IMRs move (or not) according to changes in vaccination schedules. As Catherina points out,

For example, in the early 1980ies, Germany’s infant mortality was about 5 times as high (10000 infants died per year) than it is today (2000 died in 2009 with approximately the same birth rate), however (in Miller’s and Goldman’s twisted logic), the vaccination schedule contained far fewer vaccines in the first year (essentially just DT and polio, since the whole cell pertussis was not given between 1974 and 1991, the aP not yet introduced, the MMR given in year 2, no hib, nor hepB, nor PCV given either), while Germany was already very much a “developed country”.

4. Miller and Goldman do not consider the whole world. It’s tempting to say that they’re on stronger ground here — that you want to compare wealthy, industrialized countries to other wealthy, industrialized countries. But they don’t seem to be particularly interested even in other industrialized and/or wealthy countries whose IMRs fall below that of the U.S. — say, countries in Eastern Europe, or the wealthy Arab states — to see whether their correlation holds up further down the list. Gorski:

[S]ince the focal point of the analysis seems to be the U.S., which, according to Miller and Goldman, requires more vaccine doses than any other nation, then it would make sense to look at the 33 nations with worse IMRs than the U.S.

Be that as it may, I looked at the data myself and played around with it. One thing I noticed immediately is that the authors removed four nations, Andorra, Liechenstein, Monaco, and San Marino, the justification being that because they are all so small, each nation only recorded less than five infant deaths. Coincidentally, or not, when all the data are used, the r2=.426, whereas when those four nations are excluded, r2 increases to 0.494, meaning that the goodness of fit improved.

In other words, even among the countries above the U.S., Miller and Goldman cherry pick the data, dropping small countries that don’t make the data fit the way they want it to. (4 countries out of 33 is an 8th of the data being excluded, in case you were counting.)

Are these decisions reasonable? Would including Russia or Andorra have made the data clearer, or muddied the waters? I’m not sure, but in light of other methodological decisions, this is questionable at best.

5. What’s with the grouping? Why sort the countries into groups based on the number of vaccines, and then plot the average IMR of each group, instead of just plotting all the data points separately? Gorski again:

[F]or some reason the authors, not content with an weak and not particularly convincing linear relationship in the raw data, decided to do a little creative data manipulation and divide the nations into five groups based on number of vaccine doses, take the means of each of these groups, and then regraph the data. Not surprisingly, the data look a lot cleaner, which was no doubt why this was done, as it was a completely extraneous analysis. As a rule of thumb, this sort of analysis will almost always produce a much nicer-looking linear graph, as opposed to the “star chart” in Figure 1. Usually, this sort of data massaging is done when a raw scatterplot doesn’t produce the desired relationship.

Indeed. Of particular note is Group 2, countries with a vaccination schedule of 15-17 “doses” in the first year. Group 2 only includes 5 countries, and one of those countries is Singapore, which has the best IMR in the world (2.31) and calls for its infants to receive 17 vaccines doses in their first year, according to Miller and Goldman’s counting. Because Group 2 is so small, Singapore is clearly dragging down the average IMR of the whole group — from 4.30 to 3.90. Take out Singapore, which is clearly an enormous outlier, and Group 2 has about the same IMR as Group 3, which makes the linear relationship a lot less neat. Also, 4.30 is very similar to Denmark’s 4.34, and Denmark only requires 12 vaccines in the first year. And speaking of Singapore, if this linear correlation based on vaccination schedules is so strong, why does Singapore have such a drastically low IMR with 17 vaccine doses in the first year, when Italy and San Marino have drastically high IMRs (5.51 and 5.53, respectively) with only a single dose more (18) per year? Naturally, there will be outliers in any linear regression, but it seems that when you get done smoothing out the outliers here by dropping data points and sorting the data into bins, you’ve essentially hidden half the statistical reality.

6. They fall prey to the “ecological fallacy.” Gorski once more:

The ecological fallacy can occur when an epidemiological analysis is carried out on group level data rather than individual-level data. In other words, the group is the unit of analysis. Clearly, comparing vaccination schedules to nation-level infant mortality rates is the very definition of an ecological analysis.

In other words, measuring correlations between variables on the population level tells you nothing about the correlation on an individual level, and indeed is likely to vastly overstate the likelihood of such a correlation. For example, let us suppose that Italians have fewer heart attacks than do Englishmen, and yet eat pasta at a much greater rate. Can we conclude that pasta is preventive against heart attacks? No, because, among other things, you haven’t demonstrated that the pasta-eating individuals in the Italian population are the ones getting fewer heart attacks. Perhaps there’s a smaller subset of Italians who eat hardly any pasta at all, yet get plenty of vigorous exercise, and therefore drag down the national average incidence of heart disease.

Similarly, if you want to find out if a heavier vaccine schedule in the first year correlates with higher infant mortality — or, to be even more specific, whether it correlates with higher rates of SIDS, since Miller and Goldman argue that SIDS and unexplained deaths caused by vaccine “toxicity” are probably the real culprit here — you should do a study following outcomes for individual kids who receive different schedules of vaccines. Trying to track a phenomenon, if there is one, by comparing different whole populations is both inefficient and brutally error-prone.

To their credit, Miller and Goldman attempt to address this problem in a section titled “Ecological Bias.” To their discredit, their explanation is simply awful:

Although most of the nations in this study had 90%–99% of their infants fully vaccinated, without additional data we do not know whether it is the vaccinated or unvaccinated infants who are dying in infancy at higher rates. However, respiratory disturbances have been documented in close proximity to infant vaccinations, and lethal changes in the brainstem of a recently vaccinated baby have been observed. Since some infants may be more susceptible to SIDS shortly after being vaccinated, and babies vaccinated against diarrhea died from pneumonia at a statistically higher rate than non-vaccinated babies, there is plausible biologic and causal evidence that the observed correlation between IMRs and the number of vaccine doses routinely given to infants should not be dismissed as ecological bias.

[emphasis mine]

So after admitting that they have in no way correlated these higher rates of infant mortality with actual vaccination on the individual level, Miller and Goldman attempt to razzle-dazzle the reader with a lot of scary-sounding stuff. But, for example, the “lethal changes in the brainstem” occurred in a single child after a vaccination — to infer anything from that would be a classic case of “post hoc, ergo propter hoc” reasoning. I’m sure you can find a single case of a child who died of bullet wounds after being vaccinated, too.

And the babies who died of pneumonia at a statistically significantly higher rate after receiving the rotavirus vaccine? That was in a single study out of eight studies conducted on the safety of Rotarix, the vaccine in question. When you compile all eight studies, the relative risk of pneumonia between Rotarix and placebo is exactly 1, according to this exhaustive FDA briefing (PPT — skip to slide 59).

I’m not going to bother batting at the other examples, but you see where this is going. And the problem of the ecological fallacy is probably the most damning, because even if all the other problems in this paper were fixed, this alone would be enough to keep it from making any sense as science.


Finally, I’d like to discuss that CDC report I promised to come back to, and pile on a criticism of my own that neither Catherina nor Dr. Gorski really dealt with. Namely, we know the risk factors that bring the U.S.’s IMR up. Alice Park discusses them in a 2009 article for Time:

Starting in 2008, the March of Dimes began tracking three of the major contributors to the high preterm birth rate — lack of insurance among women of childbearing age, rates of cigarette smoking and the rate of babies born preterm, but at the tail end of pregnancy, between 34 and 36 weeks….

By far the biggest contributor to the high premature birth rate is the rate of so-called late-preterm births. About 70% of babies born too early in the U.S. are born between 34 and 37 weeks. There are many reasons for these early deliveries, making it particularly difficult to target one or even a few factors and address them head-on. The increase in multiples — twins, triplets or more — is one contributor. The rise in assisted reproductive technologies, such as in vitro fertilization, is another; these techniques are associated with both an increased risk of multiples as well as a higher risk of premature delivery, even of singletons….

This is relatively undisputed, as far as I can tell from reading through literature on America’s woeful infant mortality rate. What do Miller and Goodman make of this? From the paper:

Preterm birth rates in the United States have steadily increased since the early 1980s…. Preterm
babies are more likely than full-term babies to die within the first year of life. About 12.4% of US births are preterm…. Preventing preterm births is essential to lower infant mortality rates. However, it is important to note that some nations such as Ireland and Greece, which have very low preterm birth rates (5.5% and 6%, respectively) compared to the United States, require their infants to receive a relatively high number of vaccine doses (23) and have correspondingly high IMRs. Therefore, reducing preterm birth rates is only part of the solution to reduce IMRs.

There are several squirrelly points packed into this paragraph. First, note the phrase “within the first year of life,” which, while part of a technically correct definition of infant mortality, leads us to the question: why are we counting all deaths in the first year in this study anyway? Surely the correct measure of whether vaccines influence mortality would exclude all deaths prior to the first vaccine — i.e., all deaths that occur at or immediately after birth.

Second, the cherry-picking of Ireland and Greece as countries with low preterm birth rates and high IMRs, and then imputing those figures to vaccination rates is obviously putting the cart before the horse. If you’re trying to draw correlations of this kind, why not include a table of preterm birth rates and use them to factor out that difference in IMRs before trying to measure a difference attributable to vaccine schedules? I mean, if you have those preterm birth rates handy, which Miller and Goldman seem to, although they don’t provide a footnote for the Ireland and Greece numbers.

Anyway, here’s an interesting graphic from that CDC paper Miller and Goldman cited to show that reporting differences did not account for the bulk of the difference in IMRs. It shows what the US infant mortality rate would look like if we had Sweden’s level of preterm births:

What does this tell us? It tells us that, exactly as the CDC, the CBO, and the March of Dimes have concluded, much of the difference in IMR between the U.S. and other countries can be attributed to pre-term birth rates. And what does that tell us about this supposed correlation between vaccination and IMR?

It tells us that having an aggressively interventionist medical culture in the U.S. leads, somewhat paradoxically, to higher IMR. Remember that many of those preterm births are the result of fertility treatments. And U.S. physicians are more aggressive about attempting to resuscitate very small babies, even though most will die anyway; this leads to a much higher count of live births followed by death than in countries that treat those unbreathing preemies as still births. And aggressive monitoring of fetal health, and a greater willingness to either induce early labor or perform caesareans, may also play a role.

And then there’s this interesting paper from the New England Journal of Medicine that finds that, paradoxically, the rapidly increasing numbers of new neonatal ICUs in the U.S. may be responsible for at least some of the rise in infant morbidity and mortality:

In regions with a greater supply of beds and neonatologists, infants with less serious illness might be more likely to be admitted to a neonatal intensive care unit and might be subjected to more intensive diagnostic and therapeutic measures, with the attendant risks of errors and iatrogenic complications, as well as impaired family–infant bonding.

In short, if there is a correlation between vaccination schedules and IMR — a fact not proven here — there may be a simple explanation (e.g., a more aggressive approach to medicine overall) that does not require invoking unproven and unexplained “toxicity” in vaccines.


Where does all this leave us, in terms of what I was talking about at the beginning, the relationship between science and our everyday lives? Well, it counsels skepticism, certainly, when “news” of a disturbing “scientific” discovery shows up on parenting forums or in our inboxes. And of course it challenges each of us to become more scientifically literate in our reading — which is why I occasionally undertake these close examinations of scientific subjects related to parenting.

But this process is exhausting. To really delve into this paper, to take it apart and understand it to my own satisfaction, has taken two days and 3500 words. I can’t possibly do this with each piece of scientific information (or misinformation) that comes my way. For the most part, I’m forced to shrug and rely on professionals at the CDC, the FDA, and the doctor’s office to steer me the right way. But what happens when the professionals start to seem untrustworthy or themselves misinformed? What do you do when your need for expert knowledge is undermined by an almost paranoid sense that the experts are not on your side? And how do you avoid going too far in the other direction and falling victim to things like vaccine denialism?

I’ll try to talk more about that in the next couple of entries in this series.

your little vanities

Here’s a lovely little article by Mark Oppenheimer about the allure of dandyism for frumpy 30-something dads. The bulk of it is a review of Glenn O’Brien’s How To Be A Man, but I think this paragraph from the beginning is a pretty amazing encapsulation of the hopelessness of modern middle-class living:

If parenthood meant I could no longer afford the things I badly wanted, that would be regrettable, but not exactly complicated. My problem is rather different: I actually have very simple pleasures, and I can still afford all of them. Whereas some people enjoy backpacking in Thailand, leased BMWs, and triple-mint real estate, I like skim mochas at the local coffee shop in the winter, Starbucks Frappuccinos in the summer, ice cream at the local parlor year-round, a few new books a year, and midprice new clothes bought at T.J. Maxx or at chain stores you can find in the average upscale mall. I have enough money that I could buy everything I want. But I now have children, and no money saved for, say, college-tuition payments. And yet even if I forewent every frappuccino and pair of corduroys for the next 20 years, I fear I would not save enough money for one year of college for one daughter. So while in one sense every frappuccino is money wasted, in another sense every penny saved is for naught.