Why Wait for “Economic Growth” to Raise Your Income?

Something annoys me about how the media reports economic growth statistics. All the major outlets are talking about the recent good news from the Census Bureau. Supposedly middle-income households have seen their wages increase for the first time in decades. (Here’s one such story. Every major outlet has reported on this, as far as I can tell.)

I think this is the wrong way to think about income growth, especially with regard to your personal income. A nation-wide average is not a number that you can personally control with any decision you make. Your contribution to that is probably a rounding error, even if you are an enormously influential policy maker like the Fed chairman or the president. On the other hand, you have *enormous* control over your personal income. Do you want to see *your* personal income rise with double-digit growth for several decades? Then pick a lucrative profession and start hustling!

Do you really expect your earnings to increase without making any kind of change in your life? Well, in that case you’re asking other people to work harder so that your income will grow. You’re essentially asking other people to do the heavy lifting so you can keep doin’ what you’re doin’. I can't help but think this attitude is a little bit selfish. That's not to say you won't share in the growth anyway. You most likely will. Some incredibly productive individuals will invent products that you use daily, that entertain you for hours, that replace several other bulky and expensive products. (Are you reading this on a smartphone? A laptop computer? Then you really are the beneficiary of such individuals.) Your life really will keep improving, probably even if you don’t make adjustments that make you personally more productive. Economic growth is great that way, and I certainly approve of pro-growth policies (lower taxes, less burdensome regulation, lower government spending, etc.). But it’s not something you should feel entitled to. The world doesn’t owe it to you. 

If a very large number of people were hustling, as described above, to improve their individual careers, there would be more good news regarding increasing wages. It would be accomplished by private policy rather than public policy. It’s great to have *both* kinds of policies be “pro-growth,” but individuals should concern themselves with the one they can actually affect. If you’re waiting for the rising tide to lift your boat, you’ll be waiting a very long time. 

People Choose Their Career Paths, and Therefore Choose What Income They Earn

If people can choose their personal income (as opposed to that number being assigned to them by some cosmic roll of the dice), then it makes no sense to worry about income inequality. I'm using "choose" to mean "select from available options"; obviously you can't just pick some arbitrarily high number. I present the following as “Exhibit A” for the claim that people do, in fact, choose their personal income:

https://www.dwsimpson.com/salary

(Scroll down until you see the salary ranges.) I know a lot of smart, underemployed young people who could easily knock out at least the first two or three exams and land a decent analyst job. They’d improve their salaries enormously. They’d also massively improve their options (where to live, who would date/marry them, etc.). It might take a few hundred hours of studying to pass exams 1 and 2. For a well-equipped math person, exam 1 probably requires about 100-200 hours of study, similar for exam 2, at least back when I took them a few years ago. That sounds like a lot, but the opportunity cost is low if you’re current career prospects aren’t so good. And you don’t have to keep going if you decide the exams are boring. You can land a job as a well-paid Excel jockey after completing only two or three. (I personally landed my first actuarial job after passing a single exam.)

These are solid middle-class jobs, well above the median for personal income. All it requires is to hunker down and study for a bit. This is by no means “out-of-reach.” It’s within striking distance of a lot of struggling people, and they don’t reach for it. I can only conclude that they don’t wanna. That’s not a moral judgment. I’m not at all saying they *should* want this career path over whatever it is they’re doing now. And that’s actually my point. We *shouldn’t* be second-guessing other people’s career decisions, nor should we be bemoaning their “inadequate” personal income. For whatever reason, this person had decided to spurn a perfectly lucrative career path for whatever it is s/he is doing right now.

I’m not saying that everyone in the world has this option within arms-reach. I’m sure there are some people who just aren’t smart enough to pass the exams, no matter how hard they study. Some people just don’t have a knack for math, and it’s too late to learn (although I personally think this is overblown and most people can improve their math skills more than they realize). Some people have spotty employment histories, or perhaps a history of being fired or arrested. Such a history will follow you no matter how resolutely you decide to shape up and fly right. (You know, starting now. Or maybe tomorrow.) And maybe some people have personality issues that make them difficult to employ. That’s all fine. Not everyone in the world can turn themselves into actuaries with a few months of study, and I’m not claiming everyone should. The actuarial career path isn’t the only option in the world for improving your future prospects. It happens to be the one that was most readily available to me when I was looking for a grad school exit-strategy, but there are all kinds of options like this one at all levels of education. Learn to code at coding bootcamp, or take a bunch of Coursera classes. Or get certified in a skilled trade (HVAC, plumbing, electrician, etc.). I’m using the “become an actuary” example because it’s relevant to a lot of people who I happen to know, people who could improve their outlook if they really tried. But these *kinds* of unexploited career options are available to everyone. If you really thought about it, you could make yourself more employable and get a more lucrative career. It would take some time, but you could do it.

I think it makes a lot less sense to complain about income inequality when you admit that people have a lot of control over that variable, at least in the long run. That’s not to say we’d all have equal incomes if we all tried just as hard. Some people are the beneficiaries of chance, be it the luck of being born talented or the idiosyncratic luck that rewards random people at random times. But it’s not all luck. I see many cases of equally talented, equally endowed individuals, and one decides to zig while the other decides to zag. So one ends up a doctor making $200,000+ per year, and the other lives on his mom’s couch playing video games and earning zero. It makes little sense to complain about the “unjust” distribution of incomes when you zoom in on the details. An individual’s very high or very low annual income typically become understandable the more you know about them. Rarely will you see that someone’s lot in life is something that was simply “done to” them. 

When a "Drug Overdose" Isn’t

Below are some passages I highlighted in my copy of Karch’s Pathology of Drug Abuse, 5^th edition, specifically from the chapter on cocaine. I’ll give away the punchline: this is another post arguing that drug overdose death statistics are probably overstated. I wrote about that here with some passages from the chapter on opioids. Without too much throat-clearing, let's dig in:

[A] handful of important pharmacokinetic studies have been published. In one of these, an uncontrolled clinical study, plasma cocaine concentrations in 111 symptomatic cocaine users were studied and an attempt made at correlation of plasma concentrations with clinical symptoms (Blaho et al., 2000). The study was unsuccessful to the extent that no correlation between dose and effect in real cocaine abusers was demonstrated. Failing to find a difference is, presumably, a result of cocaine tolerance, a process that begins to emerge after the first dose (Howell and Ezell, 1990; Mendelson et al., 1998). Using human volunteers, Van Dyke et al. (1982) showed many years ago that tachyphylaxis occurs after even single dose of cocaine.

In other words, cocaine users rapidly develop a tolerance to the drug, so it’s impossible to specify a threshold for “overdose.” (Tachyphylaxis is a fancy word for diminishing responses to successive doses of a drug.)

The results of these studies suggest that (1) chronic users may consume multigram quantities of cocaine with relative impunity; (2) a variety of cocaine metabolites previously thought to be insignificant (EME, norcocaine) are, in fact, formed in fairly substantial quantities; and finally, (3) the half-life of cocaine may be much variable than had previously been thought. All of these variables are partly a function of the route of administration. 

This would make it impossible to tell if a dead body with very high blood levels of cocaine are actually overdoses or heavy users who die of unrelated causes.

Although the plasma cocaine level approximately doubled following the second cocaine administration, the ratings of positive drug effects, heart rate, and blood pressure did not increase after the second cocaine administration. Clearly, acute within-session tolerance develops during repeated administration of intranasal cocaine (Foltin and Haney, 2004).

This passage illustrates just how rapidly cocaine tolerance forms in a user. You might have the image of a coke-fiend chasing a high and consuming a Tony Montana-esque quantity of cocaine. I’ve heard such descriptions of cocaine users, although I suspect these are mostly exaggerations. At any rate, if the users are rapidly developing a tolerance to the drug’s physiological effects, they are also developing a tolerance to the toxic effects.

[H]ighly accurate measurements are seldom of any help in differentiating deaths due to drugs from those deaths where the presence of drugs is simply an incidental finding or, as is increasingly recognized, an interaction between two drugs to produce a third and even more toxic drug. Why are such precise measurements of so little value? Because, except for episodes of massive overdose (as might occur in a drug mule) where the mechanism of death is perfectly clear, most cocaine-related deaths occur in chronic drug users in whom death is a consequence of neurochemical and anatomic changes induced over a period of months or even years.

So here he just comes out and says that the tissue concentrations of cocaine can’t be used to determine the cause of death. I wonder how many medical examiners understand this point, and how many just mark the cause of death a cocaine overdose when it’s a handy and convenient answer? The number of cocaine-related deaths in 2014 was 5,992, according to CDC figures. (It actually went up, from 4,494 in 1999 to a peak of 8,591 in 2006, then back down to 5,992 in 2014, just to give you a sense of what it’s done over the past 15 years.) I’m curious if most of these are really cocaine overdoses, or if most of these are mislabeled and the numbers are tracking with usage but not necessarily with mortality?  As in, “There are more corpses with cocaine in them in 2006, fewer in 2014, but we really have no idea if cocaine was the cause of death in the vast majority of these deaths.” Then again:

Long-term cocaine users have changes in their hearts (Karch et al., 1998) and in their brains (Volkow et al., 1993) that favor the occurrence of sudden death. If the abuser is truly unlucky, he or she may be heterogeneous for one of several abnormal hERG ion channels (Guo et al., 2006) or polymorphic catecholamine receptors (Ghimire et al., 2012). These changes explain why, in both the living and the dead, it is absolutely impossible to correlate a specific blood or plasma concentration with a specific type of toxicity or even speculate whether cocaine-related toxicity occurred at all (Jenkins and Goldberger, 1997; Karch et al., 1998; Blaho et al., 2000).

So there is a countervailing force here that can lead to *understating* the number of cocaine deaths. Someone could have cumulative organ damage from a cocaine habit, but have no cocaine in their system at all. They could have gotten totally clean after a long period of cocaine abuse, but the damage to their hearts and brains can still kill them later. I suspect this is a small countervailing force because the number of long-term cocaine abusers is so small, but obviously this is a giant question mark.

Given these realities, the accurate certification of a drug-related death requires knowledge of (1) the decedent’s past medical history, (2) an account of what happened at the scene, (3) a thorough postmortem examination, and (4) the results of DNA testing to rule out hereditary forms of heart disease or even myocarditis; the cost of such testing is rapidly decreasing to affordable levels. Though it will still be some time until it becomes widely available.

My impression is that most autopsies aren’t this thorough, and Karch reinforces this impression with the following passage:

The definition of just what constitutes a “complete” autopsy is not as simple or clear as it once was. Does the examination of one section of myocardium constitute a “complete” examination of the heart? When a young person dies suddenly, is it proper to refer to their heart as normal when cardiac ion channels have not been measured? In unexplained cases of drug death, should the examination be considered complete if the P450 metabolizer status is not determined? The answer to all of these questions is “no.” As a consequence, cause of death determinations are often based solely on toxicologic measurements, significantly raising the chances for a missed or incorrect diagnosis. Because cocaine is so widely used, cocaine-related deaths present a special set of problems.

Clearly the author thinks that typical autopsies are not adequate to determine the cause of death in a suspected cocaine overdose.

I thought the following passage was a good explanation of why cocaine users feel compelled to keep taking massive doses of the drug, “chasing the high” as it were:

There is seldom any reason for clinicians to measure plasma concentrations of cocaine or its metabolites. Unlike alcohol intoxication, where specific blood concentrations can generally be related to specific physiologic and psychological states, cocaine blood concentrations do not relate to symptoms (Karch et al., 1998; Blaho et al., 2000), not even in the laboratory setting. Accordingly, treatment must be based on the patient’s symptoms, not on the plasma level of cocaine.

When cocaine is given to volunteers, correlations can be drawn between the degree of mood elevation and peak blood levels, but only when cocaine concentrations are rising. If blood concentrations are falling, the exact same concentration that resulted in a “high” when concentrations were rising can be associated with a dysphoric reaction when concentrations are falling. Cardiovascular effects and feelings of euphoria decline more rapidly than do cocaine blood concentrations (Javaid et al., 1978), but the “rush” experienced by cocaine users follows a different time course than the cardiovascular changes.

Emphasis added. Given this, you can easily imagine someone taking more and more cocaine during one session, chasing the state of rising blood concentrations. Given the rapid onset of cocaine tolerance, it’s not clear that this is necessarily dangerous, unless the user takes a truly massive dose.

At one time, cocaine blood concentrations of more than 5 mg/L were thought to be uniformly fatal (Wetli and Mittlemann, 1981). With more experience, it has become apparent that isolated postmortem blood concentrations cannot be used to determine the cause of death at all. Tolerance on a massive scale occurs, and cocaine concentrations well in excess of 5 mg/L can be encountered in traumarelated deaths where the presence of cocaine is clearly an unrelated finding (Pagel et al., 1994; Shannon et al., 1996). For example, one case report described a man who was shot while drinking in a bar. Prior to being shot, the man’s behavior was said to have been normal. When he was autopsied several hours later, after having undergone extensive attempts at resuscitation, including aggressive fluid replacement, multiple blood specimens showed a blood cocaine concentration of 30 mg/L (Howell and Ezell, 1990).

Further driving home the point that blood concentrations can’t be used to determine the cause of death.

The following is good to keep in mind when thinking about the topic of overdose deaths:

Most cocaine-related deaths can be attributed to the occurrence of a lethal arrhythmia.

Unfortunately, lethal arrhythmias happen for reasons unrelated to cocaine. So it’s hard to tell if cocaine was the cause or just incidental.

The last section of this chapter is actually titled “When Is Cocaine the Cause of Death?” and it reiterates the point, repeated throughout the chapter, that it’s a hard question to answer.

It is distressing to see how often deaths caused by cocaine are misclassified. Misconceptions about cocaine-related deaths persist, partly because death certification practices are not standardized and partly because there is no reproducible method by which to make the decision.

I wish this was better quantified, some thing like “50% of ‘drug related’ deaths are misclassified.” Obviously nobody knows what the real number is. But it would be nice if the CDC, when reporting on drug-related fatalities, adjusted for this misclassification problem, or at least acknowledged it.

The following is mentioned in the footnote of a figure:

Except in the case of massive overdose, cocaine-related deaths are always multifactorial.

In other words, it’s never *just* cocaine. It’s always some combination of cocaine and other drugs, or cocaine interacting with a heart condition.

Consider the example of a young cocaine abuser who dies from smoldering myocarditis that has been present for many weeks. If microscopic examination is not performed, or, even worse, if no autopsy was performed except to draw blood for toxicology testing with “a blind stick,” even if the level of cocaine present is trivial, there is a very good chance that death will be attributed to the drug.

Read “smoldering myocarditis” to mean “an unrelated heart issue.” (It’s just a random condition he chose to make his point, as far as I can tell.)  The author is pointing out that sometimes the toxicology is the sole piece of evidence that medical examiners use to determine the cause of death, even though this is completely inappropriate.

In a 2014 study of 245 U.S. college athletes who had died suddenly, with no abnormalities detected at autopsy, nearly a third of the individuals had fully normal autopsies. At about the same time, researchers in Denmark reviewed nearly 439 cases where the decedent was aged 1–49 years (Bjarke et al., 201). As might be expected, nearly 70% of the deaths were the result of coronary artery disease. But in 135 of the U.S. cases, complete autopsy disclosed no anatomic abnormality, very strongly suggesting an underlying mutation (Maron et al., 2014).

In other words, people drop dead for no apparent reason, and sometimes even a thorough autopsy can’t find any underlying anatomical problems. I was glad to see the authors reference some actual studies of this phenomenon, because this is exactly what I suspect is happening in a large number of so-called “drug overdose” cases. This is precisely what I suspect is overstating the overdose numbers.

Suppose a person with a heritable cardiac channelopathy is found dead and a modest amount of [cocaine metabolite] BZE is found in autopsy blood. For many, the temptation to classify the death as drug related may be too strong to resist if they are unaware that a potentially lethal mutation is present.

All of this together reaffirms something I've suspected for a while now. When it’s hard to determine the cause of death, toxicology offers up an easy answer. The medical examiner can fill out the death certificate and go to lunch. I don't know how big a deal this is, but a serious effort should be made to correct for this problem.

There is much, much more in this chapter. It confirms my suspicion that drug overdose deaths are inaccurately measured, and probably are overstated. I hope that the authors don’t mind my generously quoting from their book. Certainly these passages are relevant to a very important public discussion about the drug overdose problem, and certainly these considerations should inform any policy response. 

(If the authors of Karch's Pathology of Drug Abuse see this blog post and want me to cut some of the quotes, I’d be happy to paraphrase instead of quoting. But I insist that the basic point underlying these quotes is relevant to a public discussion, so some form of the above needs to be publicly available. Karch was interviewed for Radley Balko's series on the opioid epidemic at the Huffington Post, where he is quoted as making the above pionts. So surely his intention is to inform the public on this point.) 

How Much Do Labor Unions Affect Wages?

Below I have some excerpts from Deirdre McCloskey’s book Bourgeois Dignity, just in time for Labor Day. I find it obnoxious the way that some commentators attribute far too much explanatory power to labor unions. There’s a bumper sticker that says, “Enjoy weekends? Thank your local union.” Sorry, but this is just implausible. The workers got richer because they became more productive. Their greater earnings led them to purchase, among other things, more leisure time. That is why wages have been rising and the average work-week has been shortening for the past two centuries. It’s plausible that labor unions, in some select cases at certain times, made these advances happen faster than they would have otherwise, but it’s completely unrealistic to credit the labor movement with all the gains since the mid-19^th century as some glib writers do.

The struggle by unions for higher wages and better working conditions has inspired many good songs and many good people. Clearly, say the songs, we gotta' go down and join the union; we need to fight for Harry Bridges and build the CIO; and we need to be a union maid when she fought for higher pay. "She'd show her card / To the National Guard, / And this is what she'd say:/ `Oh, you cant scare me: / I'm stickin to the union."' But the fight to get a higher share of the pie for union members leaves out nonunion members, who were always a high percentage of the workforce in the United States. If the size of the pie is pretty much fixed-the underlying assumption of classical economics and of union logic-then higher pay for auto workers implies lower pay for auto mechanics, not something to be celebrated in songs by Woody Guthrie and history books by progressive historians. The economist H. Gregg Lewis painstakingly estimated the effect of unions 1967-1979 on wages of their members relative to comparable nonmembers and found it to be, as an upper bound, rather small: some 14 percent. My uncle, who was himself a union electrician in Michigan, paid union wages for his employees gladly, he said, because he passed the expense on to the companies and hospitals and school buildings that he wired. Oh, good. But who pays that? Other workers. There's no one else to pay it. As Pogo famously said, "We has met the enemy, and he is us."

So, essentially unions succeeded in raising the pay of their own member by at most 14%, and that came at the expense of other workers. Meanwhile, the average wage in the developed world rose by something more like 1600% to 10,000% (a factor of 16 to 100, depending on how you account for changes in quality and other considerations).

And if, as was on the contrary the case, the pie was in fact exploding, then a shift in the size of the slice going to workers as a whole (setting aside that it would in fact go only to the minority of union members) would anyway play a small role in the betterment of even those workers. Workers in the United States and elsewhere grew radically better off from 1800 on, and 1900 on, and even from 1970 on because of the Bourgeois Deal, not because they went down and joined the union. How do I know? Answer: the nonunion people shared nearly equally in the gain, even though they were paying as consumers for the fancier wages for union electricians in Michigan. The maximum of 14 percent of "concessions" extracted by bargaining or strike doesn't come close to accounting for the great magnitude of rise in the real wage. There's not enough profit-usually 10 or 15 percent of national income-to raise the level of the rest of national income by a factor of even two, that is, 100 percent, much less the factor of eighteen it in fact rose after 18oo. Expropriating 15 percent of national income claimed by the wretched profiteers teers and transferring it to the 85 percent earned by us workers raises our income only 18 percent. That's a long, long way from 1,700 percent.

Deirdre McCloskey is making the point that labor unions can only rearrange portions of a relatively fixed pie; nothing they do is likely to grow the pie. They can negotiate with the capitalists to redistribute some of the profits from capitalists to laborers, but they can’t increase the total productivity available for distribution. People love to romanticize the 19th century labor struggle. So much blood was shed, it's irresistible to conclude that some tremendous benefit must have come from it. Alas, a little bit of numeracy and some back-of-the-envelope math implies otherwise. 

Casting More Doubt on the "Prescription Painkiller Epidemic"

When a doctor “certifies” a cause of death, his certification is based upon his evaluation of the evidence available to him, but it is still just his opinion and does not set a precedent for similar cases.

It turns out assigning a cause of death is really hard. 

I’m reading through Karch’s Pathology of Drug Abuse. This is the standard textbook on the topic. It repeatedly makes the point that toxicology results can’t be used to determine the cause of death. I’ve only read a fraction of it so far, but it’s definitely strengthened my belief that the recent rise in overdose deaths is, at least in part, a spurious trend. The book’s authors go into some detail on the mechanisms that make postmortem toxicology unreliable. This is important because there is much ink spilt about the recent supposed rise in prescription painkiller deaths, and much more recently the rise in heroin overdose deaths. It’s true that there are many more prescriptions today than there were 15 years ago; the sheer tonnage of opioids prescribed is easy enough to track, and the government does track these figures. It is far less clear that the rise in opiod-related deaths is real. It could simply be the case that, with more people walking around with opioids in their system, more deaths are being labeled “drug poisonings” even though the drugs are incidental and the real cause of death was actually something else. When a medical examiner labels a death a “drug poisoning,” they are expressing an opinion.

When you see numbers such as “There were 47,000 drug overdose deaths last year” or “There were 18,000 deaths from prescription painkillers last year”, these figures are basically a guess. For each such death, somebody (a coroner or medical examiner) looked over the body and determined it was a drug overdose, and that death went into a big database of all 2.6 million deaths that happened that year. Then later somebody ran a query against that database that counted up all the deaths that matched criteria X, Y, and Z. I sincerely wish that the people and organizations reporting these figures would be a bit more careful about issuing caveats and admitting to uncertainties in their data and methods. I hear a news story once a week or so about the prescription painkiller epidemic, and I'm getting increasingly annoyed that the news outlets aren't doing the slightest bit of vetting on the underlying numbers. Did not a single one of these reporters bother to crack a textbook on the topic? Did nobody bother to ask "How do you know if a death is a drug overdose?" The database and query are actually pretty straightforward, but the whole thing falls apart if you don’t have much confidence that the data reflect the true causes of death. It’s very likely that many of these deaths were due to some other cause, and the drug use was an incidental finding.

From the section on methadone:

Because methadone has a very high volume of distribution, concentrations can be expected to rise after death. Indeed, fourfold increases have been reported (Levine et al., 1995; Milroy and Forrest, 2000). Postmortem methadone concentrations are also site dependent and, for unexplained reasons, the increases appear to be greater in men than women (Caplehorn and Drummer, 2002). In every published series methadone blood concentrations in fatal cases completely overlap those found in methadone maintenance program participants.

So basically the blood concentrations are useless in terms of determining the cause of death. For one thing, drug users develop a tolerance, so what would be a fatal dose to a naïve user is safe to an experienced user. This is particularly true of opioids, although all drugs build some degree of tolerance in their users. The problem of “postmortem redistribution”, diffusion between blood and tissues, exacerbates this problem.

Not one single control study, even in animals, has ever shown that postmortem drug concentrations accurately reflect drug concentrations at the time of death, but a goodly number have shown quite the opposite to be true, chiefly because of the problem of postmortem redistribution (Pounder et al., 1996; Hilberg et al., 1999; Moriya and Hashimoto, 1999; Drummer and Gerostamoulos, 2002; Flanagan et al., 2003; Ferner, 2008). Postmortem redistribution is defined as the movement of a drug down a concentration gradient after death.

In other words, blood concentrations don’t follow a smooth decay curve after death.

The postmortem movement of free morphine out of the tissue, back into the plasma, makes it impossible to estimate the time of ingestion by calculating the ratio of free to conjugated morphine.

[T]he Vss [steady-state blood concentration] for methamphetamine, in healthy volunteers given fixed doses of drug and then living in a locked ward, was found to range from 2 to 11 L/kg (Schepers et al., 2003). This enormous and unpredictable degree of variability, even in the living, makes it impossible to establish any sort of relationship between postmortem drug concentrations and reported dosage, though it would seem reasonable to conclude that if low levels of drug are detected, the drug was consumed.

In other words, people given the same dose may show wildly varying blood levels of the drug, even in healthy living test subjects. This complicates setting any threshold for a toxicology screening, as in “Anything above X is a fatal dose, anything below X is nonfatal.” All the stuff about redistribution after death complicates matters even further.

This next part borders on a philosophy of causation lecture:

Could the death of a cocaine and heroin abuser, with cardiomyopathy, be related to the fact that his cardiologist had just begun treatment with carvedilol, or did the doctor at the methadone maintenance clinic administer the wrong dose of methadone? It may be impossible to say, but these complex issues exist and cannot be ignored. 

The authors even discuss how gut bacteria cause drugs and their metabolites to diffuse through the body after death (if I’m reading them correctly):

It is not uncommon to hear an “expert” offer an opinion on how much time had elapsed between the last dose of heroin/morphine and death. Such speculation is unscientific, not just because of the differences in Vss between parent drug and metabolite, because bacteria translocate. That is, they migrate through the walls of the bowel, invading the rest of the body within a few hours of death (Kellerman et al., 1976).

Two short sentences about how genetic differences between individuals can contribute to different drug metabolism:

Thus, even in the living, without knowing an individual’s ability to conjugate morphine (which would require DNA resequencing), comparing the ratio of bound morphine to free morphine is a meaningless exercise.

Genetic polymorphism is, no doubt, responsible for more than a few cases of drug toxicity, but the true incidence of this problem is not really known.

In other words, people metabolize drugs differently. A fatal dose to one person may be nonfatal to another, even before considering things like acquired tolerance. The authors go on to describe a specific genetic trait and its effect on codeine metabolism:

Individuals entirely lacking CYP2D6 activity (7%–10% of Caucasians) are called PMs and are not likely to get much pain relief from codeine because they cannot convert enough of it into morphine. But it is also possible to have multiple duplications of CYP2D6, making the individual into an ultrametabolizer who can transform abnormally large amounts of codeine into morphine. Thus it is quite conceivable that a person with a gene duplication might experience an overdose even though only a modest dose of codeine had been taken.

The author gives two examples of deaths that might be labeled an “overdose” and explains why the true cause of death isn’t so clear:

If toxicology results cannot be considered in a vacuum, neither can autopsy findings. When a doctor “certifies” a cause of death, his certification is based upon his evaluation of the evidence available to him, but it is still just his opinion and does not set a precedent for similar cases. If the decedent was a known cocaine user, the body was noted to have frothy pulmonary edema, blood cocaine concentration is 1 mg/L, and a crack pipe was found at his side, the decision is not difficult. But what if the blood cocaine concentration had been 0.050 mg/L, there was minimal pulmonary edema, and no other apparent stigmata of drug abuse or anatomic abnormalities were observed, but concentric cardiac hypertrophy was evident? How would the pathologist determine which abnormality was causal—the one he could see and weigh or the hERG channel–cocaine interaction he knows might exist, but cannot measure?

Another example that illustrates how difficult it is to determine the cause of death:

In the same fashion, suppose the pathologist was confronted with a decedent who had a remote history of heroin abuse and only mild pulmonary edema with a blood morphine concentration of 20 ng/mL evident at autopsy. In the absence of other identifiable anatomic changes, the pathologist would, no doubt, determine the manner of death as heroin overdose and an accidental death. But that would be incorrect for at least two reasons. First, unless hair testing had been performed, the pathologist would have no idea whether the decedent was a regular user and therefore tolerant or whether the decedent was naïve and intolerant. Second, the cocaine that was present could have unmasked one of many genetic defects that can interfere with the metabolism of morphine or exaggerate its effects (Oertel et al., 2009). Whether such a death would be classified as natural or accidental could be a matter for debate. What is not debatable is that the autopsy pathologist has no way to look at the body and determine whether or not the decedent suffered from a P-gp variant or an SCN9A mutation, at least not without performing genetic resequencing first.

There is much, much more. In fact, everything above is from the chapter on opioids. Other chapters are full of similar warnings about assigning a cause of death or interpreting blood concentrations of a drug. I’ve written several posts about how the recent rise in drug poisoning deaths could be spurious, here, here, here, here, and here . I still think that part of the increase in real, but some large fraction of it is spurious. Those news outlets who are fanning the flames of a moral panic need to cool their jets until we really understand what’s going on. 

I'm still reading this book. More to come if I find more interesting topics.

Income Inequality is Not a Problem

The problem with identifying “income inequality” as a social problem is that it misses all the real problems and it implicates non-problems as problems. The desire to alleviate poverty is legitimate, but the blaming of rich people isn’t.

Some people have a hard time in life, for a variety of reasons. Some people have serious emotional issues that make them difficult to employ. Some people have serious absentee/tardiness issues, or just general conscientiousness problems, that make them unreliable as employees. Some people, for whatever reason, failed to acquire any kind of relevant education (college or vocational) and thus have no useful job skills. Some people have a relevant education, but for whatever reason refuse to work at a meaningfully remunerative job (I have seen so much of this, and it is almost always baffling to me). Some people are government workers in cozy jobs whose cost-of-living-adjustment suddenly stops because the government goes broke. All of this is merely to observe and explain, not to blame. Sometimes it really *is* the person’s fault, and sometimes it isn’t. Either way, it’s wrong-headed to tell these people, “You’d be doing a lot better if these rich people weren’t hoarding society’s resources!” Or “If only the political system weren’t dominated by rich interests, it would work better for you, and you’d be sharing more of the wealth.” That’s not what these people need to hear. This kind of scapegoating is shameless pandering when a politician does it and self-congratulating escapism when the “underpaid” workers themselves do it. Either way it’s grossly irresponsible. There are usually actions the person can take to improve their circumstances, and we should encourage that. We shouldn’t be telling them, in effect, “Your problem is due to someone else’s greed, and only a massive change in government policy will fix it.” Without casting any moral judgment, I want to point out the causal mechanism proposed within the income inequality framing is simply mistaken. It just isn’t true that the rich are richer *because* the poor are poorer.

If you aren’t careful, it’s easy to take on a zero-sum worldview (inadvertently or explicitly). It’s easy to think “If he had less, we’d all have more.” Or “Society’s income is $16 trillion per year. We just need to dole it out more equitably.” We don’t live in a zero-sum world. “Society’s income” isn’t something that belongs to all of us; it’s not something that is wrongly and arbitrarily doled out unequally to make a few random winners rich. There really are people whose annual productivity is in the millions of dollars. If large companies didn’t shell out to place the most talented possible individual in their executive roles, they could lose out on millions or even billions of dollars. And without an appropriate incentive to perform, that talented executive might make avoidable million dollar errors. It’s easily possible that the *very* best person for the job of, say, running Microsoft will contribute $10 million more a year to the expected bottom line than the second best person. Getting that person for $5 million would be a steal for the shareholders and for the software users who are using the improved product and the employees of Microsoft who are made more productive by the CEO’s actions. Getting that very best person to put in their very best effort could easily be worth another $10 million. If the difference between a motivated and an unmotivated executive is $10 million to the company’s bottom line, then a generous bonus in the millions of dollars is economically justified. Perhaps the very best executive has a 1% chance of totally destroying the value of a large company over their tenure (say Microsoft, with a market cap of $450 billion), but the second best has a 2% chance of totally destroying the company. This consideration alone makes that top executive worth ([2%-1%] * $450 B = )  $4.5 billion. If Microsoft can acquire this person by making them a billionaire once or twice or even thrice over, it’s worth it. Sorry to burst anyone’s populist bubble, but those very large executive compensation packages make economic sense. You’re *richer* because of them, not poorer. I think it’s not hard to understand that an executive’s productivity should scale up with the total value of the company, and that their take-home pay should reflect this productivity. People react with outrage to these big compensation packages, but economically speaking they are justified.

Consider now a more modest form of inequality: those salary differentials between the professions. These are a feature, not a bug. They are a market signal directing people to where work is most dearly needed. Very high salaries for doctors, lawyers and actuaries are signals that “The world needs one more doctor/lawyer/actuary more than it needs one more teacher/secretary/cashier.” If the pay differential were too small, you wouldn’t have enough people who are willing to undergo the long years of training necessary to enter these professions, and you wouldn’t find enough people to do the often thankless, boring, or even dirty tasks that these jobs entail (and while working longer hours than an average worker).  More to the point, people aren’t being assigned these professions at birth; they choose their profession *knowing* that these salary differentials exist. It’s extremely churlish to choose a low-paying profession while complaining that a higher-paying profession earns more. People don’t just fall into these positions. They end up there after having followed a long and arduous path. Your current profession is a sum of many past choices and your past effort. 

Some people make the mistake of interpreting salary differentials in terms of value judgments, as in “Isn’t education just as important as medicine?” It’s the wrong question, and answering it doesn’t tell you anything useful about how much doctors should be paid vs how much educators should be paid. The actual question is more like, “What is the social value of *one additional doctor* vs *one additional teacher*?” And more to the point, “What salary will attract the extra doctor we need, and what salary will attract the extra teacher we need?” It’s not as though there are a fixed number of slots to fill, and we can just fill them all with any arbitrarily chosen salary figures. The actual number of people willing to enter the profession changes, moves up and down, in response to the salaries offered, and in turn those salaries adjust up or down with the number of people willing to enter the profession. (This is the standard intersecting-supply-and-demand-curves stuff from econ 101.) Inserting your own moralistic value judgment into this consideration would be arbitrary and wouldn’t help you answer the question “What *should* these relative salaries be?”

I have no doubt that there are some people who make an undeserved fortune by adjusting the rules to favor themselves. Perhaps an auto producer or textile company profits from an import quota or tariff. Or perhaps a mega-farm gets paid by the government to leave thousands of useful acres of farmland fallow. Or onerous regulations make it hard for small start-ups to challenge incumbents. It’s often the case that the companies benefiting from these market restrictions are the same companies that actively lobbied for those policies. These gains are ill-gotten. But it’s the “ill-gotten” part that’s the problem, *not* the “gains” part. By fixating wrongly on inequality, we would falsely impugn the honest business owners who earn their fortunes honorably through voluntary transactions. And we might wrongly overlook these kinds of ill-gotten gains if the thief fails to enrich himself compared to his competitors. In both cases, “inequality” is a terrible proxy for the real problem. For both kinds of errors, the inequality framing *completely misses* the problem. 

Countervailing Forces

I think it’s very likely that under drug legalization, the mix of drugs people are taking could change, but total drug-related harms wouldn’t increase. It’s far more likely these harms would decrease substantially. There are countervailing forces here, so we have to be clear about what these forces are and somehow estimate their magnitudes. (I’ll give an incomplete list what those forces are below, but this won’t be a thorough, rigorous cost-benefit analysis.)

Consider the forces that would decrease drug-related harms:

1)      Some currently illegal drugs are extremely non-toxic, contrary to popular belief. Their legal status, while not exactly making them “unavailable”, does raise their relative cost. Legalization, at least for these drugs, would shift consumption toward these and away from the current legal drugs (alcohol, tobacco, and pharmaceuticals), which are more toxic and more prone to addiction problems.

2)      Related to 1), but the same point for drugs that are potentially harmful. Someone might satisfy their need to get intoxicated on a low dose of cocaine or heroin, while needing a very much larger (and overall more harmful) dose of alcohol to achieve the same satisfaction. Don’t scoff at the notion that substituting from alcohol to heroin or from nicotine to methamphetamine could have net positive health and social effects. These drugs are not harmful if properly administered, and some of them (particularly opioids) don’t cause cumulative organ damage.

3)      Currently illegal drugs are made *far more* dangerous by prohibition than they would be in a legal market. Drug interdiction causes the dosage to fluctuate wildly, which is the cause of a lot of overdoses. Often the active ingredient is a completely different chemical than the user realizes (fentanyl sold as heroin, or experimental designer drugs sold as MDMA). Impurities and adulterants are hard to control in a black market. Dealers have a preference for very concentrated doses of the drugs, because they are easier to transfer and smuggle, so these higher-concentration versions of drugs dominate the market.

4)      It’s easier to advise people against self-harming behaviors in a legal market. Warning labels against specific harmful behaviors can be put on the packaging and purchasing the substance puts the buyer in front of a pharmacist who can advise them. Someone who buys two drugs that interact can be told “Don’t mix those.” (Considering that most drug poisoningsare multi-substance interactions, this would be a very important behavioral tweak.) Relatedly, it becomes easier to usher someone into drug rehab if their habit doesn’t make them a criminal. More people are likely to seek necessary help if doing so doesn’t risk legal sanctions.

5)      The legal sanctions are themselves harmful to people’s lives, and these would obviously disappear under full legalization. These include decades in prison, low-level harassment of millions of innocent people, and the occasional beating or shooting of a drug suspect. We’d do away with this class of social harms entirely.

6)      Black market violence is a huge driver of our overall crime rates. Estimates vary, but by all accounts are big. Read “Drug War Crimes” by Jeffrey Miron for the full story, but something like ¼ to ¾ of our murders can be blamed on the drug war, and that’s not even the entire class of black-market social costs.

Now consider the force that would lead to an increase in drug-related harms:

1)      Someone who otherwise wouldn’t have tried cocaine (or some other illegal addictive substance) now tries it and develops a self-harming habit. This is the opposite of 2) above. These people require a large, harmful quantity of illegal drugs to become satisfied. In other words, they are willing to undergo the self-harm for cocaine (and heroin, etc.), but not for the effects of alcohol or something else that is relatively inexpensive under our current regime.

For drug legalization to be a bad idea, the one harm-increasing force would have to dominate all the harm-reducing forces. I find this implausible. Don’t interpret this as a “This list is longer than that list, therefore…” argument. It’s possible in principle for the one harm to overwhelm all the benefits, even though it’s one item. I could arbitrarily express it as four items with some clever manipulation, or compress my list of benefits. We have to weight these things somehow, not simply count them. Still, I think drug legalization comes out ahead. The one “harm-increasing” force is almost surely small. There just aren’t that many people who 1) are willing to endure enormous amounts of self-harm and 2) are deterred significantly by weak legal sanctions. (Here is a more rigorous treatment of the problem, stated in terms of demand curves and total costs.)

Prohibition probably causes people to substitute some drugs in place of others, but it doesn’t alter their underlying willingness to undergo self-harm. If you look at evidence from alcohol and tobacco, it appears that the self-harm dominates the dollar price. No doubt this result generalizes to other addictive substances.  The goal of drug policy should be to reduce the social harms of drugs, not to reduce drug use *per se*. This goal can be achieved by allowing people to achieve their desired state of intoxication in the least harmful way possible. If we had a wider array of intoxicants (some of them almost entirely non-toxic) available to us, this would be a lot easier.

The fear is that light dabbling in these other kinds of drugs will inevitably lead to full-fledged addiction, with all the overdoses and other health problems. But this “try it once and you’re hooked” story is a myth. It doesn’t describe the vast majority of illegal drug use. Normal, well-adjusted people have nothing to worry about. It’s the impulsive people with self-control problems that we need to worry about, and these people are mostly already hurting themselves. Drugs don’t dominate the will and turn the former type of person into the latter. There is just an enormous amount to gain here and very little to lose. Legalizing drugs is the lowest of the low-hanging fruit. It's long past due that we pluck it already.