Would Universal Health-Care Coverage Actually Improve Health?
By Jim Manzi
There is a debate going on in the blogosphere between Ezra Klein, Arnold Kling, Karl Smith, Tim Carney, and others about, to put it crudely, whether health care really affects health that much. This is, in part, a proxy debate for whether it is worth it for the U.S. government to provide generous universal health-care financing for all of its citizens (or, I suppose, residents).
Either position can be caricatured. On one hand, no sane person would want to be without the advances of modern medicine. Recently, a little girl I know had scarlet fever. A century ago, this would very possibly have meant burying a small corpse; today, it implies a ten-day cycle of swallowing medicine at breakfast and dinner. There are few people on earth who have as much reason to be proud of how they spend their work week as pharmaceutical researchers.
On the other hand, the link from alternative methods of health-care finance, through the actual differences in provision of medical care these imply in the contemporary U.S., to the actual differences in health outcomes these treatment differences would cause, isn’t nearly so obvious. The net health effect of providing universal health-care coverage versus some alternative financing system is an empirical question, not a philosophy debate.
I’ve written a lot about why randomized experiments are so critical to understanding cause-and-effect relationships in social policy. In the case of health-care financing, the reason is that what system of health-care financing you have (high-quality “go to any doctor” plan; good HMO; catastrophic-only plan; VA; go to an emergency room because you are uninsured, etc.) is bound up with a myriad of other factors that influence health. A randomized experiment allows us to isolate the impact of the system of health-care financing.
To my knowledge, the only large-scale randomized experiment in the U.S. that has tested the actual effects on health of providing various kinds of health-care financing was the RAND Health Insurance Experiment (HIE). In this experiment, thousands of families were randomly assigned to one of five different health-insurance plans that ranged from something like a plan that provides free health care, to something like a pure catastrophic-only plan in which consumers pay out-of-pocket for day-to-day healthcare. The study tracked what exact health-care services each group used, and how their health varied over a period of 3–5 years.
Ezra Klein describes this experiment as “the best evidence we have,” and writes that it “suggests that health-care coverage does much more for the health of poorer people than it does for the health of well-compensated, highly educated people.” His statement is correct, but as a summary of the results of this experiment, seems to me to be radically incomplete. In fact, the experimenters wrote of the findings that “cost sharing reduced the use of nearly all health services,” but “the reduction in services induced by cost sharing had no adverse effect on participants’ health.” Think about that. Providing people coverage of their medical costs caused no average improvement in health.
Klein is correct that there appeared to be a net health benefit for the poorest participants, but this was for a tiny proportion of the population, and for a small subset of medical conditions. According to the study, “The poorest and sickest 6 percent of the sample at the start of the experiment had better outcomes under the free plan for 4 of the 30 conditions measured.” There are technical reasons why conclusions from such a experiment are not reliable for post hoc subgroups in the way that they are for average comparison of a test group versus a control group; but even if we were to accept this finding as valid, it’s not obvious to me that we would want to devise a health-care financing system for the United States around helping 6 percent of the population partially ameliorate about 10 percent of their potential health problems, as opposed to developing some specific supplementary programs for these issues, if they could be addressed feasibly.
Klein clearly has a very sophisticated take on the issue, and wrote in 2009 that health-care reform is not primarily about improving health, but in reducing how much we spend on it. As he put it, “The purpose of health reform, in other words, is to pay for health care — not to improve the health of the population.” Fair enough. But the real debate, then, would be about whether market forces or bureaucratic control would be better at reducing costs, not about which would be better at promoting health for the “poorest and sickest” or anybody else. It wouldn’t be about getting better health outcomes.
A single experiment like the RAND HIE is not definitive. Among other things: it finished in 1982, and we live in a different world; any such experiment requires replication; it might be that the important health effects take much longer than five years to materialize, and so on. But as an observer of the health-care debates, it always struck me as fascinating that the fact that the “best evidence we have” showed that providing health care coverage doesn’t actually improve average health wasn’t treated as more central.
Fascinating, but not surprising. In one social-policy topic after another, experts argue that some program will transform some area of public life, and solve persistent problems. They often have impressive theoretical arguments supported by complex empirical evidence. But what I believe randomized experiments have shown in many such areas — ranging from welfare to criminology to education — is that proposed policy interventions rarely work, and when they do, they tend to produce improvements that are very small as compared either to size of the problem or to the dreams of the advocates. This evidence is often ignored by those who have dedicated their lives to solving these problems, likely because it is so frustrating to almost everyone involved.
SOURCE . Note the corollary of the Rand findings: If people overall did not improve but the poorest did, then some other group did less well
My fingers and toes ached in the cold - until I took Viagra!
The pain first started whenever Anne Mawdsley was out in cold weather. ‘My fingers would turn red and felt like they were burning,’ she says. ‘It sounds like just a minor inconvenience, but I was in excruciating pain. I had to give up working as a PE teacher because being outdoors in cold weather was so difficult. I became a swimming teacher instead.’
However, the problem continued to worsen, and Anne ‘really struggled’ to look after her two sons, then both under two-and-a-half. ‘The pain seemed to reach a peak at night — my fingers would throb, and I’d be shattered because I couldn’t sleep.’
She then developed ulcers on her fingers; one finger even became gangrenous as a result. Anne’s doctor suggested the finger be amputated. ‘Although I was desperate, this sounded like medieval medicine. I was just horrified,’ says Anne, 68, of Alsager, Cheshire.
She managed to avoid this drastic solution, but for the past 30 years Anne has battled to find an effective treatment for her condition, which had also spread to her toes. And two years ago she discovered an unlikely solution — the impotence drug Viagra.
Like ten million Britons, Anne suffers from Raynaud’s syndrome, a disorder triggered by a sudden drop in temperature. The blood vessels in the fingers and toes contract, cutting off blood supply. It can also affect the tiny arteries in the nose, ears and tongue.
Typically, Raynaud’s causes the fingers or toes to turn white and numb. Then, as the blood flow returns, they turn blue and eventually red, accompanied by a burning sensation. Attacks can last from a few minutes to an hour.
Nine out of ten cases are in women, with most sufferers having their first attack before the age of 40. Although attacks peak in the cold winter months, symptoms can be triggered by everyday tasks such as taking food out of the freezer, air conditioning, or even stress — all of which cause blood vessels to contract.
There are two types of Raynaud’s. Primary Raynaud’s, which tends to run in families, is generally quite mild. Most patients can cope by wrapping up warm, although some develop painful weeping ulcers, which can become infected.
Secondary Raynaud’s is far more serious and painful, but about ten times less common. Indeed, it’s only in the past 20 years that doctors have discovered there is a difference between the two.
The secondary form of Raynaud’s, which Anne has, is usually caused by an auto-immune disease such as scleroderma, which causes a hardening of the skin, muscle and internal organs.Here, Raynaud’s is a symptom of the underlying disease. The secondary form is worse, as circulation is less likely to return to normal completely between attacks, so patients can be left in permanent pain.
When Anne appeared on a TV programme to highlight Raynaud’s and received more than 400 letters from people desperate for information, she set up the Raynaud’s & Scleroderma Association, which raises money for research and offers advice to patients.
Meanwhile her own condition worsened. She developed difficulties swallowing and had to have her oesophagus dilated to be able to do so properly.
Two years ago Anne was invited to take part in a trial at the Royal Free Hospital, led by Professor Denton, using the erectile dysfunction drug sildenafil — more commonly known as Viagra.
Viagra helps by increasing blood supply to the body’s extremities. ‘I had to smile when I was offered Viagra, but by that stage I was so desperate I would have tried anything,’ says Anne.
She took the tablets three times a day and immediately noticed improvements in her symptoms. ‘Although the numbness and pain in my fingers didn’t disappear completely, it was a lot less severe, and I can now use my hands more for things like typing,’ she says.
‘Luckily, I haven’t suffered any side-effects you can sometimes get with Viagra, such as dizziness or headaches — and I haven’t noticed any effect on my sex life either!’
The trial compared Viagra with a placebo and results show a benefit, explains Professor Denton. He presented the results at a scientific meeting, and a full paper will soon be published. ‘This is an off-label use of Viagra — meaning the drug is not licensed for this purpose,’ he adds. ‘Viagra would be reserved for treating patients with the most severe types of Raynaud’s and/or scleroderma who had already tried more conventional treatments — we’re not advocating it for everyone.’