Thinking Carefully About “Long COVID”

Several months ago, a newspaper columnist reached out to me after noticing a few of my tweets on a condition — “Long COVID” — then, as now, in the news.  I’m a pulmonary and critical care physician, and had tweeted that researchers should show greater caution in making assertions about the still mysterious syndrome; the journalist asked whether I thought that medical professionals more broadly were somehow skeptical of the condition.  “I’m asking as much as a person as a journalist,” they messaged, “because I’m more terrified of this syndrome than I am of death…”

They are not the only one.  Media stories about “Long COVID,” and the patients who call themselves “COVID long-haulers,” have been appearing at an accelerating pace, and what they describe is frightening.  Articles by one of the most respected writers on the pandemic, Ed Yong at the Atlantic, have been particularly influential.  In “Long-Haulers Are Redefining COVID-19,” Yong describes a disease that strikes even those with “mild” COVID-19 — that is to say, those who don’t need hospitalization or oxygen, much less a ventilator, and who recover at home without medical intervention.  Or, rather, in this case, who don’t seem to recover.  One such individual, he notes, described some five months of “extreme fatigue, bulging veins, excessive bruising, an erratic heartbeat, short-term memory loss, gynecological problems, sensitivity to light and sounds, and brain fog.”  For some, Yong noted, “months of illness could turn into years of disability.”  

But can, indeed, a “mild” Sars-Cov-2 infection cause such a debilitating (and potentially lifelong), mysterious, multi-organ syndrome?  Can it, as other news reports have suggested, lead to severe psychosis or a dementia-like condition months after a mild and otherwise resolved bout?  To even begin to answer these questions, we have to recognize that what is being described as “long-COVID” often conflates several distinct entities that are worth differentiating, even if they sometimes overlap.  As important, we need greater acknowledgement that the medical harm of this pandemic goes beyond the direct damage inflicted by the SARS-CoV-2 virus itself.

“Long COVID” has no universal definition, but is often used to describe those whose symptoms last more than a few weeks or months after a bout with COVID-19.  That many individuals have such protracted symptoms after this infection is hardly surprising.  After all, critical illness of any cause can be devastating.  Almost everyone who dies of COVID-19 develops a condition called “acute respiratory distress syndrome” (ARDS), a particularly severe form of pneumonia involving severe inflammation of both lungs that often requires mechanical ventilation. Many studies have shown that ARDS can have long-term effects on the body: one 2003 study found that many survivors of ARDS, at a year out from discharge from the ICU, had significant physical impairment; lung function improved over time but remained abnormal for some.  Meanwhile, as the lungs fail in ARDS, other organs often go down with it, including the kidneys and the heart.  In other words, while many with severe COVID-19 make good recoveries, other survivors of this (and other) critical illnesses can require specialized rehabilitation or care for months or even years.  There is no mystery or surprise here.

At the same time, however, some people have also had protracted symptoms following less severe COVID-19.  An Italian study showed that most patients still had at least one symptom, like fatigue or shortness of breath, two months out from a hospitalization for COVID-19. A more recent Lancet study found that six months following hospitalization for COVID-19, many patients had persistent symptoms, including fatigue and anxiety, and some (particularly those with more severe acute cases) had reductions in lung function.  Again, however, this is not qualitatively specific to COVID-19: recovery from pneumonia from bacteria or other respiratory viruses is often slow. According to one 1997 study, many individuals with pneumonia have symptoms such as cough, fatigue, and shortness of breath that can persist for three months (or longer) after onset.  And even recovery from an upper respiratory tract (URI) infection — a cold — can take a while.  A protracted “post-viral” cough following a cold is a common reason for a referral to a pulmonologist.  The experience of an acute respiratory illness will be different from person to person, and there is no “rule” on when exactly a patient’s respiratory symptoms, fatigue, and general “sick feeling” should resolve by. 

It is also true, however, that we have also seen rare cases of permanent organ damage inflicted by SARS-CoV-2 — including instances of severe myocarditis, inflammation of the heart muscle leading to heart failure and a condition called cardiomyopathy, and strokes — even among those who did not have severe pneumonia, or even any evident respiratory disease.  These can also (rarely) be caused by infections from other respiratory viruses (viruses are a leading cause of acute myocarditis in general).  But in any event, these are specific, diagnosable complications affecting specific organs, not a multi-systemic medical mystery. And outside the critically-ill population, who — as noted, can suffer basically every form of organ failure — they are very uncommon.

Yet if these ailments are sometimes included in reports of “long COVID” in the media, most narratives evoke something entirely different:  a debilitating syndrome seemingly affecting multiple organ systems for months on end — and perhaps indefinitely — but absent any specific diagnosis such as cardiomyopathy or stroke.  As noted, these individuals are often described as having what would be characterized as a mild, flu-like COVID-19 illness, and to have not been hospitalized.  Their plight is what the columnist who contacted me, and many others I’ve spoken to, think of when “Long Covid” is discussed — and it’s the focus of reporting like that of Yong’s.

What are we to make of this entity?  

Reasons to Slow Down on the Long-COVID Narrative

Media reports exploring this type of Long COVID have been appearing at a steady clip.  The symptoms of this condition are often, if not mostly, non-respiratory in nature, and the demographics of those affected are basically the opposite of those most at risk from dying from COVID in some cohorts.  For instance, whereas severe COVID-19 disproportionately strikes Black, Hispanic, low-income, and older individuals, “long-haulers” appear to have distinct demographics: a recent preprint study, for instance, identified a long-COVID cohort that is predominantly white, high-income, and non-elderly.  The headline of a story in Buzzfeed in August captures this demographic divergence.  “COVID Is Making Younger, Healthy People Debilitatingly Sick For Months. Now They’re Fighting for Recognition.” More than a hundred of the “long-haulers” described to that reporter a complex of unremitting symptoms suggestive of a mostly-non-respiratory, multi-organ chronic process: palpitations, headaches, severe fatigue, difficulty sleeping, hair loss, and, again, brain fog. 

Some news reports, meanwhile, have described even more alarming symptoms.  In October, a story in the New York Times described a dementia-like illness following a mild infection:  “It’s becoming known as Covid brain fog: troubling cognitive symptoms that can include memory loss, confusion, difficulty focusing, dizziness and grasping for everyday words.” And last month, another Times article went further still, asserting a linkage between mild coronavirus infection and “severe psychotic symptoms.”  One individual described in the article had a minor coronavirus infection in the spring that had completely resolved.  But then, “months later, she heard a voice that first told her to kill herself and then told her to kill her children.” Such stories, no doubt, chill readers to the bone.  

But, for several reasons, such reporting needs to be more cautious. 

First, a cause-and-effect relationship is typically unestablished in these articles.  The Times article contending that mild and resolved COVID-19 infections can lead to extreme psychosis months later left out some important context.  According to one international study, the incidence of psychotic disorders is around 27 per 100,000 persons per year, which would suggest that in the US, there are tens of thousands of new diagnoses of psychosis every year.  In 2020, a solid proportion of those new diagnoses will have occurred in individuals with a prior coronavirus infection.  Obviously, although the temporal link will no doubt feel powerfully suggestive to patients and their doctors, this does not establish causality.

Another reason to question the causal link between the virus and some “Long COVID” symptoms stems from the fact that some, and perhaps many labelled with long COVID appear to never have been infected with the SARS-CoV-2 virus.  For instance, in his August Atlantic article, Yong cites a survey of COVID “long-haulers” that found that some two-thirds of these individuals had negative coronavirus antibody tests, which are blood tests that reveal prior infection.  Meanwhile, the aforementioned study published on a pre-print server, organized by a group of Long COVID patients named Body Politic that recruited participants from online long COVID support groups, similarly found that some two-thirds of the long-hauler study participants who had undergone serological testing reported negative results.

Now it’s no doubt true that while serological tests are reported as highly sensitive and specific, they are imperfect; there are both false positives and false negatives.  Hence, some of those classified as negative may have indeed a prior infection.  Moreover, there is growing evidence that antibodies can wane over time — to an extent.  For instance, the aforementioned Lancet study that examined long-term symptoms among individuals hospitalized with documented COVID-19 found that more than 90% of those tested at baseline still had positive IgG antibodies (the long-lasting type) six-months after infection.  A CDC study of healthcare workers, on the other hand, found that among a group of healthcare workers who had been screened for antibodies and found positive, 72% had positive antibodies around two months later, although the proportion was much higher (98%) among the subgroup with previous confirmed COVID-19.  Another preprint study, published by researchers from the Rockefeller University, examined the performance of four commonly used antibody tests for outpatients with documented SARS-CoV-2 infections.  About a month after a positive COVID-19 test, antibodies were positive in 95-100% individuals with three of four tests, and 85% with one of the four tests.  After 81 days (or more), sensitivity remained >90% for three out of four tests, but worsened to 71% for one test. 

So again, these tests are not perfect, but they do appear to remain positive for a majority of individuals with documented infections for months in most studies.  Hence, even accounting for antibody waning, it is highly improbable that 100% of a large group of seronegative individuals without a prior diagnosed infection are false negatives; some — and it’s hard to know how many — will be true negatives.  But why does this matter?  Well, for one thing, it makes clear that it is possible for at least some individuals to incorrectly attribute chronic symptoms to SARS-COV-2.  That’s hardly surprising, but there is more to be said of the issue. 

Consider that the Body Politic study of long-haulers not only reported that most individuals who had antibody testing were seronegative, but also that there was virtually no difference in symptoms whatsoever between those with a diagnosed SARS-COV-2 infection and those who were seronegative.  A finding of no association between a reasonably reliable serological marker of a prior acute infection and a particular complex of chronic symptoms has one rather likely explanation: that the acute infection may not be the predominant driver of the chronic symptoms in that cohort.

But if true, how could we explain the fact that such individuals might perceive a direct causal link? Quite easily: our ability, as individuals, to link our particular chronic symptoms with a past infection from a particular microbial agent — in this case, SARS-CoV-2 — is fallible.  After all, the symptoms reported as distinct to “Long COVID” are nonspecific, and could stem from any number of factors and diseases.  Before COVID-19, the majority of Americans, for instance, had one or more unpleasant gastrointestinal symptoms.  More than one in ten of us felt “very tired or exhausted” every or most days. Hair loss — which has been noted in several articles about long-COVID — can be caused by multiple medical issues and stressors.  Headache has been described as an “almost universal human experience”, while “chronic daily headaches” affect 4% of adults, or millions of people a year.  “Brain fog” is not rare, and certainly not specific to any particular condition.  For these reasons, it’s important that “long COVID” studies have adequate controls of some sort, which to date has typically not been the case.  But the bigger point is that physical suffering is, sadly, very common in our society.  That is the case today, but was also the case before the outbreak.  Many people develop new physical symptoms (which often come in groups) each year — and this past year will be no exception.  But even beyond the direct effects of the SARS-CoV-2 virus, there is reason to think that 2020-21 will be even worse than the typical year in this respect.  

The Role of Anguish

This brings me to the elephant in the room.  Could mental distress, anguish, and illness be one contributing factor behind new physical suffering for some individuals this past year?  It’s a dicey question to ask — the invocation of depression and anxiety as causes of physical symptoms is sometimes seen as a form of “medical gaslighting.”  It is, however, nothing of the sort.  There is no question that mental suffering can produce physical suffering that is often undistinguishable from any other.  Those who have had a severe panic attack know it can cause chest pain and shortness of breath — indeed, those are among the cardinal signs.  Such symptoms as weight change, sleeping problems, “psychomotor retardation”, persistent fatigue, and concentration problems (what one might call “brain fog”) are actual DSM-V criteria for major depression.  The physical manifestations of mental suffering can also be chronic and insidious.  A study in the New England Journal found that across multiple continents, about half of those with depression have unexplained physical symptoms, and for more than half, that physical symptoms actually predominated over the mental ones.  For some, in other words, the experience of psychological suffering may be mostly experienced physically.

And on that note, let’s acknowledge that this is a time of incredible trauma, sorrow, and hardship.  The loved ones of more than 400,000 Americans are in mourning.  Tens of millions have lost their jobs.  This has been a period of prolonged social isolation with no obvious parallel in history.  One study, published in early September, suggested that the proportion of Americans suffering from symptoms of depression has skyrocketed, from 8.5% in 2018 to 27.8% 2020.  Whatever the long-term effects of COVID-19 may or may not be for those with mild infections — and certainly there is much to still be learned — we should expect a surge in both mental anguish and physical suffering that, while connected to the epidemic, will not always be directly connected to viral infection itself.  

Needless to say, all such symptoms — all of this suffering — is in every sense real.  There will be, as is often the case, lack of clarity about the distinct cause of suffering in each individual; often, there may be multiple causes, stretching from the virologic to the psychosocial.  Every such patient of course deserves careful, empathetic evaluation and appropriate treatment and referrals.  And more broadly, policies to stem psychosocial suffering stemming from the pandemic and the recession and social isolation it has generated are urgently required. 

What we know is bad enough

But fear-instilling assertions about illness that go beyond the evidence at hand are never helpful: we should not be positing that a mild COVID-19 infection can have frightening chronic sequelae like severe psychosis or profound cognitive impairment, or lead to a potentially lifelong, debilitating and mysterious syndrome, without firm scientific evidence.  Unfounded linkages can also be medically harmful, leading to the provision of unproven and hazardous medical therapies, as we’ve seen in the case of patients with chronic symptoms and a prior diagnosis of Lyme disease.  Some of these patients have suffered serious consequences from long-term antibiotic treatments, and others have been the victim of unproven alternative therapies ranging from colloidal silver to stem cell transplantation by unscrupulous providers.  It is far from unlikely that we could see something similar for those labelled as having “long COVID,” again to these patients’ detriment.

Make no mistake, what we know about COVID-19 today is more than enough to justify doing what we can to quash it: it is the respiratory pandemic of a century.  And of course, rigorous research on its long-term effects, including among those with mild disease, is no doubt needed. At the same time, we need to start thinking more critically — and speaking more cautiously — about long-COVID.  

Note: A shorter, revised version of this post was published in STAT on March 22, 2021.

Baffler: “Bill of Health”

I have an article in the new issue of the Baffler about what the COVID-19 pandemic reveals about the unjust and dysfunctional way we finance our nation’s hospitals — and why we need to change it. I provide a glimpse of what the COVID-19 pandemic looked like inside our hospital’s wall, a brief history of hospital financing from the Middle Ages to the invention of the DRGs in the 1970s, and why the “inverse care law” is so active in America.

New Article: “US law enforcement crowd control tactics at anti-racism protests: a public health threat”

We had a correspondence piece in The Lancet citing tactics used by US law enforcement agencies as a public health threat on Friday. In brief:

-Rubber bullets and related projectiles (bean bag rounds, foam batons, sponge rounds) can maim and kill. We highlight 12 severe injuries, as reported in the media, from these projectiles in the last few days of May. We call for a ban on these projectiles.

-We note dangers of chemical irritant use (tear gas, pepper spray), which cause coughing and sneezing and mask removal and may exacerbate viral spread. We join the American Thoracic Society in calling for a moratorium on tear gas.

-Jails are coronavirus incubators. Mass arrests will worsen the COVID-19 pandemic and must be avoided.

-We call for a reallocation of some of the >$100 billion spent annually on policing on educational, social, and health programs.



New study: “18.2 Million Individuals at Increased Risk of Severe COVID-19 Illness Are Un- or Underinsured”

We had a study published last week in the Journal of General Internal Medicine, which found that some 18 million people who are at increased risk of severe COVID-19, whether because of age or chronic illness, are uninsured or underinsured. Not surprisingly, these individuals are disproportionately people of color and those with low incomes. It was covered in Newsweek, Modern Healthcare, Marketwatch, and some other outlets.

New Paper: “COVID-19 and US Health Financing: Perils and Possibilities”

Along with David Himmelstein and Steffie Woolhandler, I have a new paper out today in the International Journal of Health Services exploring issues of health coverage, access, and financing related to the COVID-19 pandemic. It outlines the legislation and proposals meant to address these issues — what each would accomplish, and how they might fall short.

It’s available here at the PNHP website.

Health Affairs Blog: “Medicare for All: If Not Now, When?”

Medicare for All has significant advantages, many agree — but given the enormous political obstacles, shouldn’t we be focused on more moderate reforms? I respond to this critique in today’s Health Affairs blog.

One data point worth noting — although Senator Bernie Sanders often notes that there are 87 million people who are uninsured or underinsured, that figure excludes children and seniors. The actual overall number is greater than 100 million — or nearly 1/3 Americans — with deficient helath coverage.

Doctors “Prescribe” Medicare for All

Our open-letter—signed by more than 2,000 physicians—was published today as a full-page ad in the New York Times.

Among the signatories of the letter, which was organized by PNHP, includes leading figures in American medicine, including founder of Partners in Health Dr. Paul Farmer, developer of the defibrillator Dr. Bernard Lown, former editor-in-chief of the New England Journal of Medicine Dr. Marcia Angell, former NYC Health Commissioner Dr. Mary Bassett, and many more …

In conjunction with yesterday’s announcement that the American College of Physicians, the largest medical specialty society in the country, had endorsed Medicare-for-All, it is becoming increasingly clear that there has been a turn of the tides in the American medical profession on the single-payer question.

Jonathan Cohn describes these developments in an article in the Huffington Post.

Link to all the signatories:

New Study in Health Affairs: “The Effect Of Veterans Health Administration Coverage On Cost-Related Medication Nonadherence”

Our new research was published in Health Affairs this week. Using national data, we found that patients with VA coverage – which provides medications with no or low copays to veterans – were less likely than those with other forms of insurance to go without needed medications, especially among those with serious chronic diseases. VA coverage also reduced or attenuated racial and income-based disparities in prescription drug access.

We contend that the VA pharmacy benefit should be considered as a model to address the crisis in prescription drug affordability.

The study was covered in STAT:…/veterans-drugs-cost-patient-ad…/…

Here’s the press release:…/pfan-pwv010320.php

And here’s a link to the study itself:…/a…/10.1377/hlthaff.2019.00481

New Study: The Effect of Large-scale Health Coverage Expansions in Wealthy Nations on Society-Wide Healthcare Utilization

Our third paper examining how universal coverage affects the society-wide use of healthcare — a question with big implications for predicting the cost of Medicare-for-All — was just published in the Journal of General Internal Medicine. Co-authored with Steffie Woolhandler and David Himmelstein, this is a review of 13 universal coverage expansions taking place in 11 nations over 8 decades, beginning with the 1938 New Zealand Social Security Act and extending to the 2014 implementation of the ACA. We find that these expansions led to modest, and in some cases no, society-wide increase in utilization, even as they redirected care to those who needed it. Medicare for All is likely more affordable than previously predicted.

New Study: Effects of the 1966 Medicare/Medicaid and the 2014 Affordable Care Act Coverage Expansions on Physician Use

Our new study was published yesterday online in the American Journal of Public Health.  We analyzed the effects of the 1966 Medicare/Medicaid and the 2014 Affordable Care Act coverage expansions on the utilization of physician services — both visits and procedures.  We found that although these coverage expansions redirected care to the newly covered, they did not increase overall society-wide use.   Considered together with our study of how these expansions affected hospital utilization (together with other work on the utilization effects of Canadian single-payer, the NHS, and pre-ACA Medicaid expansions), this research suggests that estimates of the cost of coverage expansions may often be in error.

New Study: Utilization Effects of the 1966 and 2014 Coverage Expansions

Last week, colleagues and I published a study in the Annals of Internal Medicine based on analyses of large health surveys conducted around the time of the implementation of Medicare/Medicaid in 1966 and the Affordable Care Act in 2014.  Overall, we demonstrated that these expansions led to shifts in hospital utilization towards newly covered populations, but no net overall increase from either coverage expansion—a finding with important ramifications for today’s debate about the cost of universal coverage.

We published an op-ed about our work in the Boston Globe, and the study was additionally covered by Reuters,  Morning Consult, and other outlets.

Also this kind shout-out from Rep. Pramila Jayapal!


We’re Failing Young People with Diabetes

Our study, comparing hospitalization rates for diabetic ketoacidosis in the US to Manitoba, Canada, was just published in the Journal of General Internal Medicine.  I have an op-ed up today on the study in the Washington Post.

Diabetic ketoacidosis is a dangerous complication of diabetes that is typically preventable with regular use of insulin.

Among teenagers, we found that the ketoacidosis hospitalization rate was slightly higher in the US compared to Canada. However, as teenagers became young adults, the hospitalization rate soared by 90% in the US, but only rose 23% in Canada. Differences in our health systems – particularly the disruptions in coverage that are common when adolescents become young adults, could help explain this difference.

Andrea Christopher was the co-first author; other co-authors include Alan Katz, Dan Chateau, Chelsey McDougall, David Bor, David Himmelstein, Steffie Woolhandler, and Danny McCormick.

Screen Shot 2019-04-23 at 6.35.52 AM

The Nation: “We Don’t Need Private Health Insurance”

Earlier this month, Sarah Kliff published an informative article at Vox on the ways that private health insurance has persevered in nations with universal coverage.  On Monday, I had an article in The Nation that made something of a counter-argument: leaving a significant role for private insurance requires that we poke holes in the single-payer public plan, which helps nobody but the corporate insurers.

Blog: Physician Pay Under Single-Payer

A question that comes up in discussions of healthcare reform—and the transition to single-payer—is the potential savings via reductions in compensation for physicians’ labor.  Some assert that the transition to single-payer would, or should, involve historic reductions in pay.  To have an informed discussion, however, we have to first know how much we currently spend on physician salaries.

There are a few different ways to estimate this.  According to CMS’s National Health Expenditures (NHE) accounts, spending on “physician and clinical services” was $664.9 billion in 2016, or about 20% of our health spending.  20% is also the figure that health economist Uwe Reinhardt used a while back, presumably using CMS’ figure.   According to CMS, that figure includes spending on physician offices and outpatient care centers, but also on independent medical and diagnostic laboratories, which muddies the waters.  At the same time, it excludes salaried doctors at hospitals or nursing homes.  But importantly, according to Reinhardt, it reflects expenditures on offices and clinics (including practice overhead), not take-home income.  Reinhardt states that physician income is about half of this spending, which would be 10% of NHE.  For 2016, that would be roughly $330 billion.

Clearly there are several assumptions in that estimate that might make it either too high or too low.  An alternative approach is to multiply the number of practicing doctors by their pay.  According to the Bureau of Labor Statistics, there were 713,800 physician jobs in 2016, while median pay was “equal to or greater than $208,000 per year.”  Hence, this pay figure is presumably an underestimate.  Additionally, mean pay could be higher than median pay depending on the distribution of salaries.  Putting that aside for a moment, multiplying 713,800 by $208,000 gives us $148 billion in physician salaries, or roughly around 5% of 2016 NHE, half that of Reinhardt’s figure.  For the reasons stated, however, we should consider this an underestimate.

Dean Baker, in a piece in Politico, takes this same approach, using somewhat higher numbers.  He notes that there are more than 900,000 doctors, linking to a figure that puts the number of doctors at 1,045,910 in 2013.  However, that sources also notes that there were 148,000 inactive physicians, which would put the number of active physicians slightly shy of 900,000.  Although higher than the BLS figure, that’s similar to a figure from the Kaiser Family Foundation, which reports that there were 968,743 “professionally active” physicians in 2018.  Baker assumes that doctors are paid around $250,000 a year, on average, based on a figure from Medscape’s 2016 Physician Compensation Report.  So, if there are 900,000 doctors paid at $250,000 a year, we have a figure of $225 billion, or a bit less than 7% of 2016 NHE.  That figure is about halfway between the NHE/Reinhardt estimate and the estimate using BLS figures.  (Note: This is based on Baker’s figures, which for income is from 2016.  However, if we use the 2018 KFF figure, 2018 Medscape salary figure, and 2018 NHE, the story doesn’t change much – salaries come to a bit less than 8% of NHE).  

In sum, then, it would appear that physician salaries account for somewhere between 5 – 10 % of healthcare spending.  Let’s assume it is Reinhardt’s 10%, so as to err on the side of greater potential savings via reduced pay.  As he notes, that would mean that if we were to dramatically slash physician pay in a historically unprecedented fashion — say by 20% — US healthcare spending would fall by a grand total of 2%.  Reinhardt argued that in return for that 2% reduction in healthcare spending we would have a “wholly demoralized medical profession,” and so considered this approach a “poor strategy.”

Others may disagree.  Yet regardless of one’s opinion on what physician pay should be, these numbers demonstrate that it is by no means necessary to reduce physician reimbursement, much less slash it, to make single-payer affordable.  After all, even a historic reduction in physician salaries would produce only a 2% reduction in health spending.  Such a pay cut would presumably coincide with a modest increase in utilization under single-payer, which would mean more work for less pay.  It’s hard to see how this wouldn’t alienate the medical profession and turn them against single-payer, possibly dooming its prospects.

It is probably for this reason that major transitions to public universal healthcare systems in history—i.e. US Medicare, the Canadian universal healthcare system, and the United Kingdom’s National Health Service—did not reduce compensation for healthcare workers’ labor.1  We should consider the wisdom of that approach today as we get into the nitty gritty of designing the American single-payer system.2,3,4



1. As an article in the Independent notes, Nye Bevan “was pragmatic enough to know that he could not run the NHS without consultants, doctors and nurses.”  He made concessions to the doctors and increased the nurses’ pay.

2. As a side-note, reducing economic inequality absolutely must be a priority. To accomplish that, however, I would argue that we should pursue progressive taxes—including on unearned income from wealth—as opposed to specifically targeting the wages of well-paid healthcare workers, particularly given that pursuing the latter could potentially scuttle the passage of single-payer healthcare, a reform that itself would do a great deal to reduce inequality.

3. Keep in mind I am referring to take home reimbursement, not overall reimbursement. By reducing provider-side administrative costs, which a single-payer system will accomplish, physician fees can fall somewhat without reducing payment for labor.  After all, some fee reduction will be the way that provider-side administrative savings are realized.  Matt Bruenig argues that the provider rate cuts assumed in the Mercatus Center single-payer report could probably be wholly accounted for by administrative savings.  I’m also not referring to for-profit physician-owned hospitals or other for-profit healthcare delivery businesses, which should not be allowed in the system—I’m speaking about compensation for labor.  Finally, there should certainly be attenuation in pay disparities, but basically everybody already agrees on that.  After all, simply moving to a single rates system will mean equalizing pay for providers who care for richer and poorer patient populations.

4. Obviously, reimbursement will not (and practically cannot) stay exactly the same—I’m speaking about avoiding large changes. Making healthcare professionals education tuition-free can help ease the transition for doctors who do less well.