Cause evidently I have nothing better to do, I answered my own question.
Here’s a chart I made of HPV vaccination rates in adolescent females by state political views. The Y-axis is the percentage of adolescent girls who have had at least one dose of the HPV vaccine. The X-axis is the state’s conservative advantage, defined by Gallup as, “The difference between the percentage of state residents describing their political views as conservative and the percentage describing their political views as liberal”. I added a linear trendline, and the R2.
New data on vaccination rates among 13-17-year-olds have been released by the CDC. In 2014, more than 87% of adolescents had received at least one dose of Tdap. More than 79% had received at least one dose of the meningococcal vaccine. But only 60% of adolescent girls had received a dose of the HPV vaccine, and only 42% of boys.
Granted, these numbers are up from 2013, when only 57% of girls and 34% of boys had received a dose of HPV vaccine. But there’s still a lot of room for improvement. There are also real geographic differences. Here’s the percentage of adolescent females having received at least one dose of the vaccine by state:
Is it just me, or do HPV vaccination rates line up pretty well along blue state/red state lines?
I’ve long been concerned about implementing public health policy without really studying it. Sometimes, it’s because I worry the policy won’t work. Sometimes, it’s because I think the policy will cost a lot of money, and it won’t be worth the results. And – sometimes – it’s because I worry that the policy might backfire. A good example of this last concern was illustrated in a recent study in the American Journal of Public Health. “The Unintended Consequences of Changes in Beverage Options and the Removal of Bottled Water on a University Campus“
Go read about all of this in my latest post over at the AcademyHealth blog!
The following originally appeared on The Upshot (copyright 2015, The New York Times Company).
In the last few years, I’ve watched a continuing battle among my friends about which is worse for you: artificial sweeteners or sugar. Unless you want to forgo all beverages that are sweet, you’re going to run into one of these. Rather than rely on anecdote or myth, we can inform this debate with research.
The available evidence points to the fact that there appears to be a correlation between sugar consumption and health problems; none can be detected with artificial sweeteners.
Let’s start with artificial sweeteners. These have, for decades, been attacked as harmful chemicals. But everything is a “chemical,” and not all of them are bad for us. One of the oldest artificial sweeteners is saccharin. Starting in the 1980s, Congress mandated that any product containing it beaccompanied by the following: “Use of this product may be hazardous to your health. This product contains saccharin, which has been determined to cause cancer in laboratory animals.”
But what was the basis for this decision? A review article published in The Annals of Oncology in 2004 noted that more than 50 studies had been published looking at saccharin in rats. Twenty of these were “one generation” studies, meaning that they did not look at the rats’ offspring. Inonly one of those studies did huge amounts of saccharin produce cancer, and it was in a type of rat that is frequently infected with a bladder parasite that would leave it susceptible to saccharin-induced bladder cancer.
But “two-generation studies,” in which rats were fed lots of saccharin and their offspring were, too, found that bladder cancer was significantly more common in second-generation rats. That prompted many countries to act.
There was a problem, though. This link has never been confirmed in humans. Moreover, it turns out that some rats are just more likely to get bladder cancer. Feed them large amounts of vitamin C, and they get bladder cancer. Studies in humans in Britain, Denmark, Canada and in theUnited States could find no association between saccharin consumption and bladder cancer once they accounted for cigarette smoking (which does cause it).
Based on these newer studies, saccharin was removed from the carcinogen list in 2000. But by that time, opinions were set. It did little to make anyone feel safe.
Other artificial sweeteners haven’t fared any better. Aspartame was introduced in the United States around the time that saccharin began taking a beating. The initial studies showed that aspartame didn’t cause cancer in animals, so it was deemed safer than saccharin. But in 1996, a study was published in The Journal of Neuropathology and Experimental Neurology titled “Increasing Brain Tumor Rates: Is There a Link to Aspartame?”
Most people ignored the question mark. Instead, they noted that the paper stated that (1) brain cancer had become more common from 1975 to 1992 and (2) that more people had started consuming aspartame recently.
There were any number of problems with this logic. Most of the increase in cancer was in people 70 years and older, who were not the main consumers of aspartame. And because aspartame was approved in 1981, blaming it for a rise in tumors in the 1970s seems impossible. Finally, much more comprehensive studies couldn’t find links. These included a case-control study from The Journal of the National Cancer Institute of children and a cohort study of more than 450,000 adults in Cancer Epidemiology Biomarkers and Prevention.
Some people still point to later rat studies with aspartame as concerning, but these are highly contested. More important, as we’ve seen from saccharin, there are also big differences between rats and humans.
A 1998 randomized controlled trial could detect no neuropsychologic, neurophysiologic or behavioral effects caused by aspartame. Even a dose at 10 times the normal consumption had no effect on children with attention deficit disorder. A safety review from 2007, published in Critical Reviews in Toxicology, found that aspartame had been studied extensively and that the evidence showed that it was safe.
It is true that people with phenylketonuria, a rare genetic disorder, need to limit their consumption of aspartame, since phenylalanine is one of its components. But for most people, aspartame isn’t a concern, even outside of cancer. It’s also true that some of the sugar alcohol sweeteners, like sorbitol or mannitol, can have a laxative effect or cause bloating when eaten in large amounts by some people. In normal use by most people, though, all of the approved artificial sweeteners are safe.
But what about sugar? We should acknowledge that when I, and many others, address sugar in contexts like these, we are talking about added sugars, not the naturally occurring sugars or carbohydrates you find in things like fruit. Those are, for the most part, not the problem. Added sugars are.
The Centers for Disease Control and Prevention reports that children are consuming between 282 calories (for girls) and 362 calories (for boys) of added sugars per day on average. This means that more than 15 percent of their dietary caloric intake is from added sugars. Adults are doing slightly better, but not by much. This consumption isn’t distributed equally, however. For instance, about half of people consume no sweetened drinks at all. The next 25 percent consume about 200 calories per day from sugar drinks. The top 5 percent of people, though, consume more than 560 calories a day, or more than four 12-ounce cans of soda.
Epidemiologic studies have found that even after controlling for other factors, one’s intake of added sugars is associated with the development of type 2 diabetes, with a 1.1 percent increase in prevalence for each can of sugar-sweetened soda. A study following people for an average of more than 14 years published last year in JAMA Internal Medicine found that those in the highest quintile of added sugar consumption had more than twice the risk of dying from cardiovascular disease than those in the lowest quintile, even after controlling for many other factors.
The accompanying editorial noted that the increased risk of death began once a person consumed the equivalent of one 20-ounce Mountain Dew in a 2,000-calorie diet, and reached more than a fourfold increase if people consumed more than one-third of their diet in added sugars.
It should come as no surprise that the intake of added sugars is significantly associated with body weight. A systematic review and meta-analysis of randomized controlled trials, published in BMJ 2012, found that sugar intake increased both fat and overall weight. Another meta-analysis of randomized controlled trials, published in The American Journal of Clinical Nutrition in 2013, found that sugar-sweetened beverages alone cause body weight to go up in adults. In comparison, ameta-analysis of randomized controlled trials of artificial or low-calorie sweeteners published last year in the same journal found that their use led to lower body weight and less overall fat.
When I argue these facts with my friends, they want to know if I put my money where my mouth is. I do. My wife and I limit our children’s consumption of soda to around four to five times a week. When we let them have soda, it’s almost always caffeine-free, because we want them to sleep. It’s also almost always sugar-free. There’s a potential, and probably real, harm from consuming added sugars; there are most likely none from artificial sweeteners.
Harold Pollack, Timothy Jost, and I have a piece in The American Prospect about why we need Medicaid and how we should improve it.
We discuss an important NBER paper by Amy Finkelstein and her colleagues that tried to measure how much Medicaid is worth to those who receive it. The authors used data from the Oregon Health Insurance Experiment. The headline findings were that
- Uninsured people who get Medicaid only gained from 20 to 40 cents in value from each dollar spent by the government.
- A principal reason why the benefit of getting insured was so small is that when uninsured people received care, they typically paid only 20 cents on the dollar for those services. Safety-net providers, state or local government, friends, relatives, or someone else absorbed the remaining costs.
- Because a large fraction of Medicaid expenditures financed care that recipients would have received anyway (for example, by leaving bad debt at hospitals), it is unclear whether recipients themselves would have been willing to pay the full costs of Medicaid.
Finkelstein and her colleagues were careful not to draw normative conclusions from these findings. But some Medicaid critics have argued, first, that Medicaid is an inefficient way to benefit the poor. If a Medicaid dollar results in only 20 cents in benefit to a previously uninsured person, wouldn’t it be more efficient to simply give that person a dollar? And, second, Medicaid is actually a subsidy for people other than those it ostensibly helps.
We see matters differently. One important reason why the value of Medicaid appears to be so low is that Finkelstein put a much lower value on the health of Medicaid recipients than is typically used in valuations of the health of other Americans. We also argue that in many cases, we should not be troubled that Medicaid payments are going to third parties who are, after all, providing care to Medicaid recipients.
Please read the whole thing.
In Austin’s and my ongoing crusade to restore researchers’ access to substance-use data from Medicare and Medicaid, we’ve pinned our hopes on the Substance Abuse and Mental Health Services Agency (SAMHSA). A modest change to the agency’s regulations is all it would take to assure that the researchers who study addiction, Hep C, and HIV-AIDS, among many other conditions, get the data they need to improve treatment options and save lives.
But there’s another potential solution. Congress could fix the problem itself, without SAMHSA’s involvement. The approach holds some appeal. It would bypass the bureaucratic dithering that seems to be holding SAMHSA up. As important, it would also prevent the agency from pulling the same stunt in the future.
It wouldn’t take much to fix the problem. I’ve pulled together some statutory language that I think would do the trick. (Drop me a line if I’m overlooking something. Comments on this post are open for one week.)
Restoring Research Access to Medicare and Medicaid Data
(a) The Secretary of Health and Human Services shall be considered a “program director,” not a “third party payer,” within the meaning of 42 C.F.R. Part 2 for purposes of disclosing patient identifying information to qualified researchers.
(b) The Secretary shall, by January 1, 2016, restore research access to patient identifying information held by the Medicare and Medicaid programs, subject to privacy restrictions in 42 C.F.R. Part 2.
Now, Congress won’t adopt this draft language as a stand-alone law: as important as it is to share unbiased Medicare and Medicaid data, there’s not a big enough constituency pushing for the reversal of SAMHSA’s decision.
But if the language could be inserted into a bigger bill, we might be cooking with gas. Senator Tim Murphy, for example, has proposed the Helping Families in Mental Health Crisis Act, which includes a provision that would allow accountable care organizations and health information exchanges to freely share substance-use data to improve the quality of care. The language I’ve proposed would be a natural fit for the act.
In the current political climate, I’ll admit that I’m not optimistic about a congressional fix. But restoring access to critical data isn’t a partisan issue; indeed, it shouldn’t even be controversial. Maybe it’s too soon to count Congress out.
Online in JAMA Pediatrics today, “Epidemiologic Trends in Neonatal Intensive Care, 2007-2012“:
Importance Neonatal intensive care has been highly effective at improving newborn outcomes but is expensive and carries inherent risks. Existing studies of neonatal intensive care have focused on specific subsets of newborns and lack a population-based perspective.
Objectives To describe admission rates to neonatal intensive care units (NICUs) for US newborns across the entire continuum of birth weight and how these rates have changed across time, as well as describe the characteristics of infants admitted to NICUs.
Design, Setting, and Participants An epidemiologic time-trend analysis was conducted on April 1, 2015, of live births (≥500 g) from January 1, 2007, to December 31, 2012, to residents of 38 US states and the District of Columbia, recorded using the 2003 revision of the US Standard Certificate of Live Birth (N = 17 896 048).
Exposure Birth year.
Main Outcomes and Measures Crude, stratified (by birth weight), and adjusted admission rates. Trends in birth weight, gestational age, weight for gestational age, and use of assisted ventilation are presented to describe the cohort of admitted newborns.
Results Among nearly 18 million live births in 2012, there were 43.0 NICU admissions per 1000 normal-birth-weight infants (2500-3999 g), while the admission rate for very low-birth-weight infants (<1500 g) was 844.1 per 1000 live births. Overall, admission rates during the 6-year study period increased from 64.0 to 77.9 per 1000 live births (relative rate, 1.22; 95% CI, 1.21-1.22 [P < .001]). Admission rates increased for all birth weight categories. Trends in relative rates adjusted for maternal and newborn characteristics showed a similar 23% increase (95% CI, 1.22-1.23 [P < .001]). During the study period, newborns admitted to a NICU were larger and less premature, although no consistent trend was seen in weight for gestational age or the use of assisted ventilation.
Conclusions and Relevance After adjustment for infant and maternal risk factors, US newborns at all birth weights are increasingly likely to be admitted to a NICU, which raises the possibility of overuse of neonatal intensive care in some newborns. Further study is needed into the causes of the increased use observed in our study as well as its implications for payers, policymakers, families, and newborns.
I’d write more about what I think this study means, but I already did that in an editorial in the same issue of the Journal. Read it here: “The Concern for Supply-Sensitive Neonatal Intensive Care Unit Care: If You Build Them, They Will Come.”
Go read both articles!
In a well-referenced paper, Sherry Glied and Erin Miller summarized the history of health economics research and its policy impact, with emphasis in the second half on the Affordable Care Act.
The tl;dr version is that the Congressional Budget Office’s bill scoring role is the institutional mechanism by which health economics research affects policy. Without it, it’s not evident how health econ would matter. Not mentioned by Glied and Miller, is that the Office of Management and Budget’s evidence-based budgeting initiative is another mechanism by which health economics, as well as other social policy research, could affect policy. Glied and Miller’s unstated implication (or, my own inference) is that without a fairly explicit institutional role for research—like CBO’s bill scoring or OMB’s evidence based budgeting—it won’t reliably affect policy. All the stomping up and down about how research should inform policy won’t do much. It has to be institutionalized. Exceptions are possible, but rare.
One passage from the paper, about the ACA’s Cadillac (excise) tax:
As President Obama and Congress began debating health care reform in 2009, 32 prominent health economists sent the President a letter stating, “This provision offers the most promising approach to reducing private-sector health care costs while also giving a much needed raise to the tens of millions of Americans who receive insurance through their employers” (Rampell, 2009). The excise tax incorporated in the ACA directly addressed the tax treatment of health insurance. The new tax had no political constituency whatsoever—not unions, not business, not conservative taxpayers, not liberal taxpayers. It was a victory only for health economists.
The victory is both fragile and partial. The Cadillac tax isn’t yet implemented (still 2.5 years to go), it could still be repealed, and its design is imperfect, even ham-handed, for political reasons. But, w00t, health econ!
The paper is interesting throughout.
Related, this interview of Daniel Hausman by Gary Gutting on the limitations of economics is also worth your time.
“Female Viagra” and regular or “male” Viagra were both originally investigated as treatments for conditions other than sexual dysfunction. Viagra came out of studies on hypertension, and “female Viagra” for depression. But… that’s where most of the similarities end.
How so? Let’s discuss. Flibanserin, sometimes called “female Viagra”, is the topic of this week’s Healthcare Triage:
For those of you who want to read more:
- FDA Briefing Document: Joint Meeting of the Bone, Reproductive and Urologic Drugs Advisory Committee (BRUDAC) and the Drug Safety and Risk Management (DSaRM) Advisory Committee
- Would you take a pill every day to have sex once more each month?
- Pharmacology of Serotonin and Female Sexual Behavior
- Sildenafil in the treatment of erectile dysfunction: an overview of the clinical evidence
- A Pill to Boost Female Libido
- Phosphodiesterase 5 Inhibitors for the Treatment of Erectile Dysfunction: A Trade-off Network Meta-analysis