New Drugs Hold Real Promise for Metastatic Melanoma

I'm going to show you a survival curve for metastatic melanoma.

This data was analyzed in 2001, but sadly, even current 5 year-survival for metastatic melanoma sits around 15%. But some new drugs might change this.

For the video version of this post, click here.

Here's a chart examining Melanoma-associated mortality rates over time:

Compare that to breast cancer, which has seen some dramatic therapeutic advances over the past few decades:

But melanoma is riding a wave of novel immunotherapies that hold promise to change the treatment landscape substantially.

Appearing in the Journal of the American Medical Association is a type of study we don't see too much of these days.  It's not really a clinical trial. It's not really a meta-analysis.  Frankly, I'm not sure what to call it – an aggregate analysis perhaps?

The study examines 655 patients treated with the PD-1 inhibitor pembrolizumab from 2011 to 2013. Yup, that's the same pembrolizumab which was used so successfully to treat this charming former president:

A brief aside here. Pembrolizumab is a monoclonal antibody directed towards programmed cell death protein 1, PD-1. PD-1 acts to prevent immune cells from attacking your own cells – it's an immune "checkpoint" making pembrolizumab one in a class of "checkpoint inhibitors".  Basically, by blocking PD-1, pembrolizumab allows your immune system to attack your own cells. Not something you want under ordinary circumstances, but perhaps beneficial when your own cells have turned against you.

Merck has bet big on pembrolizumab, with clinical trials ongoing or planned in melanoma, non-small-cell lung cancer, small-cell lung cancer, ovarian cancer, glioma, colorectal cancer, and on and on. What happens when a company is doing so many trials like this is a kind of fractionation, where you lose the aggregate knowledge of patient experiences because they are spread out across so many trials.

So I was gratified to see this aggregate analysis which examined patients with advanced melanoma receiving pembrolizumab across four different trials. See, if you do four trials, and one is nice and positive, and the others are equivocal, and you are a for-profit drug company, maybe you're more likely to try to get that positive trial into some high-profile journal, and let the others either languish in peer-review hell or get published in an out-of-the-way rag.

What we get in JAMA, though, is a study with adequate power to demonstrate that pembrolizumab might make a difference.

Among all the patients treated with pembrolizumab (and yes, there is no control group reported here), the objective response rate was 33%. The median overall survival was 23 months, and 31 months among those for whom pembrolizumab was the first systemic cancer therapy.  Compared to the historical median survival of under a year, this represents a substantial improvement.

Interestingly, among those who responded to the drug initially, the duration of response was fairly long. In fact, at 2 years, around 70% of people who initially responded to the drug were still responding.  This is a good thing, as it demonstrates that development of resistance to therapy might be limited.

Now, before we bestow too many accolades on Merck for giving us this aggregate data, we might ask whether they would have been as forthcoming if the trials weren't quite as successful. But, placing cynicism aside for the moment, it seems that this drug, or one of its competitors will have a place at the table in the treatment of advanced melanoma.

Peanuts, Peanut Avoidance, and the Development of Allergy

I love a nice clinical trial that answers an important question and one of my favorites from the recent past was the “Learning Early About Peanut allergy” or LEAP trial, published in February of 2015 in the New England Journal.  I probably don’t need to reiterate the results of this truly landmark study, but basically, it upended about two decades worth of advice to parents to avoid exposing their infants to food containing potential allergens, such as peanuts.

For the video version of this post, click here.

The trial, which enrolled infants at high risk of peanut allergy, found that the rate of peanut allergy at 5 years was 18.8% among those randomized to peanut avoidance, but only 3.6% among those randomized to peanut consumption.  That’s a number needed to treat of around 7 making eating peanut products in the first five years of life about 7 times more efficacious than taking aspirin for an ST-Elevation MI. OK apples and oranges, or peanuts, but still.

But lingering questions remained.  Would these kids be protected in the long-term? Did the study just kick the peanut allergy ball down the field?

To answer the question, the LEAP researchers conducted the LEAP-ON study, in which individuals in the initial study were instructed to avoid all peanut products for 12 months. Without exposure to peanuts, would allergy come roaring back? Would these kids be doomed to eat peanuts three times a week for the rest of their lives?

Well, around 90% of the original trial participants signed on to the no-peanuts-for-12-months pledge. Overall, adherence was OK. As you might expect, those who had originally been randomized to avoid peanuts had an easier time staying off the sauce – 80% of them reported complete peanut avoidance. Only 40% of those who had been randomized to eat peanuts originally were able to stay away for the year. No shame there, peanuts are delicious.

Bottom line, after 12 months of avoidance there were 6 new cases of peanut allergy, but three from each group. In other words, you didn’t see a “rebound” in peanut allergy among those kids initially randomized to eating peanuts.  By the end of this study, 18.6% of those who had initially avoided peanuts and 5% of those who had eaten peanuts from a young age had confirmed allergy.

The point here is that the protection from allergy conferred from early exposure to peanuts persisted even through a year of not eating peanuts. This is a very good thing for the rare kid out there who doesn’t like peanuts – it seems like the protection you gained in infancy will stick around.

Now, I should mention that there was no control group here. I’m curious what might have happened to kids instructed to keep right on eating lots of peanuts. We also don’t know if avoidance for more than a year might let allergy recrudesce.

But taking this study with the results of the original trial, it’s not exactly a leap to say that early exposure to peanuts might dramatically curb the rising tide of peanut allergy in the developed world.

Huge Chinese Study Suggests 20% of Heart Disease due to Low Fruit Consumption

A 柚子 a day keeps the doctor away? Appearing in the New England Journal this week is a juicy study  that suggests that consuming fresh fruit once daily can substantially lower your risk of cardiovascular disease. In fact, the study suggests that 16% of cardiovascular death can be attributed to low fruit consumption. For those of you keeping score, that's pretty similar to the 17% of cardiovascular deaths that could be prevented if older people stopped smoking.

For the video version of this post, click here.

What we're dealing with here is a prospective, observational cohort of over 500,000 Chinese adults without a history of cardiovascular disease.  At baseline, they were asked how often they consumed a variety of foods, and gave a qualitative answer. Most of the analyses compare people eating fruit "daily" to those who ate fruit "rarely or never".

Those fruit-eaters were substantially different from the non-fruit eaters, but not, perhaps, in the way you might expect.  For example, waist circumference and BMI were higher in the fruit-eaters and fruit-eaters were much more likely to live in urban rather than rural areas. Fruit-eaters also ate more meat, all suggesting that, in China at least, eating more fruit might be a marker of better nutrition overall. Reporting the cardiovascular effects of more frequent eating of other foods would reveal whether this is the case, but that data was not shown.

More in line with our Western expectations, fruit-eaters had a substantially higher income, more education, and were less likely to smoke or drink alcohol.

After more than 3 million person-years of follow-up, there were 5,173 cardiovascular deaths. If you followed a group of 1000 fruit-eaters for a year, you'd expect less than 1 cardiovascular death. Following a similar-sized group of never-fruit eaters, you'd expect 3.7 deaths.

These observations withstood adjustment for socioeconomic factors, smoking, physical activity, BMI and consumption of other types of food, though unmeasured confounding always plays a role in dietary studies.

Why does it work? We don't know.  Though the frequent fruit-eaters had lower blood pressure and lower blood sugar, these factors did not explain the protective effects of the fruit.

Indeed, maybe it's not something in fruit that is beneficial at all, but something that isn't. Like sodium.  Fresh fruit isn't salty and salt-intake was not captured in this study. Missing data like that makes it hard to trust that the observed relationship is truly causal.

Still, there isn't much harm in advising patients to eat fresh fruit more regularly, which is I suppose, what makes studies like these so appealing.

Naltrexone to Prevent Opioid Relapse: A New Weapon in the Fight

There are a few experiences nearly every physician remembers. Delivering that first baby, running that first code, a stranger showing you a rash at a dinner party. Some things are universal. Likewise the first time you injected naloxone into someone suffering from an opioid overdose. For the non-medical folks, naloxone blocks the receptor in the brain that gives opiates their punch. Injecting someone with the stuff essentially puts them into immediate, full-blown withdrawal. It’s lifesaving, but rough. Think that scene from Trainspotting.

For the video version of this post, click here.

Naltrexone is naloxone’s longer-acting cousin. The oral formulation has a half-life of around four hours, and there have been several studies examining the use of this drug to treat opiate addiction. But overall the results have been disappointing. Skipping a dose is simply too easy.

But we may have a new weapon in the fight against opioid abuse in the form of extended-release naltrexone, a depot injection that lasts roughly a month. A randomized trial appearing in the New England Journal of Medicine examined the efficacy of this agent in a group of previously incarcerated individuals with opioid dependence. Needless to say, this group is at high-risk of relapse.

In this open-label trial, 153 individuals received monthly injections of extended-release naltrexone for six months, and 155 received what you might call usual care (basically counseling and referral to community support programs). The primary outcome was time to relapse – defined, liberally in my opinion, as ten days of self-reported opioid use or two consecutive positive bimonthly urine specimens.

And relapse rates were high – 43% in the extended-release naltrexone group and 64% in the usual care group. Still, that difference translates into a number needed to treat of 5 – meaning this drug is actually pretty efficacious.

Though time to relapse was the primary outcome, I was more interested in some of the ancillary measures. For instance, there was no difference in the re-incarceration rate in the two groups: both were around 25%. Naltrexone has also been advocated as a drug that might curb binge-drinking, but there was no difference in self-reported heavy drinking which occurred in about 15% of both groups.

After six months, naltrexone injections were stopped, but the participants were followed out for a year after that. Without the injections, the relapse rate in the treatment group quickly caught up with the usual care group. This drug may be a long-term proposition.

Knowing the mechanism of action of the drug, it’s not surprising that gastrointestinal side effects were much higher in the treatment group. Fortunately, there were no overdose events in the treatment group, even after treatment ended. This is a critical finding, as there is a theoretical concern that treatment with naltrexone might condition individuals to take higher doses of opioids. When naltrexone is stopped, those higher doses can be fatal. That this effect wasn’t seen should encourage those of us who might want to use this agent in clinical practice.

I should point out that extended-release naltrexone was not compared to what many consider the more standard approach to therapy – namely buprenorphine or methadone maintenance, though that trial is proceeding apace.

In the meantime, this is what we have. And with the epidemic of opioid addiction growing worse by the day, I for one am glad to have one more weapon in the fight.

Rosacea linked to Parkinson disease: Is this remotely plausible?

The title of the manuscript is:

Titles like that remind me of the time I was in South Africa and ran into an evangelical Christian basketball team. I know what both of those things are, but I’d never thought of putting them together. Nevertheless that’s the study that appears in JAMA Neurology. So are we playing epidemiology roulette, or is this a real finding? Should your patients with rosacea be concerned?

For the video version of this post, click here.

First things first, this is a study out of Denmark, a country with a nationalized and central health care system. Researchers examined… well… everyone in the country over age 18 from 1997 to 2011, so over 5.5 million people. They identified around 68,000 individuals with rosacea based upon either administrative codes or having received two prescriptions of topical metronidazole. They identified individuals with Parkinson disease based, again, on administrative codes. A sensitivity analysis looked at all those people who got medications associated with Parkinson disease, like levodopa.

Overall, those with rosacea were twice as likely to subsequently receive a diagnosis of Parkinson disease. After adjustment for a fair amount of covariates, the risk was lessened but still significant. Of course, that’s a relative risk. In absolute terms we’re talking about rosacea increasing the risk of Parkinson Disease from 3.5 cases per 10,000 person-years to 7.5 cases per 10,000 person years.

So… why?  Well, the authors note that rosacea is associated with upregulation of a group of proteins called matrix metalloproteinases (MMPs) which have a role in tissue breakdown and repair. There is also a mouse model of Parkinson disease that shows upregulation of MMPs. A prior observational study of 70 patients with Parkinson disease showed a higher than expected rate of rosacea. But basically, that’s it. This is the first large, epidemiologic study to even examine the association between these two conditions.

Now I could mention that administrative codes are poor at capturing conditions like this, that people with rosacea may have more contact with the healthcare system and thus be more likely to receive a diagnosis of Parkinson disease, and that the study lacked a negative control condition – say Alzheimer’s dementia – to lend support to the biologic plausibility argument. But I don’t want to be cynical. This paper clearly represents the first foray into an area that probably warrants a deeper look.

The important thing to remember though, is that even if this is a real finding, the impact for your patients with rosacea is quite minimal. I took the liberty of making a proportional Venn diagram here which I think is illustrative:

The big blue rectangle represents the total population of Denmark, and the circles represent the two disease conditions. There is some overlap between rosacea and Parkinson disease, but I think it should be very clear that most patients with rosacea needn’t worry. It is for this reason that I take issue with this statement:

Are IUDs dangerous for teenage girls?

In the past 5 years both the American Academy of Pediatrics and the American College of Obstetrics and Gynecology have come out in support of Long-acting reversible contraceptives (LARCs) as highly effective options for adolescent girls. LARCs, which include IUDs and implants, are undoubtedly superior to oral contraceptives and condoms when it comes to preventing pregnancy. Of course IUDs don’t prevent sexually transmitted infections. The question, then, is whether use of IUDs will commensurately decrease condom usage, and, according to an article appearing in JAMA pediatrics, the answer is yes. But as usual, the devil is in the details.

For the video version of this post, click here.

The study used the well-established Youth Risk Behavior Survey. This is a biannual survey administered to high-schoolers across the US, asking all sorts of probing questions about sex, drugs, and rock and roll.

The researchers identified 2,288 sexually active girls, and asked what method of contraception they used during their last sexual encounter. That defined their “base” form of contraception, and only one answer was allowed. Around 40% reported using condoms, 22% oral contraceptives, and 30% using withdrawal or no contraception at all. Just 1.8% used IUDs, so we’re not talking about a huge population here.

That you could only give one answer to this question is really the study’s Achilles’ heel, as individuals who used an IUD AND condoms at their last sexual encounter, but answered condoms to this question would not be classified as IUD users. This could bias the results making IUD users appear less likely to also use condoms.

Which is what was seen. 37% of oral contraceptive users also used condoms at their last sexual encounter, compared to 16% of IUD users, a highly statistically significant difference. So do IUDs discourage condom usage?

What this boils down to is why teenagers use condoms. I think if you were to survey them, you’d find that they use them to prevent pregnancy, not to prevent STIs. Knowing that IUDs are incredibly effective at preventing pregnancy may make teenagers less likely to think about using condoms.

But the direction of causality here may be opposite to what is being suggested. It is possible that docs encourage girls to get IUDs precisely because they are not reliable when it comes to using condoms, and that might be a very good thing.

But to me, the take home from this study isn’t that IUD users have low condom-use rates, it’s that EVERYONE does. A 37% condom use rate among oral contraceptive users should be frightening. This study didn’t convince me that IUDs discourage condom use, but it sure convinced me that we need to make dual-protection socially normative.

How about this: “dual-protection: it’s what the cool kids do when the cool kids do it.”

Or if you can think of a better slogan, let me know in the comment section.

Pregnancy, Multiple Sclerosis, and Vitamin D: The Latest Hype

A study appearing in JAMA neurology links better Vitamin D level in pregnant women to a lower risk of multiple sclerosis in their offspring. There are some really impressive features of this study, but there are some equally impressive logical leaps that seem to defy the force of epidemiologic gravity. Let's give  the study some sunlight.

For the video version of this post, click here.

The study was run out of Finland, which is a country that figured it might be a good idea to keep track of the health of its citizens. In fact, since 1983, nearly every pregnant woman in Finland has been registered, and a blood sample sent to a deep freezer in a national biobank. The researchers identified 193 individuals with MS, and went back into that biobank to measure their moms' vitamin D levels during pregnancy. They did the same thing with 326 controls who were matched on their date of birth, mother's age, and region of Finland.

This is from the first line of their discussion:

Wow. 90%. That sounds scary. And the news outlets seem to think it is scary too.  But that impressive result hides a lot of statistical skullduggery.

Here's the thing, Vitamin D level is what we call a continuous variable. Your level can be 5, 10, 17, 42, whatever – any number within a typical range. When you study a continuous variable, you have to make some decisions. Should you chop up the variable into categories that others have defined (like deficient, insufficient, normal), or should you chop it up into even-sized groups? Or should you not chop it up at all?

As a general rule, you have the most power to see an effect when you don't chop at all. Breaking a continuous variable into groups loses information.

When the Vitamin D level was treated as the continuous variable it is, there was no significant relationship between Vitamin D level in mom and MS in the child. When the researchers chopped it into 5 groups, no group showed a significantly higher risk of MS compared to the group with the highest level. Only when they chopped the data into 3 groups did they find that mom's who were vitamin D deficient had 1.9 times the risk of those that were insufficient. That's the 90% figure, but the confidence interval ran from 20% to 300%.

And did I mention there was no accounting for mothers BMI, smoking, activity level, genetic factors, sun exposure or income in any of these models? Despite that, the paper's conclusion states :

That statement should go right on the jump to conclusions mat.

Look, I'm not hating on Vitamin D. I actually think it's good for you. But research that adds more to the hype and less to the knowledge is most definitely not.

Inducing labor at 39 weeks - is picking your kid's birthday worth it?

Few aspects of modern medicine engender as much controversy as our labor and delivery practices. Rates of early induction of labor vary widely from country to country – even from hospital to hospital. And while some randomized trials have demonstrated that induction of labor prior to 40 weeks gestation might have favorable effects for infants with certain conditions like large-for-gestational age, we really don’t have much data on the effects of induction of labor during a normal pregnancy. But a study appearing in the New England Journal of Medicine attempts to shed light on that issue.

For the video version of this post, click here.

Run out of 39 hospitals in England, this study randomized 619 women, all age 35 or older on their first pregnancy, to labor induction at 39 weeks, or usual care.

Why do this? Well, for one thing, induction of labor prior to the official due date is pretty common. There is, perhaps, a quality-of-life argument to be made about having the ability to more or less choose when to deliver a baby. There is also some observational data that suggests that the sweet spot for delivery is around 38-39 weeks. Prior to that, complications associated with pre-term infants go up, and much beyond that and you start to see other birth complications.

Now, this study was clearly too small to detect differences in rare outcomes like neonatal or maternal mortality, but there has been some concern that induction of labor might increase the rate of c-section.

This study saw no such increase. The rate of c-section was 32% in the induction group and 33% in the usual care group – not statistically different. There were also no differences in rates of assisted vaginal delivery or NICU admissions, and every child in the study survived to hospital discharge. One fact caught my eye, though, and I think it gives us insight into the main limitation of this trial.

There was no significant difference in birth weight between the arms of the study. You’d think that the early induction arm would at least have slightly smaller babies. But in reality, the arms just weren’t that different in terms of any measured variables. Why? Well, there were women in the usual care arm who went into labor at 38 weeks. In fact, only 222 of the 305 women in the induction group got induction of labor prior to 40 weeks of gestation, as the protocol specified.

This bias, which the authors half-jokingly describe as “non-adherence”, is due to the fact that randomization into the study could occur at any time from 36-40 weeks. If you wanted to really answer the question that the authors pose, you’d randomize everyone at 39 weeks, and if they were put in the early induction arm, induce them at or near the time of randomization.

So we need to interpret this study not as saying that early induction is safe, but that a plan for early induction is safe. This is a subtle difference, for sure, but an important one if you are discussing inducing a woman who has already hit the 39 week mark. Still, in my book, a small victory for patient autonomy is a victory nonetheless.

Statins to prevent acute kidney injury after cardiac surgery

Statins, is there anything they can’t do? These agents, granted blockbuster status more than 20 years ago, are potent weapons in our fight against cardiovascular disease. But beyond their cholesterol-lowering effects, we’ve seen studies where statins act as anti-inflammatories, improve immune function and even stave off dementia.  Could the wonder-drugs prevent acute kidney injury, a dreaded complication after cardiac surgery, associated with more than a three-fold increase in mortality?

For the video version of this post, click here.

Full disclosure: I research acute kidney injury, or AKI. So welcome to my world, statins – a world where positive clinical trials are as rare as an epidemiologist at a Mr. Personality contest.

The trial, out of Vanderbilt university hospital appeared in JAMA and enrolled 617 individuals undergoing cardiac surgery. The treatment group got 80mg of atorvastatin prior to surgery, and 40mgs a day after that. The placebo group got, well, placebo. As you might imagine, the majority of patients (400) were already taking a statin.  In that case, if you were randomized to placebo, you only got placebo for the day of surgery and the day after. After that, you were back on your home statin dose.

And to boil the results down to a word: nothing. The rate of AKI was 21% in the statin arm and 20% in the placebo arm. Looking at secondary outcomes, there were no differences in rates of death, dialysis, delirium, stroke, or stay in the ICU.

This might be expected in the group that was already on statins – after all, skipping two days of the drug might not be enough to make a real difference. But if we look at the statin-naïve group, the rate of AKI was 22% in the statin group and 13% in the placebo group. This was not statistically significant but the trend here is clearly in the wrong direction. In fact, if we look at absolute creatinine change –where higher levels are worse- those on the statin had a small, but statistically significant increase in creatinine compared to those on placebo.

But take these numbers with a grain of salt. The data safety and monitoring board forced the study authors to stop recruitment of statin-naïve patients about 2/3rds of the way through the study. They did this because they saw a signal of harm from statins in that group. So the fact that we see harm may be biased by the DSMBs choice to stop that part of the study early.

Now, would I have stopped the study if I were on the DSMB?  Probably. The odds that continuing to recruit would show a benefit of statin were really low, and you don’t want to expose patients to potential harm. But despite that, we can’t accept the results of an early-termination arm of a trial with the same gusto that we would had the trial continued to completion.  In short, the jury is still out as to whether statin use is actually harmful in terms of AKI. But I can say for now I’m pretty convinced it ain’t helping anybody.

Pregnant women, don't stop eating fish!

Tuna, shark, king mackerel, tilefish, swordfish. If you’ve ever been pregnant, or known someone who has been pregnant, this list of seemingly random aquatic vertebrates is all too familiar to you. It’s the “avoid while pregnant” list of seafoods, and it’s just one of the confusing set of messages surrounding pregnancy and fish consumption.

(For the video version of this post, click here).

Because aren’t we supposed to be eating more fish? Fish are the main dietary source for omega-3 fatty acids, which can cross the placenta, and may promote healthy brain development. Of course, some of these fish contain mercury which, as Jeremy Piven taught us all, may be detrimental to cognitive development.

These contradictory facts led the US FDA, in 2014, to recommend that pregnant women consume more fish, but not more than 3 times a week.  You have to love the government sometimes.

A study appearing in JAMA pediatrics is making some waves with its claim that high levels of fish consumption, more than 3 times per week during pregnancy, is associated with more rapid neonatal growth as well as higher BMIs throughout a child’s young life. Now, contrary to what your mother-in-law has been telling you, more rapid infant growth is not necessarily a good thing, as rapid infant growth is associated with overweight and obesity in childhood and adulthood.

But fish as the culprit here? That strikes me as a bit odd. Indeed, prior studies of antenatal fish consumption have shown beneficial or null effects on childhood weight gain.  What is going on here?

The authors combined data from 15 pregnancy cohort studies across Europe and the US, leading to a final dataset including over 25,000 individuals. This is the studies greatest strength, but also its Achilles heel, as we’ll see in a moment.

But first the basic results. Fish consumption was based on a food frequency questionnaire, a survey instrument that I, and others, have a lot of concerns about. Women who reported eating less than or equal to 3 servings of fish a week had no increased risk of rapid infant growth or overweight kids.  But among those eating more than 3 servings, there was around a 22% increased risk of rapid growth from birth to 2 and overweight at age 6.

These effects were pretty small, and, more importantly, ephemeral. The authors looked not only at the percentage of obese and overweight children, but the raw differences in weight. At 6 years, though the percent of overweight and obese kids was statistically higher, there was no significant weight difference between children of mothers who ate a lot of fish and those who didn’t. When statistics are weird like this, it usually suggests that the effect isn’t very robust.

In fact, this line from the stats section caught my eye, take a look:

That means the authors used numbers predicted by a statistical model to get the weight of the children rather than the actual weight of the children. I asked the study’s lead author, Dr. Leda Chatzi, about this unusual approach and she wrote “Not all cohorts had available data on child measurement at the specific time points of interest… in an effort to increase sample size and…power in our analyses, we…estimated predicted values of weight and height”.

So we have a statistical model that contains as a covariate, another statistical model. This compounds error into the final estimate, and in a study like this, where the effect size is razor thin, that can easily bias you into the realm of significance.

And, at this point it probably goes without saying, but studies looking at diet are always confounded. Always. While the authors adjusted for some things like maternal age, education, smoking, BMI and birth weight, there was no adjustment for things like socio-economic status, sunlight exposure, diabetes, race, or other dietary intake.

What have we learned? Certainly not, as the authors suggest, that

That they wrote this in a study with no measurement of said pollutants is what we call a reach.

Look, you probably don’t want to be eating fish with high levels of mercury when you are pregnant. But if my patients were choosing between a nice bit of salmon and a cheeseburger, well, this study doesn’t exactly tip the scales.