Pediatric Newsletter #15: Food Allergies, Gluten, and Pizza

March 29, 2015  |  General  |  No Comments

Welcome to the latest edition of my newsletter for parents about pediatric topics. In it I highlight and comment on new research, news stories, or anything else about children’s health I think will interest parents. In this particular issue I tell you about a couple of new findings about allergies in children, as well as some new information about gluten sensitivity. I have over 30 years of experience practicing pediatrics, pediatric critical care (intensive care), and pediatric emergency room care. So sometimes I’ll use examples from that experience to make a point I think is worth talking about. If you would like to subscribe, there is a sign-up form on the home page.

Big News About Peanut Allergies

This one made a big splash both in the medical news sites and in the general media. Peanut allergy is common. It has doubled in the past decade, now affecting between 1 and 3% of all children. And it can be a big deal for children who have it, even life-threatening. For years we recommended that children not be given peanut products early in life, especially if they are at risk (based on their other medical issues) for developing allergy. Unfortunately, avoiding peanuts in the first year of life doesn’t make a child less likely to develop the allergy. So what, if anything, can?

This recent, very well done study published in the prestigious New England Journal of Medicine is really ground-breaking. It took 4 to 11-month-old children at high risk for developing peanut allergy and divided them into 2 groups. One group got the “standard” approach — being told to avoid peanut exposure. The other group was fed peanuts 3 times per week. It was done in the form of either a peanut snack or peanut butter.

At age 5 years (the long follow-up time is a particularly strong feature of the study) the children who had been fed the peanuts had nearly a 90% reduction in the development of peanut allergy. This is a huge difference.

The study also was able to provide a scientific explanation for the difference. The children fed the peanuts developed protective antibodies that cancel out the ones that provoke the allergic response.

Washing Dishes by Hand May Reduce the Risk of Food Allergies

This report comes from Pediatrics, the journal of the American Academy of Pediatrics. There has been a long-standing theory about how allergies develop in children called the “hygiene hypothesis.”

The notion is that children, particularly in Western countries, are more prone to allergies (and asthma) because their exposure to microbes is delayed by our more sanitized environment.

In this study from Sweden, children in households that washed dishes by hand rather than using a dishwasher experienced a lower risk of subsequent allergies. The authors speculated that there was a causal association. They couldn’t prove that, but they also noted that early exposure to fermented foods and if the family bought food directly from farms also correlated with less allergies. I’m not totally convinced, but it is an interesting study worth thinking about. I expect to see more on the topic.

Does the Age at Which You Introduce Gluten Into Your Child’s Diet Affect Future Risk of Gluten Sensitivity?

Gluten sensitivity is in the news, with signs everywhere advertising “gluten free” as if this is always a good thing. I hear a lot of misconceptions about gluten sensitivity. Gluten is a protein found in grains such as wheat and barley. There is a condition, called celiac disease or sprue, in which a person can develop moderate or severe intestinal symptoms triggered by gluten. It is one of the eighty or so autoimmune diseases. The incidence of celiac disease in the US is about 0.7%. The risk of developing celiac disease is closely linked to a genetic predisposition to getting it. Importantly, if you don’t have the disorder, there is no benefit to eliminating gluten from your diet. In fact, the great majority of people who think they have sensitivity to gluten . . . don’t.

But for those children who do have a higher risk for developing celiac disease because of their genetic makeup it has long been a question if delaying gluten exposure will affect their chances of actually getting the disease. A good recent study gives an answer to that question, and the answer is no. There is no correlation.

If you think your child (or you) have problems with gluten there is a useful blood test that looks for a specific antibody. However, many people who have the antibody never get symptoms of celiac disease. The ultimate test is an intestinal biopsy.

My take-away conclusion is that all this gluten-free stuff you see in, for example, restaurants, is just the latest dietary fad. For over 99% of us there is no health benefit to avoiding gluten.

So How Much Pizza Do Teenagers Eat?

This is kind of a quirky item. If nothing else, it demonstrates how weird the medical literature can be sometimes. Every parent knows kids, teenagers in particular, mostly love pizza. A recent article in Pediatrics, a fairly respected journal, used food surveys to find how much pizza kids eat and the percentage of their daily calories they get on average from pizza.

The answer? The authors claim that in 2010 21% of kids ages 12-19 reported eating pizza sometime in the past 24 hours. That number is actually down from a similar survey in 2003. What about calories? For those kids who reported eating pizza, it accounted for about 25% of their daily calories, and that hasn’t changed. The authors primly suggest that we should make pizza more nutritious. I wish them luck with that. And I’m 63 years old and still like pizza.

SLAPPS in Medicine: Can medical researchers ever be at risk for being sued for libel?

March 5, 2015  |  General  |  No Comments

It has become a common technique for large companies or other powerful organizations, when they meet public opposition, to use a strategy called strategic lawsuits against public participation, or SLAPP for short. I have seen one of these in action. In the case I observed, a large development company wanted to obtain a parcel of public land by offering the US Forest Service a swap for an obviously inferior piece of land the company owned. Many citizens objected and organized against the proposal. Their actions had a reasonable chance of blocking the land swap. The company responded by suing the leaders of the citizens’ group — a SLAPP. The key concept of these suits is not that the instigators expect to win them They almost never do, even on the rare occasions when they make it to trial. But just the threat of a lawsuit and huge monetary damages has a chilling effect on ordinary people, who do not have armies of lawyers. It puts them through stress and, most importantly, great financial cost to contest the SLAPP. It has the effect of frightening off opposition.

Could a similar process happen in medical research? A recent example suggests that this is possible. The details are presented here. The authors ask this question:

Does fear of libel lawsuits influence what gets published in medical journals? We suggest it may, especially when the conclusions run counter to corporate interests.

The particular case involved a study in which the researchers investigated the relationship between TV advertisements for fast food and children’s perception of the product. As it happens, 99% of fast food advertising directed at children comes from only two companies: MacDonald’s and Burger King. The investigators concluded that the companies failed to comply with the guidelines of the Children’s Advertising Review Unit of the Better Business Bureau. The authors then submitted their findings to Pediatrics, a journal of the American Academy of Pediatrics. The manuscript review process stopped when the legal department of the Academy recommended that the names of the fast food companies be removed from the paper. The lawyers were concerned about being sued by one or both of these fast food giants. However, the authors believed that naming names was important and they withdrew the paper from consideration. Here is what they were told by the journal editor:

In the event that a defamation claim is brought as a result of the publication of this article, the publishing company could be named as defendants. Based on these findings and advice from counsel, we recommend the article not be published.

The article eventually was published by the journal PLOS One, with the company names included. This series of events raises important questions for medical research. Remember the point of SLAPPs is not to actually win a libel suit. Rather, it is to put the SLAPP target though trouble and expense sufficient to warn them off. Valid medical research cannot be libel. There is actually a 1994 court decision (Underwager v Salter) that states scientific disagreements should be decided in the scientific, not the legal arena. And truth is always a defense against libel.

I have no idea if this sort of thing is an isolated instance or happens more frequently. I have long been concerned that, with the decline of federal NIH support for medical research, industrial financial support carries the risk of compromising the work. This is what cannot be allowed to happen:

. . . any article that reaches negative conclusions about a company’s practices or products risks rejection, as it is company practice today to strategically threaten libel suits to ward off legitimate criticism.

This is serious issue, one all of us who use the medical research literature need to think about.

Vaccines, quarantines, and compulsion in supporting the public health

February 9, 2015  |  General  |  2 Comments

I posted a version this one last year, but the recent outbreak of measles has once again ignited the debate of just what the government has the right to do or not do in compelling individual actions in support of public health. This is an old question, and it’s worth considering it in historical context.

One aspect of the endless vaccine debate is the aspect of coercion some parents feel about requiring children to be vaccinated before they can go to school. The government mandates vaccination. But this isn’t really an absolute requirement. Although all 50 states ostensibly require vaccination, all but 2  (Mississippi and West Virginia) allow parents to opt out for religious reasons, and 19 states allow this for philosophical reasons. (See here for a list.) Still, in general vaccines are required unless the child has a medical reason not to get them, such as having a problem with the immune system. Is this an unprecedented use of state power? I don’t think it is.

In fact, historically there have been many examples of the government inserting itself into healthcare decisions of individuals and families in order to protect the public health. Some of these go back many years. Quarantine, for example, goes back to medieval times, centuries before the germs were discovered. It has since 1944 been a power of the federal government; federal agents may detain and send for medical examination persons entering the country suspected of carrying one of a list of communicable diseases. Quarantine has also been used by local and state governments, particularly in the pre-antibiotic era. Diphtheria is a good example, as you can see from the photograph above. Quarantine can be abused, and has in fact been abused in the past for discrimination against certain minority groups. A brief paper from the American Bar Association details some of those instances here. The paper even suggests that it should be abolished for these reasons. But the practice is a very old one.

Of course the government mandates many things for the protection of public health. Milk is pasteurized (although there are raw milk enthusiasts who object), water is purified, and dirty restaurants can be closed. Like quarantine, these measures restrict our personal freedom a little, but what about government-mandated medical treatment? That sounds a bit more like the situation with compulsory vaccination of children. As it happens, there are more recent examples of compulsory treatment, particularly involving tuberculosis.

A couple of decades ago I was involved in a case of a woman with active tuberculosis who refused to take treatment for it. Worse, her particular strain of TB was one highly resistant to many antibiotics, so if that spread it would represent a real public health emergency. The district judge agreed. He confined the woman to the hospital against her will so she could be given anti-TB medications until she was not longer infectious to others. At the time I thought this was pretty unusual. When I looked into it, though, I found that there have been many instances of people with TB being confined against their will until they were no longer a threat to others. The ABA link above lists several examples of this.

So it’s clear to me there is a long tradition of the state restricting personal freedom in the service of protecting the public health. Like everything, of course, the devil is in the details. To me the guiding principle is that your right to swing your fist ends where my nose begins.

Pediatric Newsletter #13: childhood sleep, concussions, and more

January 31, 2015  |  General  |  No Comments

Here is the latest of my more or less monthly newsletter on pediatric topics. In it I highlight and comment on new research, news stories, or anything else about children’s health that I think will interest parents. If you want to subscribe to it and get it in the form of an email each month there is a sign-up form at the very bottom of my home page.


New Study Shows How and Why Sleep Patterns Change During Adolescence 

Every Parent of a teenager knows that they tend to go to sleep later and are harder to rouse out of bed in the morning. It turns out that as elementary school children become early and then mid-teenagers theses changing sleep patterns are a normal result of the hormonal changes their bodies are going through.According the data in a new study, conducted with 94 children in all, children are programmed to get less sleep as they mature.

A typical 9-year-old fell asleep at 9:30 p.m. on a weekday upon first enrolling in the study and would wake up at 6:40 a.m. By age 11, the same child would go to sleep at 10 p.m. The net result for that child – and many others in the cohort of 38 children who joined the study at 9 or 10 years old – would be steadily less sleep every night.
The study is one of the few to track individual kids for longer than a year. It showed wide individual differences in these trajectories. For some children, the data show, the shift to a later bedtime without a later wakeup time was abrupt, possibly putting them at a greater disadvantage relative to their peers in school.

The American Academy of Pediatrics has suggested later school start times for teenagers, advising school start times no earlier than 8:30 for middle and high school students.

For Kids With Simple Concussions, a Couple of Days Rest is Enough

The past few years have brought increasing attention on concussions, particularly the long-term effects of repeated concussions. We need to take them seriously. But they are common, and the vast majority of children recover without any further brain issues. The optimal way to care for children following a concussion is still unknown, although there is one key principle: a child should not do anything that could lead to another head injury, such as returning to contact sports, until the symptoms of the concussion have resolved. Common symptoms are headache, vomiting, and difficulty concentrating.

Some authorities have long recommended extensive bed rest following a concussion. A new study indicates that this is not needed and does not help the brain heal any faster. In fact, the authors noted that children placed on strict bed rest tended to focus on their symptoms even more, which is not surprising to me.

You can read more about concussions — what they are, what they mean — in a blog post I wrote here.


Stress During Pregnancy Can Effect Fetal Development

This study is in mice, not people, but it has very suggestive findings. The bottom line was that pregnant mice who had high levels of stress hormones had smaller offspring, and low birth weight is an important marker for later problems in infants. The effect was not because the stressed mothers ate less — they actually ate more. Although the causes of low birth weight are many, it makes sense that a stressful environment for the fetus might be one of them.


Starting Serious Contact Football Before the Age of 12 Linked to Later Brain Problems

While we’re talking about concussions and head injury (see above) another important study in the journal Neurology found, at least in NFL players a correlation between later degenerative brain problems and the age at which the player first began to play. At least minor head injury is almost inevitable in football. It is likely that there are many injuries that don’t reach the level of concussion but which, over time, add up. The identification of age 12 as the threshold for increasing risk for later problems makes sense from what we know about brain development in children.


Small Screens in a Child’s Bedroom interfere With Sleep

We should probably file this one in the common sense department, but if you allow your child to have a small screen in the bedroom, such as from a smart phone, it will interfere with his or her sleep. I know we found that to be the case with my own son. I guess it’s good to know that research confirms that.


Massive Study Confirms Safety of Measles Vaccine

Measles is very much in the news these days after the outbreak of the infection in California, which was linked to higher numbers of unvaccinated children. An inevitable byproduct has been the resurrection of fear of the vaccine. Multiple past studies have debunked any links with autism or any other serious ailments. So this study is timely.

Researchers at Kaiser-Permanente studied a total of nearly 800,000 vaccine doses over 12 years and found no serious issues.


The mathematics and politics of allocation of organs for transplant

January 13, 2015  |  General  |  No Comments

We have a problem in this country with how precious organs for transplant are allocated. The problem has been brewing for years, and is well recognized in the transplant community, the physicians and institutions that perform them. Two recent opinion pieces review the issue well — here and here. Since PICUs such as mine are closely involved in the practice of organ transplant, both from the donor and the recipient sides, pediatric intensivists like me have a great interest in the process. Above all else, we want it to be fair, because the supply of organs always falls short of the need. Many patients die on the waiting list.

The way the system works now is “locals first.” The country is divided into 58 geographical zones called donation service areas, which are in turn grouped into 11 regions. When an organ becomes available, the system called the United Network for Organ Sharing (UNOS) first tries to match the organ with the most needy person in first the service area and then the zone. Transplanted organs need to match the recipient in several key ways or they will be rejected. If there is no patient match in either of these, the organ can be listed nationally for a match. If there is one, we have a sophisticated system in place to scramble the team at the distant facility to fly to the place where the donor is to pick up the organ and get it back in time to transplant it, although there are some constraints to timing depending upon the particular organ.

The boundaries of these zones and regions were drawn decades ago. The problem is that some geographic areas have longer lists of patients waiting for organs than do others, and different places also vary in how many organs for transplant they produce. So, even though there is a “sickest first” priority system, a less sick patient in a region with a shorter list and for whom an organ matches may get that organ ahead of a much sicker patient in a less fortunate region. Patients can also choose to be listed in a region where they don’t live, as long as they can be at the hospital within several hours. Steve Jobs, for example, chose to be listed for a liver transplant in Tennessee rather than where he lived in Northern California, which has an average waiting time 6 years, because he was more likely to get a new liver in Memphis, which has an average waiting time of 3 months. When the call came, he chartered a jet to fly him there in time.

This doesn’t seem fair. But there are strong political reasons for the debate going on in the transplant community over the issue. If the system is changed, some smaller transplant centers might close down and some regions could become net exporters of organs. For example, the head of the transplant program at the University of Kansas estimates that his institution would lose 30-40% of its transplant practice.

There are some ethical issues to consider, too. For one, an individual physician is responsible for the care of his or her patient. It’s personal. How can a surgeon say to one them that, although there is a match for an organ in the same city, that organ is going to go half-way across the country to a recipient to whom the surgeon has no medical duty other than the abstract social principle of fairness? (To be fair, though, justice is one of the four principles of medical ethics.)

From the ongoing debate it seems clear that the system will be revised. For institutions, there will be winners and losers. But for patients, which is after all why we do transplants, it will be fairer. From one of the essays:

One way or another, I believe, the U.S. organ-transplantation system needs to change. The availability of the benefits of organ transplantation should depend neither on a patient’s ability to charter a private jet nor on whether he or she is lucky enough to live near a hospital that, thanks to our “local first” system, has a relatively short waiting list. When it comes to lifesaving transplants, geography should not be destiny.

Some clues why exercise helps depression

Some clues why exercise helps depression

January 5, 2015  |  General  |  No Comments

Researchers have known for many years that regular exercise helps relieve some of the symptoms of depression, but there has been little cellular or biochemical data on why that might be so, other than the generalization that exercising just makes us feel better about ourselves. There are some new and interesting findings that shed some light on what may be happening. The graphic above, from this article, illustrates the details.

Tryptophan is an amino acid, one of the building blocks of proteins. It is normally metabolized, broken down, in the tissues, including muscle. The system that does this is called the kynurenine pathway because the product of this process is called kynurenine. This substance penetrates the brain, is itself broken down, yielding some molecules that have been implicated in several brain disorders, including depression. This is shown on the left side of the graphic.

On the right side of the graphic you see what happens with exercise. Muscle that is being actively exercised produces enzymes called KATs that take the kynurenine and, before it can penetrate into the brain, change into a similar substance called kynurenic acid. The latter substance does not go into the brain and activate depression-causing pathways.

I think this is quite interesting. It is always fascinating when we find biochemical and cellular explanations for something we’ve observed before but for which we had no explanation.

The promises and pitfalls of healthcare quality performance measures

December 29, 2014  |  General  |  No Comments

The quality-measurement enterprise in U.S. health care is troubled. Physicians, hospitals, and health plans view measurement as burdensome, expensive, inaccurate, and indifferent to the complexity of care delivery. Patients and their caregivers believe that performance reporting misses what matters most to them and fails to deliver the information they need to make good decisions.

Thus begins a recent editorial in the New England Journal of Medicine. It was accompanied by another entitled “Getting More Performance from Performance Measurement.” These represent the rumblings of discontent with the status of current efforts to measure the quality of healthcare patients are getting.

Everyone wants high-quality healthcare. It’s obvious in the abstract. But how do we know what that is? It’s well known that healthcare delivery varies widely across the country. This was shown many years ago by the Dartmouth Atlas of Healthcare, which documented astonishing differences in how medicine was practiced, and of course therefore how much it cost, even between places right next door to each other. These variations persist today. Why? The diseases and disorders being treated don’t vary like that. It turns out, unsurprisingly, that local medical culture and traditions play a huge role. When a new physician comes to the area, he or she tends to fall in line with how things are done there. The obvious goal here should be to deliver the best and most effective healthcare — not skimping on useful care but not overdoing things and adding risk to the patient in the bargain. How can we do that? These days everybody is trying to figure that out, and our current efforts, as discussed in the above articles, aren’t doing as well as they could.

A key distinction to understand is the difference between process measures and outcome measures. A process measure is something that keeps track of a particular activity that we know or assume will lead to better outcomes. A good example is washing our hands. Documenting that we did that is a process measure. We know, however, that it will decrease the number of hospital-acquired infections, an outcome measure. Marking the surgical site before surgery is a process measure; eliminating wrong-site surgeries is an outcome measure. Unfortunately, very quickly things get more complicated than these simple examples. One chronic complaint from physicians is that we are held responsible for outcomes over which we have no power to influence the results. Another complaint is that, as with medical credentialing (I wrote about that swamp here), there are a host of players involved in performance measures and many have their own metrics that differ from each other. From the second essay:

The current measurement paradigm, however, does not live up to its potential. Many observers fear that a proliferation of measures is leading to measurement fatigue without commensurate results. An analysis of 48 state and regional measure sets found that they included more than 500 different measures, only 20% of which were used by more than one program. Similarly, a study of 29 private health plans identified approximately 550 distinct measures, which overlapped little with the measures used by public programs.

A mess like that is a prescription for cynicism among hospitals and physicians — and failure. We need a much smaller, much more manageable set of measurements that everybody agrees are real indicators of good medical care. I think this means, among other things, that we can’t have every payer concocting their own scheme. That is asking for chaos.

We have had some successes in linking a process measure to an outcome measure. A good example is planned delivery of infants who were almost, but not quite, at term. Sometimes there is a good medical reason for doing this. But in the past this was often done for the convenience of the doctor or the parents. Sometimes that meant a baby was delivered too early and had to spend time in a neonatal intensive care unit. As a result of close monitoring of early deliveries, of making sure they were really medically necessary, the rate of early delivery has fallen to a quarter of what it was several years ago. That’s real progress, and it came from performance improvement projects. The author is optimistic:

The science and practice of performance measurement have advanced substantially in the past decade, and increased transparency regarding results means that we know more quickly what works and what doesn’t. Furthermore, all stakeholder groups are now invested in getting more performance out of measurement, which should ultimately drive the care improvement that patients need and deserve.

Maybe. I know this is all inevitable and good for patients in the long run. But I think we will have many more growing pains — false leads, useless measurements — before we get there.


New recommendations for the treatment of bronchiolitis: we should do less because it doesn’t help

December 2, 2014  |  General  |  No Comments

Every fall I write about bronchiolitis because it is one of the most common respiratory ailments affecting infants and children under about two years of age. It is the most common reason infants end up in the hospital during the winter and early spring months. Every year we get severe cases in the PICU. Pediatricians have struggled for decades to figure out how to treat bronchiolitis but we don’t have any specific therapies that work very well. (We have some promising treatments on the horizon, though, as I wrote about here.) Recognizing this, the American Academy of Pediatrics has significantly revised its recommendations of what we should and should not do for children with bronchiolitis. Before I describe these new recommendations, however, I should review what bronchiolitis is and why it can make small children, particularly infants, so sick.

Bronchiolitis is caused by a viral infection of the small airways, the bronchioles. By far the most common virus to do this is one we call respiratory syncytial virus, or RSV. To scientists, RSV is a fascinating virus with several unique properties. One of these is its behavior in the population. When it’s present, RSV is everywhere. Then it suddenly vanishes. There are exceptions to everything in medicine — I have seen sporadic cases during the off-months — but generally RSV arrives with a bang in mid-winter and then leaves suddenly in the spring. It’s the only virus that consistently and reliably causes an epidemic every year, although it often alternates more severe with milder visitations. RSV epidemics often have some regional variability. For example, often one city will have a much more severe epidemic than do others in other regions of the country.

Another aspect of RSV that interests medical scientists is how poor a job our immune systems do in fighting it off. Virtually all children are infected with RSV during the first few years of life. Not only that, all of us are reinfected multiple times during our lives. Attempts at devising a vaccine for RSV have all been unsuccessful. In fact, early versions of an experimental vaccine seemed to make the disease worse in some infants, raising the possibility that some aspect of our immune response to the virus actually contributes to the symptoms.

RSV has a high attack rate — the term scientists use for the chances that a susceptible person will get the infection if exposed to it. That, plus our generally poor defenses against it, explain the frequent epidemics. Every year a new crop of susceptible infants enters the population.

So what is bronchiolitis? What does it look like? In medical terminology, adding the ending “itis” to a word means that whatever comes before is inflamed. Thus tonsillitis is an inflammation of the tonsils and appendicitis means an inflamed appendix. So bronchiolitis is an inflammation of the bronchioles, the final part of the system of air-conducting tubes that connect the lungs with the outside world. Beyond the bronchioles are the aveoli, the grape-like clusters of air sacs where the business of the lungs — getting oxygen into our bodies and carbon dioxide out — takes place.

Bronchiolitis is a disorder of blocked small airways. This prevents air from getting in and out normally, primarily out.  The principal source of the blockage is that the bronchiole tubes are blocked from swelling of the walls and from debris caused by the RSV infection — bits of broken airway cells and mucous plugs. This picture shows what it looks like:

Infants are the ones who have the most trouble breathing with bronchiolitis. There are several reasons for this, but a key one is the construction of an infant’s chest. When small airways get blocked, we use our chest muscles — tightening them — to force air in and out of our lungs. We are helped in doing this by the fact that our lungs are encased in a fairly rigid rib cage; when we use our muscles to squeeze or expand our chest the system works like a bellows. Infants can’t do this well because the ribs across the entire front half of their chest are not yet solid bone — they are still soft cartilage.  So when a small infant tries to move air against anything that is restricting airflow, like clogged bronchioles, his chest tends to sink inwards, causing what we call retractions. These are easiest to see just below the last ribs. They especially have trouble forcing air out, so their chests become hyperexpanded with air, making it look as if their chests are puffed out a little. The other reason infants have so much trouble handling debris in their bronchioles is that these tubes are already much smaller to start with, so they get more easily clogged up than do the larger airways of older children.

How does a child with bronchiolitis look? Typically they are breathing faster than the normal respiratory rate of 25-35; often they are puffing along at 60-70 breaths per minute. They also will show those chest retractions and have a cough. Fever is uncommon. They may look a bit dusky from not having enough oxygen in the blood. They often have trouble feeding because they are breathing so fast. The fast breathing, along with the poor feeding, often makes them become dehydrated. Our breath is completely humidified, so when we breathe fast we lose more water.

What can we do to treat bronchiolitis? You read above that we have no specific medicine that will kill the virus. What we have to offer is what we call supportive care: treating the symptoms until the infection clears. Some of that supportive care has been based on how we treat asthma, another condition where air has trouble getting into and out of the lungs. Some years ago we learned that these asthma treatments, such as albuterol breathing treatments and steroids, helped very few children. Even though we knew that fact, a common thing was to try the asthma drugs and see if they helped an individual child, then continue them if it appeared they did.

The new recommendations come down strongly on the side of not even trying these asthma drugs because compelling research argues against it. More than that, the new recommendations say not to take a chest x-ray because it doesn’t help the child and may cause more risk; taking a chest x-ray often leads to physicians over-diagnosing pneumonia and giving antibiotics when they aren’t called for. The new recommendations even suggest we stop testing for the RSV virus, which has been commonly done, because it doesn’t affect anything we do. One thing the recommendations continue from the past is providing good hydration, as well as oxygen if the child needs it — some do, but many do not.

One important point to make, especially for me as a pediatric intensivist, is that these recommendations only apply to children with milder disease. Some children with bronchiolitis become extremely ill and require help with their breathing, either with soft plastic prongs in their nose that deliver oxygen and air pressure or with a mechanical breathing machine. For those children we do what it takes to keep their blood oxygen levels in the safe range.

Old ways die hard, and it will be interesting to see if physicians follow these new recommendations. My guess is that, over time, we will. More and more we are learning that therapies that add risk and cost, without adding any benefit, are not the way to go.

Pediatric Newsletter #12: genetic vs environmental causes for autism and more

November 23, 2014  |  General  |  No Comments

Here is the latest of my more or less monthly newsletter on pediatric topics. In it I highlight and comment on new research, news stories, or anything else about children’s health that I think will interest parents. If you want to subscribe to it and get it in the form of an email each month there is a sign-up form at the very bottom of my home page.

How much of autism is caused by genetic factors and how much by environmental ones?

Autism is always very much in the news. There is intense controversy about its cause, although the bottom line is that we don’t know. It also appears to be increasing, although we don’t know how much of this is what we call ascertainment bias — finding something more when we look for it more. A big part of the controversy is the relative contributions of genetic vs environmental factors.

recent study from Sweden offers useful information about this. The study was immense, over two million children, far larger than any previous ones.

The bottom line is there appears to be more or less a 50/50 split in the relative contributions of nature and nurture. That is, genetics contributes 50% of the causative factors, environment 50%. This is an important finding. Overall, a child with a sibling with autism has a 10-fold higher chance for getting the disorder than does a child without such a family history. The middle part of the article is dense, but the first part and the conclusions are understandable by non-physicians.

Those laundry detergent pods can be quite dangerous for your toddler

recent study examined how common poisoning or other injuries are from those convenient laundry detergent pods. I have seen one severe case myself, causing breathing problems bad enough to land the child on a mechanical ventilator. This study surveyed poison control centers to find out the extent of the problem. It is not trivial.

Between 2012 and 2013 there were over 17,000 exposures to these things, a 600% increase from the previous year, indicating how popular they have become. I can see why they are popular — I use them myself. It’s a lot easier to toss one of them into the wash than pour out detergent from a bottle.

But that convenience comes at a potential risk. Toddlers put anything and everything into their mouths, and the alluring, brightly colored pods quickly dissolve when wet. The survey revealed that there were over a hundred children who required emergency placement of a breathing tube and one death.

So if you use those convenient items, make extra sure your toddler can’t get at them.

Finally we have vaccines for all strains of the deadly meningococcus

Infections from a bacteria called Neisseria meningitides (aka meningococcus) are horrible and often fatal. I have seen probably 20 children die in my career from this, and at least as many suffer terrible complications, such as loss of arms or legs.  This is the bacteria you have probably read stories in the paper about because it can cause lethal mini-epidemics in schools and any place children and adolescents come together in close contact. The infections come in a couple of varieties: meningitis alone, meningitis with septicemia, or septicemia alone. Of the three, the last is generally the worst, with a high mortality rate and serious aftereffects in survivors.

There are five strains of meningococcus that cause disease. We have had a vaccine for four of them for many years. But one of them, group B, has been difficult to develop an effective vaccine for, and this strain is a common cause of disease. The big news, and it is big, is that we now have a vaccine for group B. Meningococcal vaccine is recommended for adolescents — see your doctor about getting it for your child.

All about caffeine: what is it, where is it, and how does it work?

This one is more for you parents than it is for your children. I ran across an excellent and readable summary of what we know about caffeine. First of all, the stuff is everywhere. It is a brain stimulant that is found in many food and drink products, although the most common sources are coffee, tea, and now energy drinks like Red Bull. Here are some fun facts about it.

  1. 68 million Americans drink 3 cups of coffee per day
  2. 21 million Americans drink more than 6 cups per day
  3. 50% of caffeine users experience unpleasant symptoms when they stop, typically headaches, which can last for a week
  4. 5 grams of it can be fatal, but that is 30-40 cups of coffee
Risk of autism: how much is inherited and how much is from environmental causes?

Risk of autism: how much is inherited and how much is from environmental causes?

November 19, 2014  |  General  |  No Comments

Autism was first reported in the medical literature 70 years ago. In 1943 a child psychologist named Leo Kanner described a child with social difficulties and repetitive, stereotypic movements; the following year Hans Asperger described four such children. Since then we have gradually learned more about what we now call autism spectrum disorders (ASD), although we still do not know what causes it. From early on it was apparent that the risk for developing autism was higher among children who had other family members with the disorder. But how much higher? Twice as high? Ten times as high? Recently a very good study from Sweden has given us solid information about genetic risk for ASD. The study’s title is “The Familial Risk of Autism“.

Sweden has a very centralized and complete health care and medical record system. This allows tracking of relatives beyond the immediate family — cousins and grandparents — as well as siblings and half-siblings. One thing to note, however, is that Swedish society is much more homogeneous than ours, something that we should keep in mind when we interpret the results. The researchers also made no attempt to understand what environmental factors could be playing a role in ASD. The power of the study is that the authors asked a simple question: What is the risk for an individual child for having ASD and how is that risk affected by having other family members with the disorder?

The authors studied just over two million Swedish children born between 1982 and 2006. That is a huge study group, much higher than earlier ASD studies. What they measured was the relative recurrence risk for autism. This is the risk for the disorder among children with family members who have it compared to the risk for children with no family members with ASD. If the risk is the same for both groups, there is no genetic component. The extent to which the risk is greater for children who have affected family members is the contribution of genetic factors. This risk should get higher the closer the relationship — a sibling should cause a higher risk than, say, a first cousin. There is an important caveat to keep in mind here. Close family members often share the same environment as well as the same genes. A standard way to get around this problem is to study closely related individuals, especially identical twins, raised in separate environments. The authors weren’t able to do that, but it is still a very powerful and compelling study simply because of its huge size.

So what did they find? The risk for ASD in a given child was 10-fold higher if there was an affected full sibling, 3-fold higher if there was an affected half-sibling, and 2-fold higher if there was an affected first cousin. Plugging these numbers into a series of calculations, the authors determined that, overall, the contribution of genetic factors to ASD was 50%; that of environmental factors was 50%. So, half and half.

Autism is a complicated disorder. Like other neurological problems with both genetic and environmental components, such as schizophrenia, it is most likely a complex interplay of environmental influences on a genetically susceptible brain. There is an enormous amount of ongoing research to identify what is happening and what we can do about it, and I fully expect useful answers and treatments within the next few years. Studies such as this one are crucial to figuring it out.