Fever today is not the same fever of 30 years ago.
What does this mean?
To begin with, one must understand that fever itself (for the most part) is not dangerous. Fever, defined as 100.4 degrees Farenheit or higher, is not a disease in and of itself; rather it is a symptom or a sign of an underlying disease. Viewing fever as a disease will lead to accepting common misconceptions and evoke unneccessary anxiety.
Several times a week in my office I see children with a fever reaching 104-105 degrees who recover without incident. Studies have indicated that fever itself is not worrisome until a child reaches 107 or higher. Fortunately, fever greater than 107 will usually occur only in a child with an underlying neurological deficit or, very rarely, an environmental heatstroke (e.g. being locked in a car inadvertently in the middle of a Houston summer).
When your child has a fever, his body is telling you that he is sick (or sometimes overheated by external causes). In the majority of cases, a fever indicates that your child has become infected with a germ. There are other causes of fever as well. For example, after your child has received immunizations, he may exhibit a non-worrisome fever for a day or two. In this case the body is reacting to either dead or weakened germs or germ fragments that have been purposefully introduced to create beneficial lasting immunity.
Most parental anxiety with fever revolves around the fear that there may be potential harm to the child as a result of the fever. Specifically, the parent is often worried about damage to the brain.
In truth, fever will rarely damage or hurt the child (as mentioned above), although the underlying germ causing the fever potentially could. Which is why as a pediatrician, I am seldom concerned about the fever itself; I am always far more concerned about the source of the fever. My job as a pediatrician, when presented with a febrile child, is to deduce the source of the fever and then to decide whether the source is of concern or not (and it most often is not).
If the fever is coming from a brain infection, pneumonia or kidney infection, I am very worried about the child because all of these infections are quite serious and potentially life-threatening if not treated properly. However, if the fever is coming from a cold virus or stomach virus (which is far more likely, statistically), I am not worried about the child because most of these infections resolve on their own with time and pose little to no threat to the well-being of a child.
Which brings me back to my opening statement: fever today is not the same fever of 30 years ago.
The reason is simple: vaccines. The current gamut of immunizations, while currently controversial (although the tide is finally shifting - thank goodness), are perhaps the greatest advancement of modern medicine in the past century. The vaccinations we currently administer confer protection against the deadly germs which our parents' generation grew up with. Germs which cause meningitis, diphtheria, tetanus, pneumonia, measles, whooping cough, epiglottitis . . . and the list goes on and on.
In present day, when a child who follows the recommended vaccine schedule presents to me with fever, there are many germs that I can automatically factor out while making my diagnosis. As a result of immunizations, I already know what a child CANNOT possibly have as the source of the fever. As a result, I can focus on a much more narrow list of the usual suspects as I begin my detective work.
Imagine playing the game Clue, knowing that Professor Plum, Colonel Mustard and Mrs. Peacock are already behind bars. It just makes the game that much easier (although not as easy as peeking in the envelope like my brother often did). Likewise, if I can evaluate a fever already knowing that measles, mumps and diptheria are out of the running, it makes my job a lot easier. Which is why as a pediatrician I have a leg up on my father, who had to do the same job without the benefits of many of the newer vaccines.
Of course, as antibiotic resistance is on the rise, the landscape of our usual suspects is beginning to change once again, hence the vital need for judicious use of antibiotics (but that is a topic for a separate blog). Nonetheless, fever today represents a far more limited field of possible dangerous causes than the fever of 30 years ago. That is why I sympathize when a grandmother is still apprehensive of her grandchild's fever. She lived through the years of measles, mumps and diphtheria. Many of them remember what a fever could represent in their days and understandably harbor anxiety about their grandchild's temperature.
But as a new generation grows up with a legion of vaccinated and protected children (for the most part), there will hopefully be a societal shift in the right direction concerning the fear of fever.
Let me conclude by noting that fever can still and sometimes does represent meningitis, pneumonia or a dangerous infection. As far as vaccines have advanced, there is still more work to be done. So when a child with a fever is acting sick (i.e. not playing, not eating, appears ill, doesn't smile, lacks energy) he or she must be evaluated by a doctor.
However, over time, with the proper communciation between a well-informed pediatrician and an attentive mother, a parent can begin to grasp when to be worried and when not to be worried. This maternal instinct can be honed over time if a mom is equipped with the right information and the proper guidance from her pediatrician.
I am proud to say that in my practice I now have many veteran mothers who don't come in for every fever (although they initially may have), but only when there is an accompanying noticeable change in the activity level of her child. I could write oodles of blogs to delineate this skill, but there is a level of understanding that can only come from repeated communication and hands-on experience.
The end result is a family that has a far lower level of anxiety about fever and a far higher understanding of what fever truly is and represents. It is a benefit to the parent and to the pediatrician alike. It saves the mom unneccesary trips to my office, copay money and frustration while it frees up my appointment slots for the kids who truly need to be seen.
There are many aspects of fever I did not cover in this blog, but hopefully this can serve as a primer in building a firmer knowledge base for the anxious parent who wants to learn more!
Wednesday, August 20, 2008
Friday, July 4, 2008
Post #9 "Dry Drowning": How Worried Should You Really Be?
On June 1, 2008 10-year old Johnny Jackson got water in his lungs while swimming in the pool. He walked home, took a bath, and went to bed; he died in his sleep during a nap an hour later. The county coroner reported water in the boy's lungs.
On June 5, 2008 todayshow.com reported the following:
"According to the Centers for Disease Control, some 3,600 people drowned in 2005, the most recent year for which there are statistics. Some 10 to 15 percent of those deaths was classified as “dry drowning,” which can occur up to 24 hours after a small amount of water gets into the lungs. In children, that can happen during a bath."
While the 3,600 number is fairly accurate (3,582 to be exact), the 10-15% statistic is erroneous and the CDC enterprise communication officer Sandy Bonzo has since issued a statement as such. There are no statistics on the percentage of "dry drownings".
Soon after Johnny's unfortunate drowning, there was a full-on media blitz with the Today Show spearheading the charge. The media did what the media does best: it struck the "Moms you had better take note for your chid's sake or else suffer the consequences" nerve. What followed was a slew of stories on multiple websites, newspapers and local news channels on "dry drowning". . . the story at 10 and you had better not miss it if you care about your child. . .
Although the phrase "dry drowning" is an ideal term for a newscaster hoping to invoke fear in the heart of the average mother, it is a somewhat misleading phrase. In fact, there are so many different phrases used to describe drowning (such as wet drowning, dry drowning, near drowning, secondary drowning, passive drowning) that it leads to ambiguity in what physiologically has actually occurred in each individual case. In an attempt to simplify matters, the 2002 World Congress on Drowning held in Amsterdam defined drowning as the process of experiencing respiratory impairment from submersion/immersion in liquid.
So what do people mean by "dry drowning" then?
It's hard to pinpoint exactly as there is no set definition, but it seems to be any situation where a person cannot breathe and water does NOT enter the lungs. In this sense "dry drowning" could conceivably apply to laryngospasms (spasms of your windpipe) and such external causes such as a lung puncture or a heavier-than-air gas filling the lungs. Even in an underwater drowning, it is conceivable that a person could suffer laryngospasms and die from oxygen deprivation without water entering the lungs, and hence be classified as a dry drowning when in fact the person was fully submerged underwater. You can see how there is ambiguity and confusion in using these terms, which is why the 2002 Congress uses one universal definition.
So exactly what happened in Johnny's case then?
Most likely Johnny did swallow some water while he played in the pool and some of the water made it into his lungs (which then technically is not a "dry drowning" even though the death occured out-of-water). This water then led to a loss of pulmonary function after the "loss or inactivation of surfactant" of the alveoli in the lungs. Surfactant is an amphiphilic compound which reduces the surface tension of your lungs allowing you to breathe. Basically, it helps your lungs to expand easily allowing oxygen to enter. The water that made it into Johnny's lung disrupted the ability of his natural surfactant and therefore as he napped, he was unable to breathe properly leading to his unfortunate demise.
This type of situation is uncommon, however there are no exact statistics on it. And although it can be a scary concept to every mother whose child goes swimming during the summertime and then on occasion takes a nap, things must be put into perspective.
First, most drownings do not occur this insidiously. Rather, the majority of drownings happen where it is clear that the child has been submerged under water. In this sense, things can be done to avoid the obvious drowning: close supervision, fences/covers/alarms around unused pools, CPR training, etc.
Second, even in a case such as Johnny's, there will be some warning signs: accidental ingestion of water, forceful coughing >1 minute right after coming out of the water, difficulty breathing, extreme fatigue and changes in behavior. If your child clearly is having an excessive amount of coughing and difficulty breathing right after swimming, it would be evident to the observant mother.
Finally, there is more risk in driving your child to the local movie theater than there is in monitored water play.
The bottom line is that like many other risks that the media has over-hyped, "dry drowning" is a real risk but a very unlikely one if you follow safe water practices. One good thing about this media blitz has been an increased awareness about general water safety, which only benefits summer activities. In this sense, hopefully Johnny's life will serve as a beacon to every mother and child swimming this summer.
On June 5, 2008 todayshow.com reported the following:
"According to the Centers for Disease Control, some 3,600 people drowned in 2005, the most recent year for which there are statistics. Some 10 to 15 percent of those deaths was classified as “dry drowning,” which can occur up to 24 hours after a small amount of water gets into the lungs. In children, that can happen during a bath."
While the 3,600 number is fairly accurate (3,582 to be exact), the 10-15% statistic is erroneous and the CDC enterprise communication officer Sandy Bonzo has since issued a statement as such. There are no statistics on the percentage of "dry drownings".
Soon after Johnny's unfortunate drowning, there was a full-on media blitz with the Today Show spearheading the charge. The media did what the media does best: it struck the "Moms you had better take note for your chid's sake or else suffer the consequences" nerve. What followed was a slew of stories on multiple websites, newspapers and local news channels on "dry drowning". . . the story at 10 and you had better not miss it if you care about your child. . .
Although the phrase "dry drowning" is an ideal term for a newscaster hoping to invoke fear in the heart of the average mother, it is a somewhat misleading phrase. In fact, there are so many different phrases used to describe drowning (such as wet drowning, dry drowning, near drowning, secondary drowning, passive drowning) that it leads to ambiguity in what physiologically has actually occurred in each individual case. In an attempt to simplify matters, the 2002 World Congress on Drowning held in Amsterdam defined drowning as the process of experiencing respiratory impairment from submersion/immersion in liquid.
So what do people mean by "dry drowning" then?
It's hard to pinpoint exactly as there is no set definition, but it seems to be any situation where a person cannot breathe and water does NOT enter the lungs. In this sense "dry drowning" could conceivably apply to laryngospasms (spasms of your windpipe) and such external causes such as a lung puncture or a heavier-than-air gas filling the lungs. Even in an underwater drowning, it is conceivable that a person could suffer laryngospasms and die from oxygen deprivation without water entering the lungs, and hence be classified as a dry drowning when in fact the person was fully submerged underwater. You can see how there is ambiguity and confusion in using these terms, which is why the 2002 Congress uses one universal definition.
So exactly what happened in Johnny's case then?
Most likely Johnny did swallow some water while he played in the pool and some of the water made it into his lungs (which then technically is not a "dry drowning" even though the death occured out-of-water). This water then led to a loss of pulmonary function after the "loss or inactivation of surfactant" of the alveoli in the lungs. Surfactant is an amphiphilic compound which reduces the surface tension of your lungs allowing you to breathe. Basically, it helps your lungs to expand easily allowing oxygen to enter. The water that made it into Johnny's lung disrupted the ability of his natural surfactant and therefore as he napped, he was unable to breathe properly leading to his unfortunate demise.
This type of situation is uncommon, however there are no exact statistics on it. And although it can be a scary concept to every mother whose child goes swimming during the summertime and then on occasion takes a nap, things must be put into perspective.
First, most drownings do not occur this insidiously. Rather, the majority of drownings happen where it is clear that the child has been submerged under water. In this sense, things can be done to avoid the obvious drowning: close supervision, fences/covers/alarms around unused pools, CPR training, etc.
Second, even in a case such as Johnny's, there will be some warning signs: accidental ingestion of water, forceful coughing >1 minute right after coming out of the water, difficulty breathing, extreme fatigue and changes in behavior. If your child clearly is having an excessive amount of coughing and difficulty breathing right after swimming, it would be evident to the observant mother.
Finally, there is more risk in driving your child to the local movie theater than there is in monitored water play.
The bottom line is that like many other risks that the media has over-hyped, "dry drowning" is a real risk but a very unlikely one if you follow safe water practices. One good thing about this media blitz has been an increased awareness about general water safety, which only benefits summer activities. In this sense, hopefully Johnny's life will serve as a beacon to every mother and child swimming this summer.
Wednesday, June 11, 2008
Post#8 A Car Seat Conundrum
Henary B, Sherwood C, Crandall J, et al. Car safety seats for children: rear facing for best protection. Inj Prev. 2007;13(6): 398-402
A 2007 study on injury prevention, cited above, shows that children ages 1-2 years of age who were placed in a forward-facing car seat had a 5.32 times greater risk for serious injury as opposed to children in a rear-facing car seat. Five times the risk. WOW.
It is common practice to keep children rear-facing until 1 year of age AND 20 lbs. However, after children turn 1, most moms can't wait to turn the car seat forward. The change in position allows greater visibility of the child, more interaction with the child (perhaps a negative in terms of accident prevention), easier access to the child (again maybe not so good for accidents), and a perception that the child will now be happier with the new and improved view of the mother and the world through the front windshield. I certainly thought our first child cried less after we turned her forward.
But this new finding indicates that the child will be safer facing the world through the rear window, as children in Sweden do until 4 years of age. In fact, the study found that for children under 12 months, the safety factor of a rear-facing car seat was only 1.79 times higher than a forward-facing car seat. Meaning, from a statistical standpoint, it is even more important to keep them rear-facing from 1-2 years of age then it is before they turn 12 months.
This data poses a conundrum: At what point does the comfort and well-being of the child/family trump a statistical safety factor?
There is no question in my mind that my first child hated her car seat for the first 12 months of her life. No, hated is too weak of a word. Loathed. My wife and I counted the days until we could turn her forward, and in fact we cheated by graduating her a few weeks shy of her first birthday. Life in our car became significantly more serene once we made the change, and driving no longer raised our blood pressure.
And though the above study clearly demonstrates we took a risk in making the switch, I could argue a significant counterpoint. I believe the harrowing cries produced by my daughter while driving posed a risk in and of themselves. The amount of anxiety that her crying generated was a driving distraction which could have (but never did) led to an accident.
Did her crying offset the potential 5X increase in risk we took by turning her forward? I'm not sure and never will be. Would I change what we did with her based on this new data? Perhaps, but probably not.
However, I do plan to keep my third child (and would have with my second child) rear-facing for as long as he (and my wife) will tolerate. Seems the boys (child #2 and #3) are more content facing the world from the rear. (I'm not sure if there are any implications here about their future!)
And like many pieces of advice available to mothers out there, each must be weighed and individually determined for each family. Not only that, depending on the demeanor of the child in his/her car seat, an individual family may use different timelines to make the switch forward for each of their children.
One thing is clear: I do believe that this information is pertinent, and pediatricians need to make it available to their patient population so that each family can make an informed decision as to what is best and ultimately safest for them.
A 2007 study on injury prevention, cited above, shows that children ages 1-2 years of age who were placed in a forward-facing car seat had a 5.32 times greater risk for serious injury as opposed to children in a rear-facing car seat. Five times the risk. WOW.
It is common practice to keep children rear-facing until 1 year of age AND 20 lbs. However, after children turn 1, most moms can't wait to turn the car seat forward. The change in position allows greater visibility of the child, more interaction with the child (perhaps a negative in terms of accident prevention), easier access to the child (again maybe not so good for accidents), and a perception that the child will now be happier with the new and improved view of the mother and the world through the front windshield. I certainly thought our first child cried less after we turned her forward.
But this new finding indicates that the child will be safer facing the world through the rear window, as children in Sweden do until 4 years of age. In fact, the study found that for children under 12 months, the safety factor of a rear-facing car seat was only 1.79 times higher than a forward-facing car seat. Meaning, from a statistical standpoint, it is even more important to keep them rear-facing from 1-2 years of age then it is before they turn 12 months.
This data poses a conundrum: At what point does the comfort and well-being of the child/family trump a statistical safety factor?
There is no question in my mind that my first child hated her car seat for the first 12 months of her life. No, hated is too weak of a word. Loathed. My wife and I counted the days until we could turn her forward, and in fact we cheated by graduating her a few weeks shy of her first birthday. Life in our car became significantly more serene once we made the change, and driving no longer raised our blood pressure.
And though the above study clearly demonstrates we took a risk in making the switch, I could argue a significant counterpoint. I believe the harrowing cries produced by my daughter while driving posed a risk in and of themselves. The amount of anxiety that her crying generated was a driving distraction which could have (but never did) led to an accident.
Did her crying offset the potential 5X increase in risk we took by turning her forward? I'm not sure and never will be. Would I change what we did with her based on this new data? Perhaps, but probably not.
However, I do plan to keep my third child (and would have with my second child) rear-facing for as long as he (and my wife) will tolerate. Seems the boys (child #2 and #3) are more content facing the world from the rear. (I'm not sure if there are any implications here about their future!)
And like many pieces of advice available to mothers out there, each must be weighed and individually determined for each family. Not only that, depending on the demeanor of the child in his/her car seat, an individual family may use different timelines to make the switch forward for each of their children.
One thing is clear: I do believe that this information is pertinent, and pediatricians need to make it available to their patient population so that each family can make an informed decision as to what is best and ultimately safest for them.
Sunday, May 25, 2008
Post #7 The Vaccine Controversy
An excellent article covering the controversy over vaccines and autism. I have 3 children and they are all following the A.C.I.P. immunization schedule. They are all healthy and doing well. . . slightly mischievous, but healthy!
VACCINES & AUTISM: Myths and Misconceptions
The Anti-Vaccination Movement
Despite the growing scientific consensus that vaccines are safe and that neither vaccines nor mercury cause autism, a stubborn vocal minority claims otherwise, threatening the effectiveness of this public health program.
STEVEN NOVELLA
Steven Novella, MD, is an assistant professor of neurology at Yale University School of Medicine. He is the host of The Skeptics’ Guide to the Universe, a weekly science podcast (www.theskepticsguide.org), author of the NeuroLogica blog (www.theness.com/ NeuroLogicaBlog), and president of the New England Skeptical Society www.theness.com).
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Michelle Cedillo has autism, which her parents believe is the result of her childhood vaccines. In June 2007 they had the opportunity, along with eight other families, to make their case to the Autism Omnibus—a U.S. Court of Federal Claims that was presided over by three “special masters” appointed for the purpose. These nine cases are the first test cases that will likely determine the fate of 4,800 other claims made over the past eight years for compensation for injuries allegedly due to childhood vaccines.
Vaccines are one of the most successful programs in modern health care, reducing, and in some cases even eliminating, serious infectious diseases. Public support for the vaccination program remains strong, especially in the United States where vaccination rates are currently at an all-time high of >95 percent (CDC 2004). Yet, despite a long history of safety and effectiveness, vaccines have always had their critics: some parents and a tiny fringe of doctors question whether vaccinating children is worth what they perceive as the risks. In recent years, the anti-vaccination movement, largely based on poor science and fear-mongering, has become more vocal and even hostile (Hughes 2007).
Of course, vaccines are not without risk (no medical intervention is), although the benefits far outweigh those risks. Because vaccines are somewhat compulsory in the United States—although opting out is increasingly easy—a National Vaccine Injury Compensation Program was established to streamline the process for compensation for those who are injured due to vaccines (USDOJ 2007). It is this program to which the Cedillo and 4,800 other families are applying for compensation.
In the last decade, the anti-vaccine movement, which includes those who blame the MMR (mumps-measles-rubella) vaccine for autism, has largely merged with those who warn that mercury toxicity is the cause of many of the ills that plague mankind. The two groups have come together over the issue of thimerosal, a mercury-based preservative in some vaccines. They believe that it was the use of thimerosal in childhood vaccines that led to the apparent autism epidemic beginning in the 1990s.
Autism is a complex neurological disorder that typically manifests in the first few years of life and primarily involves a deficiency of typical social skills and behavior. In the 1990’s, the number of autism diagnoses significantly increased, from between one and three to about fifteen cases per ten thousand, although the true incidence is probably between thirty and sixty per ten thousand (Rutter 2005). During this same period, the number of vaccines given in the routine childhood schedule also increased. This led some to assume, or at least speculate, causation from correlation—perhaps the vaccines or something in them created this “epidemic” of autism.
We can now say, from multiple independent lines of evidence, that vaccines do not cause autism. For one thing, the autism “epidemic” probably does not represent a true increase in the disorder, but rather an artifact of expanding the diagnosis (now referred to as autism spectrum disorder, ASD) and increased surveillance (Taylor 2006).
In 1998, researcher Andrew Wakefield and some of his colleagues published a study in the prestigious English medical journal Lancet that claimed to show a connection between the MMR vaccine and autism (Wakefield 1998). Wakefield’s theory was that the MMR vaccine, which contains a live virus, can cause in susceptible children a chronic measles infection. This in turn leads to gastrointestinal disturbances, including what he calls a “leaky gut” syndrome, which then allows for certain toxins and chemicals, like those from bread and dairy that are normally broken down by the gut, to enter the bloodstream where they can access and damage the developing brain.
Although the study was small and the evidence was considered preliminary, this article sparked a firestorm. As a result of the study and the media coverage that followed (and continues to this day), MMR compliance in Great Britain plummeted, resulting in a surge of preventable disease (Friederichs 2006).
Subsequent to the seminal article in the Lancet, many follow-up studies were performed testing the autism-MMR vaccine correlation. As the follow-up studies began to be published, however, it became increasingly clear that there was no link between MMR and autism. For example, a study in the British Medical Journal found that autism rates continued to climb in areas where MMR vaccination rates were not increasing (Taylor 1999). Another study found no association with MMR and autism or GI (gastrointestinal) disorders (Taylor 2002). Other studies showed no difference in the diagnosis rate of autism either before or after the MMR vaccine was administered (Honda 2005), or between vaccinated and unvaccinated children (Madsen 2002). Most recently, a study found that there was no decrease in autism rates following removal of the MMR vaccine in Japan (Honda 2005).
In 2001, the Institute of Medicine (IOM) reviewed all of the MMR-autism data available to date and concluded that there was no association and essentially closed the case (IOM 2001)—a conclusion confirmed by still later studies, such as the Honda study in Japan cited above.
If Wakefield had simply been wrong in his preliminary findings, he would be innocent of any wrongdoing—scientists are not faulted if their early findings are not later vindicated. However, in May 2004, ten of Wakefield’s co-authors on his original paper withdrew their support for its conclusions. The editors of Lancet also announced that they withdrew their endorsement of the paper and cited as part of the reason an undisclosed potential conflict of interest for Wakefield, namely that at the time of its publication he was conducting research for a group of parents of autistic children seeking to sue for damages from MMR vaccine producers (Lancet 2004).
It gets worse. Investigative reporter Brian Deer has uncovered greater depths to Wakefield’s apparent malfeasance. Wakefield had applied for patents for an MMR vaccine substitute and treatments for his alleged MMR vaccine-induced gut disorder (Deer 2007). So, not only was he allegedly paid by lawyers to cast doubt on the MMR vaccine, but he stood to personally gain from the outcome of his research.
Andrew Wakefield. (Credit: Tom Miller) [Photo via Newscom]
Further, during the Cedillo case testimony, Stephen Bustin, a world expert in the polymerase chain reaction (PCR), testified that the lab Wakefield used to obtain the results for his original paper was contaminated with measles virus RNA. It was therefore likely, Bustin implied, that the PCR used by Wakefield was detecting this contamination and not evidence for measles infection in the guts of children with autism who had been vaccinated, as Wakefield claimed. And finally, Nicholas Chadwick testified that the measles RNA Wakefield found matched the laboratory contamination and did not match either any naturally occurring strain or the strain used in the MMR vaccine—a fact of which he had informed Wakefield (USCFC 2007).
All of this, plus other allegations still coming out, has caused Britain’s General Medical Council to call Wakefield before its “Fitness to Practise” panel for review of his alleged professional misconduct (GMC 2007).
Believers in the MMR-autism hypothesis dismiss the findings of the larger and more powerful epidemiological studies that contradict a link. Instead, they have turned Andrew Wakefield into a martyr, dismissing the evidence of his wrongdoing as a conspiracy against him designed to hide the true cause of autism from the public. Wakefield is unrepentant and maintains his innocence (Gorski 2007).
With the MMR-autism hypothesis scientifically dead, attention soon shifted to thimerosal, a mercury-based preservative found in some childhood vaccines (although not the MMR vaccine). There is little doubt, and no controversy, that mercury, the major component of thimerosal, is a powerful neurotoxin, or poison to the brain. However, toxicity is always a matter of dose. Everything becomes toxic in a high enough dose; even too much water or vitamin C can kill you. So the real question is whether the amount of mercury given to children in vaccines containing thimerosal was enough to cause neurological damage.
Author of the book Evidence of Harm: Mercury in Vaccines and the Autism Epidemic David Kirby (center) speaks as president Harvey Fineberg (left) of the Institute of Medicine listens during an interview by moderator Tim Russert (right) on NBC’s Meet the Press August 7, 2005, at the NBC studios in Washington, D.C. Fineberg and Kirby talked about the rising number of autism diagnoses among children and the controversial charges of a government conspiracy to allow mercury exposures from childhood vaccines to more than double between 1988 and 1992. The Institute of Medicine reviewed all MMR-autism data and concluded that there was no association. (Photo by Alex Wong/Getty Images for Meet the Press) [Photo via Newscom]
Proponents of the mercury hypothesis argue that the ethylmercury found in thimerosal was given in doses exceeding Environmental Protection Agency limits. This load of mercury should be considered with prenatal vaccine loads possibly given to mothers, and to other environmental sources of mercury, such as seafood. Furthermore, underweight or premature infants received a higher dose by weight than larger children. Some children, they argue, may have a specific inability to metabolize mercury, and perhaps these are the children who become autistic.
Fear over thimerosal and autism was given a huge boost by journalist David Kirby with his book Evidence of Harm (Kirby 2005). Kirby tells the clichéd tale of courageous families searching for help for their sick children and facing a blind medical establishment and a federal government rife with corruption from corporate dollars. Kirby echoes the core claim that as the childhood vaccine schedule increased in the 1990s, leading to an increased cumulative dose of thimerosal, autism diagnoses skyrocketed.
In the end, Evidence of Harm is an example of terrible reporting that grossly misrepresents the science and the relevant institutions. As bad as Kirby’s position was in 2005, in the last two years the evidence has been piling up that thimerosal does not cause autism. Rather than adjusting his claims to the evidence, Kirby has held fast to his claims, which has made him a hero alongside Wakefield of the mercury-autism-connection crowd as he has squandered his credibility.
There have now been a number of epidemiological and ecological studies that have all shown no correlation between thimerosal and autism (Parker 2004 and Doja 2006). I have already mentioned that the current consensus holds that there is no real autism epidemic, just an artifact of how the diagnosis is made. If there’s no epidemic, there’s no reason to look for a correlation between thimerosal and autism. This has been backed up by The Institute of Medicine, which has also reviewed all the available evidence (both epidemiological and toxicological) and concluded that the evidence does not support the conclusion that thimerosal causes autism (IOM 2004).
Especially damning for the thimerosal hypothesis are the recent studies that clearly demonstrate that early detection of autism is possible long before the diagnosis is officially made. Part of the belief that vaccines may cause autism is driven by the anecdotal observation by many parents that their children were normal until after they were vaccinated—autism is typically diagnosed around age two or three. However, more careful observations indicate that signs of autism are present much earlier, even before twelve months of age, before exposure to thimerosal (Mitchell 2006). In fact, autism expert Eric Fombonne testified in the Autism Omnibus hearings that Michelle Cedillo displayed early signs of autism clearly visibly on family video taken prior to her receiving the MMR vaccine (USCFC 2007).
Meanwhile, evidence is accumulating that autism is largely a genetic disorder (Szatmari 2007). This by itself does not rule out an environmental factor, but it is telling that genetic research in autism has proven so fruitful.
Mercury alarmists, in the face of this negative evidence, have been looking for rationalizations. Some have argued that the thimerosal in prenatal vaccines may be to blame, but recent evidence has shown a negative correlation there as well (Miles 2007).
What we have are the makings of a solid scientific consensus. Multiple independent lines of evidence all point in the same direction: vaccines in general, and thimerosal in particular, do not cause autism, which rather likely has its roots in genetics. Furthermore, true autism rates are probably static and not rising.
A demonstrator carries a sign protesting the use of mercury in vaccines past the U.S. Capitol in Washington July 20, 2005. Some three hundred people marched demanding that mercury not be used in vaccines anymore amid concern that it is the cause of autism and other neurological diseases in children. However, numerous studies show no correlation between Thimerosol and autism. (Nicholas Kamm/AFP/Getty Images) [Photo via Newscom]
The only researchers who are publishing data that contradicts this consensus are the father-and-son team of Mark and David Geier. They have looked at the same data and concluded that thimerosal does correlate with autism. However, the hammer of peer-review has come down on their methods and declared them fatally flawed, thus rendering their conclusions invalid or uninterpretable (Parker 2004). Also, like Wakefield, their reputations are far from clean. They have made something of a career out of testifying for lawyers and families claiming that vaccines caused their child’s autism, even though the Geiers’ testimony is often excluded on the basis that they lack the proper expertise (Goldacre 2007). The Geiers were not even called as experts in the Autism Omnibus hearings.
The Geiers are now undertaking an ethically suspect study in which they are administering chelation therapy to children with autism in conjunction with powerful hormonal therapy allegedly designed to reduce testosterone levels. Chelation therapy removes mercury, and so it is dependent upon the mercury hypothesis, which is all but disproved. Moreover, there is no clinical evidence for the efficacy of chelation therapy. The treatment is far from benign and is even associated with occasional deaths (Brown 2006).
With the scientific evidence so solidly against the mercury hypothesis of autism, proponents maintain their belief largely through the generous application of conspiracy thinking. The conspiracy claim has been made the loudest by Robert F. Kennedy Jr. in two conspiracy-mongering articles: Deadly Immunity published on Salon.com in 2005 (Kennedy 2005), and more recently Attack on Mothers (Kennedy 2007). In these articles, RFK Jr. completely misrepresents and selectively quotes the scientific evidence, dismisses inconvenient evidence as fraudulent, accuses the government, doctors, and the pharmaceutical industry of conspiring to neurologically damage America’s children, and accuses scientists who are skeptical of the mercury claims of attacking the mothers of children with autism.
Despite the lack of evidence for any safety concern, the FDA decided to remove all thimerosal from childhood vaccines, and by 2002 no new childhood vaccines with thimerosal were being sold in the U.S. This was not an admission of prior error, as some mercury proponents claimed; instead, the FDA was playing it safe by minimizing human exposure to mercury wherever possible. The move was also likely calculated to maintain public confidence in vaccines.
This created the opportunity to have the ultimate test of the thimerosal autism hypothesis. If rising thimerosal doses in the 1990s led to increasing rates of autism diagnosis, then the removal of thimerosal should be followed within a few years by a similar drop in new autism diagnoses. If, on the other hand, thimerosal did not cause autism, then the incidence of new diagnoses should continue to increase and eventually level off at or near the true rate of incidence. In 2005, I personally interviewed David Kirby on the topic, and we both agreed that this would be a fair test of our respective positions. Also, in an e-mail to science blogger Citizen Cain, Kirby wrote, “If the total number of 3-5 year olds in the California DDS [Department of Developmental Services] system has not declined by 2007, that would deal a severe blow to the autism-thimerosal hypothesis” (Cain 2005).
Well, five years after the removal of thimerosal, autism diagnosis rates have continued to increase (IDIC 2007). That is the final nail in the coffin in the thimerosal-vaccine-autism hypothesis. The believers, however, are in full rationalization mode. David Kirby and others have charged that although no new vaccines with thimerosal were sold after 2001, there was no recall, so pediatricians may have had a stockpile of thimerosal-laden vaccines—even though a published inspection of 447 pediatric clinics and offices found only 1.9 percent of relevant vaccines still had thimerosal by February 2002, a tiny fraction that was either exchanged, used, or expired soon after (CDCP/ACIP 2002).
Those who argue for the link have put forth increasingly desperate notions. Kirby has argued that mercury from cremations was increasing environmental mercury toxicity and offsetting the decrease in mercury from thimerosal. The Geiers simply reinterpreted the data using bad statistics to create the illusion of a downward trend where none exists (Geier 2006). Robert Kennedy Jr. dodges the issue altogether by asking for more studies, despite the fact that the evidence he asks for already exists. He just doesn’t like the answer. Kennedy and others also point to dubious evidence, such as the myth that the Amish do not vaccinate and do not get autism. Both of these claims are not true, and the data RFK Jr. refers to is nothing more than a very unscientific phone survey (Leitch 2007).
The Autism Omnibus hearings have concluded, and while we await the decision due early next year, I am optimistic that science and reason will win the day. Just as shown in the 2005 Dover trial of intelligent design where the full body of scientific evidence was given a thorough airing in court and subjected to rules of evidence and the critical eyes of experienced judges, science tends to win out over nonsense. By all accounts, the lawyers for those claiming that vaccines caused their children’s autism put on pathetic performances with transparently shoddy science, while the other side marshaled genuine experts and put forth an impressive case.
But the stakes are high, and not just for the 4,800 families. If the petitioners win these test cases despite the evidence, it will open the floodgates for the rest of the 4,800 petitioners. This will likely bankrupt the Vaccine Injury Compensation Program and will also risk our vaccine infrastructure. Pharmaceutical companies will be reluctant to subject themselves to the liability of selling vaccines if even the truth cannot protect them from lawsuits.
Thimerosal still exists as a necessary preservative in multi-shot vaccines outside the United States, especially in poor third-world countries that cannot afford stockpiles of single-shot vaccines. Anti-thimerosal hysteria therefore also threatens the health of children in poor countries.
And of course a victory for the anti-vaccination activists would undermine public confidence in what is arguably the single most effective public health measure devised by modern science. This decrease in confidence will lead, as it has before, to declining compliance and an increase in infectious disease.
The forces of irrationality are arrayed on this issue. There are conspiracy theorists, well-meaning but misguided citizen groups who are becoming increasingly desperate and hostile, irresponsible journalists, and ethically compromised or incompetent scientists. The science itself is complex, making it difficult for the average person to sift through all the misdirection and misinformation. Standing against all this is simple respect for scientific integrity and the dedication to follow the evidence wherever it leads.
Right now the evidence leads to the firm conclusion that vaccines do not cause autism. Yet, if history is any guide, the myth that they do cause autism will likely endure even in the face of increasing contradictory evidence.
References
Brown, M.J., T. Willis, B. Omalu, and R. Leiker. 2006. Deaths resulting from hypocalcemia after administration of edetate disodium: 2003–2005. Pediatrics. 118(2):e534–36.
Centers for Disease Control. 2004. MMWR Weekly, November 12. 53(44):1041–1044. Available at www.cdc.gov/mmwr/preview/mmwrhtml/mm5344a4.htm.
Centers for Disease Control and Prevention Advisory Committee on Immunization. 2002. Practice Records of the meeting held on February 20–21, 2002, Atlanta Marriott North Central Hotel. Available at www.kevinleitch.co.uk/grabit/acip-min-feb.pdf.
Citizen Cain. 2005. Slouching Toward Truth—Autism and Mercury, November 30. Available at http://citizencain.blogspot.com/2005/11/slouching-toward-truth-autism-and_30.html.
Deer, B. 2007. Andrew Wakefield & the MMR scare: part 2. Available at http://briandeer.com/wakefield-deer.htm.
Doja, A., and W. Roberts. 2006. Immunizations and autism: a review of the literature. Canadian Journal of Neurological Sciences 33(4):341–46.
Friederichs, V., J.C. Cameron, and C. Robertson. 2006. Impact of adverse publicity on MMR vaccine uptake: a population based analysis of vaccine uptake records for one million children, born 1987–2004. Archives of Diseases of Children 200691(6):465–68. Epub 2006 April 25.
Geier, D.A., and M.R. Geier. 2006. An assessment of downward trends in neurodevelopmental disorders in the United States following removal of thimerosal from childhood vaccines. Medical Science Monitor 12(6):CR231–9. Epub 2006 May 29.
General Medical Council. 2007. July 16. Available at www.gmcpressoffice.org.uk/apps/news/events/index.php?month=7&year=2007&submit=Submit.
Goldacre B. 2007. Opinions from the medical fringe should come with a health warning. The Guardian, Saturday, February 24. Available at www.guardian.co.uk/science/2007/feb/24/badscience.uknews.
Gorski, D. 2007. Andrew Wakefield: The Galileo gambit writ large in The Observer. Respectful Insolence, July 9, 2007. Available at http://scienceblogs.com/insolence/2007/07/andrew_wakefield_the_galileo_gambit_writ.php.
Honda, H., Y. Shimizu, and M. Rutter. 2005. No effect of MMR withdrawal on the incidence of autism: a total population study. Journal of Child Psychology and Psychiatry 46(6):572–79.
Hughes, V. 2007. Mercury Rising. Nature Medicine 13(8):896–7. Epub 2007 August 31.
Infectious Diseases and Immunization Committee, Canadian Paediatric Society (CPS). 2007. Autistic spectrum disorder: No causal relationship with vaccines. Paediatrics & Child Health 12(5): 393–95. Available at www.cps.ca/english/statements/ID/pidnote_jun07.htm.
Institute of Medicine. 2001. Immunization Safety Review: Measles-Mumps-Rubella Vaccine and Autism. April 23. Available at www.iom.edu/CMS/3793/4705/4715.aspx.
Institute of Medicine. 2004. Immunization Safety Review: Vaccines and Autism. May 17. Available at www.iom.edu/CMS/3793/4705/20155.aspx.
Kennedy, R.F. 2005. Deadly immunity. June 16. Salon.com. Available at http://dir.salon.com/story/news/feature/2005/06/16/thimerosal/index3.html?pn=1.
———. 2007. Attack on mothers. June 19. The Huffington Post. Available at www.huffingtonpost.com/robert-f-kennedy-jr/attack-on-mothers_b_52894.html.
Kirby, David. 2005. Evidence of Harm: Mercury in Vaccines and the Autism Epidemic: A Medical Controversy. New York: St. Martin’s Press.
Lancet Editors, 2004. Lancet 363(9411).
Leitch K. 2007. Autism amongst the Amish. Left Brain/Right Brain. 22. Available at www.kevinleitch.co.uk/wp/?p=5353.
Madsen, K.M., A. Hviid, M. Vestergaard, D. Schendel, J. Wohlfahrt, P. Thorsen, J. Olsen, and M. Melbye. 2002. A population-based study of measles, mumps, and rubella vaccination and autism. New England Journal of Medicine 347(19):1477–1482.
Miles, J.H., and T.N. Takahashi. 2007. Lack of association between Rh status, Rh immune globulin in pregnancy and autism. American Journal of Medical Genetics, Part A1. 143(13):1397–407.
Mitchell, S., J. Brian, L. Zwaigenbaum, W. Roberts, P. Szatmari, I. Smith, and S. Bryson. 2006. Early language and communication development of infants later diagnosed with autism spectrum disorder. Journal of Developmental and Behavioral Pediatrics 27(2 Suppl):S69–78.
Parker, S.K., B. Schwartz, J. Todd, and L.K. Pickering. 2004. Thimerosal-containing vaccines and autistic spectrum disorder: a critical review of published original data. Pediatrics 114(3):793–804.
Rutter, M. 2005. Incidence of autism spectrum disorders: changes over time and their meaning. Acta Paediatrica 94(1):2–15.
Szatmari, P., et. al. 2007. Mapping autism risk loci using genetic linkage and chromosomal rearrangements. Nature Genetics 39, 319–28.
Taylor, B. 2006. Vaccines and the changing epidemiology of autism. Child Care, Health, and Development 32(5):511–19.
Taylor, B., E. Miller, C.P. Farrington, M.C. Petropoulos, I. Favot-Mayaud, J. Li, and P.A. Waight. 1999. Autism and measles, mumps, and rubella vaccine: no epidemiological evidence for a causal association. Lancet 12;353(9169):2026–2029.
Taylor, B., E. Miller, R. Lingam, N. Andrews, A. Simmons, and J. Stowe. 2002. Measles, mumps, and rubella vaccination and bowel problems or developmental regression in children with autism: population study. British Medical Journal 16; 324(7334):393–96.
United States Court of Federal Claims. 2007. Cedillo v. Secretary of Health and Human Services, Transcript of Day 6. June 18, 2007. Available at ftp://autism.uscfc.uscourts.gov/autism/transcripts/day06.pdf.
United States Court of Federal Claims, 2007. Cedillo v. Secretary of Health and Human Services, Transcript of Day 8. June 20, 2007. Available at ftp://autism.uscfc.uscourts.gov/autism/transcripts/day08.pdf.
USDOJ, About the National Vaccine Injury Compensation Program. Available at www.usdoj.gov/civil/torts/const/vicp/about.htm.
Wakefield, A.J., S.H. Murch, A. Anthony, J. Linnell, D.M. Casson, M. Malik, M. Berelowitz, A.P. Dhillon, M.A. Thomson, P. Harvey, A. Valentine, S.E. Davies, and J.A. Walker-Smith. 1998. Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet 351(9103):637–41.
VACCINES & AUTISM: Myths and Misconceptions
The Anti-Vaccination Movement
Despite the growing scientific consensus that vaccines are safe and that neither vaccines nor mercury cause autism, a stubborn vocal minority claims otherwise, threatening the effectiveness of this public health program.
STEVEN NOVELLA
Steven Novella, MD, is an assistant professor of neurology at Yale University School of Medicine. He is the host of The Skeptics’ Guide to the Universe, a weekly science podcast (www.theskepticsguide.org), author of the NeuroLogica blog (www.theness.com/ NeuroLogicaBlog), and president of the New England Skeptical Society www.theness.com).
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Michelle Cedillo has autism, which her parents believe is the result of her childhood vaccines. In June 2007 they had the opportunity, along with eight other families, to make their case to the Autism Omnibus—a U.S. Court of Federal Claims that was presided over by three “special masters” appointed for the purpose. These nine cases are the first test cases that will likely determine the fate of 4,800 other claims made over the past eight years for compensation for injuries allegedly due to childhood vaccines.
Vaccines are one of the most successful programs in modern health care, reducing, and in some cases even eliminating, serious infectious diseases. Public support for the vaccination program remains strong, especially in the United States where vaccination rates are currently at an all-time high of >95 percent (CDC 2004). Yet, despite a long history of safety and effectiveness, vaccines have always had their critics: some parents and a tiny fringe of doctors question whether vaccinating children is worth what they perceive as the risks. In recent years, the anti-vaccination movement, largely based on poor science and fear-mongering, has become more vocal and even hostile (Hughes 2007).
Of course, vaccines are not without risk (no medical intervention is), although the benefits far outweigh those risks. Because vaccines are somewhat compulsory in the United States—although opting out is increasingly easy—a National Vaccine Injury Compensation Program was established to streamline the process for compensation for those who are injured due to vaccines (USDOJ 2007). It is this program to which the Cedillo and 4,800 other families are applying for compensation.
In the last decade, the anti-vaccine movement, which includes those who blame the MMR (mumps-measles-rubella) vaccine for autism, has largely merged with those who warn that mercury toxicity is the cause of many of the ills that plague mankind. The two groups have come together over the issue of thimerosal, a mercury-based preservative in some vaccines. They believe that it was the use of thimerosal in childhood vaccines that led to the apparent autism epidemic beginning in the 1990s.
Autism is a complex neurological disorder that typically manifests in the first few years of life and primarily involves a deficiency of typical social skills and behavior. In the 1990’s, the number of autism diagnoses significantly increased, from between one and three to about fifteen cases per ten thousand, although the true incidence is probably between thirty and sixty per ten thousand (Rutter 2005). During this same period, the number of vaccines given in the routine childhood schedule also increased. This led some to assume, or at least speculate, causation from correlation—perhaps the vaccines or something in them created this “epidemic” of autism.
We can now say, from multiple independent lines of evidence, that vaccines do not cause autism. For one thing, the autism “epidemic” probably does not represent a true increase in the disorder, but rather an artifact of expanding the diagnosis (now referred to as autism spectrum disorder, ASD) and increased surveillance (Taylor 2006).
In 1998, researcher Andrew Wakefield and some of his colleagues published a study in the prestigious English medical journal Lancet that claimed to show a connection between the MMR vaccine and autism (Wakefield 1998). Wakefield’s theory was that the MMR vaccine, which contains a live virus, can cause in susceptible children a chronic measles infection. This in turn leads to gastrointestinal disturbances, including what he calls a “leaky gut” syndrome, which then allows for certain toxins and chemicals, like those from bread and dairy that are normally broken down by the gut, to enter the bloodstream where they can access and damage the developing brain.
Although the study was small and the evidence was considered preliminary, this article sparked a firestorm. As a result of the study and the media coverage that followed (and continues to this day), MMR compliance in Great Britain plummeted, resulting in a surge of preventable disease (Friederichs 2006).
Subsequent to the seminal article in the Lancet, many follow-up studies were performed testing the autism-MMR vaccine correlation. As the follow-up studies began to be published, however, it became increasingly clear that there was no link between MMR and autism. For example, a study in the British Medical Journal found that autism rates continued to climb in areas where MMR vaccination rates were not increasing (Taylor 1999). Another study found no association with MMR and autism or GI (gastrointestinal) disorders (Taylor 2002). Other studies showed no difference in the diagnosis rate of autism either before or after the MMR vaccine was administered (Honda 2005), or between vaccinated and unvaccinated children (Madsen 2002). Most recently, a study found that there was no decrease in autism rates following removal of the MMR vaccine in Japan (Honda 2005).
In 2001, the Institute of Medicine (IOM) reviewed all of the MMR-autism data available to date and concluded that there was no association and essentially closed the case (IOM 2001)—a conclusion confirmed by still later studies, such as the Honda study in Japan cited above.
If Wakefield had simply been wrong in his preliminary findings, he would be innocent of any wrongdoing—scientists are not faulted if their early findings are not later vindicated. However, in May 2004, ten of Wakefield’s co-authors on his original paper withdrew their support for its conclusions. The editors of Lancet also announced that they withdrew their endorsement of the paper and cited as part of the reason an undisclosed potential conflict of interest for Wakefield, namely that at the time of its publication he was conducting research for a group of parents of autistic children seeking to sue for damages from MMR vaccine producers (Lancet 2004).
It gets worse. Investigative reporter Brian Deer has uncovered greater depths to Wakefield’s apparent malfeasance. Wakefield had applied for patents for an MMR vaccine substitute and treatments for his alleged MMR vaccine-induced gut disorder (Deer 2007). So, not only was he allegedly paid by lawyers to cast doubt on the MMR vaccine, but he stood to personally gain from the outcome of his research.
Andrew Wakefield. (Credit: Tom Miller) [Photo via Newscom]
Further, during the Cedillo case testimony, Stephen Bustin, a world expert in the polymerase chain reaction (PCR), testified that the lab Wakefield used to obtain the results for his original paper was contaminated with measles virus RNA. It was therefore likely, Bustin implied, that the PCR used by Wakefield was detecting this contamination and not evidence for measles infection in the guts of children with autism who had been vaccinated, as Wakefield claimed. And finally, Nicholas Chadwick testified that the measles RNA Wakefield found matched the laboratory contamination and did not match either any naturally occurring strain or the strain used in the MMR vaccine—a fact of which he had informed Wakefield (USCFC 2007).
All of this, plus other allegations still coming out, has caused Britain’s General Medical Council to call Wakefield before its “Fitness to Practise” panel for review of his alleged professional misconduct (GMC 2007).
Believers in the MMR-autism hypothesis dismiss the findings of the larger and more powerful epidemiological studies that contradict a link. Instead, they have turned Andrew Wakefield into a martyr, dismissing the evidence of his wrongdoing as a conspiracy against him designed to hide the true cause of autism from the public. Wakefield is unrepentant and maintains his innocence (Gorski 2007).
With the MMR-autism hypothesis scientifically dead, attention soon shifted to thimerosal, a mercury-based preservative found in some childhood vaccines (although not the MMR vaccine). There is little doubt, and no controversy, that mercury, the major component of thimerosal, is a powerful neurotoxin, or poison to the brain. However, toxicity is always a matter of dose. Everything becomes toxic in a high enough dose; even too much water or vitamin C can kill you. So the real question is whether the amount of mercury given to children in vaccines containing thimerosal was enough to cause neurological damage.
Author of the book Evidence of Harm: Mercury in Vaccines and the Autism Epidemic David Kirby (center) speaks as president Harvey Fineberg (left) of the Institute of Medicine listens during an interview by moderator Tim Russert (right) on NBC’s Meet the Press August 7, 2005, at the NBC studios in Washington, D.C. Fineberg and Kirby talked about the rising number of autism diagnoses among children and the controversial charges of a government conspiracy to allow mercury exposures from childhood vaccines to more than double between 1988 and 1992. The Institute of Medicine reviewed all MMR-autism data and concluded that there was no association. (Photo by Alex Wong/Getty Images for Meet the Press) [Photo via Newscom]
Proponents of the mercury hypothesis argue that the ethylmercury found in thimerosal was given in doses exceeding Environmental Protection Agency limits. This load of mercury should be considered with prenatal vaccine loads possibly given to mothers, and to other environmental sources of mercury, such as seafood. Furthermore, underweight or premature infants received a higher dose by weight than larger children. Some children, they argue, may have a specific inability to metabolize mercury, and perhaps these are the children who become autistic.
Fear over thimerosal and autism was given a huge boost by journalist David Kirby with his book Evidence of Harm (Kirby 2005). Kirby tells the clichéd tale of courageous families searching for help for their sick children and facing a blind medical establishment and a federal government rife with corruption from corporate dollars. Kirby echoes the core claim that as the childhood vaccine schedule increased in the 1990s, leading to an increased cumulative dose of thimerosal, autism diagnoses skyrocketed.
In the end, Evidence of Harm is an example of terrible reporting that grossly misrepresents the science and the relevant institutions. As bad as Kirby’s position was in 2005, in the last two years the evidence has been piling up that thimerosal does not cause autism. Rather than adjusting his claims to the evidence, Kirby has held fast to his claims, which has made him a hero alongside Wakefield of the mercury-autism-connection crowd as he has squandered his credibility.
There have now been a number of epidemiological and ecological studies that have all shown no correlation between thimerosal and autism (Parker 2004 and Doja 2006). I have already mentioned that the current consensus holds that there is no real autism epidemic, just an artifact of how the diagnosis is made. If there’s no epidemic, there’s no reason to look for a correlation between thimerosal and autism. This has been backed up by The Institute of Medicine, which has also reviewed all the available evidence (both epidemiological and toxicological) and concluded that the evidence does not support the conclusion that thimerosal causes autism (IOM 2004).
Especially damning for the thimerosal hypothesis are the recent studies that clearly demonstrate that early detection of autism is possible long before the diagnosis is officially made. Part of the belief that vaccines may cause autism is driven by the anecdotal observation by many parents that their children were normal until after they were vaccinated—autism is typically diagnosed around age two or three. However, more careful observations indicate that signs of autism are present much earlier, even before twelve months of age, before exposure to thimerosal (Mitchell 2006). In fact, autism expert Eric Fombonne testified in the Autism Omnibus hearings that Michelle Cedillo displayed early signs of autism clearly visibly on family video taken prior to her receiving the MMR vaccine (USCFC 2007).
Meanwhile, evidence is accumulating that autism is largely a genetic disorder (Szatmari 2007). This by itself does not rule out an environmental factor, but it is telling that genetic research in autism has proven so fruitful.
Mercury alarmists, in the face of this negative evidence, have been looking for rationalizations. Some have argued that the thimerosal in prenatal vaccines may be to blame, but recent evidence has shown a negative correlation there as well (Miles 2007).
What we have are the makings of a solid scientific consensus. Multiple independent lines of evidence all point in the same direction: vaccines in general, and thimerosal in particular, do not cause autism, which rather likely has its roots in genetics. Furthermore, true autism rates are probably static and not rising.
A demonstrator carries a sign protesting the use of mercury in vaccines past the U.S. Capitol in Washington July 20, 2005. Some three hundred people marched demanding that mercury not be used in vaccines anymore amid concern that it is the cause of autism and other neurological diseases in children. However, numerous studies show no correlation between Thimerosol and autism. (Nicholas Kamm/AFP/Getty Images) [Photo via Newscom]
The only researchers who are publishing data that contradicts this consensus are the father-and-son team of Mark and David Geier. They have looked at the same data and concluded that thimerosal does correlate with autism. However, the hammer of peer-review has come down on their methods and declared them fatally flawed, thus rendering their conclusions invalid or uninterpretable (Parker 2004). Also, like Wakefield, their reputations are far from clean. They have made something of a career out of testifying for lawyers and families claiming that vaccines caused their child’s autism, even though the Geiers’ testimony is often excluded on the basis that they lack the proper expertise (Goldacre 2007). The Geiers were not even called as experts in the Autism Omnibus hearings.
The Geiers are now undertaking an ethically suspect study in which they are administering chelation therapy to children with autism in conjunction with powerful hormonal therapy allegedly designed to reduce testosterone levels. Chelation therapy removes mercury, and so it is dependent upon the mercury hypothesis, which is all but disproved. Moreover, there is no clinical evidence for the efficacy of chelation therapy. The treatment is far from benign and is even associated with occasional deaths (Brown 2006).
With the scientific evidence so solidly against the mercury hypothesis of autism, proponents maintain their belief largely through the generous application of conspiracy thinking. The conspiracy claim has been made the loudest by Robert F. Kennedy Jr. in two conspiracy-mongering articles: Deadly Immunity published on Salon.com in 2005 (Kennedy 2005), and more recently Attack on Mothers (Kennedy 2007). In these articles, RFK Jr. completely misrepresents and selectively quotes the scientific evidence, dismisses inconvenient evidence as fraudulent, accuses the government, doctors, and the pharmaceutical industry of conspiring to neurologically damage America’s children, and accuses scientists who are skeptical of the mercury claims of attacking the mothers of children with autism.
Despite the lack of evidence for any safety concern, the FDA decided to remove all thimerosal from childhood vaccines, and by 2002 no new childhood vaccines with thimerosal were being sold in the U.S. This was not an admission of prior error, as some mercury proponents claimed; instead, the FDA was playing it safe by minimizing human exposure to mercury wherever possible. The move was also likely calculated to maintain public confidence in vaccines.
This created the opportunity to have the ultimate test of the thimerosal autism hypothesis. If rising thimerosal doses in the 1990s led to increasing rates of autism diagnosis, then the removal of thimerosal should be followed within a few years by a similar drop in new autism diagnoses. If, on the other hand, thimerosal did not cause autism, then the incidence of new diagnoses should continue to increase and eventually level off at or near the true rate of incidence. In 2005, I personally interviewed David Kirby on the topic, and we both agreed that this would be a fair test of our respective positions. Also, in an e-mail to science blogger Citizen Cain, Kirby wrote, “If the total number of 3-5 year olds in the California DDS [Department of Developmental Services] system has not declined by 2007, that would deal a severe blow to the autism-thimerosal hypothesis” (Cain 2005).
Well, five years after the removal of thimerosal, autism diagnosis rates have continued to increase (IDIC 2007). That is the final nail in the coffin in the thimerosal-vaccine-autism hypothesis. The believers, however, are in full rationalization mode. David Kirby and others have charged that although no new vaccines with thimerosal were sold after 2001, there was no recall, so pediatricians may have had a stockpile of thimerosal-laden vaccines—even though a published inspection of 447 pediatric clinics and offices found only 1.9 percent of relevant vaccines still had thimerosal by February 2002, a tiny fraction that was either exchanged, used, or expired soon after (CDCP/ACIP 2002).
Those who argue for the link have put forth increasingly desperate notions. Kirby has argued that mercury from cremations was increasing environmental mercury toxicity and offsetting the decrease in mercury from thimerosal. The Geiers simply reinterpreted the data using bad statistics to create the illusion of a downward trend where none exists (Geier 2006). Robert Kennedy Jr. dodges the issue altogether by asking for more studies, despite the fact that the evidence he asks for already exists. He just doesn’t like the answer. Kennedy and others also point to dubious evidence, such as the myth that the Amish do not vaccinate and do not get autism. Both of these claims are not true, and the data RFK Jr. refers to is nothing more than a very unscientific phone survey (Leitch 2007).
The Autism Omnibus hearings have concluded, and while we await the decision due early next year, I am optimistic that science and reason will win the day. Just as shown in the 2005 Dover trial of intelligent design where the full body of scientific evidence was given a thorough airing in court and subjected to rules of evidence and the critical eyes of experienced judges, science tends to win out over nonsense. By all accounts, the lawyers for those claiming that vaccines caused their children’s autism put on pathetic performances with transparently shoddy science, while the other side marshaled genuine experts and put forth an impressive case.
But the stakes are high, and not just for the 4,800 families. If the petitioners win these test cases despite the evidence, it will open the floodgates for the rest of the 4,800 petitioners. This will likely bankrupt the Vaccine Injury Compensation Program and will also risk our vaccine infrastructure. Pharmaceutical companies will be reluctant to subject themselves to the liability of selling vaccines if even the truth cannot protect them from lawsuits.
Thimerosal still exists as a necessary preservative in multi-shot vaccines outside the United States, especially in poor third-world countries that cannot afford stockpiles of single-shot vaccines. Anti-thimerosal hysteria therefore also threatens the health of children in poor countries.
And of course a victory for the anti-vaccination activists would undermine public confidence in what is arguably the single most effective public health measure devised by modern science. This decrease in confidence will lead, as it has before, to declining compliance and an increase in infectious disease.
The forces of irrationality are arrayed on this issue. There are conspiracy theorists, well-meaning but misguided citizen groups who are becoming increasingly desperate and hostile, irresponsible journalists, and ethically compromised or incompetent scientists. The science itself is complex, making it difficult for the average person to sift through all the misdirection and misinformation. Standing against all this is simple respect for scientific integrity and the dedication to follow the evidence wherever it leads.
Right now the evidence leads to the firm conclusion that vaccines do not cause autism. Yet, if history is any guide, the myth that they do cause autism will likely endure even in the face of increasing contradictory evidence.
References
Brown, M.J., T. Willis, B. Omalu, and R. Leiker. 2006. Deaths resulting from hypocalcemia after administration of edetate disodium: 2003–2005. Pediatrics. 118(2):e534–36.
Centers for Disease Control. 2004. MMWR Weekly, November 12. 53(44):1041–1044. Available at www.cdc.gov/mmwr/preview/mmwrhtml/mm5344a4.htm.
Centers for Disease Control and Prevention Advisory Committee on Immunization. 2002. Practice Records of the meeting held on February 20–21, 2002, Atlanta Marriott North Central Hotel. Available at www.kevinleitch.co.uk/grabit/acip-min-feb.pdf.
Citizen Cain. 2005. Slouching Toward Truth—Autism and Mercury, November 30. Available at http://citizencain.blogspot.com/2005/11/slouching-toward-truth-autism-and_30.html.
Deer, B. 2007. Andrew Wakefield & the MMR scare: part 2. Available at http://briandeer.com/wakefield-deer.htm.
Doja, A., and W. Roberts. 2006. Immunizations and autism: a review of the literature. Canadian Journal of Neurological Sciences 33(4):341–46.
Friederichs, V., J.C. Cameron, and C. Robertson. 2006. Impact of adverse publicity on MMR vaccine uptake: a population based analysis of vaccine uptake records for one million children, born 1987–2004. Archives of Diseases of Children 200691(6):465–68. Epub 2006 April 25.
Geier, D.A., and M.R. Geier. 2006. An assessment of downward trends in neurodevelopmental disorders in the United States following removal of thimerosal from childhood vaccines. Medical Science Monitor 12(6):CR231–9. Epub 2006 May 29.
General Medical Council. 2007. July 16. Available at www.gmcpressoffice.org.uk/apps/news/events/index.php?month=7&year=2007&submit=Submit.
Goldacre B. 2007. Opinions from the medical fringe should come with a health warning. The Guardian, Saturday, February 24. Available at www.guardian.co.uk/science/2007/feb/24/badscience.uknews.
Gorski, D. 2007. Andrew Wakefield: The Galileo gambit writ large in The Observer. Respectful Insolence, July 9, 2007. Available at http://scienceblogs.com/insolence/2007/07/andrew_wakefield_the_galileo_gambit_writ.php.
Honda, H., Y. Shimizu, and M. Rutter. 2005. No effect of MMR withdrawal on the incidence of autism: a total population study. Journal of Child Psychology and Psychiatry 46(6):572–79.
Hughes, V. 2007. Mercury Rising. Nature Medicine 13(8):896–7. Epub 2007 August 31.
Infectious Diseases and Immunization Committee, Canadian Paediatric Society (CPS). 2007. Autistic spectrum disorder: No causal relationship with vaccines. Paediatrics & Child Health 12(5): 393–95. Available at www.cps.ca/english/statements/ID/pidnote_jun07.htm.
Institute of Medicine. 2001. Immunization Safety Review: Measles-Mumps-Rubella Vaccine and Autism. April 23. Available at www.iom.edu/CMS/3793/4705/4715.aspx.
Institute of Medicine. 2004. Immunization Safety Review: Vaccines and Autism. May 17. Available at www.iom.edu/CMS/3793/4705/20155.aspx.
Kennedy, R.F. 2005. Deadly immunity. June 16. Salon.com. Available at http://dir.salon.com/story/news/feature/2005/06/16/thimerosal/index3.html?pn=1.
———. 2007. Attack on mothers. June 19. The Huffington Post. Available at www.huffingtonpost.com/robert-f-kennedy-jr/attack-on-mothers_b_52894.html.
Kirby, David. 2005. Evidence of Harm: Mercury in Vaccines and the Autism Epidemic: A Medical Controversy. New York: St. Martin’s Press.
Lancet Editors, 2004. Lancet 363(9411).
Leitch K. 2007. Autism amongst the Amish. Left Brain/Right Brain. 22. Available at www.kevinleitch.co.uk/wp/?p=5353.
Madsen, K.M., A. Hviid, M. Vestergaard, D. Schendel, J. Wohlfahrt, P. Thorsen, J. Olsen, and M. Melbye. 2002. A population-based study of measles, mumps, and rubella vaccination and autism. New England Journal of Medicine 347(19):1477–1482.
Miles, J.H., and T.N. Takahashi. 2007. Lack of association between Rh status, Rh immune globulin in pregnancy and autism. American Journal of Medical Genetics, Part A1. 143(13):1397–407.
Mitchell, S., J. Brian, L. Zwaigenbaum, W. Roberts, P. Szatmari, I. Smith, and S. Bryson. 2006. Early language and communication development of infants later diagnosed with autism spectrum disorder. Journal of Developmental and Behavioral Pediatrics 27(2 Suppl):S69–78.
Parker, S.K., B. Schwartz, J. Todd, and L.K. Pickering. 2004. Thimerosal-containing vaccines and autistic spectrum disorder: a critical review of published original data. Pediatrics 114(3):793–804.
Rutter, M. 2005. Incidence of autism spectrum disorders: changes over time and their meaning. Acta Paediatrica 94(1):2–15.
Szatmari, P., et. al. 2007. Mapping autism risk loci using genetic linkage and chromosomal rearrangements. Nature Genetics 39, 319–28.
Taylor, B. 2006. Vaccines and the changing epidemiology of autism. Child Care, Health, and Development 32(5):511–19.
Taylor, B., E. Miller, C.P. Farrington, M.C. Petropoulos, I. Favot-Mayaud, J. Li, and P.A. Waight. 1999. Autism and measles, mumps, and rubella vaccine: no epidemiological evidence for a causal association. Lancet 12;353(9169):2026–2029.
Taylor, B., E. Miller, R. Lingam, N. Andrews, A. Simmons, and J. Stowe. 2002. Measles, mumps, and rubella vaccination and bowel problems or developmental regression in children with autism: population study. British Medical Journal 16; 324(7334):393–96.
United States Court of Federal Claims. 2007. Cedillo v. Secretary of Health and Human Services, Transcript of Day 6. June 18, 2007. Available at ftp://autism.uscfc.uscourts.gov/autism/transcripts/day06.pdf.
United States Court of Federal Claims, 2007. Cedillo v. Secretary of Health and Human Services, Transcript of Day 8. June 20, 2007. Available at ftp://autism.uscfc.uscourts.gov/autism/transcripts/day08.pdf.
USDOJ, About the National Vaccine Injury Compensation Program. Available at www.usdoj.gov/civil/torts/const/vicp/about.htm.
Wakefield, A.J., S.H. Murch, A. Anthony, J. Linnell, D.M. Casson, M. Malik, M. Berelowitz, A.P. Dhillon, M.A. Thomson, P. Harvey, A. Valentine, S.E. Davies, and J.A. Walker-Smith. 1998. Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet 351(9103):637–41.
Sunday, March 2, 2008
Post#6 Does Infant/Mother Nutrition Affect Allergy-Related Problems?
Sorry for the long delay between entries. Our family has recently been blessed with baby #3! My wife and I are now the proud parents of Ellie, Matthew, and now Michael Jung.
For years I have been telling my mothers that there is weak evidence available to support the implementation of restrictive diets (either for the breastfeeding mother or the baby) in hopes of preventing allergy-related problems in their newborn.
Recently, the American Academy of Pediatrics came out with a comprehensive statement further validating this advice. I felt this information was so refreshing and liberating - much like the recent recall on cough/cold medications - that I wanted to pass this on to the readers of this blog! Breastfeeding moms, eat what you want, and do it with a clear conscience!! Now go hit the buffets!!
Frank Greer M.D., the principle author on this article, is the chairman of the American Academy of Pediatrics Committee on Nutrition. The below statement was developed in cooperation with the academy’s Section on Allergy and Immunology.
The highlights of the article (posted below) are this:
1. The idea that egg, fish, and foods containing peanut protein should not be introduced before 1 year of age is not based on good science.
2. Maternal dietary restrictions during pregnancy do not appear to play a significant role in the prevention of atopic [allergy-related] disease in infants.
3. There is no convincing evidence for the use of soy-based infant formula for the purpose of allergy prevention.
4. For infants beyond 4-6 months of age, there is insufficient data to support a protective effect of any dietary intervention for the development of atopic disease.
5. In Infants who are at risk of developing atopic disease, the current evidence does not support the hypothesis that exclusive breast-feeding protects against allergic asthma occurring beyond the age of 6 years.
6. For a child who has developed an atopic disease that might be precipitated or exacerbated by ingested proteins (via human milk, infant formula, or specific complementary foods), treatment could require specific identification and restriction of causal food proteins .
For those who want to read the entire article. . .
This policy is a revision of the policy posted on August 1, 2000.
CLINICAL REPORT
PEDIATRICS Vol. 121 No. 1 January 2008, pp. 183-191 (doi:10.1542/peds.2007-3022)
CLINICAL REPORT
Effects of Early Nutritional Interventions on the Development of Atopic Disease in Infants and Children: The Role of Maternal Dietary Restriction, Breastfeeding, Timing of Introduction of Complementary Foods, and Hydrolyzed Formulas
Frank R. Greer, MD, Scott H. Sicherer, MD, A. Wesley Burks, MD and the Committee on Nutrition and Section on Allergy and Immunology
ABSTRACT
This clinical report reviews the nutritional options during pregnancy, lactation, and the first year of life that may affect the development of atopic disease (atopic dermatitis, asthma, food allergy) in early life. It replaces an earlier policy statement from the American Academy of Pediatrics that addressed the use of hypoallergenic infant formulas and included provisional recommendations for dietary management for the prevention of atopic disease. The documented benefits of nutritional intervention that may prevent or delay the onset of atopic disease are largely limited to infants at high risk of developing allergy (i.e., infants with at least 1 first-degree relative [parent or sibling] with allergic disease).
Current evidence does not support a major role for maternal dietary restrictions during pregnancy or lactation. There is evidence that breastfeeding for at least 4 months, compared with feeding formula made with intact cow milk protein, prevents or delays the occurrence of atopic dermatitis, cow milk allergy, and wheezing in early childhood. In studies of infants at high risk of atopy and who are not exclusively breastfed for 4 to 6 months, there is modest evidence that the onset of atopic disease may be delayed or prevented by the use of hydrolyzed formulas compared with formula made with intact cow milk protein, particularly for atopic dermatitis. Comparative studies of the various hydrolyzed formulas also indicate that not all formulas have the same protective benefit. There is also little evidence that delaying the timing of the introduction of complementary foods beyond 4 to 6 months of age prevents the occurrence of atopic disease. At present, there are insufficient data to document a protective effect of any dietary intervention beyond 4 to 6 months of age for the development of atopic disease.
Key Words: atopy • food allergies • breastfeeding • complementary foods • hydrolyzed formula • atopic dermatitis • asthma
Abbreviations: AAP—American Academy of Pediatrics • IgE—immunoglobulin E • OR—odds ratio • CI—confidence interval
INTRODUCTION
Over the past several decades, the incidence of atopic diseases such as asthma, atopic dermatitis, and food allergies has increased dramatically. Among children up to 4 years of age, the incidence of asthma has increased 160%, and the incidence of atopic dermatitis has increased twofold to threefold. The incidence of peanut allergy has also doubled in the past decade. Thus, atopic diseases increasingly are a problem for clinicians who provide health care to children.
It has been recognized that early childhood events, including diet, are likely to be important in the development of both childhood and adult diseases.
This clinical report will review the nutritional options during pregnancy, lactation, and the first year of life that may or may not affect the development of atopic disease. Although atopic diseases have a clear genetic basis, environmental factors, including early infant nutrition, may have an important influence on their development and, thus, present an opportunity to prevent or delay the onset of the disease. This clinical report replaces an earlier policy statement from the American Academy of Pediatrics (AAP) that addressed the use of hypoallergenic infant formulas and included provisional recommendations for dietary management for the prevention of atopic disease. This report is not directed at the treatment of atopic disease once an infant or child has developed specific atopic symptoms.
DEFINITIONS
The following definitions are used throughout this clinical report (adapted from work by Muraro et al)
Allergy: A hypersensitivity reaction initiated by immunologic mechanisms.
Atopy: A personal or familial tendency to produce immunoglobulin E (IgE) antibodies in response to low-dose allergens, confirmed by a positive skin-prick test result.
Atopic disease: Clinical disease characterized by atopy; typically refers to atopic dermatitis, asthma, allergic rhinitis, and food allergy. This report will be limited to the discussion of conditions for which substantial information is available in the medical literature.
Atopic dermatitis (eczema): A pruritic, chronic inflammatory skin disease that commonly presents during early childhood and is often associated with a personal or family history of other atopic diseases.
Asthma: An allergic-mediated response in the bronchial airways that is verified by the variation in lung function (measured by spirometry) either spontaneously or after bronchodilating drugs.
Cow milk allergy: An immunologically mediated hypersensitivity reaction to cow milk, including IgE-mediated and/or non––IgE-mediated allergic reactions.
Food allergy: An immunologically mediated hypersensitivity reaction to any food, including IgE-mediated and/or non––IgE-mediated allergic reactions.
Hypoallergenic: Reduced allergenicity or reduced ability to stimulate an IgE response and induce IgE-mediated reactions.
Infants at high risk of developing allergy: Infants with at least 1 first-degree relative (parent or sibling) with documented allergic disease.
The following definitions are from various industry sources:
Partially hydrolyzed (PH) formula: Contains reduced oligopeptides that have a molecular weight of generally less than 5000 d.
Extensively hydrolyzed (EH) formula: Contains only peptides that have a molecular weight of less than 3000 d.
Free amino acid––based formula: Peptide-free formula that contains mixtures of essential and nonessential amino acids.
DIETARY RESTRICTIONS FOR PREGNANT AND LACTATING WOMEN
The earliest possible nutritional influence on atopic disease in an infant is the diet of the pregnant woman. However, studies generally have not supported a protective effect of a maternal exclusion diet (including the exclusion of cow milk and eggs) during pregnancy on the development of atopic disease in infants, as summarized in a 2006 Cochrane review. Although previous AAP publications have suggested that pregnant women avoid peanuts, a more recent study has reported that there is no association between the maternal consumption of peanuts during pregnancy and childhood peanut allergy.
Previous AAP publications have advised lactating mothers with infants at high risk of developing allergy to avoid peanuts and tree nuts and to consider eliminating eggs, cow milk, and fish from their diets while nursing. Dietary food allergens can be detected in breast milk, including peanuts, cow milk protein, and egg. Two studies found a preventive effect of maternal dietary exclusion of milk, egg, and fish while breastfeeding on the development of atopic dermatitis in the infant. Other studies found no association between the development of atopic diseases and a maternal exclusion diet. A 2003 study found no association between breastfeeding and peanut allergy, and there was no difference in peanut intake during lactation between mothers with and without children with peanut allergy. Dietary food allergens in human milk may interact with the mucosal immune system and induce allergic reactions in infants who are known to be clinically allergic to the antigen. Rare cases of anaphylaxis to cow milk protein present in human milk have been described even in exclusively breastfed infants.
Consideration of a large number of studies on maternal diet, not all of which were randomized or included dietary restriction during lactation, demonstrated no impact on various outcomes among the majority of the studies, particularly when follow-up was beyond 4 years, and led one recent group of reviewers to conclude that there is no convincing evidence for a long-term preventive effect of maternal diet during lactation on atopic disease in childhood. A 2006 Cochrane review also concluded that there was insufficient evidence that antigen avoidance during lactation was beneficial in preventing atopic disease in the breastfed infant, with the exception of atopic dermatitis. Because the available published trials have had methodologic shortcomings, more data are necessary to conclude that the avoidance of antigens during lactation prevents atopic dermatitis in infants.
ROLE OF HUMAN MILK AND EXCLUSIVE BREASTFEEDING ON THE DEVELOPMENT OF ATOPIC DISEASE
Since the 1930s, many studies have examined the benefits of breastfeeding on the development of atopic disease. In general, these have been nonrandomized, retrospective, or observational in design and, thus, inconclusive. Of course, it is not possible to truly randomize breastfeeding, which is always a confounding variable in these studies. Acknowledging this difficulty, Kramer proposed 12 criteria to apply to studies designed to assess the relationship between atopic disease and breastfeeding. These criteria included nonreliance on late maternal recall of breastfeeding, sufficient duration of exclusive breastfeeding, strict diagnostic criteria for atopic outcomes, assessment of effects of children at high risk of atopic outcomes, and adequate statistical power. Unfortunately, no studies to date have completely fulfilled these criteria.
Atopic Dermatitis
A 2001 meta-analysis of 18 prospective studies compared the incidence of atopic dermatitis in infants who were breastfed versus infants who were fed cow milk formula. Overall, there was a protective effect of exclusive breastfeeding for 3 months (odds ratio [OR]: 0.68; 95% confidence interval [CI]: 0.52–0.88), the stronger effect having been shown for infants with a family history of allergy (OR: 0.58; 95% CI: 0.4–0.92). No protective effect of breastfeeding was seen in children who were not at risk of developing allergy (OR: 1.43; 95% CI: 0.72–2.86). A 2005 study published from Sweden found no effect of exclusive breastfeeding for 4 months on the incidence of atopic dermatitis in the first year of life with or without a family history of atopic disease. On the other hand, another 2005 study from Sweden found that exclusive breastfeeding for more than 4 months reduced the risk of atopic dermatitis at 4 years of age (OR: 0.78; 95% CI: 0.63–0.96) with or without a family history of allergy. In their review, Kramer and Kakuma also found no benefit of exclusive breastfeeding beyond 3 months of age on the incidence of atopic dermatitis in studies in which parents were not selected for risk of allergy.
A series of recent reports from the German Infant Nutritional Intervention Program also found that breastfeeding reduces the incidence of atopic dermatitis, supporting the results of the meta-analysis. In the interventional arm of this study, 1834 newborn infants identified as being at high risk of developing atopic disease were enrolled in a 3-year longitudinal, prospective study. Breastfeeding infants at risk for atopic disease were enrolled in the study before 14 days of life and, at that time, were exclusively breastfed and had no history of formula supplementation. Infants were randomly assigned at the time of entry to receive supplements of 1 of 3 hydrolyzed formulas (2 extensively hydrolyzed formulas and 1 partially hydrolyzed formula) or a cow milk formula, if formula supplementation had begun. Eight hundred eighty-nine mothers exclusively breastfed for 4 months and did not use any of the formula supplements they were randomly assigned to use. Nine hundred forty-five infants were introduced to the randomly assigned formula before 4 months and, thus, were not exclusively breastfed. Of these, 689 infants were randomly assigned to receive one of the hydrolyzed formulas, and 256 were randomly assigned to receive cow milk formula. The incidence of atopic dermatitis in infants who were exclusively breastfed, breastfed with supplemental hydrolyzed formula, and breastfed with supplemental cow milk formula was 9.5%, 9.8%, and 14.8%, respectively, at the 1-year follow-up.
Thus, exclusive breastfeeding for 4 months showed a positive effect compared with breastfeeding with supplemental cow milk formula in these infants at high risk of developing allergy. Breastfeeding with supplemental hydrolyzed formula (both partially and extensively hydrolyzed) also showed a positive effect compared with breastfeeding with supplemental cow milk formula; however, breastfeeding with supplements of hydrolyzed formulas showed no advantage compared with exclusive breastfeeding. Both groups showed a one-third decrease in the risk of atopic dermatitis compared with the risk of breastfeeding with supplements of cow milk formula. Thus, exclusive breastfeeding or breastfeeding with hydrolyzed formula is not enough to prevent the majority of cases of atopic dermatitis.
The advantages of breastfeeding are less clear for infants who are not selected for high risk of developing atopic disease, as shown in the noninterventional arm of the German Infant Nutritional Intervention Program. In this arm, mothers unselected for a history of atopy who either formula fed or partially breastfed their infants were free to select cow milk–based or hydrolyzed formulas. No differences in the incidence of atopic dermatitis occurred among the 3 groups of infants (exclusively breastfed for 4 months, cow milk formula fed with or without breastfeeding, and hydrolyzed formula fed with or without breastfeeding). This lack of effect has been attributed to reverse causation; thus, mothers who knew that their infants were at risk of developing allergy were more likely not only to breastfeed but also to breastfeed for a longer period of time. Alternatively, mothers who were not going to breastfeed or were going to supplement with formula were more likely to choose hydrolyzed formula if they believed that their children were at risk of developing atopy. This reverse causation effect may explain why some studies have found an increased incidence of atopic dermatitis in breastfed infants.
In summary, for infants at high risk of developing atopy, there is evidence that exclusive breastfeeding for at least 4 months or breastfeeding with supplements of hydrolyzed infant formulas decreases the risk of atopic dermatitis compared with breastfeeding with supplements of standard cow milk–based formulas. On the basis of currently available evidence, this is less likely to apply to infants who are not at risk of developing atopy, and exclusive breastfeeding beyond 3 to 4 months does not seem to lead to any additional benefit in the incidence of atopic eczema.
Asthma
The evidence for the protective effects of human milk on the development of asthma is more controversial. A 2001 meta-analysis of 12 prospective studies that met preestablished criteria found that exclusive breastfeeding for at least 3 months was protective against the development of asthma between 2 and 5 years of age (OR: 0.70; 95% CI: 0.60–0.81). The effect of breastfeeding was even stronger when the analysis was limited to children from families with a history of atopic disease (OR: 0.52; 95% CI: 0.35–0.79). No benefit was seen in children from families without a history of atopic disease (OR: 0.99; 95% CI: 0.48–2.03). Two more studies not included in this meta-analysis supported these results. On the other hand, a 2002 Cochrane review found no benefit of exclusive breastfeeding beyond 3 months on the incidence of asthma in families not preselected for a history of atopic disease.
Two additional reports in the literature with a more accurate definition of asthma made a distinction between the wheezy bronchitis associated with viral infections in younger children and that of the allergic disease seen in older children associated with respiratory spirometric changes. In the first of these studies, a cohort of 1246 children in Tucson, Arizona, was followed from birth to 13 years of age. The study found that an association between breastfeeding and asthma at 13 years of age depended on the presence of maternal asthma in children with atopic disease. Infants whose mothers had asthma were at greatest risk of developing asthma by 13 years of age if they had been breastfed exclusively for 4 months (OR: 8.7; 95% CI: 3.4–22.2). When infants with atopic disease whose mothers had asthma were exclusively breastfed for any length of time (either greater than or less than 4 months), the risk of developing asthma between 6 and 13 years of age was also increased (OR: 5.7; 95% CI: 2.3–14.1). An increased risk of developing asthma was not found in breastfed children of mothers without asthma. However, in this same study during the first 2 years of life, exclusive breastfeeding was associated with significantly lower rates of recurrent wheezing of infancy (OR: 0.45; 95% CI: 0.2–0.9), similar to results from a recent study performed in Perth, Australia.
In the second of these studies, a long-term longitudinal study from New Zealand, 1037children from a general population (not selected for risk of allergic disease) were followed from 3 to 26 years of age. Five hundred four infants were breastfed for 4 weeks or more, and 533 infants were formula fed from the time of birth or breastfed for less than 4 weeks. Breastfeeding for more than 4 weeks significantly increased the risk of developing asthma at 9 years (OR: 2.40; 95% CI: 1.36–4.6) and at 21 years (OR: 1.83; 95% CI: 1.35–2.47). This increased risk was not related to the presence of maternal atopic disease, unlike in the Tucson study. The study has been criticized for retrospective determination of breastfeeding and unclear definitions of atopic heredity. There was also no evidence of a "dose-response" effect of breastfeeding on the incidence of atopy or asthma.
In summary, at the present time, it is not possible to conclude that exclusive breastfeeding protects young infants who are at risk of atopic disease from developing asthma in the long term (>6 years of age), and it may even have a detrimental effect. On the other hand, breastfeeding seems to decrease the wheezing episodes seen in younger children (<4 years of age) that are often associated with respiratory infections.
Food Allergy
Food allergy, similar to atopic dermatitis and asthma, is more likely to occur in infants with a family history of atopic disease. In a prospective study of infants born to families with a history of atopic disease, it was determined that 25% will develop food allergy between birth and 7 years of age. Because both atopic dermatitis and asthma are closely associated with the development of food allergy, it is difficult to sort out the effect of breastfeeding on the development of food allergy. As reviewed above, maternal dietary exposure during pregnancy and lactation is unlikely to contribute significantly to the development of food allergy in the infant, although many food antigens can be found in human milk.
In theory, human milk should inhibit food antigen absorption; however, prospective studies have failed to show a protective effect of human milk–specific antibodies to cow milk on infant sensitization. Investigations of the role of breastfeeding on the outcomes of allergies to specific foods have been few, and the results may have been influenced by additional dietary variables such as length and degree of breastfeeding exclusivity. In reviewing the available studies, Muraro et al concluded that exclusively breastfeeding for at least 4 months in infants who are at risk of developing atopic diseases is associated with a lower cumulative incidence of cow milk allergy until 18 months of age. A Cochrane review included only 1 study with a blinded challenge (using the double-blind, placebo-controlled food-challenge technique) and concluded that at least 4 months of exclusive breastfeeding did not protect against food allergy at 1 year of age. Overall, firm conclusions about the role of breastfeeding in either preventing or delaying the onset of specific food allergies are not possible at this time.
ROLE OF HYDROLYZED FORMULA ON THE DEVELOPMENT OF ATOPIC DISEASE
The role of partially hydrolyzed and extensively hydrolyzed formulas for the prevention of atopic disease has been the subject of many studies in both formula-fed and breastfed infants in the last 15 years. Most studies with published results have been of infants at high risk of developing allergy.
Approximately 100 studies in the literature have examined the role of hydrolyzed formulas on the development of atopic disease. However, using the criteria of a 2006 Cochrane review, only 14 randomized or quasi-randomized (eg, using alternation) trials in term infants compared the use of partially or extensively hydrolyzed formula with the use of human milk or an adapted cow milk formula. All of these trials have followed up with at least 80% of study participants. It is important to note that none of these studies reported any adverse effects, including any adverse effect on infant growth. No long-term studies have compared partially or extensively hydrolyzed formula to exclusive breastfeeding. Thus, there is no evidence that the use of these formulas is any better than human milk in the prevention of atopic disease.
Three studies of 251 infants examined the effect of partially hydrolyzed formula on reduction of the occurrence of any allergy compared with cow milk formula in infants at high risk of developing allergy. Two of these studies found no significant effect, and a third study found an OR of 0.45 (95% CI: 0.22–0.94) for partially hydrolyzed formula versus cow milk formula. Three more studies examined prolonged feeding of extensively hydrolyzed formula compared with partially hydrolyzed formula in 411 infants at high risk of developing allergy. None of these studies found a significant difference in the incidence of atopic dermatitis between the 2 feeding groups. Two of these studies of 352 infants also examined other manifestations of atopic disease and did not show a significant difference in the occurrence of food allergy, cow milk allergy, or asthma between the groups of infants who were fed extensively or partially hydrolyzed formula.
A very large published study from the German Infant Nutritional Intervention Program raised additional issues. In the interventional arm of this study, 945 newborn infants were identified as being at high risk of developing atopic disease and were enrolled in a longitudinal, prospective study through 12 months of age. Although the majority of infants were breastfed initially, formula was introduced in the first 4 weeks to most infants. The infants were randomly assigned to receive 1 of 3 hydrolyzed formulas (n = 689) or cow milk formula (n = 256). The 3 hydrolyzed formulas were a partially hydrolyzed whey-based formula, an extensively hydrolyzed whey-based formula, and an extensively hydrolyzed casein-based formula. The incidence of atopic dermatitis was significantly reduced in those using the extensively hydrolyzed casein-based formula (OR: 0.42; 95% CI: 0.22–0.79; P < .007) and the partially hydrolyzed whey-based formula (OR: 0.56; 95% CI: 0.32–0.99; P < .046) but not the extensively hydrolyzed whey-based formula (OR: 0.81; 95% CI: 0.48–1.4; P < .44), compared with the incidence in those in the cow milk formula group.
However, the overall results for prevention of allergic disease (atopic dermatitis, urticaria, and food allergy) for the 3 hydrolyzed formulas compared with cow milk formula were less impressive (extensively hydrolyzed whey-based: OR: 0.86; 95% CI: 0.52–1.4; partially hydrolyzed whey-based: OR: 0.65; 95% CI: 0.38–1.1; and extensively hydrolyzed casein-based: OR: 0.51; 95% CI: 0.28–0.92; P < .025). Thus, this study indicated that different hydrolysates have different effects on atopic disease, and there may be an advantage for the extensively hydrolyzed casein-based formula. However, as the study demonstrated, it is difficult to show that partially hydrolyzed formulas have a very large effect on the reduction of atopic disease in infants who are fed formula or mixed feedings of human milk and formula, even if they are at high risk of developing allergic disease. If atopic disease associated with cow milk allergy has occurred, partially hydrolyzed formula is not recommended, because it contains potentially allergic cow milk peptides. More studies are needed to determine if any of the hydrolyzed formulas have any effect on the incidence of atopic disease later in childhood and adolescence and whether the modest effects of the use of extensively or partially hydrolyzed formulas in early childhood can be confirmed and are sustained. Such studies should also include a cost/benefit analysis of the use of the more expensive hydrolyzed formulas. It should be noted that the potential benefit of these formulas has only been documented in infants at risk of developing atopic disease.
Additional studies are needed among unselected infants or infants at low risk. The use of amino acid–based formulas for prevention of atopic disease has not been studied. Soy formulas, on the other hand, have a long history of use for atopic disease in infants. In a recent meta-analysis of 5 randomized or quasi-randomized studies, the authors concluded that feeding with soy formula should not be recommended for the prevention of atopy in infants at high risk of developing allergy.
ROLE OF INTRODUCTION OF COMPLEMENTARY FOODS ON ATOPIC DISEASE
Many studies have examined the duration of breastfeeding and its effect on atopic disease. However, few studies have examined the timing of the introduction of complementary foods as an independent risk factor for atopic disease in breastfed or formula-fed infants. An expert panel from the European Academy of Allergology and Clinical Immunology has recommended delayed introduction of solid foods for 4 to 6 months in breastfed or formula-fed infants. The AAP has also recommended that solid foods be delayed until 4 to 6 months of age and that whole cow milk be delayed until 12 months of age. Before publication of this clinical report, AAP recommendations for infants who are at risk of developing atopic disease were to avoid eggs until 2 years of age and avoid peanuts, tree nuts, and fish until 3 years of age. These guidelines for solid food introduction and avoidance of specific allergens were based on the evidence of a few studies with various limitations. Three newer studies have reported mixed results regarding the timing of the introduction of solid foods and development of childhood atopic disease.
In a prospective (nonrandomized) study of infants at risk of developing atopic disease by Kajosaari, atopic dermatitis and history of food allergy were reduced at 1 year of age if the introduction of solid foods was delayed until 6 months compared with at 3 months of age. However, in a 5-year follow-up study, no difference was seen in the incidence of atopic dermatitis or symptoms of food allergy. In a second prospective study of a birth cohort of 1210 unselected children between 2 and 4 years of age, there was more atopic dermatitis but not asthma in infants who were fed 4 or more solid foods compared with no solid foods before 4 months of age. This difference was maintained in a 10-year follow-up study in 85% of the original study infants.
In a study of 257 preterm infants (34.4 weeks’ gestational age; birth weight: 2.3–2.4kg), the introduction of 4 or more, compared with fewer than 4, solid foods before 17 weeks after term was associated with a higher risk of atopic dermatitis (unconfirmed by skin-prick testing) at 12 months after term (OR: 3.49; 95% CI: 1.51–8.05). Also in this study, the introduction of solid foods before 10 weeks of age or atopic disease in either parent increased the risk of atopic dermatitis in infants (OR: 2.94; 95% CI: 1.57–5.52).
In a more recent prospective, longitudinal cohort study in which atopic dermatitis was confirmed by skin testing, 642 infants were followed until 5.5 years of age. The history of the introduction of solid foods was carefully recorded during the first year of life. Most children had at least 1 parent with a positive skin-prick test result. Rice cereal was introduced at a median age of 3 months, milk was introduced at a median age of 6 months, and egg was introduced at a median age of 8 months. However, the later introduction of solids had no effect on the prevalence of asthma or atopic dermatitis (confirmed by skin-prick testing), although there was an increased risk of atopic dermatitis in relation to the late (6–8 months) rather than the earlier introduction of eggs (OR: 1.6; 95% CI: 1.1–2.4) or milk (OR: 1.7; 95% CI: 1.1–2.5).
Finally, an ongoing prospective, cohort study of 2612 infants (without a risk of developing atopic disease) found no evidence to support delayed introduction of solid foods beyond 6 months of age for prevention of atopic disease. However, in the same study, the effect of delayed introduction of solid foods for the first 4 months of life was less clear. Another study has even suggested that children exposed to cereal grains before 6 months of age (as opposed to after 6 months of age) are protected from the development of wheat-specific IgE.
In summary, the evidence from these conflicting studies, in balance, does not allow one to conclude that there is a strong relationship between the timing of the introduction of complementary foods and development of atopic disease. This raises serious questions about the benefit of delaying the introduction of solid foods that are thought to be highly allergic (cow milk, fish, eggs, and peanut-containing foods) beyond 4 to 6 months of age; additional studies are needed.
SUMMARY
It is evident that inadequate study design and/or a paucity of data currently limit the ability to draw firm conclusions about certain aspects of atopy prevention through dietary interventions. In some circumstances in which there are insufficient studies (pregnancy and lactation avoidance diets, timing of introduction of specific complementary foods), the lack of proven efficacy does not indicate that the approach is disproved. Rather, more studies would be needed to clarify whether there is a positive or negative effect on atopy outcomes. The following statements summarize the current evidence within the context of these limitations.
At the present time, there is lack of evidence that maternal dietary restrictions during pregnancy play a significant role in the prevention of atopic disease in infants. Similarly, antigen avoidance during lactation does not prevent atopic disease, with the possible exception of atopic eczema, although more data are needed to substantiate this conclusion.
For infants at high risk of developing atopic disease, there is evidence that exclusive breastfeeding for at least 4 months compared with feeding intact cow milk protein formula decreases the cumulative incidence of atopic dermatitis and cow milk allergy in the first 2 years of life.
There is evidence that exclusive breastfeeding for at least 3 months protects against wheezing in early life. However, in infants at risk of developing atopic disease, the current evidence that exclusive breastfeeding protects against allergic asthma occurring beyond 6 years of age is not convincing.
In studies of infants at high risk of developing atopic disease who are not breastfed exclusively for 4 to 6 months or are formula fed, there is modest evidence that atopic dermatitis may be delayed or prevented by the use of extensively or partially hydrolyzed formulas, compared with cow milk formula, in early childhood. Comparative studies of the various hydrolyzed formulas have also indicated that not all formulas have the same protective benefit. Extensively hydrolyzed formulas may be more effective than partially hydrolyzed in the prevention of atopic disease. In addition, more research is needed to determine whether these benefits extend into late childhood and adolescence. The higher cost of the hydrolyzed formulas must be considered in any decision-making process for their use. To date, the use of amino acid–based formulas for atopy prevention has not been studied.
There is no convincing evidence for the use of soy-based infant formula for the purpose of allergy prevention.
Although solid foods should not be introduced before 4 to 6 months of age, there is no current convincing evidence that delaying their introduction beyond this period has a significant protective effect on the development of atopic disease regardless of whether infants are fed cow milk protein formula or human milk. This includes delaying the introduction of foods that are considered to be highly allergic, such as fish, eggs, and foods containing peanut protein.
For infants after 4 to 6 months of age, there are insufficient data to support a protective effect of any dietary intervention for the development of atopic disease.
Additional studies are needed to document the long-term effect of dietary interventions in infancy to prevent atopic disease, especially in children older than 4 years and in adults.
This document describes means to prevent or delay atopic diseases through dietary changes. For a child who has developed an atopic disease that may be precipitated or exacerbated by ingested proteins (via human milk, infant formula, or specific complementary foods), treatment may require specific identification and restriction of causal food proteins. This topic was not reviewed in this document.
Committee on Nutrition, 2006–2007
Frank R. Greer, MD, Chairperson
Robert D. Baker, Jr, MD, PhD
Jatinder J. S. Bhatia, MD
Stephen Robert Daniels, MD, PhD
Marcie B. Schneider, MD
Janet Silverstein, MD
Dan W. Thomas, MD
Liaisons
Sue Ann Anderson, PhD, RD
Food and Drug Administration
Donna Blum-Kemelor, MS, RD
US Department of Agriculture
Margaret P. Boland, MD
Canadian Paediatric Society
Laurence Grummer-Strawn, PhD
Centers for Disease Control
Capt Van S. Hubbard, MD, PhD
National Institutes of Health
Benson M. Silverman, MD
Food and Drug Administration
For years I have been telling my mothers that there is weak evidence available to support the implementation of restrictive diets (either for the breastfeeding mother or the baby) in hopes of preventing allergy-related problems in their newborn.
Recently, the American Academy of Pediatrics came out with a comprehensive statement further validating this advice. I felt this information was so refreshing and liberating - much like the recent recall on cough/cold medications - that I wanted to pass this on to the readers of this blog! Breastfeeding moms, eat what you want, and do it with a clear conscience!! Now go hit the buffets!!
Frank Greer M.D., the principle author on this article, is the chairman of the American Academy of Pediatrics Committee on Nutrition. The below statement was developed in cooperation with the academy’s Section on Allergy and Immunology.
The highlights of the article (posted below) are this:
1. The idea that egg, fish, and foods containing peanut protein should not be introduced before 1 year of age is not based on good science.
2. Maternal dietary restrictions during pregnancy do not appear to play a significant role in the prevention of atopic [allergy-related] disease in infants.
3. There is no convincing evidence for the use of soy-based infant formula for the purpose of allergy prevention.
4. For infants beyond 4-6 months of age, there is insufficient data to support a protective effect of any dietary intervention for the development of atopic disease.
5. In Infants who are at risk of developing atopic disease, the current evidence does not support the hypothesis that exclusive breast-feeding protects against allergic asthma occurring beyond the age of 6 years.
6. For a child who has developed an atopic disease that might be precipitated or exacerbated by ingested proteins (via human milk, infant formula, or specific complementary foods), treatment could require specific identification and restriction of causal food proteins .
For those who want to read the entire article. . .
This policy is a revision of the policy posted on August 1, 2000.
CLINICAL REPORT
PEDIATRICS Vol. 121 No. 1 January 2008, pp. 183-191 (doi:10.1542/peds.2007-3022)
CLINICAL REPORT
Effects of Early Nutritional Interventions on the Development of Atopic Disease in Infants and Children: The Role of Maternal Dietary Restriction, Breastfeeding, Timing of Introduction of Complementary Foods, and Hydrolyzed Formulas
Frank R. Greer, MD, Scott H. Sicherer, MD, A. Wesley Burks, MD and the Committee on Nutrition and Section on Allergy and Immunology
ABSTRACT
This clinical report reviews the nutritional options during pregnancy, lactation, and the first year of life that may affect the development of atopic disease (atopic dermatitis, asthma, food allergy) in early life. It replaces an earlier policy statement from the American Academy of Pediatrics that addressed the use of hypoallergenic infant formulas and included provisional recommendations for dietary management for the prevention of atopic disease. The documented benefits of nutritional intervention that may prevent or delay the onset of atopic disease are largely limited to infants at high risk of developing allergy (i.e., infants with at least 1 first-degree relative [parent or sibling] with allergic disease).
Current evidence does not support a major role for maternal dietary restrictions during pregnancy or lactation. There is evidence that breastfeeding for at least 4 months, compared with feeding formula made with intact cow milk protein, prevents or delays the occurrence of atopic dermatitis, cow milk allergy, and wheezing in early childhood. In studies of infants at high risk of atopy and who are not exclusively breastfed for 4 to 6 months, there is modest evidence that the onset of atopic disease may be delayed or prevented by the use of hydrolyzed formulas compared with formula made with intact cow milk protein, particularly for atopic dermatitis. Comparative studies of the various hydrolyzed formulas also indicate that not all formulas have the same protective benefit. There is also little evidence that delaying the timing of the introduction of complementary foods beyond 4 to 6 months of age prevents the occurrence of atopic disease. At present, there are insufficient data to document a protective effect of any dietary intervention beyond 4 to 6 months of age for the development of atopic disease.
Key Words: atopy • food allergies • breastfeeding • complementary foods • hydrolyzed formula • atopic dermatitis • asthma
Abbreviations: AAP—American Academy of Pediatrics • IgE—immunoglobulin E • OR—odds ratio • CI—confidence interval
INTRODUCTION
Over the past several decades, the incidence of atopic diseases such as asthma, atopic dermatitis, and food allergies has increased dramatically. Among children up to 4 years of age, the incidence of asthma has increased 160%, and the incidence of atopic dermatitis has increased twofold to threefold. The incidence of peanut allergy has also doubled in the past decade. Thus, atopic diseases increasingly are a problem for clinicians who provide health care to children.
It has been recognized that early childhood events, including diet, are likely to be important in the development of both childhood and adult diseases.
This clinical report will review the nutritional options during pregnancy, lactation, and the first year of life that may or may not affect the development of atopic disease. Although atopic diseases have a clear genetic basis, environmental factors, including early infant nutrition, may have an important influence on their development and, thus, present an opportunity to prevent or delay the onset of the disease. This clinical report replaces an earlier policy statement from the American Academy of Pediatrics (AAP) that addressed the use of hypoallergenic infant formulas and included provisional recommendations for dietary management for the prevention of atopic disease. This report is not directed at the treatment of atopic disease once an infant or child has developed specific atopic symptoms.
DEFINITIONS
The following definitions are used throughout this clinical report (adapted from work by Muraro et al)
Allergy: A hypersensitivity reaction initiated by immunologic mechanisms.
Atopy: A personal or familial tendency to produce immunoglobulin E (IgE) antibodies in response to low-dose allergens, confirmed by a positive skin-prick test result.
Atopic disease: Clinical disease characterized by atopy; typically refers to atopic dermatitis, asthma, allergic rhinitis, and food allergy. This report will be limited to the discussion of conditions for which substantial information is available in the medical literature.
Atopic dermatitis (eczema): A pruritic, chronic inflammatory skin disease that commonly presents during early childhood and is often associated with a personal or family history of other atopic diseases.
Asthma: An allergic-mediated response in the bronchial airways that is verified by the variation in lung function (measured by spirometry) either spontaneously or after bronchodilating drugs.
Cow milk allergy: An immunologically mediated hypersensitivity reaction to cow milk, including IgE-mediated and/or non––IgE-mediated allergic reactions.
Food allergy: An immunologically mediated hypersensitivity reaction to any food, including IgE-mediated and/or non––IgE-mediated allergic reactions.
Hypoallergenic: Reduced allergenicity or reduced ability to stimulate an IgE response and induce IgE-mediated reactions.
Infants at high risk of developing allergy: Infants with at least 1 first-degree relative (parent or sibling) with documented allergic disease.
The following definitions are from various industry sources:
Partially hydrolyzed (PH) formula: Contains reduced oligopeptides that have a molecular weight of generally less than 5000 d.
Extensively hydrolyzed (EH) formula: Contains only peptides that have a molecular weight of less than 3000 d.
Free amino acid––based formula: Peptide-free formula that contains mixtures of essential and nonessential amino acids.
DIETARY RESTRICTIONS FOR PREGNANT AND LACTATING WOMEN
The earliest possible nutritional influence on atopic disease in an infant is the diet of the pregnant woman. However, studies generally have not supported a protective effect of a maternal exclusion diet (including the exclusion of cow milk and eggs) during pregnancy on the development of atopic disease in infants, as summarized in a 2006 Cochrane review. Although previous AAP publications have suggested that pregnant women avoid peanuts, a more recent study has reported that there is no association between the maternal consumption of peanuts during pregnancy and childhood peanut allergy.
Previous AAP publications have advised lactating mothers with infants at high risk of developing allergy to avoid peanuts and tree nuts and to consider eliminating eggs, cow milk, and fish from their diets while nursing. Dietary food allergens can be detected in breast milk, including peanuts, cow milk protein, and egg. Two studies found a preventive effect of maternal dietary exclusion of milk, egg, and fish while breastfeeding on the development of atopic dermatitis in the infant. Other studies found no association between the development of atopic diseases and a maternal exclusion diet. A 2003 study found no association between breastfeeding and peanut allergy, and there was no difference in peanut intake during lactation between mothers with and without children with peanut allergy. Dietary food allergens in human milk may interact with the mucosal immune system and induce allergic reactions in infants who are known to be clinically allergic to the antigen. Rare cases of anaphylaxis to cow milk protein present in human milk have been described even in exclusively breastfed infants.
Consideration of a large number of studies on maternal diet, not all of which were randomized or included dietary restriction during lactation, demonstrated no impact on various outcomes among the majority of the studies, particularly when follow-up was beyond 4 years, and led one recent group of reviewers to conclude that there is no convincing evidence for a long-term preventive effect of maternal diet during lactation on atopic disease in childhood. A 2006 Cochrane review also concluded that there was insufficient evidence that antigen avoidance during lactation was beneficial in preventing atopic disease in the breastfed infant, with the exception of atopic dermatitis. Because the available published trials have had methodologic shortcomings, more data are necessary to conclude that the avoidance of antigens during lactation prevents atopic dermatitis in infants.
ROLE OF HUMAN MILK AND EXCLUSIVE BREASTFEEDING ON THE DEVELOPMENT OF ATOPIC DISEASE
Since the 1930s, many studies have examined the benefits of breastfeeding on the development of atopic disease. In general, these have been nonrandomized, retrospective, or observational in design and, thus, inconclusive. Of course, it is not possible to truly randomize breastfeeding, which is always a confounding variable in these studies. Acknowledging this difficulty, Kramer proposed 12 criteria to apply to studies designed to assess the relationship between atopic disease and breastfeeding. These criteria included nonreliance on late maternal recall of breastfeeding, sufficient duration of exclusive breastfeeding, strict diagnostic criteria for atopic outcomes, assessment of effects of children at high risk of atopic outcomes, and adequate statistical power. Unfortunately, no studies to date have completely fulfilled these criteria.
Atopic Dermatitis
A 2001 meta-analysis of 18 prospective studies compared the incidence of atopic dermatitis in infants who were breastfed versus infants who were fed cow milk formula. Overall, there was a protective effect of exclusive breastfeeding for 3 months (odds ratio [OR]: 0.68; 95% confidence interval [CI]: 0.52–0.88), the stronger effect having been shown for infants with a family history of allergy (OR: 0.58; 95% CI: 0.4–0.92). No protective effect of breastfeeding was seen in children who were not at risk of developing allergy (OR: 1.43; 95% CI: 0.72–2.86). A 2005 study published from Sweden found no effect of exclusive breastfeeding for 4 months on the incidence of atopic dermatitis in the first year of life with or without a family history of atopic disease. On the other hand, another 2005 study from Sweden found that exclusive breastfeeding for more than 4 months reduced the risk of atopic dermatitis at 4 years of age (OR: 0.78; 95% CI: 0.63–0.96) with or without a family history of allergy. In their review, Kramer and Kakuma also found no benefit of exclusive breastfeeding beyond 3 months of age on the incidence of atopic dermatitis in studies in which parents were not selected for risk of allergy.
A series of recent reports from the German Infant Nutritional Intervention Program also found that breastfeeding reduces the incidence of atopic dermatitis, supporting the results of the meta-analysis. In the interventional arm of this study, 1834 newborn infants identified as being at high risk of developing atopic disease were enrolled in a 3-year longitudinal, prospective study. Breastfeeding infants at risk for atopic disease were enrolled in the study before 14 days of life and, at that time, were exclusively breastfed and had no history of formula supplementation. Infants were randomly assigned at the time of entry to receive supplements of 1 of 3 hydrolyzed formulas (2 extensively hydrolyzed formulas and 1 partially hydrolyzed formula) or a cow milk formula, if formula supplementation had begun. Eight hundred eighty-nine mothers exclusively breastfed for 4 months and did not use any of the formula supplements they were randomly assigned to use. Nine hundred forty-five infants were introduced to the randomly assigned formula before 4 months and, thus, were not exclusively breastfed. Of these, 689 infants were randomly assigned to receive one of the hydrolyzed formulas, and 256 were randomly assigned to receive cow milk formula. The incidence of atopic dermatitis in infants who were exclusively breastfed, breastfed with supplemental hydrolyzed formula, and breastfed with supplemental cow milk formula was 9.5%, 9.8%, and 14.8%, respectively, at the 1-year follow-up.
Thus, exclusive breastfeeding for 4 months showed a positive effect compared with breastfeeding with supplemental cow milk formula in these infants at high risk of developing allergy. Breastfeeding with supplemental hydrolyzed formula (both partially and extensively hydrolyzed) also showed a positive effect compared with breastfeeding with supplemental cow milk formula; however, breastfeeding with supplements of hydrolyzed formulas showed no advantage compared with exclusive breastfeeding. Both groups showed a one-third decrease in the risk of atopic dermatitis compared with the risk of breastfeeding with supplements of cow milk formula. Thus, exclusive breastfeeding or breastfeeding with hydrolyzed formula is not enough to prevent the majority of cases of atopic dermatitis.
The advantages of breastfeeding are less clear for infants who are not selected for high risk of developing atopic disease, as shown in the noninterventional arm of the German Infant Nutritional Intervention Program. In this arm, mothers unselected for a history of atopy who either formula fed or partially breastfed their infants were free to select cow milk–based or hydrolyzed formulas. No differences in the incidence of atopic dermatitis occurred among the 3 groups of infants (exclusively breastfed for 4 months, cow milk formula fed with or without breastfeeding, and hydrolyzed formula fed with or without breastfeeding). This lack of effect has been attributed to reverse causation; thus, mothers who knew that their infants were at risk of developing allergy were more likely not only to breastfeed but also to breastfeed for a longer period of time. Alternatively, mothers who were not going to breastfeed or were going to supplement with formula were more likely to choose hydrolyzed formula if they believed that their children were at risk of developing atopy. This reverse causation effect may explain why some studies have found an increased incidence of atopic dermatitis in breastfed infants.
In summary, for infants at high risk of developing atopy, there is evidence that exclusive breastfeeding for at least 4 months or breastfeeding with supplements of hydrolyzed infant formulas decreases the risk of atopic dermatitis compared with breastfeeding with supplements of standard cow milk–based formulas. On the basis of currently available evidence, this is less likely to apply to infants who are not at risk of developing atopy, and exclusive breastfeeding beyond 3 to 4 months does not seem to lead to any additional benefit in the incidence of atopic eczema.
Asthma
The evidence for the protective effects of human milk on the development of asthma is more controversial. A 2001 meta-analysis of 12 prospective studies that met preestablished criteria found that exclusive breastfeeding for at least 3 months was protective against the development of asthma between 2 and 5 years of age (OR: 0.70; 95% CI: 0.60–0.81). The effect of breastfeeding was even stronger when the analysis was limited to children from families with a history of atopic disease (OR: 0.52; 95% CI: 0.35–0.79). No benefit was seen in children from families without a history of atopic disease (OR: 0.99; 95% CI: 0.48–2.03). Two more studies not included in this meta-analysis supported these results. On the other hand, a 2002 Cochrane review found no benefit of exclusive breastfeeding beyond 3 months on the incidence of asthma in families not preselected for a history of atopic disease.
Two additional reports in the literature with a more accurate definition of asthma made a distinction between the wheezy bronchitis associated with viral infections in younger children and that of the allergic disease seen in older children associated with respiratory spirometric changes. In the first of these studies, a cohort of 1246 children in Tucson, Arizona, was followed from birth to 13 years of age. The study found that an association between breastfeeding and asthma at 13 years of age depended on the presence of maternal asthma in children with atopic disease. Infants whose mothers had asthma were at greatest risk of developing asthma by 13 years of age if they had been breastfed exclusively for 4 months (OR: 8.7; 95% CI: 3.4–22.2). When infants with atopic disease whose mothers had asthma were exclusively breastfed for any length of time (either greater than or less than 4 months), the risk of developing asthma between 6 and 13 years of age was also increased (OR: 5.7; 95% CI: 2.3–14.1). An increased risk of developing asthma was not found in breastfed children of mothers without asthma. However, in this same study during the first 2 years of life, exclusive breastfeeding was associated with significantly lower rates of recurrent wheezing of infancy (OR: 0.45; 95% CI: 0.2–0.9), similar to results from a recent study performed in Perth, Australia.
In the second of these studies, a long-term longitudinal study from New Zealand, 1037children from a general population (not selected for risk of allergic disease) were followed from 3 to 26 years of age. Five hundred four infants were breastfed for 4 weeks or more, and 533 infants were formula fed from the time of birth or breastfed for less than 4 weeks. Breastfeeding for more than 4 weeks significantly increased the risk of developing asthma at 9 years (OR: 2.40; 95% CI: 1.36–4.6) and at 21 years (OR: 1.83; 95% CI: 1.35–2.47). This increased risk was not related to the presence of maternal atopic disease, unlike in the Tucson study. The study has been criticized for retrospective determination of breastfeeding and unclear definitions of atopic heredity. There was also no evidence of a "dose-response" effect of breastfeeding on the incidence of atopy or asthma.
In summary, at the present time, it is not possible to conclude that exclusive breastfeeding protects young infants who are at risk of atopic disease from developing asthma in the long term (>6 years of age), and it may even have a detrimental effect. On the other hand, breastfeeding seems to decrease the wheezing episodes seen in younger children (<4 years of age) that are often associated with respiratory infections.
Food Allergy
Food allergy, similar to atopic dermatitis and asthma, is more likely to occur in infants with a family history of atopic disease. In a prospective study of infants born to families with a history of atopic disease, it was determined that 25% will develop food allergy between birth and 7 years of age. Because both atopic dermatitis and asthma are closely associated with the development of food allergy, it is difficult to sort out the effect of breastfeeding on the development of food allergy. As reviewed above, maternal dietary exposure during pregnancy and lactation is unlikely to contribute significantly to the development of food allergy in the infant, although many food antigens can be found in human milk.
In theory, human milk should inhibit food antigen absorption; however, prospective studies have failed to show a protective effect of human milk–specific antibodies to cow milk on infant sensitization. Investigations of the role of breastfeeding on the outcomes of allergies to specific foods have been few, and the results may have been influenced by additional dietary variables such as length and degree of breastfeeding exclusivity. In reviewing the available studies, Muraro et al concluded that exclusively breastfeeding for at least 4 months in infants who are at risk of developing atopic diseases is associated with a lower cumulative incidence of cow milk allergy until 18 months of age. A Cochrane review included only 1 study with a blinded challenge (using the double-blind, placebo-controlled food-challenge technique) and concluded that at least 4 months of exclusive breastfeeding did not protect against food allergy at 1 year of age. Overall, firm conclusions about the role of breastfeeding in either preventing or delaying the onset of specific food allergies are not possible at this time.
ROLE OF HYDROLYZED FORMULA ON THE DEVELOPMENT OF ATOPIC DISEASE
The role of partially hydrolyzed and extensively hydrolyzed formulas for the prevention of atopic disease has been the subject of many studies in both formula-fed and breastfed infants in the last 15 years. Most studies with published results have been of infants at high risk of developing allergy.
Approximately 100 studies in the literature have examined the role of hydrolyzed formulas on the development of atopic disease. However, using the criteria of a 2006 Cochrane review, only 14 randomized or quasi-randomized (eg, using alternation) trials in term infants compared the use of partially or extensively hydrolyzed formula with the use of human milk or an adapted cow milk formula. All of these trials have followed up with at least 80% of study participants. It is important to note that none of these studies reported any adverse effects, including any adverse effect on infant growth. No long-term studies have compared partially or extensively hydrolyzed formula to exclusive breastfeeding. Thus, there is no evidence that the use of these formulas is any better than human milk in the prevention of atopic disease.
Three studies of 251 infants examined the effect of partially hydrolyzed formula on reduction of the occurrence of any allergy compared with cow milk formula in infants at high risk of developing allergy. Two of these studies found no significant effect, and a third study found an OR of 0.45 (95% CI: 0.22–0.94) for partially hydrolyzed formula versus cow milk formula. Three more studies examined prolonged feeding of extensively hydrolyzed formula compared with partially hydrolyzed formula in 411 infants at high risk of developing allergy. None of these studies found a significant difference in the incidence of atopic dermatitis between the 2 feeding groups. Two of these studies of 352 infants also examined other manifestations of atopic disease and did not show a significant difference in the occurrence of food allergy, cow milk allergy, or asthma between the groups of infants who were fed extensively or partially hydrolyzed formula.
A very large published study from the German Infant Nutritional Intervention Program raised additional issues. In the interventional arm of this study, 945 newborn infants were identified as being at high risk of developing atopic disease and were enrolled in a longitudinal, prospective study through 12 months of age. Although the majority of infants were breastfed initially, formula was introduced in the first 4 weeks to most infants. The infants were randomly assigned to receive 1 of 3 hydrolyzed formulas (n = 689) or cow milk formula (n = 256). The 3 hydrolyzed formulas were a partially hydrolyzed whey-based formula, an extensively hydrolyzed whey-based formula, and an extensively hydrolyzed casein-based formula. The incidence of atopic dermatitis was significantly reduced in those using the extensively hydrolyzed casein-based formula (OR: 0.42; 95% CI: 0.22–0.79; P < .007) and the partially hydrolyzed whey-based formula (OR: 0.56; 95% CI: 0.32–0.99; P < .046) but not the extensively hydrolyzed whey-based formula (OR: 0.81; 95% CI: 0.48–1.4; P < .44), compared with the incidence in those in the cow milk formula group.
However, the overall results for prevention of allergic disease (atopic dermatitis, urticaria, and food allergy) for the 3 hydrolyzed formulas compared with cow milk formula were less impressive (extensively hydrolyzed whey-based: OR: 0.86; 95% CI: 0.52–1.4; partially hydrolyzed whey-based: OR: 0.65; 95% CI: 0.38–1.1; and extensively hydrolyzed casein-based: OR: 0.51; 95% CI: 0.28–0.92; P < .025). Thus, this study indicated that different hydrolysates have different effects on atopic disease, and there may be an advantage for the extensively hydrolyzed casein-based formula. However, as the study demonstrated, it is difficult to show that partially hydrolyzed formulas have a very large effect on the reduction of atopic disease in infants who are fed formula or mixed feedings of human milk and formula, even if they are at high risk of developing allergic disease. If atopic disease associated with cow milk allergy has occurred, partially hydrolyzed formula is not recommended, because it contains potentially allergic cow milk peptides. More studies are needed to determine if any of the hydrolyzed formulas have any effect on the incidence of atopic disease later in childhood and adolescence and whether the modest effects of the use of extensively or partially hydrolyzed formulas in early childhood can be confirmed and are sustained. Such studies should also include a cost/benefit analysis of the use of the more expensive hydrolyzed formulas. It should be noted that the potential benefit of these formulas has only been documented in infants at risk of developing atopic disease.
Additional studies are needed among unselected infants or infants at low risk. The use of amino acid–based formulas for prevention of atopic disease has not been studied. Soy formulas, on the other hand, have a long history of use for atopic disease in infants. In a recent meta-analysis of 5 randomized or quasi-randomized studies, the authors concluded that feeding with soy formula should not be recommended for the prevention of atopy in infants at high risk of developing allergy.
ROLE OF INTRODUCTION OF COMPLEMENTARY FOODS ON ATOPIC DISEASE
Many studies have examined the duration of breastfeeding and its effect on atopic disease. However, few studies have examined the timing of the introduction of complementary foods as an independent risk factor for atopic disease in breastfed or formula-fed infants. An expert panel from the European Academy of Allergology and Clinical Immunology has recommended delayed introduction of solid foods for 4 to 6 months in breastfed or formula-fed infants. The AAP has also recommended that solid foods be delayed until 4 to 6 months of age and that whole cow milk be delayed until 12 months of age. Before publication of this clinical report, AAP recommendations for infants who are at risk of developing atopic disease were to avoid eggs until 2 years of age and avoid peanuts, tree nuts, and fish until 3 years of age. These guidelines for solid food introduction and avoidance of specific allergens were based on the evidence of a few studies with various limitations. Three newer studies have reported mixed results regarding the timing of the introduction of solid foods and development of childhood atopic disease.
In a prospective (nonrandomized) study of infants at risk of developing atopic disease by Kajosaari, atopic dermatitis and history of food allergy were reduced at 1 year of age if the introduction of solid foods was delayed until 6 months compared with at 3 months of age. However, in a 5-year follow-up study, no difference was seen in the incidence of atopic dermatitis or symptoms of food allergy. In a second prospective study of a birth cohort of 1210 unselected children between 2 and 4 years of age, there was more atopic dermatitis but not asthma in infants who were fed 4 or more solid foods compared with no solid foods before 4 months of age. This difference was maintained in a 10-year follow-up study in 85% of the original study infants.
In a study of 257 preterm infants (34.4 weeks’ gestational age; birth weight: 2.3–2.4kg), the introduction of 4 or more, compared with fewer than 4, solid foods before 17 weeks after term was associated with a higher risk of atopic dermatitis (unconfirmed by skin-prick testing) at 12 months after term (OR: 3.49; 95% CI: 1.51–8.05). Also in this study, the introduction of solid foods before 10 weeks of age or atopic disease in either parent increased the risk of atopic dermatitis in infants (OR: 2.94; 95% CI: 1.57–5.52).
In a more recent prospective, longitudinal cohort study in which atopic dermatitis was confirmed by skin testing, 642 infants were followed until 5.5 years of age. The history of the introduction of solid foods was carefully recorded during the first year of life. Most children had at least 1 parent with a positive skin-prick test result. Rice cereal was introduced at a median age of 3 months, milk was introduced at a median age of 6 months, and egg was introduced at a median age of 8 months. However, the later introduction of solids had no effect on the prevalence of asthma or atopic dermatitis (confirmed by skin-prick testing), although there was an increased risk of atopic dermatitis in relation to the late (6–8 months) rather than the earlier introduction of eggs (OR: 1.6; 95% CI: 1.1–2.4) or milk (OR: 1.7; 95% CI: 1.1–2.5).
Finally, an ongoing prospective, cohort study of 2612 infants (without a risk of developing atopic disease) found no evidence to support delayed introduction of solid foods beyond 6 months of age for prevention of atopic disease. However, in the same study, the effect of delayed introduction of solid foods for the first 4 months of life was less clear. Another study has even suggested that children exposed to cereal grains before 6 months of age (as opposed to after 6 months of age) are protected from the development of wheat-specific IgE.
In summary, the evidence from these conflicting studies, in balance, does not allow one to conclude that there is a strong relationship between the timing of the introduction of complementary foods and development of atopic disease. This raises serious questions about the benefit of delaying the introduction of solid foods that are thought to be highly allergic (cow milk, fish, eggs, and peanut-containing foods) beyond 4 to 6 months of age; additional studies are needed.
SUMMARY
It is evident that inadequate study design and/or a paucity of data currently limit the ability to draw firm conclusions about certain aspects of atopy prevention through dietary interventions. In some circumstances in which there are insufficient studies (pregnancy and lactation avoidance diets, timing of introduction of specific complementary foods), the lack of proven efficacy does not indicate that the approach is disproved. Rather, more studies would be needed to clarify whether there is a positive or negative effect on atopy outcomes. The following statements summarize the current evidence within the context of these limitations.
At the present time, there is lack of evidence that maternal dietary restrictions during pregnancy play a significant role in the prevention of atopic disease in infants. Similarly, antigen avoidance during lactation does not prevent atopic disease, with the possible exception of atopic eczema, although more data are needed to substantiate this conclusion.
For infants at high risk of developing atopic disease, there is evidence that exclusive breastfeeding for at least 4 months compared with feeding intact cow milk protein formula decreases the cumulative incidence of atopic dermatitis and cow milk allergy in the first 2 years of life.
There is evidence that exclusive breastfeeding for at least 3 months protects against wheezing in early life. However, in infants at risk of developing atopic disease, the current evidence that exclusive breastfeeding protects against allergic asthma occurring beyond 6 years of age is not convincing.
In studies of infants at high risk of developing atopic disease who are not breastfed exclusively for 4 to 6 months or are formula fed, there is modest evidence that atopic dermatitis may be delayed or prevented by the use of extensively or partially hydrolyzed formulas, compared with cow milk formula, in early childhood. Comparative studies of the various hydrolyzed formulas have also indicated that not all formulas have the same protective benefit. Extensively hydrolyzed formulas may be more effective than partially hydrolyzed in the prevention of atopic disease. In addition, more research is needed to determine whether these benefits extend into late childhood and adolescence. The higher cost of the hydrolyzed formulas must be considered in any decision-making process for their use. To date, the use of amino acid–based formulas for atopy prevention has not been studied.
There is no convincing evidence for the use of soy-based infant formula for the purpose of allergy prevention.
Although solid foods should not be introduced before 4 to 6 months of age, there is no current convincing evidence that delaying their introduction beyond this period has a significant protective effect on the development of atopic disease regardless of whether infants are fed cow milk protein formula or human milk. This includes delaying the introduction of foods that are considered to be highly allergic, such as fish, eggs, and foods containing peanut protein.
For infants after 4 to 6 months of age, there are insufficient data to support a protective effect of any dietary intervention for the development of atopic disease.
Additional studies are needed to document the long-term effect of dietary interventions in infancy to prevent atopic disease, especially in children older than 4 years and in adults.
This document describes means to prevent or delay atopic diseases through dietary changes. For a child who has developed an atopic disease that may be precipitated or exacerbated by ingested proteins (via human milk, infant formula, or specific complementary foods), treatment may require specific identification and restriction of causal food proteins. This topic was not reviewed in this document.
Committee on Nutrition, 2006–2007
Frank R. Greer, MD, Chairperson
Robert D. Baker, Jr, MD, PhD
Jatinder J. S. Bhatia, MD
Stephen Robert Daniels, MD, PhD
Marcie B. Schneider, MD
Janet Silverstein, MD
Dan W. Thomas, MD
Liaisons
Sue Ann Anderson, PhD, RD
Food and Drug Administration
Donna Blum-Kemelor, MS, RD
US Department of Agriculture
Margaret P. Boland, MD
Canadian Paediatric Society
Laurence Grummer-Strawn, PhD
Centers for Disease Control
Capt Van S. Hubbard, MD, PhD
National Institutes of Health
Benson M. Silverman, MD
Food and Drug Administration
Saturday, November 3, 2007
Post#5 The Blame Game
As parents, we rarely want to see our children sick. Not only does it affect our children's temporary well-being, it often thwarts our everyday routine. Of course, we all know and accept (for the most part) that catching colds and vomiting are an immutable fact of life. As a pediatrician, I view children combating regular illnesses as a rite of passage; with each passing fever and sniffle, our immune systems become stronger, more mature and smarter.
Regardless, when our children become sick, it is sometimes hard not to dissect the past 72 hours in an effort to deduce which of our friends' children made little Johnny sick. Sometimes it is simply an innocent fact-finding mission with little malice or misgiving. Other times, however, we rack our brains, pursuing a mini witch hunt, until we have concluded who passed the unfortunate germ to our child.
From a public health standpoint, it is a well researched fact that an average healthy child will come down with 6-8 viral illnesses each year; if the child attends daycare, this number jumps to 8-12 viral episodes. Furthermore, it is also known that children will often shed a virus for several weeks, even after they themselves appear perfectly healthy. Viruses, especially during the winter time, are rather hardy and can survive for several hours on fomite surfaces, including door handles, countertops, grocery carts, toys, and wherever else they happen to slobber, touch, or lick (in other words everywhere!).
Thus, when investigating the possible places or people that a child may have acquired a germ, it really is a total crapshoot. And assigning fault, especially if there is any ill will involved (pun intended!), is a dangerous and inaccurate game to play.
I often counsel my families that they should resign themselves to the fact that their children will become sick multiple times each year, with the bulk of the illnesses occurring during the winter time (the lower humidity and increased tendency for people to remain indoors leads to a greater survivability and sharing of germs). With this in mind, I believe that it is an impractical standard for people to avoid public gatherings when their children have a simple viral illness (or vice-versa, to impose this standard on others). The fact of the matter is, most of the time, whether their "sick appearing" snotty child joins the party or not, there will be plenty of germs abounding regardless.
If we truly want to avoid becoming ill, we would have to essentially live in a bubble. Even the most cautious, Purell-addicted family will encounter their fair share of germs each year. And even if they only socialize with well-appearing children, some of these kids may still be shedding germs from an illness they got over several weeks prior.
A simple but practical set of guidelines I pass on to parents is as follows:
1. Babies under 3 months should avoid contact with sick children. Anyone who plans to physically touch the baby should always wash their hands thoroughly before playing with the child, no matter how healthy they appear.
2. If a child is harboring a significant illness such as chicken pox or scarlet fever, they should be quarantined from other children until they are no longer contagious. For a full list of illnesses that should be quarantined, a pediatrician should be consulted with a quick phone call. The scope of this discussion is too exhaustive for a simple blog.
3. If a child is playing happily but has some mild symptoms (i.e. runny nose, cough, mild non-bloody diarrhea), they should NOT be quarantined and free to attend church, school, birthday parties, political functions, poetry readings, etc.
There are other circumstances that also need more detail; for example, an immunocompromised member lives in the household. However, the above general rules cover most circumstances.
It is this author's opinion that playing the blame game with colds and viral illnesses can not only be inaccurate, but ultimately fruitless. Rather focus on the upside! Your child's immune system has just been battle tested one additional time, and this can only strengthen him in the long run. Perhaps, rather than consigning blame, you should send the offending germ donor a thank you note. And maybe a little Purell.
Regardless, when our children become sick, it is sometimes hard not to dissect the past 72 hours in an effort to deduce which of our friends' children made little Johnny sick. Sometimes it is simply an innocent fact-finding mission with little malice or misgiving. Other times, however, we rack our brains, pursuing a mini witch hunt, until we have concluded who passed the unfortunate germ to our child.
From a public health standpoint, it is a well researched fact that an average healthy child will come down with 6-8 viral illnesses each year; if the child attends daycare, this number jumps to 8-12 viral episodes. Furthermore, it is also known that children will often shed a virus for several weeks, even after they themselves appear perfectly healthy. Viruses, especially during the winter time, are rather hardy and can survive for several hours on fomite surfaces, including door handles, countertops, grocery carts, toys, and wherever else they happen to slobber, touch, or lick (in other words everywhere!).
Thus, when investigating the possible places or people that a child may have acquired a germ, it really is a total crapshoot. And assigning fault, especially if there is any ill will involved (pun intended!), is a dangerous and inaccurate game to play.
I often counsel my families that they should resign themselves to the fact that their children will become sick multiple times each year, with the bulk of the illnesses occurring during the winter time (the lower humidity and increased tendency for people to remain indoors leads to a greater survivability and sharing of germs). With this in mind, I believe that it is an impractical standard for people to avoid public gatherings when their children have a simple viral illness (or vice-versa, to impose this standard on others). The fact of the matter is, most of the time, whether their "sick appearing" snotty child joins the party or not, there will be plenty of germs abounding regardless.
If we truly want to avoid becoming ill, we would have to essentially live in a bubble. Even the most cautious, Purell-addicted family will encounter their fair share of germs each year. And even if they only socialize with well-appearing children, some of these kids may still be shedding germs from an illness they got over several weeks prior.
A simple but practical set of guidelines I pass on to parents is as follows:
1. Babies under 3 months should avoid contact with sick children. Anyone who plans to physically touch the baby should always wash their hands thoroughly before playing with the child, no matter how healthy they appear.
2. If a child is harboring a significant illness such as chicken pox or scarlet fever, they should be quarantined from other children until they are no longer contagious. For a full list of illnesses that should be quarantined, a pediatrician should be consulted with a quick phone call. The scope of this discussion is too exhaustive for a simple blog.
3. If a child is playing happily but has some mild symptoms (i.e. runny nose, cough, mild non-bloody diarrhea), they should NOT be quarantined and free to attend church, school, birthday parties, political functions, poetry readings, etc.
There are other circumstances that also need more detail; for example, an immunocompromised member lives in the household. However, the above general rules cover most circumstances.
It is this author's opinion that playing the blame game with colds and viral illnesses can not only be inaccurate, but ultimately fruitless. Rather focus on the upside! Your child's immune system has just been battle tested one additional time, and this can only strengthen him in the long run. Perhaps, rather than consigning blame, you should send the offending germ donor a thank you note. And maybe a little Purell.
Wednesday, October 3, 2007
Post#4 Did My Doctor Miss the Diagnosis?
Every so often, I will walk into an exam room to meet a new patient who has come to elicit a second opinion. Many will readily explain what they are concerned about, who their primary doctor is, what they were told, why they are worried and for what they are seeking a second opinion. Others will tread more lightly, offering vague clues as to why they are seeking a second opinion - either they are slightly embarrassed to second guess their doctor, or they fear that too many facts will bias my mind, thus tainting the objective second opinion they seek.
There have been a few times, after listening to a parent's story and examining them, it seems clear that the previous doctor did not accurately diagnose or work-up the patient before me. I use the word "seems" because there are two sides to every story, and were I to ask their doctor his/her take on the matter, my judgment on the matter may sway.
However, more often than not, my overall impression usually does not find fault in the previous doctor; rather, I often assess mentally that the patient's disease(s) has probably evolved from their initial presentation, and had the family followed-up with their primary doctor, the correct diagnosis would have eventually been made.
I need to qualify this blog with a few thoughts:
1. Pediatrics is a different beast than adult medicine. In adults, debilitating diagnoses such as cancer, heart disease, stroke, etc. are more common, hence there is a greater propensity in adult medicine to misdiagnose a life altering ailment.
2. Doctors do make mistakes. This is not an attempt to exonerate myself or all pediatricians from errors. We are all human and every doctor has their share of war stories. Of course, we all try to keep these stories to a minimum.
3. I practice in an area of Houston where, for the most part, my surrounding colleagues are all excellent well-trained physicians, for whom I hold mutual respect. There is excellent camaraderie and perpetual educational conferences where we freely exchange information and medical trends. Thus, when a patient of their's seeks my second opinion, it is rare that I discover an egregious error.
4. Most of the mistakes I have personally witnessed are not from when patients have seen another pediatrician, rather they are seen at follow-up visits after a family has visited a non-pediatric emergency room where the physician on call did not regularly see children. The suburban strip mall after-hour clinics tend to be the most frequent offender. Of course, I have also met and know some excellent doctors in each of these settings. It just tends to be more of a crapshoot.
To fully demonstrate the point of this blog, I will delve for a moment into the minutiae of pediatric medicine. Let's take a look for a moment at the pathophysiology of bacterial pneumonia. Pneumonias can actually be categorized into 3 general groups divided by etiology (cause): bacterial, viral and atypical bacteria. Of these 3 groups, the one that can turn into an ICU nightmare is the bacterial pneumonia. The other 2 etiologies are of less clinical significance and, for the most part, are not dangerous. However, should a bacterial pneumonia not be properly treated, a normally healthy child can suffer significant consequences including the infrequent ICU hospitalization.
So how does a bacterial pneumonia evolve?
1. First, a child will catch the common cold (caused by one of many viruses). This will turn his nose into a faucet, which causes many to suffer from post-nasal drip, where the mucus runs from the back of their nose down their throat and into their lung. This essentially turns their trachea (windpipe) into a water slide, or more specifically, a mucus slide.
2. Second, the water slide of mucus/phlegm will accumulate in a pocket of their lung. Interestingly, the very cough that many parents want to alleviate and squelch, offers the best protection against the formation of these biological cesspools. In effect, cough is protective and beneficial! God is smart!!
3. A bacteria (often being harbored harmlessly in the child's nose) will ride the water slide down from the nose into the lung. Should it find an acceptable domicile of collected mucus, it will set up house and began to multiply. Once a sufficient army of bacteria are formed, the germs will infiltrate the surrounding lung tissue, firmly establishing a pneumonia.
This entire process usually takes 1-2 weeks, however should the offending agent be an aggressive bacteria, the timeline can be significantly shorter. The pathophysiology for ear infections and sinus infections is also very similar. So should a parent bring in a child during the first few days of this timeline, the appropriate diagnosis would be an upper respiratory infection (cold) caused by a virus, and thus the appropriate treatment would be tender loving care and watchful waiting.
As the child evolves from having a cold into a pneumonia, there is usually a clear change in their overall appearance. Often they will appear less energetic, have shallow labored breaths, their appetite/play will decrease, and there may be a second peak of fever. Most mothers will pick up on this and bring them back to their pediatrician for a second check. However, should the mother decide to switch doctors at this point, it may appear that the original doctor who diagnosed a cold made a mistake, when in actuality the disease has evolved since the initial presentation.
Second opinions are certainly warranted in certain situations, especially if you feel that your doctor is not adequately addressing a deteriorating illness. Either a lack of guidance and roadmapping may leave a parent feeling slightly lost and scared, or the doctor may simply be missing the boat on the underlying diagnosis.
However, it is more often the case that your child has simply progressed from their initial presentation, and allowing your own doctor to observe the change in symptoms will often be your safest recourse. Having seen how your child originally presented and then being able to see the change in presentation, will proffer your physician a bird's eye view on the entire history of the illness. Hopefully, you have enough faith in your pediatrician that you trust he has made the correct original diagnosis, and will also make a change in his assessment, should the opportunity necessitate itself. If this faith does not exist, it may be time to find a doctor in whom you can put it!
This blog is not to deter you from seeking second opinions, but rather to help you understand that sometimes a change in clinical diagnosis is not always indicative of a mistake but rather an evolution in the natural history of a disease process. And it may be in your child's best interest to stick with one doctor through thick and thin, especially if you've already found a doctor who you trust.
There have been a few times, after listening to a parent's story and examining them, it seems clear that the previous doctor did not accurately diagnose or work-up the patient before me. I use the word "seems" because there are two sides to every story, and were I to ask their doctor his/her take on the matter, my judgment on the matter may sway.
However, more often than not, my overall impression usually does not find fault in the previous doctor; rather, I often assess mentally that the patient's disease(s) has probably evolved from their initial presentation, and had the family followed-up with their primary doctor, the correct diagnosis would have eventually been made.
I need to qualify this blog with a few thoughts:
1. Pediatrics is a different beast than adult medicine. In adults, debilitating diagnoses such as cancer, heart disease, stroke, etc. are more common, hence there is a greater propensity in adult medicine to misdiagnose a life altering ailment.
2. Doctors do make mistakes. This is not an attempt to exonerate myself or all pediatricians from errors. We are all human and every doctor has their share of war stories. Of course, we all try to keep these stories to a minimum.
3. I practice in an area of Houston where, for the most part, my surrounding colleagues are all excellent well-trained physicians, for whom I hold mutual respect. There is excellent camaraderie and perpetual educational conferences where we freely exchange information and medical trends. Thus, when a patient of their's seeks my second opinion, it is rare that I discover an egregious error.
4. Most of the mistakes I have personally witnessed are not from when patients have seen another pediatrician, rather they are seen at follow-up visits after a family has visited a non-pediatric emergency room where the physician on call did not regularly see children. The suburban strip mall after-hour clinics tend to be the most frequent offender. Of course, I have also met and know some excellent doctors in each of these settings. It just tends to be more of a crapshoot.
To fully demonstrate the point of this blog, I will delve for a moment into the minutiae of pediatric medicine. Let's take a look for a moment at the pathophysiology of bacterial pneumonia. Pneumonias can actually be categorized into 3 general groups divided by etiology (cause): bacterial, viral and atypical bacteria. Of these 3 groups, the one that can turn into an ICU nightmare is the bacterial pneumonia. The other 2 etiologies are of less clinical significance and, for the most part, are not dangerous. However, should a bacterial pneumonia not be properly treated, a normally healthy child can suffer significant consequences including the infrequent ICU hospitalization.
So how does a bacterial pneumonia evolve?
1. First, a child will catch the common cold (caused by one of many viruses). This will turn his nose into a faucet, which causes many to suffer from post-nasal drip, where the mucus runs from the back of their nose down their throat and into their lung. This essentially turns their trachea (windpipe) into a water slide, or more specifically, a mucus slide.
2. Second, the water slide of mucus/phlegm will accumulate in a pocket of their lung. Interestingly, the very cough that many parents want to alleviate and squelch, offers the best protection against the formation of these biological cesspools. In effect, cough is protective and beneficial! God is smart!!
3. A bacteria (often being harbored harmlessly in the child's nose) will ride the water slide down from the nose into the lung. Should it find an acceptable domicile of collected mucus, it will set up house and began to multiply. Once a sufficient army of bacteria are formed, the germs will infiltrate the surrounding lung tissue, firmly establishing a pneumonia.
This entire process usually takes 1-2 weeks, however should the offending agent be an aggressive bacteria, the timeline can be significantly shorter. The pathophysiology for ear infections and sinus infections is also very similar. So should a parent bring in a child during the first few days of this timeline, the appropriate diagnosis would be an upper respiratory infection (cold) caused by a virus, and thus the appropriate treatment would be tender loving care and watchful waiting.
As the child evolves from having a cold into a pneumonia, there is usually a clear change in their overall appearance. Often they will appear less energetic, have shallow labored breaths, their appetite/play will decrease, and there may be a second peak of fever. Most mothers will pick up on this and bring them back to their pediatrician for a second check. However, should the mother decide to switch doctors at this point, it may appear that the original doctor who diagnosed a cold made a mistake, when in actuality the disease has evolved since the initial presentation.
Second opinions are certainly warranted in certain situations, especially if you feel that your doctor is not adequately addressing a deteriorating illness. Either a lack of guidance and roadmapping may leave a parent feeling slightly lost and scared, or the doctor may simply be missing the boat on the underlying diagnosis.
However, it is more often the case that your child has simply progressed from their initial presentation, and allowing your own doctor to observe the change in symptoms will often be your safest recourse. Having seen how your child originally presented and then being able to see the change in presentation, will proffer your physician a bird's eye view on the entire history of the illness. Hopefully, you have enough faith in your pediatrician that you trust he has made the correct original diagnosis, and will also make a change in his assessment, should the opportunity necessitate itself. If this faith does not exist, it may be time to find a doctor in whom you can put it!
This blog is not to deter you from seeking second opinions, but rather to help you understand that sometimes a change in clinical diagnosis is not always indicative of a mistake but rather an evolution in the natural history of a disease process. And it may be in your child's best interest to stick with one doctor through thick and thin, especially if you've already found a doctor who you trust.
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