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Thursday, June 5, 2008

Rational decision making

In light of several comments on a recent post, it seems as though a more complete discussion of cost-benefit analysis might be useful. It is a process that is useful in many aspects of biology, from resource management to health issues.

The basic premise is that to make decisions, you need to estimate both qualitatively and quantitatively the potential costs and benefits of the possible choices, and use that information to make the best choice. The magnitudes of both cost and benefits are important, because balancing a large cost against a small benefit will result in a different choice than when the cost is small but the benefit is large.

The mistake most people make when making choices is to consider only the potential benefits, or the costs, but not both simultaneously. For example, the anti-vaccine movement exists mainly because of fears of side effects, specifically autism (a link which has not been established). Yet even if all the potential side effects do occur, they are extremely rare, relative to the benefit received in resistance to disease, many of which can be fatal. True, if only a few school children are unvaccinated they may get by given that disease is less likely to travel through a group that is mostly vaccinated. But this cheating can be harmful even for some vaccinated children, for vaccines that are not 100% effective (such as whooping cough).

The point is that to focus on a vanishingly small cost to vaccination which confers a huge benefit in protection from common disease is a completely irrational choice.

Another context where cost-benefit analysis applies is in the area of climate change. Here, the problem is a bit tougher, because the costs and benefits of trying to do something about it, versus not doing anything, are harder to estimate. One major consideration in this case, of course, is that we only get one chance to do something (and the opportunity to do it may already be vanishing rapidly). We don't get to figure out what we did wrong this time and fix it the next. So what do we do? We first must acknowledge the possibility that climate change could be catastrophic, no matter how small. This is a potentially huge cost to ignoring the issue. The benefit to ignoring it is easier to grasp - short term economic pains in readjusting our energy usage around the world, which is clearly a monumental task, would be avoided.

The benefit to doing all we can to avert a possible worldwide catastrophe is two-fold; first, we potentially save a lot of the planet, and second, many of the measures taken could have positive geopolitical results as well, e.g. reduction in demand for oil, and spurring economic growth in new alternative-energy industries. The cost mirrors the benefit for not doing anything - it is the difficult inertia needed to radically change the way we produce and use energy. The biggest part of the problem in looking at these costs and benefits is that if we choose to do something, the costs are biggest here and now, while the benefit seems far down the road. Most of the people setting policy in the powerful industrial countries that could take a stronger lead on this will likely be dead before the jury comes in on the outcome.

This video goes into more detail about these trade-offs, and convincingly makes the argument that the eventual benefits of doing something now outweigh the costs.

A similar case involves the control of invasive species. Even though most of the time the benefit in controlling them early far outweighs the potential cost of doing nothing, and having to control them later, we still tend to ignore them until they are too late to control. The reason for this is that our political system for government (which is responsible for making and acting on these decisions) overly discounts future benefits. So, time after time, we wait to see whether an introduced species gets out of control before we do anything to control it, and end up spending millions more than it would have cost to control it early on.

Another health example is cancer treatment. With all the progress that has been made, we still know very little about what we are doing in this area. In this case, people tend to focus on hoping for a strong benefit, and accept all sorts of hellish treatment (a significant cost) that may or may not benefit them. But this is one case in which it is very difficult to be objective, because we are dealing with our own mortality, and we buy into the idea that anything that can possibly help is worth doing. Is it possible to make a rational decision? For some people it is, but they are in the minority.

And come to think of it, it is way too much to ask the multi-headed government beast to be rational too. At least it is easy to make the rational choice about anti-bacterial soap.

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Tuesday, April 22, 2008

Stop using antibacterial soaps now. Really.

In recent years, there has been a small bit of backlash against the ubiquitous use of antibacterial soaps. Indeed, research beginning in 2002 has continued to confirm that based on both effectiveness and potential negative side effects, there really is no reason to use these soaps and plenty of reasons not to.

The active antibacterial agent in question is triclosan. The only real question that can result from numerous scientific studies about triclosan is whether or not its potential negatives are strong enough to stop using it. (Indeed, the only piece (opinion) questioning the validity of the research showing both potential resistance problems and toxic byproducts of triclosan (Swofford, 2005) was written by a member of the soap industry.) However, given unambiguous results showing that soap containing triclosan is indistinguishable in its effectiveness against bacteria as regular soap (and, frankly, given that most illnesses most household users of antibacterial soaps are concerned about are actually caused by viruses, which do not respond to antibacterials) any potentially negative side-effects of its use should be unacceptable.

Here is the problem. Humans are dumping all kinds of chemicals into our (and other organisms') water supply, that are not removed during sewage treatment (even when the water properly goes through sewage treatment). Among these is triclosan (Gomez et al., 2007), which has been found in large proportions of human urinary samples (Calafat et al., 2008). Not only do we know nothing about how ingesting all these various chemicals may be affecting us over the long term, we cannot begin to know the complex ways in which they are interacting with each other to create new, and potentially more toxic compounds. Both laboratory (DeLorenzo et al., 2008) and field research (Kinney et al., 2008) suggests that triclosan bioaccumulates, which means its concentration could increase up the food chain (the same phenomenon responsible for the crash of bald eagle populations a few decades ago, due to DDT). Other laboratory studies suggest that it reacts with light and chlorine (ubiquitous in our drinking water) to form types of dioxin, a toxic compound (Sanchez-Prado et al., 2006). These studies are just scratching the surface of potential interactions between triclosan and other ubiquitous pharmaceuticals such as painkillers and sex hormones from birth control. Laboratory studies have also demonstrated that bacteria such as E coli and Salmonella can become resistant to triclosan (Yazdankhah et al., 2006).

Proponents of antibacterial soaps claim that none of these studies have shown that toxicity is common in the field, and resistance also has only been shown in the laboratory. So, let's get this straight: we should continue to use this completely useless agent, because research has not yet shown that it is definitely harmful in the short term. Brilliant reasoning. The abstract of a recent review paper sums up the state of our knowledge quite nicely:

Abstract (Aiello et al., 2007)
Background. Much has been written recently about the potential hazards versus benefits of antibacterial (biocide)-containing soaps. The purpose of this systematic literature review was to assess the studies that have examined the efficacy of products containing triclosan, compared with that of plain soap, in the community setting, as well as to evaluate findings that address potential hazards of this use-namely, the emergence of antibiotic-resistant bacteria. Methods. The PubMed database was searched for English-language articles, using relevant keyword combinations for articles published between 1980 and 2006. Twenty-seven studies were eventually identified as being relevant to the review. Results. Soaps containing triclosan within the range of concentrations commonly used in the community setting (0.1%-0.45% wt/vol) were no more effective than plain soap at preventing infectious illness symptoms and reducing bacterial levels on the hands. Several laboratory studies demonstrated evidence of triclosan-adapted cross-resistance to antibiotics among different species of bacteria. Conclusions. The lack of an additional health benefit associated with the use of triclosan-containing consumer soaps over regular soap, coupled with laboratory data demonstrating a potential risk of selecting for drug resistance, warrants further evaluation by governmental regulators regarding antibacterial product claims and advertising. Further studies of this issue are encouraged.


If the only weapon we have to stop this idiotic dumping of even a potentially harmful chemical into our water systems and environment is consumer demand, then let's use it. Stop using anti-bacterial soaps now, and maybe the fools producing them will stop, because it is no longer profitable.

References

Aiello, A.E., Larson, E.L. & Levy, S.B. (2007) Consumer antibacterial soaps: Effective or just risky? Clinical Infectious Diseases, 45:S137-S147.

Calafat, A.M., Ye, X., Wong, L.Y., Reidy, J.A. & Needham, L.L. (2008) Urinary concentrations of Triclosan in the US population: 2003-2004. Environmental Health Perspectives, 116:303-307.

DeLorenzo, M.E., Keller, J.M., Arthur, C.D., Finnegan, M.C., Harper, H.E., Winder, V.L. & Zdankiewicz, D.L. (2008) Toxicity of the antimicrobial compound triclosan and formation of the metabolite methyl-triclosan in estuarine systems. Environmental Toxicology, 23:224-232.

Gomez, M.J., Bueno, M.J.M., Lacorte, S., Fernandez-Alba, A.R. & Aguera, A. (2007) Pilot survey monitoring pharmaceuticals and related compounds in a sewage treatment plant located on the Mediterranean coast. Chemosphere, 66:993-1002.

Kinney, C.A., Furlong, E.T., Kolpin, D.W., Burkhardt, M.R., Zaugg, S.D., Werner, S.L., Bossio, J.P. & Benotti, M.J. (2008) Bioaccumulation of pharmaceuticals and other anthropogenic waste indicators in earthworms from agricultural soil amended with biosolid or swine manure. Environmental Science & Technology, 42:1863-1870.

Sanchez-Prado, L., Llompart, M., Lores, M., Fernandez-Alvarez, M., Garcia-Jares, C. & Cela, R. (2006) Further research on the photo-SPME of triclosan. Analytical And Bioanalytical Chemistry, 384:1548-1557.

Swofford, W. (2005) Triclosan research misreported? Environmental Science & Technology, 39:271A-272A.

Yazdankhah, S.P., Scheie, A.A., Hoiby, E.A., Lunestad, B.T., Heir, E., Fotland, T.O., Naterstad, K. & Kruse, H. (2006) Triclosan and antimicrobial resistance in bacteria: An overview. Microbial Drug Resistance-Mechanisms Epidemiology and Disease, 12:83-90.

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Wednesday, April 16, 2008

Merck's "fraud" is standard industry practice

This is a comment, based on personal experience in this area, on the latest news about Vioxx - that Merck hired "ghostwriters" to write the scientific papers about Vioxx and thus were perpetrating "fraud."

A new freely available report (Ross, J.S., MD, MHS; K.P. Hill, MD, MHS; D.S. Egilman, MD, MPH; H.M. Krumholz, MD, SM. 2008. Guest authorship and ghostwriting in publications related to Rofecoxib: A case study of industry documents From rofecoxib litigation. Journal of the American Medical Association 299(15):1800-1812) suggests that methods employed by Merck to use scientific journals to promote its products show just how scummy this company is, in case you didn't already believe it.

This is an issue that interests me because I was once a paid ghostwriter of a paper for a biotech company (which shortly after went belly up, and apparently the paper was never published). Based on the report's definition, ("Ghostwriting has been defined as the failure to designate an individual (as an author) who has made a substantial contribution to the research or writing of a manuscript") it is my impression from my own experience that biotech companies (including pharmaceutical) routinely pay "ghostwriters" to write papers intended for publication in medical journals. In my own case, the doctor whose name was to go on the paper did supposedly collect the data, and I was provided with a brief summary of the findings which I expanded into a full paper, which was then edited further by staff at the company.

Is such a process unethical? The way I saw it at the time, it was more an instance of the doctors collecting the data being too busy and/or subpar writers who could not be depended on to get the research written up and submitted to a journal for review in a timely manner, which is in the interest of the company promoting the product. On the one hand, this didn't seem to be a big deal given that the doctor who "authored" the paper did actually collect the data, and even contributed discussion points in the summary, which made him a valid author on the paper. On the other hand, the experience did make me cynical about papers in medical journals, which from then on I viewed as rather poorly conducted and reviewed advertisements for industry products (a common theme on this blog). In my mind, the question of who actually wrote the words of the paper to present the data is insignificant compared to the fact that papers published in medical journals are held to an incredibly low standard of scientific rigor compared to, say, those published in ecology journals. Part of the reason for this is obvious - scientific rigor is much more difficult in human studies, in which researchers are ethically more limited than ecologists in the types of manipulations available. Somewhat of a lower standard is probably necessary for progress in the field.

But another reason never discussed for poor medical studies is that journals and the medical industry seem to have a reciprocal back-scratching arrangement: the journal gets a lot of press coverage when it publishes yet another "significant" paper, and the biotech industry gets the promotion of their products. The authors and reviewers, by the way, are tied up in the same knot as well; they are scientists who need to publish to progress in their career, and are also often funded by the biotech industry. "Conflict of interest" probably doesn't begin to describe the complex web of interactions among all these parties.

A big problem with this system is that it creates a slippery slope. There certainly may have been instances when Merck's methods were less defensible, for example:
Documents were found describing Merck compensating investigators with honoraria for agreeing to serve as authors on review manuscripts ghostwritten on their behalf by medical publishing companies. Honoraria varied, ranging from $750 to $2500. One author refused his honorarium from Scientific Therapeutics Information stating, "I really do not feel it is appropriate to be paid for this type of effort."

Unfortunately, when you are so close to the line to begin with, crossing it becomes almost unavoidable. Paying the printed authors to put their name on any publication would certainly be crossing it.

Still, one wonders what planet Dr. Ross and the other authors have been on, given that they seem to imply that Merck should be singled out for using these methods to promote its products - they are shocked, shocked! to find what they did. Perhaps their disclosure statement sheds some light:
Although every effort was made to present this information objectively and fairly, it is important to note that all of the authors of this article have been compensated for their work as consultants/expert witnesses at the request of plaintiffs in litigation against Merck related to rofecoxib [Vioxx].

OK, they finally then admit that they may have heard of something like this before:
...it is reasonable to expect that the authorship practices observed in this case study may be used by other pharmaceutical companies as well. A recent press account seems to confirm as much, as does the presence of an industry specializing in medical writing.


They end with the extremely ironic statement, "We are hopeful that our findings encourage discussion of ways in which to improve the integrity of research." Simply, the "integrity" of medical research is a joke, and has been for a long time. Companies and journals will continue this charade as long as it stays profitable.

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Thursday, February 21, 2008

Diet Soda is Clearly an Evil Plot to Kill Us All

One common theme of this blog recognizable to regular readers is that medical studies based on giant data sets, especially those including self-reporting data, are quite limited in their implications for how an individual should live his or her life to promote optimum health. A recent article publicized as linking diet soda consumption to greater risk of diabetes and heart disease, and mortality in general, is a good example of this.

The problem with the study (Lutsey, P.L., L.M. Steffen and J. Stevens, 2008. Dietary intake and the development of the metabolic syndrome: The atherosclerosis risk in communities study. Circulation 117:754-761) is not that it is necessarily wrong. It is that it is too hard to tell what importance the findings have in the context of all the other health information with which we are bombarded daily.

Aside from the problems inherent in self-reporting diet data -- which the authors acknowledge in the discussion but which obviously had no effect on likelihood of publication or promotion of the press release -- the authors reveal a troubling bias in their assumptions and use of terminology. They conducted a factor analysis on dietary components in an attempt to see which parts of a diet are more highly correlated with a condition called metabolic syndrome (fat, high blood pressure, high cholesterol, etc.) or "MetSyn". So far so good. But the next problem here is that human beings had to classify the types of food people ate, and these classifications are based on assumptions already about what foods are good and bad for you. For example, "red meat" of course does not take into account what species of mammal was eaten, or the conditions under which it was raised, which surely affect its nutritional and fat content. They use a category "low-fat diary" because they believe there is a reason to distinguish it from non-low-fat dairy.

The use of categories is necessary for their methodology, but it illustrates the problem with nutritional data collection which to this point is always colored by currently held biases about good and bad food. To make matters worse, when their factor analysis revealed two broad dietary patterns (based on their categories) among the people studied, they chose to label these "Western" and "Prudent" dietary patterns. Guess which dietary pattern they have already decided is bad for you, and likely to cause MetSyn?

Although their results showing more people on the "Western" diet to acquire "MetSyn" show a correlation, they are quick to label certain food groups (e.g. dairy) as "protective". But of course this is based on the studies in the past that have shown certain types of food to have negative effects on human health (usually, though, only when consumed in high quantities). Of course then none of the results were too surprising, except for the finding of diet soda, consumption of which in their model increased risk for MetSyn even more than consumption of sweetened drinks. This was the splashy result that got the newspaper headline.

I have no problem with their explanation, it makes perfect sense. They first admit that the data might be confounded, because diabetics are more likely to drink diet soda than nondiabetics, so which came first? But they also cite a rat study which suggested that artificial sweetener screws up our body's ability to determine the caloric content of what we are consuming - our mouth says "caloric" and our body says "not" and thus our body may simply stop trusting our mouth. It's a much more interesting explanation, and makes some intuitive sense, so that makes it easy to ignore the explanation that the data are confounded. The study gets published anyway, and promoters at the journal find the line in the results and discussion that will attract media attention, and bingo.

Those of us who think artificial (= man made) sweetners are potentially nasty unknowns to be avoided if possible, love a result like this. But that still doesn't mean that if you drink a lot of diet soda you are doomed to be fat and get diabetes. Even when we really know very little about what we are studying, even when our methods are poor, and the results questionable (in some cases contradicted by other studies, as the authors cite), and based on broad assumptions, these studies get published, because they get headlines. Bad methods are considered acceptable to medical journals because there are not necessarily feasible methods that are valid. Assumptions may be based in part on established medical knowledge, but they are mostly based on previous, poorly conducted studies such as this one, not to mention constant propaganda from our media and government about what is good for us, and which is so obviously correct that they completely revamp the propaganda every couple of decades or so. We think we are learning more and more and more when we "confirm" these same assumptions, yet in truth we haven't even begun to understand the complexity and variation in the human body. Just ask a scientist researching disease cures, who actually has to get it right for anyone to care about her research. Eating dairy products is "protective"? Check that with someone from a genetic heritage of lactose intolerance.

Never forget that these studies are blunt, blunt instruments, that tell us nothing about what works for an individual. A good rule of thumb for most diets is, simply, variety, and not too much of any one thing. That, not forcing down a gallon of skim milk every day, should be the first step for anyone trying to feel better through a diet better suited to his body.

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Thursday, December 13, 2007

The Continuing Misuse of Body Mass Index

Some researchers (Flegal et al., 2005 and 2007) have claimed, using data for Body Mass Index (BMI) and death rates, that it is somehow beneficial to be "overweight." This is the type of announcement that will always make headlines in the popular press. As usual, these studies are fraught with flaws that would only be accepted in a publication about humans, and are meaningless in the terms that really matter to all of us, which is what decisions individuals should make about their lifestyles in order to have the best chance of living long, healthy lives.

The major reason why studies like these are meaningless is because of the arbitrary nature of definitions: "underweight" = BMI <18.5; "normal" = BMI 18.5-25; "overweight" = BMI 25-30; and "obese" = BMI > 30. There may not be much reason to quibble with the extremes on this scale. As expected, the majority of "excess deaths" were associated with the extremes in weight - both "underweight" and "obesity grade 2" (BMI>35). But of course what makes the headlines is the fact that over the time period studied, "overweight" people had fewer excess deaths of most diseases than "normal" people.

The first question anyone should ask is, what exactly does BMI measure? BMI is nothing more than a ratio of your weight by your height (squared). It takes nothing else into account. As originally conceived, the BMI was not intended for assessing individuals medically. It has become a popular measure in the media because it is somewhat useful for describing population-level trends - such as the well known trend in the U.S. toward more obesity over the last few decades. BMI data in this context can show us that there is something about the lifestyle of Americans which is causing us to gain weight, and in a rational world would lead to measures to provide plenty of decent food and opportunities for reasonable levels of physical activity for everyone in the country.

But for an individual, BMI is not particularly useful, because it does not take into account the individual variation in body type (for example, bone density or muscle density, which contribute far more to weight than fat), not to mention activity level or overall conditioning, or even gender. All the talk of BMI has emphasized calculating one's own BMI, for example at the federal government's CDCsite, which, based on the arbitrary, government-created ranges listed above, spits out an assessment that you are "normal," "overweight," etc. Of course the caveat on most of these sites is given that for "highly trained athletes" BMI may be "high"; it is implied that this condition is sufficiently rare that the great majority of us need not take it into account.

On any football team, even at the lowest level (such as my NAIA college), every player would be considered "overweight," and many are classified as "obese." Perhaps this is a straw man, but I would challenge someone who seriously believes in the BMI as an individual health measure to calculate it for anyone who regularly goes to a gym or just has more than moderate physical activity. Based on my own experience, I suspect that a lot of Americans who ended up in the "overweight" category were fit; hence, the "earth-shattering" results that it is beneficial to be "overweight."

Of course, these papers are indeed using the typical huge sample sizes to make their point, so aren't they using BMI correctly, to study general population trends? If only they said so in the discussion, or at least included the caveat about the arbitrary divisions in BMI classes, one could more easily put these papers into the proper context, which is that there are health risks associated with the extremes of BMI. But of course they don't. The truth is that only you and your doctor can assess your personal health risks and the benefits to changing your lifestyle (if that is even realistically possible for most people). The media saying to everyone, "hey, it's better to be overweight!" are missing the point. If you are interested in maintaining or improving your health, stop using BMI calculators. Just eat well and get enough exercise to feel good.

References

Flegal, K.M., B.I. Graubard, D.F. Williamson, and M.H. Gail, 2005. Excess deaths associated with under weight, over weight, and obesity. Journal of the American Medical Association 293:1861-1867.

Flegal, K.M., B.I. Graubard, D.F. Williamson, and M.H. Gail, 2007. Cause-specific excess deaths associated with under weight, over weight, and obesity. Journal of the American Medical Association 298:2028-2037.

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Friday, October 19, 2007

You are responsible for how your children eat

Once again, the mass media can't tell real science from a junior high fair project. Genetics is the new path to a guilt-free style of life and child-rearing; it has been mass-marketed to people who want to evade all responsibility for persistent unpleasant conditions ranging from obesity to bad behavior, not to mention sexism. This is especially true in the field of child-rearing, where there has been a backlash against the offensive "blame the mother" explanations for problem children espoused decades ago. As usual, though, the backlash has swung too far in the other direction, making parents completely blameless. Bad papers supporting this faddish view continue to be published simply because they generate positive press.

The latest condition to be given a free pass is picky eating by children, in a study (Cooke, L.J., C.M.A. Haworth, and J. Wardle, 2007. Genetic and environmental influences on children's food neophobia. American Journal of Clinical Nutrition 86:428-433) using the differences between the eating behavior in identical twin pairs and in fraternal twin pairs. The idea is that twins in each pair are both presumably reared in the same environment, and so if there is a bigger difference in fear of new foods (="neophobia") between fraternal twins than there is between identical twins, this behavior must be genetic, thus, it's not the parent's fault that a child is picky.

The press release demonstrates the first problem with this paper:
"People have really dismissed this as an idea because they have been looking at the social associations between parents and their children," Dr. Cooke said. "I came from a position of not wanting to blame parents."

This of course explains the absurd conclusions of this paper - apparently, the first author had decided what the results should be before the study was conducted.

As usual with human health papers, the authors commit the fallacy of believing that a bigger sample size is better. They admit up front that a previous paper failed to find that genetics played a role in picky eating, but discount it by asserting that its sample size of 91 was too small. This of course is a circular argument; the authors are defining 91 as too small a sample size because no effect was found.

The data from the study are from parents completing questionnaires on the pickiness of each of their twin children, answering four questions on a scale of 1 to 4. They determined that fraternal twins were more different in their food choice than identical twins, based on a difference in survey score of 0.03 on that scale. Such a minute difference could of course only be detected by an enormous sample size, which they had - 5390 twin pairs. When a huge sample size is needed to detect a difference, it is unlikely that difference is biologically meaningful. This result is thus consistent with that of the previous paper which was unable to detect a difference with its sample of 91 twin pairs. It is especially egregious that the authors try to pass off their result as meaningful, when two other analyses associated with the paper that did not contribute to the support of their theory, but were statistically significant, were dismissed because these results were "statistically significant only because of the large sample size."

The other fundamental problem with the study is the fact of its reliance on evaluations of pickiness by parents. Think about it for a moment: parents with identical twins often dress them the same, give them the same toys, and refer to them as a unit, while parents with fraternal twins are much less likely to do so. The tiny difference that was found could be merely due to a bias by parents of identical twins, in their unconscious assumption that the children are naturally similar. This is separate from the possibility that there would probably be a greater correlation between identical twins than fraternal twins in personality traits that manifest themselves as food pickiness, apart from any genetic determination of pickiness per se. And, while the questions addressed the children's behavior toward new food, there was no data on how often the children actually encountered new food.

Obviously there are clear genetic differences in how individuals taste food. This is known from research on taste receptors. Given this, it is actually surprising that a study that set out to show genetic differences in food exploration found such a slight effect. Nevertheless, the publicity surrounding this non-result will lead people to believe that they cannot control their children's stated food preferences, and thus must give in to them. This is an unfortunate implication, because it could lead to an even larger number of adults in the next generation subsisting on McNuggets from the drive-thru as they drain the health system with their obesity-related conditions.

You do have a choice about whether or not your children will eat anything besides tater tots. Give them the food you have cooked for the family, and if they don't want to eat it, fine. They really will not starve to death between dinner and breakfast. (For a lot more advice in this vein, read Ellyn Satter.)

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Thursday, September 27, 2007

Alcohol and pregnancy - what do we really know?

One media-blasted notion that most women now seem to take at face value is the importance of not drinking a drop of alcohol during pregnancy. The most ironic part of the propoganda is that those passing it along know it is a double-edged sword: they try to keep an impossible balance between convincing you that one beer will cause irreparable harm to your fetus, and assuring you that if you had some drinks before you were pregnant, you shouldn't acutally worry.

This contradiction might make some women wonder where the truth lies. While it is clear that excessive alcohol consumption can result in Fetal Alcohol Syndrome (FAS), a suite of birth defects mainly affecting the brain (learning and memory), but Wikipedia's definition of the condition is misleading in that it states: "It is unknown whether amount, frequency or timing of alcohol consumption during pregnancy causes a difference in amount of damage done to the fetus." A perusal of the current literature on the topic of alcohol and pregnancy makes it quite clear that generally there is a positive relationship between the amount of alcohol consumed during pregnancy and the likelihood and severity of defects. In addition, it is also known that the most important brain development occurs in the first trimester, and thus that is almost certainly the most critical period to avoid consumption of alcohol.

What has been unknown since the FAS-prevention media blitz started is whether or not there is a threshold level of alcohol consumption below which there is no damage to the child. Frankly, there doesn't seem to have been a lot of interest in this among medical professionals, because it is simpler just to tell women not to drink at all than it is to consider nuances that might cause women to think it is okay to drink, and then drink too much, whatever too much is. The one certainty is that if a woman does not drink at all, there is no danger of impairments to the fetus caused by alcohol.

There have been occasional papers, however, focusing on the moderate drinkers, in order to possibly establish a safety threshold for alcohol consumption. One research project in particular is interesting because it is an ongoing longitudinal study that began when 580 mothers involved joined the study at 4 months pregnant. The most recent paper I was able to access on the study has data from when the focal children were 14 years old (Wilford, J.A., Richardson, G.A., Leech, S.L., Day, N.L., 2004. Verbal and visuospatial learning and memory function in children with moderate prenatal alcohol exposure. Alcoholism: Clinical and Experimental Research. 28:497-507.) This study is a genuine attempt to uncover potentially subtle effects on children whose mothers had around three drinks or less a week during pregnancy.

The positive aspects of the paper is that 1) it separates drinking by trimester, which is developmentally relevant and 2) it compares continuous variables in a regression analysis - e.g. drinking amounts are not placed into arbitrary categories, rather the actual volume drunk is used for the data.
The problems with the paper are pretty much the same ones that plague so many medical papers. First, by necessity, drinking levels are self-reported. Given that the first assessment was at 4 months - after the first trimester - the accuracy of the data is not convincing. Not only was each woman required to remember amounts drunk months previously (questionable even for those not experiencing the undulating body chemistry of pregnancy) but at the point these women were pregnant there was already some media blitzing discouraging drinking during pregnancy. The authors do not address the problem of potential underreporting bias.

Mainly, though, the problems are statistical. The authors used a large suite of learning and memory tests to score the children. They then regressed every variable they could think of against the scores, because of the need to correct for all the other potential factors influencing the scores, for example: race, mother's IQ, child's age, child's current substance use, mother's current substance use, etc. in addition to mother's alcohol and other substance use over each trimester. This makes for an extremely large number of statistical tests performed, although the number is unreported and thus must be estimated. The "significant" results alone number 31. For the six learning and memory tests that had "significant" results, all included mother's use of alcohol in the first trimester (but not the second or third in any case). This leads to a long discussion of the mechanism by which moderate drinking has caused "learning and memory deficits" in these children, etc.

But assuming the learning and memory tests are valid evaluations, we need to take another look at what the statistics actually showed. (Table 2 with p-value results is reproduced below.) First of all, one of the most basic statistical rules, ignored by doctors in every case I have seen, is that there is a probability of being wrong about the result. It is generally accepted that if the statistics show 95% probability of an effect, it is a valid result. The problem arises when as part of a single study, a large number of statistical tests are run, as in this case. The flip side of being 95% sure is that out of every 20 statistical tests conducted, we can expect, on average, for one of them to show significance when in fact there is actually no effect. To control for this problem, many scientists employ a Bonferroni correction, which simply means dividing the base significance level (0.05) by the number of tests conducted - in this case, apparently something greater than 200, although the true number is never stated by the authors. The appropriately conservative significance level for this paper would then be 0.00025.

The highest significance level for maternal consumption of alcohol in the paper was at <0.001 for "word-pair learning," and three of the other four significant tests were at 0.05. Perhaps, though, since first trimester alcohol consumption cropped up as a relatively high probability effect for five different learning and memory indexes (out of a total of 12, I think, but again it is not clear), it could be considered a real effect. But what other effects were real? The only effect that nearly every single time passes the Bonferroni level of significance was mother's IQ, which was significant at the 0.00001 level 5 times out of 6. So, even if there is a barely measurable effect on learning and memory on the children whose mothers drank, the IQ of their mother is 5000 times more important in determining that score. Also, for a given index, equally or more important than whether the mother drank was the child's current use of alcohol or tobacco. Race was more significant for four indexes. In two of the indexes, the child's gender was more significant.

The take-home message boils down to this. A lot of factors affect your children's mental abilities. Many of these are out of your control. The first trimester of pregnancy is certainly the most sensitive period for brain development. For a lot of women, morning sickness during that time means the last thing they are interested in is alcohol. Although these results are about as sketchy as you can get, it is certainly rational for women to abstain during the first timester, just in case. It took a lot of fishing for these authors to find a result they could publish, and they never discussed it in terms of relative importance to the other factors. Ironically, the mothers who seem to worry the most about alcohol during pregnancy are the high-powered, yuppie types with the big IQs to match - who it seems have the least to worry about. After all, their mothers went to cocktail parties while pregnant, and they still got into Ivy League schools.

So next time you see a visibly pregnant woman drinking a glass of wine in public (are there any of them left who have the guts to do it?), don't insist that it is your civic duty to give her a dressing down, because she is past the first trimester anyway. The stress you cause her is probably worse for her fetus than the wine.

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Friday, September 21, 2007

How could those fat friends of mine do this to me?!

About a month ago, another new paper on obesity (Christakis, N.A. and Fowler, J.H., 2007. The spread of obesity in a large social network over 32 years. New England Journal of Medicine 357:370-379) made headlines. The paper is based on an enormous data set that started being compiled in 1948, consisting of health information of thousands of residents of the town of Framingham, Massachussets. The original purpose of the study was to learn about causes of heart disease. Everyone in the study has received complete physicals every couple of years throughout their lives, and the data collection has continued on to the second and third generation of patients, which will presumably provide some information about the genetics of heart disease in addition to external causes. Christakis and Fowler use information about relatives and friends of the study subjects, included as part of the original data set, to assert that people whose friends get fat are more likely to get fat themselves.

The authors make the case that "[t]he spread of obesity in social networks appears to be a factor in the obesity epidemic." Although they never use the specific word "disease" in reference to obesity as some sensationalizing media outlets do, the thrust of the paper is that there is yet another cause of our obesity out there that is not our fault.

The advantage of using such a data set in this paper is that there is a lot of data about a lot of people over a long time period, and it is certainly understandable that scientists might conceive of other uses than the original purpose. The disadvantage is that the data set was not really designed to draw conclusions about obesity - and one of the major problems with the study is that the authors are promoting a cultural influence - based on interpersonal relationships - on weight gain using an extremely homogeneous sample, which does not represent a real cross-section of society. But, approached with an understanding of its assumptions and limits, Framingham-type data can indeed be useful for secondary studies.

The biggest limit of this analysis is its dependence on overlapping relationships among people. Although "social-network analysis" is not a technique with which I am highly familiar, it appears to consist mainly of high levels of pseudoreplication, which is a major problem for statistical analyses. Pseudoreplication is the use of data that are not independent, violating an important assumption upon which proper statistical analysis depends. There were 5124 focal subjects, and over 12,000 people total in the study, with an average of 7.5 social ties per person. The math on this clearly indicates that some people were analyzed as friends of more than one person. Thus, these data are not exactly independent. If the data were on people scattered about the country, so that each person's social network was independent of everybody else's, pseudoreplication would be avoided. With the data used as is, the statistical assumption of independence has been violated (although one can only conclude this in a roundabout manner; the author's use of jargon and limited statistical explanation makes their methods difficult to discover).

The most sensational assertion of the paper, that physical distance from one's friend does not affect the probability of becoming obese - and thus obesity of friends cannot be explained simply by them all having bad habits together - is undermined by the actual data, which are not nearly so conclusive. The authors broke physical distance into 6 rather absurd categories: 0 miles, 0.26, 1.5 miles, 3.4 miles, 9.3 miles, and 471 miles. Effectively, only the last group has true physical distance. Their conclusion is based on a nonstatistical difference, which may just mean that variation in the data is too large to detect a difference. In fact, the variation in their data is huge, with 95% confidence intervals (the statistical standard) often ranging over 50 or more percentage points. There is only confidence that having fat friends makes you fatter if the confidence interval does not overlap with a probability of zero. Looking at category 6 (471 miles) compared to the other groups in the figure below from the paper, four of the confidence intervals overlap with zero, as opposed to not more than 1-2 in the other distance categories, and upper confidence levels of probabilities of becoming obese are much lower than with shorter distances. The difference between category 6 and the others may not have been significant, but it is quite a stretch to conclude from this that distance from the friend does not make a difference in the probability of following him or her into obesity. (The six bars in each category represent data from six different health examinations over a person's life.)

For the authors, this paper was a no-brainer in two ways, though. If you can find a way to publish another reason why it isn't really someone's fault they are obese, by implying that the condition spreads from person to person like a disease, you've struck gold. In addition, because the conclusions are not that surprising at all (although they were spun as such by the NEJM media machine) it's easier not to pay attention to the statistical problems in the paper. But surely the authors' explanation that people thing it's more acceptable to be obese if their friends are is laughable to anyone. Do you know anyone who chose to be fat? "It really must be OK to let myself go if my friend has" just does not seem like a thought many people would have. But people who are friends will do things together, and if one of them can no longer do something physical, the other will end up hanging out watching TV with them, in a lowest-common-denominator effect. Because the assertion about physical distance not mattering is essentially bogus, a much simpler one is mutual lifestyle choice. It just wouldn't be very nice to dump a close friend because she got fat and couldn't ride bikes anymore.

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Wednesday, August 22, 2007

Can we be honest about what is science?

A long term academic controversy boiled up into the New York Times recently. There are dozens of these all the time in every field, but this one, regarding Dr. J. Michael Bailey, who in 2003 published "The Man Who Would Be Queen: The Science of Gender-Bending and Transsexualism" obviously made the mainstream press because of its topic.

The portrayal of the controversy is a typical rehash pitting the Nasty Scientist Who Misuses His Credentials To Promote An Unsubstantiated Viewpoint versus the Knee Jerk PC Crowd Who Doesn't Want To Hear The Uncomfortable Truth.

My disclaimer up front is that I have not read the book, just a lot of commentary by both its supporters and detractors. For my purposes this is enough. The existence of the controversy itself brings to mind two separate questions. The first is a question about how we go about conducting science and promoting its results, especially when the research involves human subjects (which by default produce data that are complex and difficult to interpret). The second is a question about the relationship between gender identity issues and society, and will be addressed in the next post.

Any academic discussion of sexual identity will become quickly polarized, because people view statements written in generalities as personal attacks. This is why a book such as this provokes much more emotional responses than controversial books or papers about other health issues. The crux of this controversy is that proponents of the book maintain that any transsexuals who were offended by it just don't want to hear the truth about themselves, while the offended transsexuals are insulted that anyone else would presume to know more than they about their motivations. It is clear from reviews on both sides that Dr. Bailey goes somewhat out on a limb by claiming that there are only two motivations for transsexuals, and every transsexual falls into one of the two groups. It is not surprising that transsexuals who believe they fit one of the categories like the book, and those who do not believe such do not. But what truly matters is whether this book is actually science or merely opinion.

Certainly it is wise to be suspicious of those making sweeping claims about human biology based on their invariably self-selected, self-reporting sample. Such a book, if it purports to be true science, should be absolutely clear in its justification of research methods (e.g. at the minimum, general acceptance of those methods by others in the field), and equally up-front about the assumptions that were made in the analysis of the data. All data analyses, statistical or not (and I have no idea if Bailey used statistics or not), involve assumptions, that if violated, undermine the conclusions the author is drawing.

There is a widespread problem of those with scientific credentials claiming authority in areas such as this that are notorious for requiring many assumptions and inferences that cannot be directly confirmed through observation or experiment. An example of a field outside the realm of human biology is paleontology, in which scientists notoriously cling to their personal theories with a vigor less known in other areas of geology and biology. The reason is that there is a clear limit on what we can ever know about plants and animals that went extinct millions of years ago, no matter how many more fossils are discovered. Thus the field is rife with assumptions and inferences that can never be disproved.

The field of human biology is similar. Our knowledge of how the brain works is growing, and may sometime be sufficient to make well supported generalizations, but the more we learn, the more we discover how little we really know. Every individual is a unique combination of genes and environment, with no way to replicate his or her singular experience (except in the limited case of identical twins-reared apart studies). So even sincere attempts at conducting scientifically rigorous, unbiased research are extremely limited in their real scientific utility. Overlaid on top of this is the problem of distinct personalities conducting the research, with biases (quite strong when the subject is our own species) either blatant or in most cases more subtle and difficult to detect, and the reception of results also by distinct personalities with their own biases. Rigorous scientific methods are a distinct improvement over exhortations from those claiming to converse with a higher being, but even their results are often far from black and white.

Is Dr. Bailey's book science? I cannot answer that question without reading it. But my own bias is that little health research to do with humans is worthwhile at the present time. Its larger potential value is that it will lead to more interesting questions to ask in the future, when we may have better technologies for understanding the interactions between genes and environment that create the deeply complex bags of water and chemicals that we are.

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Saturday, August 18, 2007

Sleep problems and ADHD - chicken and egg?

Although evidence is purely anecdotal, it appears these days that most children sleep a lot less than children of generations past. The majority of parents I encounter (certainly not all) seem to put their children to bed around the time they go to bed, which means a lot of kids out there may be getting only eight hours of sleep or less. Data presented in Weissbluth (2003), however, show that although total sleep per day declines with age until 14 years (in teenagers it creeps back up again), the median amount of sleep needed by children never drops below about 9.5 hours by this age. At 4, median sleep time is 12.5 hours, and the 10th percentile is 10.5. So although 10% of 4-year-olds out there may need less than 10.5 hours of sleep, one encounters many more than that who are getting less.

There seems also to be some correlation between sleep disorders and ADHD (attention deficit-hyperactivity disorder) (Gau et al., 2007; Hora das Neves 2007), although the nature of this correlation is not yet well understood, if it is even real (Sadeh et al., 2006). Medical studies relying on self- (or parental-) reported data, which many of these seem to be, are unreliable at best.

There are, however, suggestions by some that some of the people labeled as ADHD may instead be suffering from poor sleeping. This may be caused by sleep disorders such as sleep apnea. But most articles on the subject, even those advocating treatment of sleep disorders before treatment of the ADHD itself, seem to assume that sleep problems are one of the symptoms of ADHD.

What if the reverse is true, that years of sleep deprivation has caused ADHD? Weissbluth (2003) seems to be one of the few authors suggesting this link. All of us know that in the short term, sleep deprivation makes people irritable, unable to concentrate, and even often hyperactive. What if kids are growing up sleep-deprived for years? Might that not be a cause of sleep disorders?

What's worse is that the popular drug for controlling ADHD, Ritalin, is a stimulant, and kids on it sleep less than those on an alternative non-stimulant ADHD drug, atomoxetine. (Sangal et al., 2006). Are we making our kids lives worse in the long run by addressing only the short-term behavioral problems?

It can be difficult for parents to sleep-train their children, and many never do. Their child is in an endless cycle of exhaustion followed by a crash. The easiest way to sleep-train a baby is to put her down and let her cry until she falls asleep. Most kids will only cry for a long time for 2-3 nights, and then they understand that it is their sleep time, and they learn to put themselves to sleep. Failure to teach a child to get to sleep on his own can lead to a lifetime of sleep problems. It is crucial for the developing brain to get an adequate amount of sleep, which is when the brain processes new knowledge and experience. Babies and small children have a lot of new information to process, and they need to sleep a lot, often for longer than they are awake. It is not a stretch to imagine subtle (or not so subtle) developmental brain damage occurring in children who are chronically sleep-deprived because their parents will not force them to go to bed before they are exhausted. Obviously ADHD is a complicated issue, and it is likely to have many causes, ranging from genetic to environmental. But the first question any parent of a hyperactive kid should ask is, does my child get enough sleep?


References

Gau, S.S.F., Kessler, R.C., Tseng, W.L., Wu, Y.Y., Chiu, Y.N., Yeh, C.B. & Hwu, H.G. (2007) Association between sleep problems and symptoms of attention-deficit/hyperactivity disorder in young adults. Sleep 30:195-201.

Hora das Neves, S.N. & Reimao, R. (2007) Sleep disturbances in 50 children with attention-deficit hyperactivity disorder. Arquivos De Neuro-Psiquiatria 65:228-233.

Sadeh, A., Pergamin, L. & Bar-Haim, Y. (2006) Sleep in children with attention-deficit hyperactivity disorder: A meta-analysis of polysomnographic studies. Sleep Medicine Reviews 10:381-398.

Sangal, R.B., Owens, J., Allen, A.J., Sutton, V., Schuh, K. & Kelsey, D. (2006) Effects of atomoxetine and methylphenidate on sleep in children with ADHD. Sleep29:1573-1585.

Weissbluth, 2003. Healthy Sleep Habits, Happy Child. Ballantine Books, New York.

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Tuesday, August 14, 2007

Infant toilet training is a valid option

Before there were washing machines to process cloth diapers, let alone disposable diapers, children in Western societies were toilet trained significantly earlier than they are now, usually by around a year old. Similarly, the great majority of children today living in non-Western societies are also toilet trained by a year. The pattern largely reflects parental convenience; age at toilet training has increased in societies in which the ease of diapering has increased. A Chinese colleague of mine has noted that as disposable diapers have become more readily available in China, toilet training is becoming delayed there as well.

This is all quite understandable. There are many time pressures on parents, and the multitude of choices we make every day about child-rearing will inevitably factor in parental needs. There is nothing wrong with this; those who advocate a purely child-centered approach to child rearing can end up with extremely self-centered children who will have trouble functioning in the real world. And a parent who never considers her own needs can end up stressed in a way that impacts a child negatively.

The problem with current toilet-training philosophy is that choice has essentially been removed by the mainstream media and medical establishment. In the U.S., we now live in a world in which it does not occur to most people to train their children early, even though it is common practice elsewhere. Why is this so?

Early toilet-training advocates such as Dr. Linda Sonna and Laurie Boucke (see references below) have traced the current late-training trend mainly to a paper published in the journal Pediatrics by Dr. T. Berry Brazelton, who was famous for a time for his child-rearing advice. This paper (Brazelton, T.B., 1962. A child-oriented approach to toilet training. Pediatrics 29:121-128) became the basis for the now widespread idea that early toilet training causes psychological damage to a child, despite the fact that Brazelton's research was supported by Proctor & Gamble, which produces Pampers. (Back then it was not required to report conflicts of interest in a published paper, so there is no hint of the affiliation in the original version.)

The problem with the paper is that it essentially sets up a straw man; Brazelton compares punitive and coercive techniques used by advocates of early training in the early 20th century, known then and now for potential damage, to waiting until a child is 2 before initiating toilet training. This is an apples and oranges comparison, because he does not examine the outcome of non-coercive early training, which is used successfully by most people around the world.

An underlying assumption of Brazelton's paper, one that is still commonly believed today, is that children do not have voluntary control of their sphincter muscles until they are 18 months or older. Anyone who has had a toilet-trained 10-month-old can tell you that this is simply untrue. What Brazelton and today's "experts" ignore is the fact that babies have been trained since birth not to exercise control, because they are wearing diapers and their parents do not care where or when they urinate or defecate. Brazelton asserts without any basis that "there is little innate in the child that leads him to want to be clean and dry" when in fact there is strong evidence from babies who are never diaper trained that in infancy they do have an instinct not to wet their bedding or clothes, and they do alert their caregiver that they need to go. Again, babies that have been in diapers for a few months lose this awareness of their bladder and bowel.

The most absurd statement Brazelton makes, which reveals his narrow agenda, is the following: "The developmental energy invested in learning to walk on his own is freed after 15 to 18 months and can be transferred to the more complex mastery of sphincter control and toilet training." According to Brazelton, we must wait to toilet train until age 2 because learning control of two muscles, one each controlling bladder and bowel release, is more complex than learning to walk, which involves the use of dozens of muscles.

The paper was essentially instruction for doctors on how to brainwash parents not to toilet train their children when they wish to, but to wait until a child is about 2 and is physiologically "ready," based on his incorrect assumptions. In the intervening decades, this idea of "readiness" has been transformed to mean, in the mainstream media, that your child will decide one day that she wants to be toilet trained. Some parents are lucky enough that this indeed happens. For many however, toilet training is a struggle because after being conditioned for 2-3 years that the place to urinate and defecate is the diaper, the child is told that he must forget this conditioning. You try the reverse right now, as you sit reading: urinate in your pants, just as an experiment. Can't do it, can you? Conditioning is a powerful behavioral control.

Disposable diapers are indeed a convenience, really a luxury. Cloth diapers are viewed as more environmentally correct, but their use generates many gallons of wastewater, as well as quantities of detergent and bleach released into the environment. Parents should be aware that there is indeed a third option: eliminating the use of diapers as early as possible. At a minimum, I strongly recommend bowel training, which we achieved almost instantly with our daughter at 9 months when we gave her the opportunity to sit on a potty at the appropriate time. The methods for this are fairly straightforward, and are discussed in detail in the recommended books below. There are also resources available at the Elimination Communication store. For some it is a matter of convenience to wait until their child can complete the whole toilet process by himself. But it also takes time, a lot of money, and produces a lot of waste to change diapers for years. All pediatricians should make parents aware that non-coercive early toilet training is a choice that many families make successfully.




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Tuesday, July 17, 2007

Parenthood is all about Me

Isn't parenthood supposed to be about raising a kid to be a healthy, happy, independently functioning, contributing member of society? These distorted, egocentric days in Yuppieville, it seems instead to be all about the reproductive process, rather than a far-off endpoint, that bolsters the parent's self esteem. All the issues surrounding having kids -- when, how, and not to mention whether -- focus on the parents' wants and needs, as if they were choosing the car which best projects their self-image.

Here's a woman who, after struggling with health problems that threatened her ability to get pregnant, was able to give birth to a healthy boy at age 40. One would think she would feel extremely fortunate. Instead:
"I had my sense of self-worth tied up with having a 'normal' family," Deborah explained. "You know, the family with two children. It was always this destination to be counted upon. It was what made tolerable all the losses along the way, the surgeries, the ostomy bags, everything. So when this path felt threatened, all those other losses suddenly took on more substance."

...days before the process was to begin, she found herself lying awake nights, frantic over whether she was doing the right thing. "What gets to me is that the three of them would be genetically related," she said, "and I would be the one. . . . It's not about passing on my genes. It's that I don't want to be an outsider in my own family. I don't want to feel less legitimate in my child's eyes."

If not sharing genes somehow makes this woman an "outsider in my own family," than clearly it is about passing on genes. In one sense this woman cannot help but feel this way. She wanted to adopt a second child, but her husband, who claimed he didn't have enough time to spend with the son they already have, insisted that the next child must share his genes. These people are both trapped into their views of what is "normal" reproductively. Do they put as much thought into actually raising these kids?

Before starting our donor cycle, my husband and I met once with a social worker, a standard requirement for couples using donor eggs -- though, again, not for those using donor sperm. Her job wasn't to screen us (she did, after all, work for the clinic and had little incentive to reject anyone) but to help us imagine how the genetic asymmetry might play out.


Do you know why it is not required for sperm donation? Because most men do not freak out about using donors the way that women do (excepting the jerk above who obviously thought his manhood was in jepoardy if the child was not his genetically). Using donated sperm has been common for much longer, so maybe it is just a lag in how used we are to these technologies. But in general, it is women who seem to obsess over these issues, and read deep significance into every possible stage of the reproductive process. One of the most absurd examples I have encountered was a remark made by a woman who had given birth recently by emergency cesarean section. Referring to my own c-section, I was corrected by her: "You should say 'cesarean birth' so that it affirms that you gave birth to the baby." I could only stare open-mouthed. I hauled my kid around in my guts for nine months (most of which time her presence made me miserable), and this woman actually thinks that someone out there thinks I did not really give birth because the baby didn't exit through my vagina? She was in me, and then came out. Even it had been through my nose, I would certainly define that as "birth."

But in a sense perhaps the woman was right. She either said what she did because she is pathetically insecure, or because in her mind a vaginal birth was somehow superior or more valid. My own doctor was needlessly apologetic when he informed me of the necessity of my having a cesarean. I read a parent magazine article that actually discussed making the choice to attempt a vaginal birth of a breech baby as if it were a positive thing.

It is not convincing to suggest that safety due to protection from surgery is an adequate reason for making such a choice. In a western hospital, complications from a cesarean are not much more common than those from vaginal birth. From the baby's perspective, however, it is significantly more dangerous. I am close to someone who was a breech delivery, and became slightly brain-damaged as a result of being choked by her own umbilical cord. Why any mother would put her own desires (this does not include maternal health risks, which are a separate issue) above what is safest for the baby is beyond me. But such desires have fed the growing popularity of giving birth at home (also promoted by articles in the same magazine), and underwater in birthing tubs.

The egg donor article continues:
"People see a child in a supermarket checkout line and almost reflexively make some comment about who he looks like or doesn't look like," said Robert Nachtigall, an adjunct clinical professor of obstetrics, gynecology and reproductive sciences at the University of California, San Francisco and a co-author of the paper. "We interpret it as a kind of shorthand by which people validate the child's position in the family, in society, by basically making comments that refer to the blood relationship that must exist between the child and his or her parents. The problem for people who have conceived with donor gametes is that they know it's not true. And the dilemma for them is how to respond, if at all."...The difference is that there's widespread cultural support for adoption in a way there isn't for donor conception.

So we are supposed to have special sympathy for those who make the choice to spend $40,000 on an ovum rather than a child? Why is it anyone's business in the first place? What happened to smiling and nodding politely? The answer is that they want to make it everyone's business because they have a bizarre need to have their choice "validat