Bioblog: Biology in the News Biology Blog

According to the editors of JournalWatch,  Light Alcohol Consumption During Early Pregnancy: The News Might Not Be So Bad – Women’s Health. (Free access summary and analysis).  This is not earth-shattering news to Bioblog.

Finally, the idea that a sip of wine during pregnancy won’t completely destroy your fetus seems to be creeping back into the mainstream.  Of course it bears pointing out that Bioblog took this position three years ago.  Back then there were no worthwhile data supporting the intense propaganda that light-to-moderate drinking is harmful.  Not only are there still not, the latest study (Robinson et al., 2010) to look for data to support this notion – and believe me, researchers have been continually grasping at straws for any wisp of a possible connection to behavioral problems, learning disabilities, etc. – not only found no hint of a connection, the numbers actually trended toward the result that the children of light drinkers had fewer behavioral problems from ages 2-14 than those of teetotalers.

But don’t rush out and start swigging a couple beers each week if you would prefer not to drink during pregnancy.  There were many statistical tests used in the paper and no Bonferroni correction was performed, and thus the authors themselves point out that some of the significant results were likely to be spurious. Although it can comfortably be said that alcohol consumption at this level is probably neutral, they and we may assume the “benefit” isn’t real because we just can’t imagine at this time a mechanism through which alcohol would be beneficial.  It doesn’t mean there isn’t one, but it certainly is most likely that the results were due to the multiple comparisons coupled with the large sample size, which increased the power of the statistics used to detect slight, and meaningless, differences.  It’s worth noting though that given self-reported data, the continuing social stigma means that it is probably more likely that women underestimated, rather than overestimated, their alcohol consumption, which means any potential for harm would be overestimated.  At least the women in this study were surveyed during their pregnancy, unlike the previously analyzed laughable study which asked women to remember how much they had had to drink fifteen years before.

This is a good opportunity to reiterate that it’s time to stop accosting visibly pregnant women who are enjoying a glass.  The most likely time for alcohol to adversely affect a fetus is the first trimester anyway (which was covered in the study), so by the time she’s showing, it’s too late for that poor dumb kid anyway.

Reference

Robinson M et al. Low–moderate prenatal alcohol exposure and risk to child behavioural development: A prospective cohort study. BJOG 2010 Aug; 117:1139.

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Is prostate cancer common in families?  It has been presumed to be so based on clusters of men in families that have been diagnosed with the disease.  But in fact, it turns out that brothers of prostate cancer patients undergo more diagnostic activities – meaning it could be that they are diagnosed more simply because they are screened more.

It’s only natural – a first-degree relative gets a cancer diagnosis, and everyone in the family gets screened soon after for that cancer. It is encouraged by doctors because of the tendency for some cancers at least to have a clear genetic component. But the funny thing about prostate cancer is that similar to breast cancer, but even more so, the more you look for it the more you will find it. So a recent study tried to tease apart this cancer detection bias from a real genetic effect. Given that it is well understood now that a cancer diagnosis is a far, far different situation than having clinically significant (i.e. potentially harmful) cancer, they asked the pertinent question of whether or not prostate cancer clusters in families are due to genetics, or due to family members looking for it after a relative has been diagnosed. Apparently, in previous epidemiological studies, data simply for cancer rates have been used, without taking into account this potential bias.

It was a large study, involving over 36,000 Swedish men, but the data are significant enough to suggest they are not spurious results due simply to huge sample size. Particularly telling was the finding that the risk of a brother being diagnosed with prostate cancer was highest in the first year after the original brother’s diagnosis. The best explanation for this is that most relatives get tested soon after their relative’s diagnosis, which reinforces the strong correlation between prostate cancer testing and diagnosis. Prostate cancer diagnosis also ran more in families of higher socioeconomic status; again, almost certainly because those with more resources are more likely to be tested.

These correlations demonstrate an almost certain strong bias in epidemiological studies that declare prostate cancer to be strongly genetically determined. As the accompanying editorial states, 70% of autopsied men in their 60s who never received a prostate cancer diagnosis did have prostate cancer. This indicates two things: first, that genetics is probably not a particularly useful indicator of the risk of prostate cancer for a given individual; and second, it is clear that epidemiological analyses should be assessing the genetics of clinically significant prostate cancer, not just any prostate cancer, which is clearly a meaningless label.

Cancer developed a reputation as a unequivocal killer in the days before scans and screens, because we only became aware of the clinically significant, usually deadly, cases. Our current medical technology has outstrapped our cultural understanding of what cancer really is. A vital cultural shift, supported by more and more information but still not accepted by the general public or even most doctors, is that we need, need, need to stop considering all cancer as a death sentence unless aggressive treatment is administered immediately. It is necessary because cancer screening and treatment is reaching into all aspects of health care like, well, a cancer. Huge amounts of money and energy will continue to be wasted, and stress to be caused, if we don’t make this shift.

And yes, the shift is clearly not possible without tort reform.

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It’s clear, despite what trial lawyers and their defenders may say, that significant cost control in health care will not be achieved without tort reform, because much overuse of medical imaging (over 25% in one recent survey), a significant source of cost, is due to the practice of defensive medicine – But despite what tort reform proponents insist, there is not a single easy solution to overuse of high-tech medical imaging, which has become a clear problem for many reasons.

The exquisite depictions of anatomy and function generated by modern imaging technologies have blinded many physicians to the limitations and potential harms of radiologic diagnosis. The greatest risk that patients face with unnecessary imaging is needless exposure to nonbeneficial downstream testing and inappropriate treatment related to misdiagnosis and the overdiagnosis of common but unimportant findings.

While the idea that imaging is becoming a crutch to overworked and less-engaged doctors is disturbing, there is another enormous downside to the overuse of medical imaging that is mostly unrecognized (by anyone aside from interested parties, such as companies involved in medical technology) and gone undiscussed at a political level. That is, there are or will be potentially greater restrictions and hurdles involved in the development and clinical approval of new potentially life-saving tools. While biotech companies have an economic interest in fighting provisions in the ACA that delay clinical use of new technology in the U.S., it would make the most sense for policy makers to focus efforts on altering the cause of the problem – current technology overuse – rather than its effect.

As is often the case, change will be difficult and not adequately effected by legislation because ultimately what is needed is a cultural shift. Certainly it is clear that radiologists, who benefit directly from overuse of imaging, will be less than willing to change their own culture, as evidenced by the completely self-serving and hostile reaction against the new mammography recommendations by the U.S. Preventative Services Task Force. The NEJM article’s suggestion that radiologists should actually be “more assertive as consultants” seems more likely to reinforce, rather than change this attitude.

In the meantime, this is another area in which patients should begin to take more charge of their own healthcare decisions. Everyone, everyone should read the book Should I Be Tested for Cancer?: Maybe Not and Here’s Why. This way you can make an informed decision, given both the advantages and disadvantages to routine cancer screening, one area in which imaging is overused. Although there are obvious downsides for public health and economics, there are also less commonly understood problems for individuals being overscreened.

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Lots of arguments are being made about whether or health care reform will be economically sustainable in the long term. Many forget that one of the big reasons for reform was that our current trajectory was clearly unsustainable, and the bill that passed is taking a shot at a much more humane system, with attempts to pay for it. Many people on the right seem to be ignoring that a big part of the bill covers pilot projects to figure out different ways to lower costs, which could be implemented on a large scale in the future. If the authors of the bill just decided ahead of time what cost savings to try without real data to support them, and required those in the bill, it would indicate much more of a top-down control approach. Ironically, that’s what those on the right accuse this administration and congress of doing, despite the creative way the provisions were written.

Here is a reasoned economic analysis, albeit a leftward one, of the future of healthcare costs.

And here is some disclosure of this economist’s background, for those who want to find a reason to claim he’s full of it. But those who would decry Jonathan Gruber’s conflict of interest probably overlap somewhat with those who don’t like that the government appointees dealing with fixing the financial regulatory structure are not businessmen who are the biggest experts on the financial markets. No matter what side you are coming from, the top experts in any area that the government needs to regulate always have ties that could be considered conflict of interest. Their expertise cannot be dissociated from the fact that they earn a living implementing it.

What’s more interesting than this is that we really are witnessing a better way to approach many of the major problems our nation is facing. It’s too bad that so many vocal opponents of change don’t seem to understand that the status quo in so many areas is killing us slowly (and in some cases not so slowly). It would be naive to think that politics are no longer a consideration in legislation, but with this bill, and with the steps taken in education, we really have the chance to be a better, science-based nation, with less cynical pandering to the lowest common denominator of our society than we have seen in decades. As a scientist I know this is a better way.

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Only sociologists would find it astounding that babies make “moral” decisions. The author, Dr. Paul Bloom, a psychologist, says, “Why would anyone even entertain the thought of babies as moral beings? ” Apparently it’s all in the definition of “moral,” because any sociobiologist would assume as much without giving the matter a second thought.

From Sigmund Freud to Jean Piaget to Lawrence Kohlberg, psychologists have long argued that we begin life as amoral animals. One important task of society, particularly of parents, is to turn babies into civilized beings…

Perhaps psychologists have, but they are not actually equipped to make this argument. Any sociobiologist would argue in fact that babies are absolutely predisposed to morality.

Why this disparity? As suggested above, it probably has to do with the definition of “moral.” Psychologists and sociologists seem to have a very abstract concept of this term, which is probably why they don’t think babies should achieve morality – they presumably lack an ability to think in abstract terms.

Sociobiologists on the other hand, people like Frans de Waal, define morality as a set of rules that are necessary to follow in order be a successful member of society. As a corollary, morality exists in all social species, not just humans. Morality is the respect an individual shows to others of the group, so that the others will in turn respect that individual. When everyone plays fair, and by the same set of rules, all members of the society benefit. It is all about reciprocity, because if I cheat you to gain an advantage, you won’t want to deal with me in the future. It is a losing strategy in the long run, even if it gives me an advantage in the short term. Just think about the well known difference between the behavior of domestic dogs and cats: dogs, animals derived from social species, are very trainable because they care so much about what other members of their group (even the human members) think about them. Cats are relatively untrainable because they are derived from solitary species, and so they perceive no reciprocal benefit to pleasing another member of the group. In short, they don’t really care what you think of them.

The babies in Bloom’s article demonstrate that morality is nothing but a set of rules to live by. A baby as young as one year old believed in a study that someone who behaved in an antisocial, unfair way, should be punished. But how does such a young baby already understand these rules so well? Because a baby that is of a social species is designed to start learning the rules governing society from day one. That is the way they will develop into successful adults, and they learn the rules by observing the behavior of older members of their group. (This is why good role models are so important in preventing antisocial behavior in humans.)

Incidentally, this is also why studies searching for “genetic” differences between genders using babies and toddlers are completely idiotic, because they make the bizarre assumption that a three-year-old has not yet had the chance to absorb the rules for behavior that apply to its specific gender. Psychologists and sociologists fail to understand this simple truth, because they are not trained in sociobiology. Perhaps if they knew more evolutionary biology they would think more deeply about the broader context of human behavior. But what is baffling is that they think they can study the brain and human interactions without understanding the basic biology of social animals.

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It’s always been easy to ridicule the use of PowerPoint in academia, but the current implications of its ubiquitous use, although delightful to Microsoft, could potentially be more serious than even they could have predicted.

First used widely among scientists in the ’90s, PowerPoint promised blessed relief from the tedium and frustration associated with slide making. When I was an undergraduate and graduate student, I literally had to make slides with a camera – meaning I printed out my text and figures from a computer (fortunately I was already blessed with that labor-saving device) and took a picture of them with a camera. (The last time I did this was actually 2001, when better technology was available but I didn’t have access to it at the fairly remote research station where I worked.)

Generally you would bracket the pictures and take other steps to make sure they came out all right, but you wouldn’t know for sure that they didn’t have to be redone until they were developed. In those days, there was no monkeying around with slides five minutes before your talk. And while there is no danger anymore of accidentally dropping the slide carousel and having slides scatter in a dozen directions, this convenience for quite awhile was traded off with the inevitable computer problems that regularly occurred at conferences I attended until the mid-2000′s. I credit the lessening of issues to better computer capacity, since Microsoft programs make files about ten times bigger than they actually need to be.

Then there was the problem of people suddenly going nuts with dozens of colors and patterns all over their slides. I mean those of you out there who thought it would be a good idea to have dark green type on a navy blue background with your university’s seal embossed over it. You know who you are. You were tired of just being able to do your slides in black and white (or blue and white, as was a common film) and you ignored the fact that the easiest slides to see, even in the computer age, still have black type on a white background.

Of course there are ways in which PowerPoint genuinely has enhanced talks. I was as delighted as anyone else the first time I saw a presentation with (working) embedded video. But at least in the realm of academics, there is a net loss. Professors now have canned PowerPoint lectures for which they hand out print-outs of all the slides, so that students now rely on passive absorption rather than active participation (at least to the degree of having to take lecture notes) to learn the material, which has been a partial contributor to the continuing slide in acceptable standards for college-level work. Students making presentations these days seem to have spent much more time choosing their fonts, colors, and animation tools than actually thinking about their material and how to teach it to the class clearly and concisely.

Perhaps nothing has changed except the ways in which we waste time. There have always been bad presentations. But a recent article in the New York Times on PowerPoint’s impacts on current military operations shows that the insidiousness of PowerPoint – which really boils down to helping effect the usurpation of substance by style – suggests that there may be serious consequences to letting a dominant piece of software affect how we see the world.

PowerPoint slides paradoxically have become mainly either essentially useless for conveying information (as above) or oversimplifications of a complex problem to a set of bullet points. When a soldier at an overseas conflict spends his entire work day, every day, in the world of PowerPoint, that means he is not able to spend much time thinking about solving problems in the real world. His whole job has become turning a three-dimensional world into a two-dimensional one that doesn’t exist.

This seems to be a microcosm of our sound-byte world. A real problem we face these days is that human brains love to reduce complexity into a neat little package that is easily digested, and especially that conforms to our current world view. Humans have been doing this for a very long time, but computers, the internet, and PowerPoint are making it a hell of a lot easier to slide back into comfortable tendencies, rather than taking on the greater challenge of trying to actually learn about something we don’t know much about. (Most of us seem to be past the point of even admitting we don’t know stuff – it seems obvious to everyone now that everyone but them is clueless.)

This blog has documented several examples of how modern technology has short-circuited natural human tendencies, increasing the toxicity of our social and political environment by providing the illusions that we can all be instant experts about all things, that non-face-to-face communication is a preferred method, and that viral fear-mongering is a helpful means to valid political ends. Add PowerPoint to the list of ways in which we are ceding control of our world to our limbic system from our cerebral cortex. Give us a little more time on this trajectory, and we’ll be back to living in caves before you know it.

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For awhile now, women have received conflicting data about how the consumption of soy products affects breast cancer. While soy is often touted as a cancer-prevention food, diagnosed Western patients in particular have generally been scared off of soy, because the plant contains phytoestrogens, which can mimic the action of estrogens.

The uncertainty surrounding the risks and benefits of phytoestrogens involves that of non-human chemicals in general that are capable of binding with human hormone receptors. When a compound other than estrogen binds with an estrogen receptor, it can have one of two effects: it can have a similar effect as estrogen itself, stimulating estrogenic effects, or it can have the opposite affect, serving as a block for estrogen, thereby reducing estrogenic effects.

It gets even more complicated than this, because there are estrogen receptors all over the human body, even in men, and there are at least two types of receptors, alpha (α) and beta (β). Furthermore, estrogenic effects of phytoestrogens are several orders of magnitude below those of true estrogen. (It is for this reason that even before the studies discussed below were published, many oncologists including Dr. Susan Love have said that women with breast cancer should not worry about eating soy foods in moderation.)

Here’s a little more about what is known about phytoestrogens. They can be divided into three main classes: isoflavones (over a thousand chemicals found in soy-based foods), lignans (fruits, vegetables, and grains), and coumestans (found in alfalfa sprouts). Of these, isoflavones appear to be the most potent. Another weak phytoestrogen is resveratrol (the compound in wine made from red grapes that is associated with anti-aging and anti-cancer effects).

Below is a chart of phytoestrogen amounts in different soy foods, taken from a phytoestrogen report by the Hospital for Special Surgery in New York. (A relatively high intake of isoflavones would be on the order of an average of 60 mg per day):

Food	Phytoestrogen Content
Miso	30 mg per 1/4 cup
Soybeans	40 mg per 1/2 cup
Soyflour	25 mg per 1/4 cup
Tempeh	40 mg per 1/2 cup
Tofu	40 mg per 1/2 cup
Soy Milk	40 mg per 1 cup
Roasted Soybeans	162 mg per 3 1/2 ounces
Textured Vegetable Protein	138 mg per 3 1/2 ounces
Green Soybeans	135 mg per 3 1/2 ounces
Tofu yogurt	16 mg per 3 1/2 ounces
Soy hot dog	15 mg per 3 1/2 ounces
Soy noodles (dry)	8.5 mg per 3 1/2 ounces

But although epidemiological studies for years have indicated that diet has a role in the likelihood of developing breast cancer, it has remained unclear whether phyotestrogens are specifically protective, or whether they are just associated with a healthy diet in general.
This is because the interaction of the many different phytoestrogens with hormones and receptors in our bodies turns out to be highly complex.

In general, the amount of estrogen in the blood seems to be reduced by the intake of phytoestrogens. There is some mixed evidence that increasing phytoestrogens may lengthen the menstrual cycle as well. This would provide indirect protection against breast cancer, as it would reduce exposure of cancer cells to estrogen over a lifetime.

The mechanism by which phytoestrogens reduce estrogen in the body seems to be that they interfere with the enzymes involved in estrogen production, particularly cytochrome P450 19 aromatase. (It is known that people with higher levels of these enzymes are more likely to have breast cancer.) They therefore function as aromatase inhibitors, similarly to the commercial drugs Femara, Arimidex, and Aromasin, which are now commonly prescribed to post-menopausal women with breast cancer.

But it is more complicated than this, of course; just as estrogens have different effects depending on how they interact with estrogen receptors in different parts of the body, some phytoestrogens can increase aromatase activity in some areas.

One potentially important difference between phytoestrogens and estrogen is that while estrogen binds equally to ER-α and ER-β receptors, phytoestrogens have a higher affinity for ER-β. A higher number of ER-α receptors is associated with more aggressive malignant tumors. ER-β receptors seem to have antiproliferative (= anticancer) effects that are induced when they are bound.

Even though phytoestrogens have a lower affinity for estrogen receptors in general, some seem to induce a greater response from those receptors than estrogen itself. The presence of estrogen seems to influence this effect. And so, phytoestrogens can promote cell growth in ER-positive cancer cells. In the case of ER-negative cells, the effect appears to be the opposite.

On top of this, phytoestrogens seem to alter estrogen-metabolizing enzymes, which affects how quickly estrogen is broken down in your system, and also the levels of estrogen metabolites, some of which are known to be carcinogenic.

All this together shows that there is still no simple answer on inhibitory vs. proliferative effects on cancer cells in general for phytoestrogens, because there is variation among the different phytoestrogens, and studies have had conflicting results even for the same compound. It is important to remember that these compounds do not function in a vacuum, and the overlying hormonal environment, which is ever changing in women, will have an influence. This means that whether phytoestrogens inhibit or stimulate cancer cells depends at a minimum on 1) the specific phytoestrogen compound, 2) its concentration in the blood, 3) whether cancer is yet present, and if so, the stage and other pathology of the tumor and 4) the general hormonal environment in the person at the time of exposure – both age and menopausal status clearly matter. Effectively this means that there is no rule for whether or not it is good or bad to consume phytoestrogens, and there probably will never be, even if we determine the effects of the compounds in a given context at a detailed level.

For example, one study found that in mice whose ovaries had been removed (and therefore rendered “post-menopausal”), the phytoestrogen genestein stimulated tumor growth, rather than inhibiting it. A possible explanation was that phytoestrogens exhibit estrogenic activity in a low estrogen environment, but anti-estrogenic activity when there is more estrogen in the blood. Other studies have shown that genestein inhibits the growth of breast cancer cells. The timing of phytoestrogen intake is thus important. Mice fed genestein when they were young had fewer breast tumors later compared with those fed it later in life.

Even when anticancer effects have been found, most studies have been done in vitro (in a petri dish, not in a human) and often much larger doses of the phytoestrogens than could be obtained by diet alone were required to demonstrate tumor-inhibiting effects.

There is also an interesting idea that phytoestrogen intake over one’s life could actually influence the ER status of breast cancer when it occurs. This is because lower estrogen levels in the blood, which can be an effect of phytoestrogens, stimulate ER expression. In a study of 124 premenopausal breast cancer patients, 18 individual and 5 classes of phytoestrogens were examined for this relationship, to find out which, if any, were more strongly associated with the development of ER-negative disease than ER-positive disease in premenopausal women with breast cancer. They looked only at the status of ER-α receptors.

The study found evidence that the isoflavones genistein and daidzein (both found in soy and other legumes) could enhance ER expression in breast cancer cells, through the above mechanism.

One recently publicized study was done on Chinese women with breast cancer, to find out how soy consumption might affect cancer recurrence. It was based on questionnaires, with a 3 year follow-up. On the surface, there was a striking result that among the highest soy consumers, taking tamoxifen did not incur an added benefit.

However, the positive effects encompassed nearly every possible group: pre- and post-menopause, ER-positive and ER-negative, and both early- and late-stage cancers. The broad consistency of this result suggests that this type of study is a blunt instrument that may still not be too useful in informing individual dietary decisions. The study had the inherent weakness of being retrospective instead of controlled, and related to that, the sample size of >5000 is large, which increases its power to detect small differences. In comparing (roughly estimated) phytoestrogens ingested between the group with the highest soy intake and the group with the lowest soy intake, the hazard ratios (likelihood of death or recurrence for highest intake group vs. lowest intake group) were at best barely significant, which suggests a low biological significance of this result, because small effects are more likely to be significant statistically when you are working with a large sample size.

In another study by the same research group of 73,223 Chinese women, adult soy food consumption, measured either by soy protein or isoflavone intake, was inversely associated with the risk of premenopausal breast cancer. No significant association with soy food consumption was found for postmenopausal breast cancer. This study was so huge that it included thousands of cancer patients. So again, one must be wary of the extreme statistical power being used in these studies, and whether such power implies more biological significance than there actually is.

In conclusion, although there is evidence that a diet rich in phytoestrogens can promote breast cell proliferation in the short-term, all the available evidence taken together still suggests that consuming a lot of phytoestrogens does not increase the risk of breast cancer, and may indeed protect against it. It is still impossible to reconcile dietary/supplement exposure with epidemiological and experimental studies, and some researchers worry that women may take high doses of ‘natural’ phytoestrogens and end up with levels high enough in their blood that might have a negative impact on their long term health.

As with all foods, moderation is the key. There is almost never any real reason for a well fed Westerner to take any supplements, and that is really the only way that one could overdose on phytoestrogens. Whether or not you have had breast cancer, a moderate amount of soy in your diet is not likely to affect your outcome dramatically. So Shelley Lewis, who as related in her breast cancer memoir made the unhappy decision to cut off all soy in her diet, should take heart that there is not likely to be any harm in enjoying edamame now and then – and it may even be beneficial.

References

Glazier MG, Bowman MA, 2001. A review of the evidence for the use of phytoestrogens as a replacement for traditional estrogen replacement therapy. Archives of Internal Medicine 161(9):1161-72.

Lee SA, Shu XO, Li H, Yang G, Cai H, Wen W, Ji BT, Gao J, Gao YT, Zheng W, 2009.
Adolescent and adult soy food intake and breast cancer risk: results from the Shanghai Women’s Health Study. American Journal of Clinical Nutrition 89(6):1920-6.

Mense SM, Hei TK, Ganju RK, Bhat HK., 2008. Phytoestrogens and breast cancer prevention: possible mechanisms of action. Environ Health Perspect. 116(4):426-33.

Rice S, Whitehead SA. , 2006. Phytoestrogens and breast cancer–promoters or protectors? Endocr Relat Cancer13(4):995-1015.

Shu XO, Zheng Y, Cai H, Gu K, Chen Z, Zheng W, Lu W, 2009. Soy food intake and breast cancer survival. JAMA. 302(22):2437-43.

Touillaud MS, Pillow PC, Jakovljevic J, Bondy ML, Singletary SE, Li D, Chang S. , 2005. Effect of dietary intake of phytoestrogens on estrogen receptor status in premenopausal women with breast cancer. Nutrition and Cancer 51(2):162-9.

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…but will the ruling against Myriad Genetics striking down patents on genes (in this case the breast/ovarian/prostate cancer-linked BRCA genes) be upheld in appeals, especially given the current pro-business makeup of the Supreme Court? Unfortunately it seems unlikely. Patents have been granted for isolated genes now for decades. The original claims were granted on the faulty basis that because isolating genes took such a lot of time and money, those who accomplished the isolation should be allowed to reap the benefits of all that work. It would almost be understandable that this argument carried water 20 years ago, when isolating and sequencing genes did indeed entail huge amounts of work – if, even then, most of that work leading to the sequence had not usually already been done by academic scientists using taxpayer funded grants. But that has always been the case.

The main problem, though, was that the patent office and the courts failed to foresee the advances in technology that made Myriad Genetics’ process for sequencing the BRCA genes essentially trivial. Once the real part of the work, locating the general area of the genome where a gene is located, has been done, the final step involves simply to turn on a whole bunch of sequencers for awhile. It still takes a little bit of money, but since when did we think it’s a good idea to award people patents on stuff they bought?

The unintended (but foreseeable) result of this patent policy has been for biotech companies to sequence genes all over the place and slap patents on them, even if they have no current intention of producing – or even knowledge of how to produce – any sort of useful product with those sequences. Sequencing a gene is just the first step in producing something medically useful, just as conducting a reference search is the first and easiest step in writing a brilliant paper. There are convincing arguments that locking up sequences with patents is actually slowing down scientific innovation, not promoting it. The great majority of those thousands of patents that this ruling calls into question are just sitting there, providing no benefit to anyone. They do, however, present a real obstacle to anyone who would like to take the lead on studying the genes in order to produce a benefit. What we are left with is people and their insurance companies being forced to pay $3000 for a test that any molecular biologist could now do in a day in their lab for less than $100. This, without any way to confirm whether or not their test is valid, since no one is allowed to develop a competing one. Once again I ask, is this really what the free market is all about?

A positive result of the decision, though, even if overwhelming corporate interests cause it ultimately to fail, will be to get this issue out into public discussion. The public needs to know that their 20% of their own DNA is now owned by corporations, meaning it is not yours to do with as you wish. This case getting press will be a good start to establishing the constitutionality of current patent law, a discussion that was really never had, but needs to be. Whether this ruling is thrown out or not, eventually it will be understood that even though corporations have now been ruled people, owning another person is still unconstitutional, since the thirteenth amendment was adopted in 1865.

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The wingnuts must just be so distracted from the recent success by Democrats (sorry, that would be “Socialists”) in destroying our country by passing health care legislation that they haven’t found time to rail about more blatant misrepresentations in the Intergovernmental Panel on Climate Change (IPCC) report. Oh, wait… these “mistakes” actually underestimate the rate of planetary destruction. I guess this section of the report is good, solid science, unlike the part where they “exaggerate.”

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Recently, as part of the health care debate, and in response to the Stupak-Pitts Amendment attempting to restrict abortions in the pending health care reform bill, arguments have recently been made that universal access to health care actually has reduced the abortion rate when implemented, at least in developed countries, and in Massachusetts.

The Massachusetts example seems better at first glance, because it is a comparison of rates pre- and post- universal coverage:

The abortion rate… declined from 3.8 per 1000 population in 2006 to 3.6 per 1000 in 2008.

Of course, the main problem with this is that it’s not clear if this is a statistically significant difference, because it is a sample size of one. But even if the data were available for multiple states/countries before and after universal coverage, the trend has to be placed in the greater context of a longer time period. As it turns out,

The Massachusetts abortion rate has…dropped by a third, from 30 per 1000 women 15 to 44 years of age in 1991 to about 20 per 1000 in 2005, with most of the decrease occurring during the late 1990s.

So the trend was a decline in Massachusetts anyway, so there’s no a priori reason to believe that the cause of the decline was the implementation of universal coverage.

But the author, Dr. Patrick Whelan, successfully makes his point: the belief motivating the Stupak Amendment is that abortions will increase as a result of expanded coverage, but not if the government refuses to pay for them, or allow subsidized plans to pay for them. The Massachusetts data at least suggest that there is no apparent basis for this belief.

The world-wide abortion-rate data from the U.N. cited by T.R. Reid in the Washington Post has the advantage of being multiple data points, but the disadvantage that there is no before-and-after data available. Reid reasonably compares the U.S. abortion rate to that of the 32 other most developed countries which all have universal coverage in at least some form. It is a compelling notion that access to care corresponds to better access to pregnancy prevention, not to mention pre- and post-natal care, and therefore, results in fewer abortions.

Alas, although he makes a convincing argument that will provide talking points for progressives, his data were cherry-picked with no objective statistical analysis. He does point out what seems to be a smoking gun that out of developed countries, that the U.S. abortion rate is the highest (at 20.8 per 1000 women), but there is nothing inherent in that observation showing that universal health coverage reduces abortions.

Thus, it seemed it would be interesting to do some statistics on the data, to see if any trend pops out. In the table below (click for larger view), the abortion rate is listed for all 61 countries for which the U.N. provided data:

The universal health care status was gleaned from various documents available online, but mainly from the World Health Organization when it was not otherwise clear. (Because in some cases the definition of “universal coverage” can be subjective, some of these designations are debatable and I welcome arguments about where particular countries are placed.)

The most valid way to statistically compare the abortion rates between countries with and without universal health coverage is with a non-parametric test, because the sample sizes are so unbalanced – 48 countries have some form of universal health coverage, while 13 do not. A Mann-Whitney U test on the ranks of the data shows that there is no statistical difference (p>0.25) in abortion rates between countries with and without universal coverage.

The caveats in this analysis are first that it depends on the accuracy of the U.N. data, which presumably do not take into account illegal or under-the-table abortions (so to speak), whose rates will clearly vary greatly from country to country. (The zero values for Brazil, Panama, and Poland are a case in point.) Second, it also depends on the definition of universal coverage, which also varies greatly from country to country. For example, although Russia has universal coverage on paper, it is well known that their system is broken, and does not in practice provide universal access to health care.

But what if we focus on developed nations, as Reid did? We can’t compare those with universal coverage to those without, since they all have it but the U.S., but we can see if time since universal coverage was available has had any effect on the current abortion rate, and we can look more closely at the type of coverage provided. The next table summarizes these data.

Here are the same data plotted graphically. First is a regression analysis including all developed countries, and second is a regression including only the developed countries guaranteeing primary (rather than just catastrophic) care.


Both plots tell essentially the same story, which is that there is no statistical relationship between abortion rate and history of healthcare access. Increasing access to abortion through universal health coverage at the very least doesn’t obviously make women run out and have a lot more. The mere existence of the Stupak-Pitts argument just reinforces the conclusion that the primary goal of anti-abortion legislation is not actually to reduce the number of abortions (and thus “save lives”) in a scientifically demonstratable way, but is instead about control over women.

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