Every so often, there’s a bit of misinformation that starts spreading around the Internet that shows up in enough places that our readers take notice and e-mail us about it. What happens is that these in essence become “requests.” We at SBM are, of course, happy to consider all requests and sometimes will actually take them on, particularly when doing so will be educational about the mission of this blog, namely discussing science-based medicine and providing much needed critical analysis to the pseudoscience that is, alas, becoming more and more common in medicine. A frequent topic of this blog is, not surprisingly, the anti-vaccine movement, which is arguably the most dangerous (to public health, at least) pseudoscience movement currently in existence. The misinformation about vaccines that anti-vaccine activists spread through websites, podcasts, radio, TV, and other media is protean, and it’s difficult to keep up with it all.

Which is probably why I hadn’t heard this bit of misinformation about the HPV vaccine from an anti-vaccine group I hadn’t heard of before (or at least didn’t remember) called SANE Vax. (I include the “Inc.” because SAFE Vax, Inc. itself insists on using it frequently in all its press releases.) If you’ve been in the biz a while, as I have, you can tell right away from the very name of this website exactly where its creators are coming from. Here’s a hint. It’s not the mission that the website claims that it is, which is stated thusly:

The Sane Vax Mission is to promote Safe, Affordable, Necessary & Effective vaccines and vaccination practices through education and information. We believe in science-based medicine. Our primary goal is to provide the information necessary for you to make informed decisions regarding your health and well-being. We also provide referrals to helpful resources for those unfortunate enough to have experienced vaccine-related injuries.

Oh, no. SANE Vax didn’t go and claim that its members believe in science-based medicine, did it? Science-based medicine. You keep using that term. I do not think it means what you think it means. (I know, I know, I use that quip far too often, but I like it.) In any case, SANE Vax appears to be anti-vaccine to the core, which should be obvious from its name. Clearly, if its creators think they’re promoting “sane vaccination,” by implication they very likely think that by comparison the current vaccination schedule is not sane. Further supporting the rather mind-numbingly obvious conclusion that SANE Vax is indeed anti-vaccine are videos featuring Andrew Wakefield, Barbara Loe Fisher, and other luminaries of the anti-vaccine movement, as well as a Vaccine Victims Memorial, the latter of which is a page taken right out of the playbook of the National Vaccine Information Center (NVIC), one of the oldest anti-vaccine groups still in existence. Meanwhile, it’s list of “vaccine groups” contains all the usual anti-vaccine suspects, like the Australian Vaccination Network, Age of Autism, ThinkTwice, Generation Rescue, and Impfschaden.

I also don’t believe for a minute that SANE Vax is, as it bills itself, a “vaccine safety” group. For one thing, in the comments of two of the SANE Vax posts I’m about to discuss, Australian skeptic Peter Bowditch shows up to ask, “Which vaccines are “necessary” and “effective” to match the ‘N’ and ‘E’ in SANE?” He has yet to receive an answer. This fulfills one of my key criteria of an anti-vaccine activist in that when, after hearing her piously pontificate that she is “not anti-vaccine,” you ask her which specific vaccines she supports and get either no answer or dancing around the question with no real answer.

So what’s got SANE Vax in an uproar? DNA. But not just any DNA. Recombinant DNA. But not just any recombinant DNA. HPV recombinant DNA. Take a look at some posts that appeared on the SANE Vax blog over the weekend and on Tuesday:

• SANE Vax to FDA: Recombinant HPV DNA found in multiple samples of Gardasil
• SANE Vax Inc. Discovers Potential Bio-hazard Contaminant in Merck’s Gardasil™ HPV 4 Vaccine (NOTE ADDED: Interestingly, this link now goes nowhere when you click on it, but only when accessed from this blog, at least as far as I can tell. When accessed from a Google search on the title or from the link on the front page of the SANE Vax website, the URL works. It also works as a secondary link from this story linking to it.
• SANE Vax Inc. Announces the Discovery of Viral HPV DNA Contaminant in Gardasil.
• SANE Vax, Inc. Reports Human Papillomavirus (HPV) DNA Contamination in Gardasil™ To FDA: Requests Public Safety Investigation.

Oh, no! DNA! The horror…the horror.

Does this sound familiar? It should. It’s almost exactly the same fear mongering nonsense that Helen Ratajczak used to try to claim that homologous recombination of fetal DNA in vaccines with the DNA in babies’ brains resulted in autoimmune inflammation that led to autism. In this case, the vaccine is the HPV vaccine, but the arguments are merely a variation on the same scientifically ignorant theme. Here’s what SANE Vax is :

SANE Vax Inc. contracted with an independent lab to test for contamination and found HPV recombinant DNA (rDNA) in 13 vaccine vials. The Gardasil vials with different lot numbers were from New Zealand, Australia, Spain, Poland, France and three states in the U.S. 100% of the samples tested positive for the presence of the genetically modified HPV DNA.

Dr. Sin Hang Lee, a pathologist at the Milford Hospital pathology laboratory well-known for using cutting-edge DNA sequencing for molecular diagnoses, was initially contracted to examine a single sample of Gardasil for possible contamination. This sample tested positive for recombinant HPV-11 and HPV-18 residues, both of which were firmly attached to the aluminum adjuvant.

Wow. Sounds pretty scary, doesn’t it? Actual HPV DNA! But not just any HPV DNA. Oh, no. We’re talking recombinant HPV-11 and HPV-18 residues, which–horror of horrors!–were attached to the dreaded aluminum adjuvant! Stop the factories! Stop injecting our little girls with that evil vaccine whose only purpose is to encourage them to go out and have unprotected sex, knowing that they won’t get HPV!

Now hold on just a minute. I got a little carried away.

Let’s take a look first. First of all, one notes that there is not a single scientific paper–or even scientific report–describing the methodology used and the specific tests used. True, in SaneVax’s letter to the FDA, Norma Erickson provides an actual picture of an actual graph from an actual DNA sequencing run in order to look all science-y, but then she also says:

The SANE Vax Inc. data, including the electropherograms of short target sequencing used to validate the HPV DNA detected in the thirteen (13) Gardasil samples, each with a different lot number, are available for your review, provided appropriate safeguards are in place to protect the proprietary processes and information utilized by our laboratory to test the samples.

Protect the “proprietary” processes used to test the samples? Why on earth does the Milford Hospital Pathology Laboratory need to use “proprietary” processes to test for recombinant DNA in the vaccine? Whenever I see a result like this attributed to proprietary, non-transparent methodology, it sends up huge red flags, particularly when it comes to doing something like detecting DNA contamination. I could do it in my own laboratory using simple polymerase chain reaction (PCR) and then sequencing the DNA sequences (if any) that I managed to amplify up! There’s no need for anything proprietary, other than choosing the PCR primers properly! I could use PCR kits right off the shelf and any of a number of PCR machines, either the old warhorse in my lab or the spiffier, newer machines that some other investigators in nearby labs have. Again, the key is choosing the right primers and working out the right conditions, but none of that is anything particularly difficult, although testing different conditions can be time consuming and require a fair amount of trial-and-error drudgery.

Before I get to the significance (or, far more likely, lack of significance) of this finding. Let’s take a look at the methodology. As is my wont when I see someone making a claim I haven’t seen before, I did a bit of Googling for Dr. Sin Hang Lee, and it turns out that he is rather well known in the Lyme disease community for having apparently invented a new test for Lyme disease. That may or may not be dubious. What is definitely dubious is that he’s also teamed up with SANE Vax—excuse me, SANE Vax, Inc.—to offer an HPV genotyping test announced on the quackery-promoting NaturalNews.com. This latter link actually suggested to me what Dr. Lee’s “proprietary” methodology might be, as it’s described as “nested PCR with short target DNA sequencing for HPV genotyping.” Going back to look at his Lyme disease DNA test, I find this paper, which also used nested PCR to detect sequences from the Lyme disease spirochete Borrelia burgdorferi.

So what is nested PCR? As readers might recall, PCR is a method to amplify nucleic acid sequences, like those of DNA or RNA. Believe it or not, the Wikipedia entry for PCR contains a pretty good description. Having a great deal of experience with PCR, I know, as does anyone who works with PCR, that the greatest power of PCR also leads to its greatest difficulties in its usage, namely its extreme sensitivity. PCR is so sensitive that it’s very, very easy to amplify a contaminant or for the primers to bind to (and thereby amplify) DNA sequences other than the one of interest. This problem goes double (or even quadruple) for nested PCR. The reason is that nested PCR involves using one set of primers to amplify a DNA sequence, and then taking some of the resultant reaction mixture and using a second set of primers that amplifies a smaller sequence within the sequence amplified in the first PCR run. The process is illustrated below. First, here’s routine PCR:

And here’s nested PCR:

The usefulness of nested PCR is two-fold: First, because two different sets of primers are used, specificity is increased and the amplification of contaminants decreased because, although there might be contaminants amplified in the first PCR run, it’s very unlikely that any of the unwanted PCR products so amplified contain binding sites for both of the new primers used in the second PCR run. Second, nested PCR can be very, very sensitive, even more sensitive than “simple” PCR, depending upon the number of amplification cycles used in each PCR step. It’s that sensitivity that allows nested PCR to amplify very tiny amounts of target sequence.

Which brings me to the lack of any detail in this report.

Let’s say, for the moment, that Dr. Lee did everything right and actually did detect a bit of recombinant DNA from the HPV DNA used to make the vaccine still remaining in the 13 vials of vaccine he tested. It’s possible. He’s apparently made a name for himself in developing PCR-based diagnostic tests and has published in the peer-reviewed literature. Would it matter? One factor to consider is how much DNA was present, which was almost certainly very, very tiny, given that it took nested PCR to detect it. However, we don’t know how much was detected, because nothing on the SANE Vax posts tells us enough to let us know approximately how much was detected. Did Dr. Lee amplify his template with 40 cycles, followed by another 40 cycles? That would imply an incredibly tiny amount of DNA, indeed, and would actually be very difficult to do without a lost of false positives. Given that, and given the probably minuscule amount of DNA detected, even assuming these aren’t false positives, there is no justification for statements like this:

In an effort to help her now very sick daughter the mother went to an MD practicing naturopath who conducted a toxicity test that eventually found HPV DNA in the girl’s blood. The significance of this finding is that it is highly unusual to find HPV DNA in the blood. HPV, if present in the body, exists in the epithelial (skin and mucosa) membranes. HPV or its DNA, by itself does not survive for any great length of time in the bloodstream. Why was the HPV DNA in her bloodstream two years post-vaccination?

My answer would be: Probably because the naturopath, like most naturopaths, didn’t have a clue what he was doing or how when he “detected” HPV DNA in the blood. If Dr. Lee had clue one, that’s what he would have said. But he didn’t. He said this instead:

According to Dr. Lee, “‘Natural HPV DNA does not remain in the bloodstream for very long. However, the HPV DNA in Gardasil™ is not ‘natural’ DNA. It is a recombinant HPV DNA (rDNA) – genetically engineered – to be inserted into yeast cells for VLP (virus-like-particle) protein production. rDNA is known to behave differently from natural DNA. It may enter a human cell, especially in an inflammatory lesion caused by the effects of the aluminum adjuvant, via poorly understood mechanisms.

“Once a segment of recombinant DNA is inserted into a human cell, the consequences are hard to predict. It may be in the cell temporarily or stay there forever, with or without causing a mutation. Now the host cell contains human DNA as well as genetically engineered viral DNA.”

This is utter nonsense. First off, as I described before, it’s not a trivial matter to get recombinant DNA into human cells and expressing the protein that its sequence codes for. It’s worth repeating what I described when I first encountered this sort of claim in a different context. For rDNA to do what Dr. Lee worries about, the minute amount of rDNA in the HPV vaccine would have to:

• Find its way into human cells in significant quantities, which is highly unlikely given the tiny amount that, even in the worst case, is there.
• Express the protein that it codes for, which would require that the DNA be intact, complete with its promoter and regulatory regions. Again, this is incredibly unlikely, given the amount of DNA we’re talking about unlikely.

I actually have some experience with direct intramuscular injection of DNA to try to get gene expression, at least in the distant past. Indeed, some of the earliest experiments studying gene regulation in rat muscle by direct injection of plasmid DNA were performed in the laboratory where I did my PhD work. I knew the graduate student who was doing it, and even now I know investigators who are working on DNA vaccines. In humans, it takes microgram quantities of intact plasmid DNA, and even then expression levels are usually low without special help, such as the “gene gun” or other techniques. Indeed, this is arguably the single biggest problem that needs to be overcome in developing effective DNA-based vaccines. Also remember that the HPV vaccine is made of non-infectious HPV-like particles, which are basically formed from the L1 surface protein of the HPV virus, which makes the outer coat of the virus particle. Even in the highly unlikely situation that the tiny amount of recombinant DNA alleged to be left behind in Gardasil could get into human cells and actually make detectable amounts of VLP, the only place it’s likely to be able to do that is in the muscle in the immediate vicinity of the injection site.

None of this prevents SANE Vax from extrapolating beyond science and reason:

SANE Vax Inc. wants to know how many adolescents who have suffered adverse reactions post Gardasil vaccination have HPV DNA in their blood. What are the medical ramifications should HPV DNA remain in the bloodstream for an extended period of time?

Does the aluminum adjuvant become the carrier for HPV DNA causing said DNA to remain in the blood and/or organs for an extended length of time?

Since viral DNA cannot replicate by itself (it needs a host cell) what happens if genetically engineered viral DNA enters a human host cell?

In a followup post, SANE Vax demands:

• What autoimmune-related disorders could result from this contamination?
• Is it possible for this contamination to initiate gene mutations which may lead to cancer?
• What genetic changes (mutagenesis) could occur should the residual HPV DNA enter and begin reproducing in a human cell?

All of this is putting the proverbial cart before the horse. First things first. Before anyone takes the claim that there is HPV DNA left in HPV vaccines and, more importantly, before anyone does anything (if, indeed, anything even needs to be done, which it probably doesn’t), an external laboratory needs to replicate Dr. Lee’s results. Interestingly, SANE Vax now appears to be backpedaling a bit:

The HPV DNA testing was performed by Dr. Sin Hang Lee, a pathologist at the Milford Hospital pathology laboratory known in using cutting-edge DNA sequencing for molecular diagnoses. This methodology was first reported to the FDA in 2006 and has been published in various peer-reviewed scientific journals, stated Erickson.

If Dr. Lee’s methodology was reported to the FDA in 2006 and has been published in peer-reviewed scientific journals, then what’s “proprietary” about it, and why is he so reluctant just to publish his results regarding the HPV vaccine? I challenge Dr. Lee and SANE Vax to publish in full the complete methodology used to make this finding, along with the results, and, no, this claim in the comments of one of the press releases doesn’t fly:

Question #3 – The results are already included as an attachment in the SANE Vax press release.

I tried to figure out what she meant, because if the results are included anywhere on the SANE Vax website, I couldn’t find them. Then I looked again at the original press release. The “attachment” there is simply a snippet of the graph from a DNA sequencing reaction. That’s not “results.” That could have come from anywhere, including just directly sequencing a plasmid containing HPV sequences. At the very least, any full report should include a description of the methodology, including sequences of the PCR primers, the temperatures and times of the PCR cycles, and gels of the PCR results, complete with positive and negative controls at each step of the nested PCR, plus sequencing of the PCR products. What SANE Vax has provided as “results” is meaningless and does not allow scientists to determine whether Dr. Lee detected what he claims to have detected. Sorry, Charlie. This won’t fly.

I find it most ironic that SANE Vax repeatedly calls on the FDA and Merck to be “transparent,” but nothing about the way SANE Vax has publicized its “results” is in the least bit transparent, nor has Dr. Lee’s methodology to obtain these results been peer-reviewed. Worse, in the SANE Vax letter to the FDA, SANE Vax demands assurances that the FDA will protect Dr. Lee’s proprietary methodology before it will provide the FDA with its results. The hypocrisy and intellectual dishonesty are staggering. More importantly, without SANE Vax’s alleged results being available to the FDA and independent scientists to examine, all we have to support the claim that there is recombinant DNA in the HPV vaccine is the word of an anti-vaccine group.

Color me not particularly worried. Until there is independent verification, it’s utterly pointless even to worry about these other questions because the source, being rabidly anti-HPV vaccine, is suspect, and there is no way to determine if the methodology used is valid and not likely to produce false positives. After all, the HPV vaccine is tested for the presence of recombinant DNA, and it’s below the limit of detection of standard techniques; otherwise, Merck, the FDA, and other scientists would have detected it before. Only a scientist affiliated with an anti-vaccine group can seemingly detect it. Moreover, even if Dr. Lee did detect what previously couldn’t be detected before, clearly he’s detecting rDNA at such a low quantity that it’s doubtful that it would be harmful in the least. Certainly, given such a tiny amount of rDNA, it’s downright silly to talk about whether the aluminum adjuvant could somehow become a “carrier” for HPV DNA that allows it to be present in the blood for an extended period of time. Given that the HPV rDNA couldn’t replicate, the law of conservation of mass is enough to dismiss this concern as ridiculous, because it would take far more DNA than could possibly be in the adjuvant to produce detectable levels in the blood for long periods of time, particularly given that the way the L1 protein is made is to use expression plasmids designed to work in yeast, most of which will not work (or will work very poorly) in human cells. Finally, even in the incredibly unlikely event that a tiny amount of L1 rDNA could be expressed by surrounding muscle cells, what would it do? It would make more L1, arguably slightly increasing the efficacy of the vaccine.

Maybe Dr. Lee should be come a homeopath. He seems to think that the more the HPV DNA is diluted, the stronger it becomes.

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The latest issue of the BMJ contains an editorial recommending that regulators (this is in the UK, but the argument applies in the US and elsewhere) should require pharmaceutical companies to provide research on direct comparison to existing therapies as part of the approval process. The authors, Sorenson, Naci, Cylus, and Mossialos, write:

When a drug comes to market, evidence on the comparative risks and benefits is needed to help regulatory authorities to safeguard public health from inferior and unsafe treatments, to ensure that health technology assessment agencies and payers make funding decisions based on the best available evidence of different treatments, and to aid clinicians’ and patients’ understanding of what therapies work best and their appropriate position in the treatment pathway.

They make a persuasive argument, but there are some interesting angles to this topic.

Comparative efficacy research is definitely valuable, for all the reasons stated by the authors above. In order to get approval, typically a new drug has to demonstrate that it is safe and more effective than a placebo treatment. For many common indications there are also often more than one drug for the same indication. Therefore there may be several drugs approved to treat migraine, gastric ulcers, hypertension, etc., all of which have been compared to placebo, but perhaps not to each other (at least not prior to approval).

Clinicians, therefore, may have difficulty in comparing available options. You can compare the relative effect size with respect to placebo, but this is fraught with confounding factors. No two trials are exactly the same: outcome measures may be different, the subject population may be different, etc.  and therefore comparing the results of two different trials is problematic. There is no substitute, therefore, for a head-to-head comparison of two or more drugs (or any treatments, for that matter) in the same trial.

The issue is also not simply a matter of which drug is better – each may have different strengths and weaknesses, or be more efficacious or safe in different subpopulations. Comparitive efficacy research is often performed, but it is done post-market. The authors are advocating that such research be required pre-market. The primary criterion they are recommending is lack of inferiority – demonstrating that the new drug is at least as effective as existing treatments.

There are advantages and disadvantages to such regulation, in my opinion. The advantages are outlined above – more information for clinicians, regulators, and payors that cannot be obtained any other way. Further they argue that pharmaceutical companies are often reluctant to initiate or sponsor head-to-head research because it is risky for them if their product comes out on bottom. They would rather have ambiguous evidence that all sides can spin to appear to favor their product.

The one potential downside I see is that it would make the drug research and approval process more expensive and longer than it already is. This could delay or even prevent the introduction of new effective drugs to the market. This is always the trade off – the more evidence we require for approval the safer and better evidenced our drug market will be, but the higher the barriers to getting potentially effective drugs to patients. Would this new requirement (for comparative efficacy research) be worth the higher barriers?

Some have also criticized the practice of pharmaceutical companies producing “copy cat” or “me too” drugs for the market, simply to capture their piece of a lucrative pie. There is some legitimacy to this criticism – decisions about which potential new drugs to research are corporate marketing decisions, not decisions made on the basis of societal welfare.  (I am not criticizing the capitalist system we employ in the US for drug development – that is a separate issue I do not intend to explore here – I am simply pointing out one relevant consequence.)

However, I find it very useful to have multiple drug options for a single indication. There are always differences, and this allows for individualization for patients. Some patients may be allergic to one drug, so having another option is critical. And also sometimes one drug simply does not work in a patient while another “copy cat” drug may (perhaps due to genetic differences).

In the end, I find direct head-to-head comparative efficacy research highly valuable, but I am not sure it should be required pre-market. That may be one burden too many on the approval process. Perhaps we should explore other mechanisms to facilitate such research, such as funding independent academic comparative efficacy research (which happens now, but could be increased through funding). Regulations could even require pharmaceutical companies to participate in some way in such research of their drugs, by providing free drugs for the trial or even contribute to funding.

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When women live together, do their menstrual cycles tend to synchronize? It’s been a long time since I first heard that claim. I didn’t believe it, for a number of reasons. I had never observed it myself, I saw no plausible mechanism to explain how it could happen, I thought the statistics to prove it would be problematic and complicated, and I suspected that confirmation bias and selective memory might have persuaded people that a spurious correlation existed. How often do women say “Oh, look! We’re having our periods at the same time”? How often do they say “Oh, look! We’re having our periods at different times”?  Now that many years have passed since my first encounter, I thought it would be fun to revisit the claim and see whether science has supported it or rejected it.

A perusal of PubMed and other Internet sources left me confused and amused.

Synchrony Is Difficult to Define

Consider that the normal menstrual cycle can vary from 21 to 35 days and can last 2 to 7 days. Consider that some women are regular and consistent, while others have variable patterns, even “regularly irregular” patterns. Consider that anovulatory cycles and other conditions often lead to menstrual irregularities that fall outside the normal range. Consider that strenuous exercise and other life events can affect menstruation. Put all that together, and you can see that often cycles will overlap simply by chance, and that it is difficult to define synchrony.

If two women have regular 28 day cycles and 7 day periods, the maximum number of days they could not overlap is 14. On average, their periods will be 7 days apart, and half the time they will be closer.

How could a 21 day cycle ever “synchronize” with a 35 day cycle? For example if you compare a woman with a regular 35 day cycle who starts on January 1 to a woman with a 21 day cycle who starts two weeks later on January 15, their next periods will coincide almost perfectly (Feb 4-10 and Feb 5-11) but they will diverge after that. Would it count if the last day of one woman’s period overlapped with the first day of another woman’s? What if half the periods coincide and half don’t? The whole thing is problematic.

What Does the Literature Say?

It all started with Martha McClintock. In a paper published in Nature in 1971 she found that “social interaction” in a college dormitory setting could have a strong effect on the menstrual cycle. A follow-up study in 1998 tended to support the hypothesis that pheromones were involved: smelling armpit secretions of other women could either lengthen or shorten cycles depending on what part of her cycle the donor was in.

I’ll summarize rather than trying to cover everything published on the subject.  A Scientific American article did a good job of reviewing the literature as of 2007. Suffice it to say that about half the published papers support the synchronization hypothesis and half don’t; and the half that do have been harshly criticized for their poor design and poor statistical analyses. So we haven’t reached a consensus, but it’s looking more likely that synchronization is a myth.

A study in a nursing journal assumes that synchronization occurs and addresses the subjective meaning of the experience to

assist nurses to understand the holistic aspects of this everyday experience of women and to design effective strategies and techniques to help women gain knowledge about their cycle functions, promote healthy attitudes toward menstruation as a process, and acknowledge and honor this natural, healthy aspect of their menstrual cycle.

I will be kind to those nurses and apply Thumper’s rule. (In Bambi, he said “If you can’t say something nice, don’t say nothing at all.”)

What About Non-Humans?

It was originally thought that other primates and other mammals demonstrated menstrual synchrony due to pheromones, but recent studies have shown that it doesn’t occur in chimpanzees, hamsters, mandrills, or golden tamarins.

Do Human Pheromones Exist?

The existence of human pheromones is controversial. Pheromones are chemical signals released by one individual that affect the behavior of another individual of the same species. They can be useful for alarms, food trails, sex attractants, and other purposes. They have been well documented in insects and even in plants. In one memorable demonstration, a drop of oleic acid was all it took to persuade other ants that a live ant was dead; they dragged it back to the trash heap over and over, ignoring the fact that it kept protesting its trips to the ant graveyard by vigorously kicking, and that it kept “coming back from the dead.”

In humans, pheromones have been postulated and even sold as sexual attractants. But there is little or no peer-reviewed evidence to suggest that any pheromone influences human behavior. No human pheromones have been identified, and the vomeronasal organ that detects pheromones in other mammals is rudimentary and nonfunctional in humans.

Other Explanations

Not knowing if it occurs hasn’t stopped people from speculating about why it occurs or about why it doesn’t. The evolutionary reasoners have chimed in with just-so stories both about why it would and wouldn’t offer a survival benefit. For instance, if everyone ovulated at the same time, it would be harder for a woman to get a man. Or being banished to the menstrual hut at the same time would allow women to bond and collaborate on social enterprises. I was particularly amused by one chain of reasoning:

Synchronization also doesn’t make sense because during their mentrual cycles, women often experience lack of energy. These spells of low energy among women in a tribe would be detrimental to a hunter-gatherer lifestyle. Furthermore, if all of the women get pregnant at the same time, they won’t be able to help each other. Given our anthropological history, evolution should select that women do not cycle together. (errors in the original)

And this comment on the Scientific American article left me rolling on the floor:

Astrology explains this for better than modern science. Normally close friends have similar sun, moon positions in their horoscopes. The moon and mars determine the menstrual cycles. Astrological harmony makes them friends than living together which in turn is the cause of synchronization. Even if they are living far in different continents they will be in sync. In India any normal astrologer can check a woman’s horoscope and can tell the date of her menstruation time ( especially used when they have to attend auspicious ceremonies) and plan the events. (errors in the original)

Conclusion

Do women’s menstrual cycles tend to synchronize when they live together? As so often in medicine, science doesn’t provide a clear answer. Even if the phenomenon occurs, and even if human pheromones cause it, so what? It’s a matter of curiosity, not of clinical importance.  When there is a reason to manipulate ovulation or menstrual timing, pharmaceutical hormones work very well. The paucity of evidence for human pheromones suggests that if they do exist, their effects must be too small in magnitude to be very important.

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