Thursday, April 2, 2015

Bizarre Things Purported to Cause Autism: Hormonal Contraceptives

EXECUTIVE SUMMARY: An article published last winter in Medical Hypotheses suggests that long-term use of hormonal contraceptives might raise the likelihood of one's future children being born autistic. There is no good reason to believe this; the only things the article offers as potential reasons for it are 1) a very tenuous temporal relationship between widespread contraceptive use and a later (much later) rise in autism prevalence; 2) a misinterpreted bit of information largely pertaining to fertility testing; and 3) "What If?" scenarios involving epigenetics. I am worried about potential political fallout, to the further detriment of children and teenagers' sex education in the US, should this idea be uncritically popularized.
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Of all the myriad forms anti-feminist backlash can take, anti-contraceptive fearmongering is probably the most irritating to me.

So when I stumbled across this appalling article in Medical Hypotheses while I was casting about for items to populate my list of proposed causes of autism, I knew I would have to write a post specifically addressing this one.

The author, Kim Strifert, says that it may be possible that taking combined oral contraceptives (the ones that include both an estrogen, typically ethinyl estradiol, and a progestin, like levonorgestrel, norethindrone, or any of these others) over a long period* of time can change the conditions inside the ova and perhaps trigger epigenetic modification of genomic DNA.

I'd love to go into more detail about how this is supposed to work, but I can't, because no such detail is provided in the article:
Given the lack of research on the effects of oral contraceptive use on progeny, it is impossible at this point to specify a mechanistic link between oral contraceptives and autism. This fact represents a meaningful limitation to the hypothesis presented in this review. However, recent research already suggests that the current understanding of the pharmacology of oral contraceptives may be over-simplified. It has been proposed, for example, that epigenetic side-effects of pharmaceuticals may be involved in the etiology of cancer, heart disease, neurological and cognitive disorders, obesity, infertility, and sexual dysfunction [7][PDF]. It has also been suggested that epigenetic assays be incorporated into the safety assessment of all pharmaceutical drugs, which might lead to new mechanistic insights in the future [7]. Finally, new evidence is emerging that oral contraceptive use directly and deleteriously affects both the ovaries and the ova [8]. Thus, we are at a point where some concrete mechanistic hypotheses may be achievable in the near future.
What she does offer in support of her hypothesis is summarized here:
  • Temporal correlation between use of oral contraceptives and increased prevalence of ASD.
  • To date no definitive cause or contributing factors for increase in ASD prevalence has been established.
  • Oral contraceptives disrupt the endocrine system -- COC's are endocrine disruptors.
  • Oral contraceptives directly and deleteriously affect both the ovaries and ova.
  • Likely effects of oral contraceptives on progeny are an open question.
  • The called-for [by Dr. Roy Hertz**] further study and controlled follow-up of the possible transgenerational effects of oral contraceptive use has not been executed.
I will address these one at a time.

The first bullet point, the temporal correlation between use of oral contraceptives and autism prevalence, is true enough, but there are temporal correlations between lots of unrelated things. There's a whole mess of 'em archived for educational and comedic effect at Tyler Vigen's website Spurious Correlations. A cursory look at that website should be all the explanation you need of why this is not very good evidence that the two variables actually have anything to do with one another.

And even if we ignore that aspect of it, the time frames of the two trends -- increasing oral contraceptive use over time and increasing prevalence of autism over time -- don't quite overlap the way we would expect them to if there really were any sort of cause-and-effect relationship between them.

If there were such a relationship, we would expect a graph showing autism prevalence rates to be sort of a muted echo of a graph showing oral contraceptive use -- lower numbers overall, and trailing by maybe 5-10 years, but roughly the same shape, with peaks corresponding to peaks in the contraceptive-use graph.

Instead of that, we see two graphs of very different shapes, with their peaks separated by a much wider margin than would be possible if Strifert's hypothesis were true.

I cannot find comprehensive data on how many women used The Pill for every year between 1960, when it was approved, and now, but I can cobble together enough information from several different places to sketch a rough outline.
A very, very loose sketch of oral contraceptive usage in the US between 1960 and 2010, stitched together from numbers provided by PBS, the CDC (PDF, PDF), the Kaiser Family Foundation and the Guttmacher Institute
I can't vouch for the strictest accuracy of this picture, but the overall shape -- up, up, up, then slowing down, then a dip, then holding steady at about 10 million -- I'm reasonably confident in. 

By way of contrast, here is a graph of autism prevalence rates from 1985 to 2012 that Emily Willingham made:
Autism prevalence, 1985-2012, by Emily Willingham

As you can see, the shapes are very, very, very different! The graph of oral contraceptive use starts shooting upwards immediately, and then slows down its rate of increase, and then hits its peak and flattens out, while the graph of autism prevalence rises very slowly before it finally begins to build up steam. Like a logarithmic vs. an exponential*** curve...

They both trend upward, but other than that, they have little in common.

Even more important than the shape is the timing. Oral contraceptive use seems to hit its peak around the mid-to-late-1970s, while autism prevalence has perhaps not even peaked yet. It has a long, slow rise with what appear to be two inflection points, one around 2001 and another at about 2005.

Twenty-five years is an awfully long lag time between getting on the Pill and having young children. My mom could easily have been taking the Pill in the mid-1970s, and she had me thirty years ago! And I was diagnosed in 1989 or 1990, when the graph of autism prevalence was still hugging the x-axis.

The women making up that first big wave of oral contraceptive users are probably more likely to be the grandmothers of the children making up the present Autism Epidemic than they are to be their mothers.

The second bullet point is not really an argument in support of a causal relationship between contraceptive use and autism in progeny -- it's just saying, "Well, we don't know what causes autism, so why not entertain my idea?"

The third bullet point -- that hormonal contraceptives are endocrine disruptors -- is kind of a tautology. Of course they are endocrine disruptors -- they wouldn't be able to suppress ovulation if they were not.

Pointing out that hormonal contraceptives are endocrine disruptors is about as helpful as running up to someone and announcing that the Tylenol they are about to take will interfere with their body's natural warning system by dulling their sensations of pain. They know that; that is why they're taking the pill in the first place!

Finally, let's return to the first passage I quoted, which is the first mention of bullet point #4, "[o]ral contraceptives directly and deleteriously affect both the ovaries and ova." The source Strifert gives for this statement -- the "new evidence" that is "emerging" -- is this article on the biotechnology news website BioscienceTechnology.com.

What that article says is very different from what Strifert seems to think it says.

Prolonged hormonal contraceptive use does indeed shrink the ovaries, lower the levels of anti-Müllerian hormone in the blood, and reduce the number of ovarian follicles at a certain stage of maturation. Those two things are considered reliable indicators of how many egg cells might be left within the ovary.

(Here is a literature review comparing the relative merits of those two biomarkers)

However, the researchers who discovered this -- Dr. Kathrine Birch Petersen and her team -- do not think these effects are permanent, and are mostly concerned with making sure people getting their fertility tested after just coming off of birth control get an accurate estimate of their ovarian reserves. Dr. Birch Petersen is especially worried that this temporary suppression of ovarian-reserve markers by long-term contraceptive use might mask a naturally low ovarian reserve, something a person wishing to become pregnant would want to know about.

Here she is, quoted in the Bioscience Technology article:
Birch Petersen's team does not believe these changes [decreased ovarian volume, lower AMH levels, lower antral follicle count] are permanent. But as a result of the study, she said, women in the Pre-conceptional Care Program who have been on the contraceptive pill are now advised that their ovaries may look older and smaller, and may possess only a few small antral follicles, with low levels of AMH for a time after stopping. They are told this likely does not affect future fertility for most women. 
But it could matter for women undergoing premature menopause. Naturally diminished ovarian reserves could be masked by the above. It is therefore possible ovarian reserve assessment should be repeated after stopping birth control pills. 
"Worldwide, 160 million women are on the pill," Birch Petersen told Bioscience. "One percent will go into early menopause before the age of 40. The pill can mask the symptoms of early menopause, and this is why women should consider repeating the tests after six months [off the pill], if they have a low ovarian reserve." 
Next up, says Birch Petersen: "To examine what happens with the ovarian reserve parameters after one, three, and six months."
And here is a short press release published last year on the Clinical Endocrinology News website:
Oral contraceptives do more than prevent unwanted pregnancy. They also make it harder to gauge a woman's ovarian reserve, based on data from 833 women aged 19-46 years seen at a single Danish fertility clinic. 
Study findings suggested that an accurate measure of a woman's ovarian reserve can occur only after she has been off an estrogen-containing [oral contraceptive], probably for at least 3 months, Dr. Kathrine Birch Petersen reported at the annual meeting of the European Society of Human Reproduction and Embryology. 
The impact of estrogen-containing OC use on reducing ovarian volume was especially pronounced in women under 30, the reduction increased with longer durations of OC use, and the ability of OC's to mask a woman's actual ovarian reserve was strong enough to potentially conceal a true case of premature ovarian insufficiency, said Dr. Birch Petersen, an ob.gyn. at the Fertility Assessment and Counseling Clinic at Righospitalet in Copenhagen. 
"When we see a woman on an OC with impaired ovarian reserve, we would presume [based on these new findings] that her real ovarian reserve was about 30% higher than what we measure. We would advise her to be retested after she was off her OC for about 3 months," Dr. Birch Petersen said during a press conference before her presentation at the meeting. 
The study included the first women seen at the clinic since it opened in 2011, excluding those who were pregnant or failed to supply adequate information. The cross-sectional cohort included 240 women on estrogen-containing OC and 593 women with natural cycles. 
The analysis focused on three parameters: blood level of anti-Müllerian hormone (AMH), antral follicle count (AFC), and ovarian volume. The multivariate, linear regression analysis adjusted for age, body mass index, smoking, age of maternal menopause, maternal smoking during pregnancy, preterm birth, and duration of OC use. 
The analysis showed that compared with the women with natural cycles, those on an OC had a 19% relative reduction in their average blood level of AMH, a 16% reduction in average AFC, and a 47% relative reduction in average ovarian volume. The women on an OC also had smaller antral follicles. All three differences were statistically significant. 
Seeing an effect from an estrogen-containing OC on all three measures makes sense because of their interrelatedness. The antral follicles produce AMH, and a reduction in antral follicle number as well as size would shrink the ovarian contents and result in reduced volume. These results would not occur in women on a progestin-only OC, she said.
This additional context makes it clear to me that the changes wrought on the ovary by estrogen-containing contraceptives are indeed temporary.

And here is one more thing I wonder -- why autism? Why would the kind of epigenetic interference Strifert seems to be postulating only result in one type of developmental disability? I know autism is a broad category, but still -- why would only development of the nervous system be affected? Why not all aspects of fetal development?

(A cynic's response to that question would be, because autism is the biggest cultural bogeyman with which to threaten prospective parents. See also: the anti-vaccine movement.)

I would not be opposed to any of the further research into contraceptive safety, uterine and ovarian physiology, or potential alternative methods for contraception!

Even though I do not think it likely at all that what she suspects is true, I think that only good could come of additional efforts to develop even safer methods of contraception that work in multiple different ways.

But what I do not want to happen, which I strongly suspect would be a more likely near-term consequence of Strifert's article gaining widespread attention, is for her warnings to be hyperbolized (instead of the question "what is the effect of long-term hormonal contraceptive use on the ova?" it would become the statement "using hormonal contraceptives means that your children will be born with developmental disabilities later on") and be taught to teenagers in sex education classes as yet another reason they should eschew any and all birth control methods. Sex education classes in the US already lie to children about the efficacy of condoms and tell them that total sexual abstinence is the only way to protect themselves, so adding one more lie to the list is hardly unthinkable.

And looking at the path Strifert's ideas have taken into the blogosphere, this impression -- that, far from echoing her call for more research and development of new contraceptive methods and for improved safety of existing methods, the blogs reporting on her article merely urge their readers to eschew hormonal methods of contraception entirely.

The only blog post I could find dealing with this specific article is this one, by Dr. Kelly Brogan, MD, who despite her medical training seems to reject all of modern, conventional medicine in favor of diet and lifestyle changes.

There are other posts that express a similar idea -- that birth control pills can cause autism in one's future children -- but credit a different source and propose a different mechanism by which it happens (usually gut bacteria rather than the epigenetic explanation loosely sketched by Strifert); those blogs are about an even mix of anti-vaccine, alternative medicine blogs that advocate rejection of all conventional medicine and Catholic blogs that reject all methods of contraception except Natural Family Planning and abstinence.


I do not think it is irrelevant that those are the types of the blogs on which this particular Bizarre Autism Hypothesis has appeared.


*Pun intended

**In a 1966 report by the U.S. Food and Drug Administration's Advisory Committee on Obstetrics and Gynecology; that report, physically archived at the University of Michigan, has been digitized and can be viewed online here.

***Or, what is more likely, a logistic curve. Populations cannot grow indefinitely.

Friday, January 23, 2015

An Incomplete List of Things that Have Been Postulated, In Earnest, as Possible Causes of Autism

(Note: Not all of these ideas are crank hypotheses; some of them are, a few were widely accepted in their day but are now regarded as crank notions, many are just people throwing things out there on the strength of statistical correlations, some have a fairly impressive body of evidence supporting them, and some are ones that I consider crankish but not everyone does -- the Extreme Male Brain theory being an example of this latter category. I do not use my "bizarre autism hypotheses" tag exclusively for bad science; just everything that strikes me as odd.)

In no particular order:

This is an incomplete list, so feel free to add anything you've heard that I have not listed here in the comments!

Saturday, November 15, 2014

This Article About the JRC Is Very Enlightening, If You Can Stand to Read It

"Prisoners of the Apparatus": The Judge Rotenberg Center, by Quentin Davies of the Autistic Self Advocacy Network

The article is very long (though very much worth reading in full, if you have the time and concentration for it), so I'm going to excerpt the section at the end that talks about what the best avenues for shutting the place down permanently would be:
Policy Recommendations
The Judge Rotenberg Center's abusive behavior is a civil rights concern, and should be addressed by policy at the federal level. As the New York Psychological Association Task Force said, the use of shock aversives on the students at the Judge Rotenberg Center would be considered corporal punishment and would be illegal if the nondisabled people were treated the same way in a school setting. Regulations that selectively allow abusive punishment for disabled students that are not allowed for nondisabled students is not only a terrible allowance of abuse, but also is a discriminatory action on the part of the United States and Massachusetts governments, regardless of whether we call this "corporal punishment" or "aversive behavioral intervention" (Ahern and Rosenthal 27). Additionally, the lack of actual instruction within the Judge Rotenberg Center, the social isolation, the food deprivation, the use of restraints and seclusion as punishment and for long periods of time mean that preventing the Judge Rotenberg Center from using shock aversives, while it would be a step in the right direction, would not be broad enough to stop the abuse at the Center. The Judge Rotenberg Center (formerly called the Behavior Research Institute) has tortured disabled children and adults for over forty years, and it needs to stop now. 
This policy must be passed at the federal level. The Judge Rotenberg Center has been located in three different states over its history, and there is a real possibility of the JRC moving again if protections were only ensured on a state level (Méndez). Currently, there is some federal policy that is applicable to the Judge Rotenberg Center, but much of that legislation has been weakened by court action. For example, in 1975, Congress passed the "Developmental Disabilities Assistance and Bill of Rights Act" (DD Act), which states, that "the Federal Government and the States have an obligation to ensure that public funds are provided only to institutional programs, residential programs, and other community programs, including educational programs in which individuals with developmental disabilities participate, that  ... meet minimum standards relating to provision of care that is free of abuse, neglect, sexual and financial exploitation, and violations of legal and human rights that subjects individuals with disabilities to no greater risk of harm than others in the general population ... and prohibition of the use of such restraint and seclusion as a substitute for a habilitation program" (Ahern and Rosenthal 29). However, in the case, Pennhurst State School and Hospital vs. Halderman, where a former Pennhurst resident alleged that the hospital was unsanitary, inhumane, dangerous, and used cruel and unusual punishment, the US Supreme Court ruled that the DD Act did not create any new legal rights or protections and [that] the language of the DD Act was "hortatory not mandatory." That court opinion, written by William Rehnquist, stated that "[t]he Act does no more than express a congressional preference for certain kinds of treatment" (Ahern and Rosenthal 30). Consequently, new legislation that has similar goals but expresses them in a way that is clear about the mandatory nature of the legislation is necessary. 
Although the President's New Freedom Commission on Mental Health has said that "restraint will be used only as safety interventions of last resort, not as treatment interventions" and the US Department of Health and Human Services Substance Abuse and Mental Health Administration has said that restraint and seclusion are "detrimental to the recovery of persons with mental illnesses" (Ahern and Rosenthal 12), no federal legislation has enforced these goals. Restraints and seclusion are still used in almost every state in the United States, and no federal law limits the use of restraints within schools (Ahern and Rosenthal 28). The Individuals with Disabilities Education Act (IDEA) states that alternatives to aversives should be considered, but does not explicitly prohibit aversives (Ahern and Rosenthal 29). None of these recommendations have protected the students at the Judge Rotenberg Center from the torturous treatment they have experienced. 
Federal law could draw from the state laws of California, Connecticut, Florida, North and South Dakota, Pennsylvania, Arizona, Rhode Island, New York, New Jersey, Nevada, and Colorado, all of which have taken steps to ban or limit the use of aversives on disabled children and adults (Cobb 9). A US Court of Appeals found in Bryant vs. New York State Department of Education (2012) that bans on aversive interventions did not violate IDEA as was alleged by the plaintiffs. The decision reads "[w]e conclude that prohibiting one possible method of dealing with disorders in behavior, such as aversive intervention, does not undermine a child's right to an individualized, free and appropriate public education, and that New York's law represents the State's considered judgment regarding the education and safety of its children that is consistent with federal education policy and the United States Constitution" (Bryant 2). Federal law prohibiting aversive interventions would provide protection throughout the US for disabled children and adults subjected to aversive techniques, including the students of the Judge Rotenberg Center.
That was a lot of densely written text, so I will attempt to paraphrase: To close the Judge Rotenberg Center, we need legislation that is 1) federal, not state; 2) comprehensive in what types of abuses it prevents (i.e., not narrowly focused on the skin shock devices); and 3) unmistakably binding and mandatory.

It needs to be those things because the JRC's own history shows that it can survive measures that do not meet all three of those criteria. If you outlaw what they do on a state level, they move. If you call attention to the barbarity of one particular method of punishment, they switch to others. If you say, "This is not a school and we will not give you a license to operate it," they re-incorporate, changing their paperwork but not their methods. If you sue them on the grounds that they violate an existing federal law (like, say, the DD Act), a court might well rule that the law is not absolute. And, finally, if you threaten to ban the device they use to administer the infamous skin shocks, on the grounds that it's not safe, they will stop using it -- but only on new students. Students who have been living there since before 2011 will continue to be shocked as before. 

It needs to be torn out, root and stem.

Carthago delenda est.

Friday, November 14, 2014

Cartoon Versions of Glycolytic Enzymes - Part I

Cross-posted from my Tumblr

Someone on Tumblr asked for help understanding glycolysis (along with a lot of other things, but I decided to focus on glycolysis first), so I had the brainwave of drawing cartoon versions of all the glycolytic enzymes.


Here are my cartoon interpretations of the enzymes catalyzing the first five steps of glycolysis:

1. Hexokinase
Hexokinase, drawn as a pair of interlocking jaws with a space for glucose and ATP
I drew this one to look like a huge snapping alligator jaw that fits together like a jigsaw puzzle, except for a small space near the back for glucose and ATP to fit into. (See the links at the bottom of this post, and also this blog -- particularly this post -- for more realistic images of hexokinase).

2. Phosphoglucose isomerase
Phosphoglucose isomerase, drawn as a stylized pair of interlocking hands
I have functional as well as structural reasons for choosing this way to represent this enzyme; besides the fact that its structure really is two identical subunits shaped roughly like twin blobs with long arms wrapped around one another — arms that remind me of thumbs sticking out from fists — I also figured that, since its function is to break the ring that makes up glucose, change a few things around and then let the ring re-form into fructose, a pair of hands looks like something that could do that. Like I drew hexokinase — whose function is to clamp itself around glucose — as a pair of jaws, I drew this one thinking to evoke some everyday-life analogy for what it does. The analogy that occurred to me was cracking an egg, which I do with two hands, using my thumbs to pry the shell open. (See the links at the bottom of this post, plus this one*, this one, and this one, for more realistic images of phosphoglucose isomerase).

3. Phosphofructokinase
Phosphofructokinase, drawn as a pinwheel with a smiley face in the middle
I drew a pinwheel to represent phosphofructokinase. I chose that shape because most of the drawings and computer models I found of its structure seemed to show a radial symmetry, of either 90 or 180 degrees depending on which image I was looking at. (See the links at the bottom of this post, plus this one, this one, this one and this one, for more realistic images of phosphofructokinase).

4. Aldolase
Aldolase, drawn as a pair of butterfly wings
I chose a butterfly for aldolase because in most of the drawings and computer models I could find of its structure, it looked like it had mirror symmetry. (See the links at the bottom of this post, plus this one and this one***, for more realistic pictures of aldolase).

5. Triose phosphate isomerase
Triose phosphate isomerase, drawn as a barrel with a face
I drew this one as a barrel, to reflect the "beta barrel" that makes up its interior structure, and contains the active site. (See the links at the bottom of this post, plus this one, this one and this entire blog -- particularly this post -- for more realistic images of triose phosphate isomerase). 

As you can hopefully see if you've been clicking on the links, I've tried to anchor all of my cartoon avatars of these enzymes in some element of their actual structure.

Here are some general links where you can see some decent representations of the structures of all ten of these enzymes:

Glycolysis (enzymes of the preparatory phase)

Glycolysis (enzymes of the payoff phase)

The Glycolytic Enzymes (PDF)

Notes

*The linked image is an illustration from an evolutionary biology textbook -- Evolution, by Nicholas H. Barton, Derek E. G. Briggs, Jonathan A. Eisen, David B. Goldstein, and Nipam H. Patel. The book has a website, where you can see some of the content -- including all the illustrations -- for free. 

This particular image is not original, though -- the ultimate source is a paper from 2006 by Christopher W. Wheat, Ward B. Watt, David D. Pollock and Patricia M. Schulte. It was published in Molecular Biology and Evolution and you can read the full text here.


**The linked image is Figure 2 from this article in Biochemical Society Transactions


Citations

Mitternacht, S., and Berezovsky, I. (2011). Coherent Conformational Degrees of Freedom as a Structural Basis for Allosteric Communication PLoS Computational Biology, 7 (12) DOI: 10.1371/journal.pcbi.1002301

Perica, T., Marsh, J., Sousa, F., Natan, E., Colwell, L., Ahnert, S., and Teichmann, S. (2012). The emergence of protein complexes: quaternary structure, dynamics and allostery Biochemical Society Transactions, 40 (3), 475-491 DOI: 10.1042/BST20120056

Wheat, C. (2005). From DNA to Fitness Differences: Sequences and Structures of Adaptive Variants of Colias Phosphoglucose Isomerase (PGI) Molecular Biology and Evolution, 23 (3), 499-512 DOI: 10.1093/molbev/msj062

Saturday, August 16, 2014

More Pictures of the Tiny Sketchbook for Drawing Tiny Things

It occurred to me after I'd made this post that it would've been a good idea to include pictures of the notebook itself along with the pictures of the things I've drawn in it.

So here they are now!
A shot of the cover of my jeweled pocket notebook. It looks like a game of Bejeweled or something ... and it sheds glitter. But it makes me happy to look at it.
Here are some pictures of it in my hand, so you can appreciate just how tiny it is.
Here's a sideways shot of the notebook, with me holding it half open. You can see a little bit of my drawing of a Christmas ornament peeking out from behind the cover.
Here it is sitting on my flat, open hand. This is my favorite shot of it. I like the natural light on the jewels.
Here it is again, engulfed by my hand. It is perhaps an average sized hand overall, though it is pretty large and meaty for a woman's hand.

It's a Tiny Sketchbook, for Drawings of Tiny Things


One of my uncles gave me this sketchbook a few years ago -- I just measured the pages, and I found out they are three inches wide by three and three-quarter inches long. Very small!

I have adapted to this notebook's extreme smallness by deciding I'm only going to draw still lifes of very small objects in it.

So far, everything is proceeding according to plan!

I have two drawings done, and I think they turned out really well!

The top one is of a Christmas ornament, a shiny round ball with a sort of swirly design painted on it with glitter, and the bottom one is of a ring I have in the shape of a scarab beetle.

I really like the bottom one. I tried using primarily stippling to shade it, and I think that was the right choice.

Tuesday, August 12, 2014

The Prudent Blogger Never Titles a Post 'Part One' ...

... because, once you do that, you have all but guaranteed that the mother of all cases of writer's block will descend on you as soon as you hit "Publish" on that first post.

Probably at least half of the posts that I've written with the intention of having them be part of a series ended up as stand-alones.

Friday, July 18, 2014

More Game of Thrones-Themed Art


This is a super quick watercolor portrait I did of Tywin Lannister from "Game of Thrones." He's all purple because I intend to do a bunch of these, choosing one character to represent each of the Seven Deadly Sins and Seven Heavenly Virtues.

They will all be painted monochromatically, in the color traditionally associated with their sin or virtue.

Tywin is Pride, so I've painted him purple. 

Thursday, July 17, 2014

A Fairly Silly Art Project I've Been Working On




It's Robb Stark from "Game of Thrones" reimagined as a comic-book superhero!

I made these because someone on Tumblr was asking for fan art of Robb Stark and Jon Snow dressed in revealing superhero costumes, and I figured I could do that.

I made up aliases and powers for them, too, to go with the costumes.

Robb's superhero alias is Grey Wind, and he can fly and control the wind. (Possibly he flies by calling on the wind to carry him?)

I'm still pretty jittery about my skill with watercolors, so I made sure to scan this in stages, so that if I screwed up irreparably at any point I'd still have the linework to fall back on.

(The finished picture is mixed media -- outlined in ink, the figure colored with colored pencils, and the background colored with watercolors.)

Here are the other places I've posted these pictures on the Internet:

On my Tumblr: Stage One Stage Two Stage Three All Together

On my Deviant Art: Stage One Stage Two Stage Three

Wednesday, July 16, 2014

Bizarre Things Purported to Cause Autism: Glyphosate in Pesticides

EXECUTIVE SUMMARY: This is the first of two posts dealing with the claim by MIT researcher Stephanie Seneff that a chemical found in Monsanto's RoundUp herbicide is implicated in the increase in autism prevalence rates in recent years.

This post does not address the claim itself, but evaluates whether Dr. Seneff is a credible source.

She does appear to have credibility and standing in the field of computer science -- particularly the subfield of natural language processing -- and has a lengthy publication history and an impressive array of citations within that field. But in public health, she mostly seems relegated to fringe conferences, the Internet and one not particularly selective journal.
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Sometimes I wonder if I should even be bothering to write about some of these autism hypotheses, because they're so fringe, and most people haven't even heard them, much less believe them to be true, but since I mostly write about these for my own amusement, and to satisfy my collector's instinct, the feeling soon passes.

Anyway, on Tumblr I came across a link to this article on some bogus "alternative health" website, about a senior research scientist at MIT who's been going around giving presentations (at conferences of dubious repute, like AutismOne and this anti-GMO symposium hosted by this day spa/alternative medical clinic in Groton, Massachusetts) about how pesticides --- specifically, pesticides containing glyphosate --- are turning everyone autistic.
This was one of the ads in the sidebar of that article

I will address the specifics of Dr. Seneff's claims in another post, because right now I see a golden opportunity to talk about source evaluation, and I'm taking it.

Every news article I could find on this topic had a headline along the lines of, "MIT researcher says chemical in RoundUp linked to autism." That's true as far as it goes (Stephanie Seneff is a researcher at MIT, and that is indeed what she says), but it also has the unfortunate effect of giving the reader the impression that MIT says those things, when really it's just her.

The closer you look at her background and publication history, the more red flags you see.

Her position at MIT is Senior Research Scientist at the MIT Computer Science and Artificial Intelligence Laboratory; she's a computer programmer, Jim, not a doctor!

Her advanced degrees are in electrical engineering and computer science, and her undergraduate degree --- the closest she gets to having any background whatsoever in biology or medicine --- is in biophysics.

Biophysics is a perfectly fine field of study --- it's an interdisciplinary melding of biology and physics --- but it's very broad, and it seems to me like it isn't so much a specialty in itself as it is a collection of specific research topics that require study from both biological and physics perspectives. 

Parts of it deal with atomic-level interactions between molecules: figuring out, in exacting detail, how any particular grouping of molecules fits together; how an enzyme or receptor forms a complex with its target molecule; how proteins arrive at, and maintain, their three-dimensional shape. Parts of it deal with electrostatic interactions between those same atoms and molecules, as in the study of ion channels, or the difference in electrostatic potential that exists across cell membranes.

Parts of it are more purely mathematical or computational, dealing with mathematical modeling and computer simulations.

That actually all sounds super interesting and cool, but the point is that most of those areas of inquiry are things that would benefit from investigation by very carefully chosen teams of experts in diverse fields, not one person, and it also seems to me like a bachelor's degree in biophysics (where the option exists -- it looks like biophysics is more often a graduate degree program) involves a fairly solid grounding in basic physics, chemistry, and molecular/cellular biology (as distinct from organismal or population biology, I mean) and then your choice of advanced courses in a very wide range of topics.

Here are some lists of degree requirements for a B.S. in biophysics from various universities that offer it, if you want to look at them yourself: Johns Hopkins University (PDF); York University in Canada (PDF); Arizona State University; Wake Forest University

The point of all the foregoing is just to show that someone could have an undergraduate degree in biophysics that is weighted more heavily toward the physics or chemistry ends of things, with only cursory attention paid to cell biology and little or none to metabolism or physiology. 

Anyway, it looks like most of her research over the years has been concerned with speech and language, and improving computer recognition of human speech. Her Ph.D. thesis, according to this webpage, was a computer model of how the human brain processes language.

She seems to have only pivoted to medical research in recent years.

What's worse, she seems to be writing about a very wide range of unrelated topics in medicine: the heart, the brain, the gut, epigenetics, nutrition, toxicology, epidemiology ... how much can one person understand of so many disparate fields, especially when that person is trained primarily in computer science and has only just (2011-2014) begun to publish about any of them?

Also, when you look at her CV, you notice a striking change in the nature of her citations, corresponding with the change in subject matter.

Following her pivot to writing about public-health issues, more and more of her writing is either self-published (on her website) or published in a single journal, Entropy, which has been called a "pay to play" journal -- one that will publish whatever you send them, regardless of merit, as long as you pay the fee.

For comparison, when she was writing about natural language processing stuff she would be getting published in peer-reviewed journals* published by prestigious academic and professional organizations like IEEE (the Institute of Electrical and Electronics Engineers), the Acoustical Society of America, the European Association for Signal Processing, the International Speech Communication Association, and the Association for Computational Linguistics.

The same holds true for her speaking engagements. 

In the past, she's spoken about natural language processing stuff at international conferences in various fields relating to linguistics and computer science --- the International Conference on Spoken Language Processing in 1990, 1992, 1994, 1996, 2000, 2002, 2004, 2006, and 2010; the Conference of the International Speech Communication Association in 2007, 2009, 2010 and 2011; the European Conference on Speech Communication and Technology in 1991, 1993, 1995, 1997, 2001, 2003 and 2005; the International Conference on Computational Linguistics in 1996; the Conference on Empirical Methods in Natural Language Processing in 2009; the Special Interest Group on Discourse and Dialogue in 2010; and the IEEE International Conference on Acoustics, Speech, and Signal Processing in 1991, 1992, 1994, 20002008 and 2012 --- whereas her presentations about glyphosate seem to be given mostly to small gatherings of laypeople or at crank conferences, like the Weston A. Price Foundation's Wise Traditions Conference. (She's spoken at five of those!)

Given all of this, the logical thing to do is take whatever she has to say about medicine with a huge grain of salt.

* This is as good a place as any to point out that peer review isn't 100% effective at screening out dodgy science; even The Lancet managed to let Andrew Wakefield's fraudulent research slip past their vetting process. And just recently there's been a huge scandal over a "peer review ring" through which a few authors were able to fabricate favorable reviews of their submissions to make sure they would be published.  

Thursday, June 19, 2014

Commissions

Doing this drawing made me really excited about drawing people riding comically enlarged animals, so I've decided I'm going to take commissions.

If you want a picture of yourself riding a comically oversized animal -- any animal, even a specific individual (like, if you want a picture of yourself riding your cat), with whatever other specifications you might care to make (what you'd like to be wearing or doing, like if you want to be carrying a banner or aiming or brandishing a weapon or something, or if you'd like to be riding your animal in a specific setting, like up a mountain or through a snowstorm or over the ramparts of Helm's Deep or whatever), PayPal me ten dollars and send me a message (in comments here, in my Tumblr askbox, on my DeviantArt profile page, in an email ... whatever) describing what you'd like me to do.

(Obviously, if I'm going to draw you, I need to know what you look like, so you'll need to send me a picture or a link to someplace where you've posted pictures online.)


My email address (which is also the address of my PayPal account) is lindsayegehring@gmail.com, if you want to take me up on this offer. 

Wednesday, June 18, 2014

Bring Me One Large Enough to Ride!

A drawing of myself riding a huge Norwegian Forest Cat, inspired by this post on Tumblr

Only Some of These Really Bother Me

(A version of this post has also appeared on my Tumblr)
Article header from io9.com: "10 Scientific Ideas That Scientists Wish You Would Stop Misusing"
There's an article on io9.com listing ten words/concepts from various fields of science that are commonly misused by laypeople, so I had to look at it and see if any of my pet peeves made it onto the list.

There were a few:
3. Quantum Uncertainty and Quantum Weirdness
[Astrophysicist Dave] Goldberg adds that there's another idea that's been misinterpreted even more perniciously than "theory." It's when people appropriate concepts from physics for new agey or spiritual purposes:
This misconception is an exploitation of quantum mechanics by a certain breed spiritualists and self-helpers, and epitomized by the abomination, [the movie] What the Bleep Do We Know? Quantum mechanics, famously, has measurement at its core. An observer measuring position or momentum or energy causes the "wavefunction to collapse," non-deterministically. (Indeed, I did one of my first columns on "How smart do you need to collapse a wavefunction?") But just because the universe isn't deterministic doesn't mean that you are the one controlling it. It is remarkable (and frankly, alarming) the degree to which quantum uncertainty and quantum weirdness get inextricably bound up in certain circles with the idea of a soul, or humans controlling the universe, or some other pseudoscience. In the end, we are made of quantum particles (protons, neutrons, electrons) and are part of the quantum universe. That is cool, of course, but only in the sense that all of physics is cool. 
4. Learned vs. Innate
Evolutionary biologist Marlene Zuk says:
One of my favorite [misuses] is the idea of behavior being "learned vs. innate" or any of the other nature-nurture versions of this. The first question I often get when I talk about a behavior is whether it's "genetic" or not, which is a misunderstanding because ALL traits, all the time, are the result of input from the genes and input from the environment. Only a difference between traits, and not the trait itself, can be genetic or learned — like if you have identical twins reared in different environments and they do something different (like speak different languages), then that difference is learned. But speaking French or Italian or whatever isn't totally learned in and of itself, because obviously one has to have a certain genetic background to be able to speak at all.
....
6. Gene

[Synthetic biologist Terry] Johnson has an even bigger concern with how the word gene gets used, however: 
It took 25 scientists two contentious days to come up with: "a locatable region of genomic sequence, corresponding to a unit of inheritance, which is associated with regulatory regions, transcribed regions and/or other functional sequence regions." Meaning that a gene is a discrete bit of DNA that we can point to and say, "that makes something, or regulates the making of something". The definition has a lot of wiggle room by design; it wasn't long ago that we thought that most of our DNA didn't do anything at all. We called it "junk DNA", but we're discovering that much of that junk has purposes that weren't immediately obvious. 
Typically "gene" is misused most when followed by "for". There's two problems with this. We all have genes for hemoglobin, but we don't all have sickle cell anemia. Different people have different versions of the hemoglobin gene, called alleles. There are hemoglobin alleles which are associated with sickle cell diseases, and others that aren't. So, a gene refers to a family of alleles, and only a few members of that family, if any, are associated with diseases or disorders. The gene isn't bad - trust me, you won't live long without hemoglobin - though the particular version of hemoglobin that you have could be problematic. 
I worry most about the popularization of the idea that when a genetic variation is correlated with something, it is the "gene for" that something. The language suggests that "this gene causes heart disease", when the reality is usually, "people that have this allele seem to have a slightly higher incidence of heart disease, but we don't know why, and maybe there are compensating advantages to this allele that we didn't notice because we weren't looking for them".
Those were the ones that resonated with me the most; others were only minor peeves or didn't actually bother me at all.

Misused Word #1, "Proof," was only a minor annoyance for me in that I'm almost never talking about mathematical proofs, and even if I were the sort of person who does use them routinely, it still seems to me like most things people talking about "proving" colloquially are impossible to express in mathematical terms.

It just seems to me like there wouldn't be very many circumstances in which mixing up the technical and colloquial meanings of "proof" would be an issue that would even arise.

(I have found that the most annoying sources of confusion in scientist/layperson conversations about proof have to do with standards of evidence, or also degrees of uncertainty. You can be more unsure of one thing than you are of another, even if you're not 100% certain about the thing you are more sure of.)

Similarly, "theory" also doesn't annoy me that much because I don't usually have much trouble adjusting to different usages of words in different contexts.

I can see how it would get really old having to explain the technical meaning of "theory" over and over again, though.
It seems like those are more about the meaning of specific words than they are about whole networks of ideas, so they are easier for me to adapt to when they surprise me in conversation.
The ones discussed in the quoted text above, though? Misuse of ideas derived from quantum mechanics, misinterpretations of evolution and natural selection, or the idea that genes are "for" specific things? Those come with so many other ideas connected to them, so many wrong things tacitly accepted as premises, that I feel like I need a ball of yarn to slowly pick my way back to the start of the conceptual maze.