Friend: “Flowers are basically a place where insects go to masturbate.”
Typical Thursday night.
Friend: “Flowers are basically a place where insects go to masturbate.”
Typical Thursday night.
My talk from Skepticon is now online! If you ever wanted a quick and dirty summary of basic genetic concepts, now’s your chance. I try to address a lot of common misconceptions about genetics and address some of the shoddy ways genetics is portrayed by the media:
That was my first time giving that talk. From the Q&A and questions I got afterward, I certainly know what sort of stuff I need to add, subtract, or explain better. If there’s still anything you don’t quite get about genetics, feel free to leave a question in a comments.
Yesterday I picked apart the Burzynski clinic’s list of “scientific studies supporting antineoplason research since 2006.” Unsurprisingly, a majority of these citations were just abstracts of conference presentations lacking peer review, and a couple studies published in terrible (and even sketchy) journals. I wasn’t able to comment on specifics about the papers since I didn’t have access through my university.
A reader sent me a pdf of the first paper from Pediatric Drugs, which is even more incriminating. For one, it’s a review paper. Review papers summarize the current state of scientific knowledge about a certain topic. Sometimes they perform meta analysis on multiple papers, but they don’t always add any new information. Burzynski’s review falls into the latter – that is, it does not have any new peer reviewed data. And the studies about antineoplastons that the paper cites are from multiple conference abstracts, a patent from 1995, his report to the FDA, and an entry in a book by Nova Science Publishers (aka, also all not peer reviewed).
The only peer reviewed research paper the review cites was on the previous list – it was the one published in the crappy alternative medicine journal. I haven’t gotten hold of the paper, but commenter joshtriska summarized it thusly:
 A report on 18 patients with “High-Grade, Recurrent, and Progressive Brainstem Glioma” picked from 4 of his clinical trials. The conclusion states that typically less than 10% of patients with this condition survive 2 years, but in his group 22% (or four whole people) survived past 5 years. The conclusion also states that “Because a small number of patients have been evaluated, a larger study is required to confirm these results”. No kidding!
And that final paper – the one published in the sketchy as hell “Cancer Therapy” journal, was also a review:
 A review paper, not a study. Antineoplastons are mentioned and a line of data from one of Burzynski’s trials is included in a table. The discussion states that the data concerning antineoplastons was from from conference abstracts, and not peer-reviewed.
The Burzynski clinic is claiming that it’s libelous to say “There are no scientific studies supporting antineoplaston treatment since 2006.” But it’s not libelous because it is true. Results that lack peer review cannot be said to support something. Abstracts at conferences are not peer reviewed. Review papers do not include new, peer-reviewed data. The only published paper he has itself states that it is inconclusive without a larger study to confirm the results.
Plus, they don’t even understand what the phrase “since 2006” means. It means published starting in 2007. From that alone we throw out the first two papers. You’re left with a review paper that cites conference abstracts, and conference abstracts.
So no, Burzynski clinic. There aren’t any scientific studies supporting antineoplaston treatment since 2006. But there are plenty falsifying it.
The Burzynski clinic has responded to the flood of skeptical bloggers with a press release. They’ve apparently fired (in so many words) Marc Stephens for his harassment, yet still plan to send attorneys after UK bloggers. I’m not sure if the targeting of UK bloggers has to do with UK libel laws, or if the Burzynski clinic is oblivious to the dozens of American bloggers also pointing out their harmful pseudoscience.
But the part of the press release that intrigued me was that they finally attempt to give some evidence for all that scientific research Burzynski has to back up his claims. Wow, a list of citations! To a non-scientist, it certainly seems impressive, what with its big words and journal names and such. But as a scientist, I was still skeptical, and decided to do some digging.
Why was I skeptical? Because not all journals are created equal. Lay people know this to an extent. It’s much more prestigious to get into journals like Science and Nature because the peer review process is way more rigorous. Your research not only has to be pretty damn air tight, but it has to make a significant contribution to scientific knowledge. We can measure how good a journal is by a metric known as an “impact factor.” It’s complicated, but generally the higher the impact factor, the better the journal.
So let’s have a look at Burzynski’s research, shall we?
1. Burzynski, SR. Treatments for Astrocytic Tumors in Chiìdren: Current and Emerging Strategies. Pediatric Drugs 2006; 8: l67-178.
Pediatric Drugs: No impact factor.
Off to a great start! (Hint: That’s sarcasm)
2. Burzynski, S.R., Janicki, T.J., Weaver, RA., Burzynski, B. Targeted therapy with Antineoplastons A10 and of high grade, recurrent, and progressive breínstem gliome. Integrative Cancer Therapies 2006; 5(1):4047.
Integrative Cancer Therapies has an impact factor of 1.716. What does this number mean? Compared to other journals in the category of Integrative & Complementary Medicine, it’s ranked 6 out of 21. Not bad, but “Integrative medicine” sets off my Pseudoscience Alarms. Suspicions confirmed, the journal describes itself as emphasizing “scientific understanding of alternative medicine and traditional medicine therapies.”
To quote the brilliant Tim Minchin:
“By definition … alternative medicine … has either not been proved to work, or has been proved not to work. You know what they call alternative medicine that’s been proved to work? Medicine.”
What happens when you compare this journal in a more legitimate category, like Oncology? Its rank unsurprisingly drops to an abysmal 134 out of 185.
3. Burzynski, SR. Recent clinical trials in diffuse intrinsic brainstem glioma. Cancer Therapy 2007;5, 379-390.
When this journal’s website loaded, I started laughing and dragged my laptop to my fellow-scientist roommate. It looks like a relic from the 90s. Even more sketchy and unprofessional than the white-text-on-black-background and ugly use of frames is its repeated mentioning of its “rapid review process.” I couldn’t find out anything about the editorial board other than there’s some guy in Greece you should submit things to. And after a lot of digging, I couldn’t find an impact factor at all.
4. Burzynski, SR., Weaver, R.A., Janicki, T.J., Jufida, G.F., Szymkowskì, B,G., Kubove, E. Phase Il studies of Antineoplasîons A10 and AS 2-1 (ANP) in chiìdren with newly diagnosed diffuse, intrinsic brainstem gliornas. Neuro-Oncology 2007;9:206.
The final nine of his citations all seem to come from the Journal of Neuro-Oncology. Upon first glance, it seems legit. It has a relatively high impact factor of 5.483, which makes it 24 out of 184 in Oncology. Not bad at all, especially for a specialized oncology journal (the neuro part).
Not bad until you search the journal for articles by Burzynski. The result?
Burzynski has not published a single paper in this journal. Every single citation is an abstract from a presentation made at a conference. For those of you not in academia, we like to hold conferences where people can present their research and network. However, you’re allowed to present preliminary results that haven’t been published yet. Any scientist can submit abstracts in order to speak at conferences, and if that single paragraph sounds interesting, you get to give a talk. It’s pretty much impossible to judge how legitimate research is from an abstract (or presentation) alone, and some conferences are not competitive at all when it comes to who gets to speak – they have plenty of spaces to accept all presenters. Journals often act as archives for conferences they’re affiliated with, and will list those abstracts.
This means that none of Burzynski’s research from this journal has actually been peer-reviewed by the journal. The fact that he never actually published this data says a lot. Seriously – if you legitimately found something that helped cure cancer, prestigious journals would be tripping over themselves to have you publish in them. The fact that you can’t publish your research anywhere except in the occasional bottom-of-the-barrel shady journal means your research is terrible.
There was a final citation that stood out to me. It was the only citation that wasn’t research that Burzynski himself had done. Another key facet of science that makes it robust is that other scientists must be able to confirm your findings. And if they falsify your hypothesis, it’s back to the drawing board. So lets look at this one last citation:
11. Ogata, Y., Shirouzu, K., Matono, M., Ushìjima, M., Uchida, S., Tsuda, H. Randomized phase H study of hepatic arterial infusion with or without antíneoplastons as adjuvant therapy after hepatectomy for liver metastases from colorectal cancer. Ann Oncol 2010;21:víiî221 .
Again, this was a presentation made at a conference, specifically the 2010 European Society for Medical Oncology. Again, that means this research has not been peer-reviewed at all. In addition to the lack of non-Burzynski studies replicating his results, the National Cancer Institute also points out multiple studies (in legitimate journals) that are not able to replicate his results.
I would really like someone to take a look at the few papers Burzynski has published to see what the science looks like. One, I can’t access the couple of journal articles he actually does have because the journals are so crappy that my university doesn’t bother subscribing to them. But two, my area is population genetics and evolution, so I’m not really equipped to do an in-depth analysis of cancer research. But as a biologist I can safely remark on the quality of the journals his research was published in, and what that means.
So, Burzynski. Do you have any actual science to support your claims?
Why am I directing my ire at the Burzynski clinic? Any one of these reasons would be enough, but let’s go through the list, shall we?
1. Pseudoscience. The Burzynski clinic claims to be able to cure cancer with “antineoplaston therapy.” What’s that? Mainly a load of bunk (emphasis mine):
Some people promote antineoplaston therapy as a cancer treatment. But available scientific evidence does not support claims that antineoplaston therapy is effective in treating or preventing cancer. Antineoplaston therapy was developed by Dr. S. R. Burzynski in the 1970’s. He believes that antineoplastons are part of the body’s natural defence mechanisms against cancer and that people with cancer don’t have enough of them. At first, he took these compounds out of urine and blood. Now, it is possible to make them in the laboratory. There are several types of antineoplastons. They are known by the letter ‘A’ and a number such as A10, AS-25 and AS2-1.
Antineoplastons are taken either as a tablet or as an injection into the bloodstream.
There have been a number of phase 1 and 2 trials in different types of cancer. These early phase trials test what dose of treatment people should have, how safe the treatment is, and how well it works. Early trials only give the treatment to small numbers of people. Although Dr Burzynski’s own clinic have reported positive results for these trials, no other researchers have been able to show that this type of treatment helps to treat cancer. Other researchers have criticised the way the Burzynski Clinic trials have been carried out. Despite researching this type of treatment for over 35 years, no phase 3 trials have been carried out or reported. A randomised clinical trial is the only way to properly test whether any new drug or therapy works.
Are we clear? There’s no evidence that “antineoplaston therapy” cures cancer, despite decades of research. Moving on.
2. Unethical behavior. Despite this lack of evidence, the Burzynski clinic will happily give you their “treatment.” The newest example of this despicable behavior is with four-year old Billie Bainbridge, who has an inoperable brain tumor.
The Burzynski clinic is happy to “treat” her – for $200,000. Which was donated by random people and even some celebrities (including the bands Gorillaz and Radiohead), who had no idea that there’s no evidence that this treatment works. Exploiting sick children for your own profit is the lowest of low.
Quackometer puts it best on why this false hope is so terrible:
False hope takes away opportunities for families to be together and to prepare for the future, no matter how desperately sad that is. It may make the lives of those treated more unpleasant and scary. (Antineoplaston therapy is not without dangerous side-effects). It exploits the goodwill of others and enriches those that are either deluded, misguided or fraudulent. It may leave a tragedy-struck family in financial ruin afterwards. Giving false hope may be more about appeasing the guilt and helplessness of ourselves rather than an act of kindness to the sick.
3. Bullying. If you can’t back up your claims with scientific evidence, it seems like the next step is propaganda and bullying. Burzynski claims he’s some of “brave maverick doctor” who’s being persecuted by the scientific community. There’s a whole propaganda documentary supporting his clinic.
But now the clinic has turned to bullying bloggers who dare question the efficacy of his treatment. Marc Stephens, who represents the Burzynski clinic, has been sending deranged pseudo-legal rants to these bloggers, threatening to sue for libel. Andy Lewis of Quackometer had his family threatened:
“Be smart and considerate for your family and new child, and shut the article down..Immediately.”
If that wasn’t enough, Marc has aggressively gone after 17-year-old blogger Rhys Morgan, including a screen capture of a Google Maps satellite view of Rhys’s house in order to intimidate him.
If Burzynski really is a visionary, his research should speak for itself. Bullying and silencing is not how science is done, despite how highly you think of your ideas. The Texas State Medical Board is holding a hearing next April to revoke his medical license – not because he’s a rebel – but because he’s unethically exploiting sick people with his pseudoscience.
If you want to learn even more about “antineoplaston therapy” and Burzynski’s history, Dr. David Gorski has an excellent and lengthy summary over at Science Based Medicine. And if you want to show these bullies that silencing tactics do not work, spread the word far and wide. Let’s teach them about this little thing called the “Streisand Effect.”
Male deep-sea squid so rarely have another squid swim by, it’s too much of a risk to miss a female. Especially since it’s hard to tell male and female squid apart, especially when you’re at the bottom of the ocean. So they fling their little sperm packets out indiscriminately, sometimes hitting other male squid.
This reads like porno specifically tailored for PZ:
The way the squid mate is something else. Little is known about the details but it seems that the male ejaculates a packet of sperm at the mating partner, and the packet turns inside out, essentially shooting the sperm contained in a membrane into the flesh of the partner, where they stay embedded until the female (if the shooter has been lucky) is ready to fertilize its eggs. If males are the recipient of these rocket sperm, they are just stuck with them. It is the kind of mating that would make a good video game.
Obviously this is proof that male bisexuals are really just desperate and indiscriminately looking for sex. Duh.
Wait, what’s that?
[Dr. Hoving] fended off that notion, reiterating that the squid has no discernible sexual orientation, and that a tentacled invertebrate that shoots sperm into its mate’s flesh really has nothing to do with human behavior.
Panic that eating calamari makes you gay in 3…2…1…
Researchers followed 1.3 million middle-aged women in the United Kingdom for several years, and found the risk of cancer increased by about 16% for every 4 inches or 10 centimeters of increased height.
But the question remains, why?
According to Jane Green, a clinical epidemiologist at Oxford University and the lead author of the study, the tallest group – women 5 feet 9 or taller – were 37% more likely to develop cancer than the shortest group – women 5 feet and shorter- regardless of factors such as age, socioeconomic status, body-mass index and amount of physical activity.
There were 97,376 incidents of cancers reported among the women, and height related increases were greatest for the following: colon, malignant melanoma, breast, endometrial, kidney, central nervous system, non-Hodgkin lymphoma, and leukemia.
The study did not investigate what specifically about height led to the increased risk, but the research add to other studies that have found a link between cancer and height. The study authors aren’t sure what exactly increases the cancer risk, but they believe there are several theories that warrant more investigation.
For one, the authors propose that “taller people have more cells, and thus a greater opportunity for mutations leading to malignant transformation.”
Another possible culprit: Hormone levels resulting from insulin-like growth factors both in childhood and in adult life.“
Growth hormones increase cell growth and rate of division, and inhibit cell death,” Green explained in an email. “Both of these might be relevant to cancer either directly or perhaps just by increasing the number of cell divisions during which mutations can occur in the cell DNA.”
John: I thought that was because the cancer cloud hangs approximately 5 feet 10 inches off of the ground.
Well, add that to the List of Reasons Jen is Totally Going to Get Cancer, after family history, repeated terrible blistering sunburns, getting your first period before age 12, biology labwork, and hours of unintentionally inhaling lots of art supply fumes in confined spaces, and being alive.
The final top donor request (the rest didn’t request a topic):
“blog about this“
Since this is from a friend and not a stranger, I can safely say this: I hate you for making me read a scientific paper and review it during Blogathon. Hate. So much hate.
But you have my word, so I’ll do it. Onto the science!
A lot of people like to ask the question “What makes men gay?” It’s pretty clear it’s not a willy-nilly lifestyle choice, but scientists still aren’t really sure what the biology behind homosexuality actually is. Is it genetic? Hormonal?
Research on the latter is what a recent review article in the journal Frontiers in Neuroendocrinology summarized. You probably heard about the starting premise, since it received a lot of attention in the media. A study in 1996 found that gay men had a greater number of older brothers than heterosexual men. This is known as the “fraternal birth order” (FBO) effect, and has been replicated in many studies. It’s independent of potentially confounding variables like year of birth, age, socioeconomic status, and parental age. Non-biological siblings had no effect on sexual orientation.
The main hypothesis for why you see this pattern is known as the maternal immune hypothesis. Just like your body mounts an immune response against bacteria or ill-matched transplants, moms may develop an immune reaction against a male specific protein that’s present during development. Those proteins are normal for a male fetus, but a mother’s body still recognizes them as foreign. The immune response may then alter parts of the brain associated with male specific proteins like the anterior hypothalamus, which has also been linked to sexual orientation.
Recent research is finding more and more support for this hypothesis. One study showed that mothers of boys do develop an immune response to H-Y antigen, which is a protein expressed in the brain that is important in male fetal development. This immune response becomes stronger and stronger with each son a mother has.
This isn’t a totally crazy hypothesis. This exact thing happens in terms of blood type:
A medical model for a maternal immune response underlying the FBO effect is Hemolytic Disease of the Newborn (HDN). When a mother does not have the Rh factor in her blood (i.e., a mother is Rh negative), after gestating and giving birth to an Rh positive (Rh +) fetus, she may mount an immune response against the Rh factor. This immune response may affect subsequent Rh + fetuses, potentially attacking their red blood cells and causing anemia. The likelihood of an immune response becomes increasingly likely with each Rh + fetus a mother gestates.
There’s a problem though. H-Y antigen isn’t just produced in the brain – it’s also expressed in the gonads. Homosexual and heterosexual men don’t have any major difference in terms of gonads or fertility. Is there a way that the immune response would only effect H-Y proteins in the brain, but not in the gonads?
Possibly. Mice testes can develop without H-Y. And male gonads don’t reach maturity until puberty, so maybe a maternal immune response wouldn’t affect sperm too much.
The most compelling point is that there are three different forms of H-Y protein. It’s possible that the different forms are localized in different tissues, with only the one in the brain being targeted by the maternal immune response. However, there’s currently no information on where different forms of H-Y protein are localized.
Despite all of this evidence, this still doesn’t provide an actual mechanism. There’s a big gap between “increased immune response” to “homosexual behavior.” What are all of the steps in between? And is H-Y the only male specific protein that a maternal immune response targets? Probably not, but more research still needs to be done.
So do we definitively know what’s going on yet? Not quite. But feel free to slap homophobes with some science the next time you hear “lifestyle choice.”
And there goes all of the Blogathoon buffer time I had built up. Curses!
Adjacent pic is from a whiteboard in a student clubroom at the University of Helsinki, Faculty of Agriculture and Forestry (or, as we call it, “Wood & Weed Science”). Someone had drawn a crude chart of plant floral induction pathway and another(?) person had made some additions, including labeling “mRNA” as “missionary RNA”. I thought your readers might want to explain in comments what exactly is “missionary RNA” :)
Missionary RNA…I wonder what it does? Maybe this is the mechanism behind gene conversion *ba dum ching* (For the non-biologists, the correct label is “messenger RNA”)
Poop jokes: A universal staple in graduate student humor.
(By the way, almost all our student clubs are curriculum-related, but we’re still mostly not huge nerds. For example, the rest of the whiteboard featured a poop joke in Finnish.)
From a top donor:
“I’d like you to write a blog entry (primer) about neutral theory aimed at the layperson.”
Okay, I’m not going to lie. I’ve been secretly hoping someone would bump this question out of the top ten, mainly because neutral theory is kind of boring and vaguely confusing and hard enough to explain while using biology buzzwords. It’s even harder to explain when you only have 30 minutes to write about it and it’s supposed to be targeting non-biologists. When I shared this question with some fellow genetics grad students, the general response was “Ewwwww.”
But I will try my best!
When most people think about evolution, they think of adaptations. Something in the environment puts selective pressure on a certain trait, and organisms with that trait are more “fit” (reproduce more). For example, rabbits that live in snowy climates are more likely to survive (and reproduce) if they have white fur that helps them blend into the snow. If a mutation randomly arises that make their fur white, or just lighter, that rabbit has an advantage over the other rabbits – the dark brown ones are going to be the first ones that are eaten.
There are lots of examples of adaptive evolution through natural selection, and people know them more because they make good stories. The most famous example of evolution, Darwin’s finches, is a case of adaptive evolution.
But not all evolution takes place because of natural selection. Evolution is at its simplest defined as the change in allele frequencies over time. That’s where neutral theory comes in. Neutral theory states that most evolutionary changes are the result of random drift of neutral mutants.
Buzzwords buzzwords, I know. So let’s take it one step at a time and pretend that we’re looking at a population of unicorns (if we’re pretending, might as well pretend all the way).
Alleles are just two different forms of a gene. Genes are usually hundreds or thousands of basepairs long, but let’s pretend we’re zooming in on three bases in a gene for fur color. If you have the sequence AAA, your fur is white. But if you have AAG, your fur is pink. AAA and AAG are different alleles.
Now let’s say all of the unicorns start as AAA, and then from mutation you get a unicorn who’s AAG. Being pink has no effect on the unicorn. He’s not more likely to get eaten, he doesn’t live longer, he doesn’t have more luck with lady unicorns. It’s a “neutral” mutation because it doesn’t change the unicorn’s fitness.
That’s where random drift comes in. Drift simply refers to the frequency of one allele changing due to random chance. That is, nothing is selecting for pinkness. Maybe that unicorn just happened to have more offspring. Maybe the population underwent a bottleneck and was reduced to just a few unicorns, the pink one happened to survive, and now his pinkness will make up a larger percentage of the population. Maybe a couple of unicorns, including the pink one, happened to get isolated on one side of a river, so that side eventually had a lot of pink unicorns, while the other has a lot of white ones. Through random chance alone, a neutral mutation can grow to high frequency or even reach 100% (what biologists call “becoming fixed in a population.”)
When you get into the mathematics, you assume that random neutral mutations occur at the same rates across individuals. This is how biologists get things like “molecular clocks” where they can tell when two species diverged from each other.
…And I have no idea if that made any sense, but I’m out of time. You have all now been exposed to (a shoddy summary of) evolutionary theory, congratulations. If anyone would like to explain further or correct me in the comments, please do so!
This is post 20 of 49 of Blogathon. Pledge a donation to the Secular Student Alliance here.