Cutting-edge science and long-pondered questions explained in plain English. Bad science gutted. Great science extolled.

Thursday, December 28, 2006

A "Cloned Beef" Sandwich

Today, the FDA approved the sale of meat and milk from cloned animals for human consumption. Though it will be years before cloned animals begin showing up in the supermarket, already some people are freaking out that they might accidently eat cloned meat.

First, let’s discuss what cloned animals are and what they are not.

Cloned animals are the identical twin of an existing animal that was born at a later time. Stephen F. Sundlof, D.V.M., Ph.D., director of FDA's Center for Veterinary Medicine, said, "Based on FDA's analysis of hundreds of peer-reviewed publications and other studies on the health and food composition of clones and their offspring, the draft risk assessment has determined that meat and milk from clones and their offspring are as safe as food we eat every day. Cloning poses no unique risks to animal health when compared to other assisted reproductive technologies currently in use in U.S. agriculture."

Cloned animals are not genetically modified. They do not have bug, plant, or sea urchin genes inserted into their DNA. Genetically modified organisms (GMOs) are already in our food chain, though the only GMOs that we commonly eat are plants, such as corn with increased resistance to corn fungus. Clones are a perfect twin of the original animal, not mutants.

So, should you be concerned about eating clones?

First of all, no. It’s just an identical twin of a normal cow, pig, or goat. (Sheep have not been approved, a ironic omission considering “Dolly the Sheep” was the first successfully cloned animal.)

Second of all, cloning is a lot more expensive than artificial insemination and other reproductive technologies already in use. People are not going to clone animals to be sent directly to the slaughterhouse. They’re going to clone their best prize bull or their astonishingly productive dairy cow a couple times, and then those animals will be over-represented in the next generation of livestock.

That over-representation of genes in future generations, the homogenizing of animal herds, is the real threat that is implicit in the unrestricted cloning of livestock. It opens the door for the mammalian equivalent of monoculture and the loss of genetic diversity, what there is, in livestock. It increases the likelihood that an emerging pathogen could spawn an epizootic (an epidemic in an animal population) and could devastate livestock herds with no natural resistance and little variation in that lack of resistance.

That’s the real danger here: loss of genetic diversity.

TK Kenyon

Saturday, November 11, 2006

Why is Snot Slimy?

Each string of mucus in your nose is a long molecule. Each of these strings has a bunch of smaller molecules called “neuraminic acid”, stuck all over it. Neuraminic acid has a negative charge. When all those negative charges interact, they repel each other, like pushing the south poles of two magnets toward each other so that the magnet poles slip away from each other. The negative charges on the neuraminic acid on the mucus strings slip away from each other when they are forced together, and so mucus feels slippery, or slimy.

Here’s another question; why does mucous have those neuraminic acids on it?

Neuraminic acid is a molecule is also on the surface (cell membrane) of your lung cells. The influenza virus (the flu virus, the coughing kind of flu, not the stomach flu,) attaches to neuraminic acid so it can infect your lung cells. Then, the virus slips inside your cells and shanghais your cells’ machines (enzymes and ribosomes) to make lots more flu viruses, until there are so many viruses that the cell explodes. Then those viruses infect other lung cells, and so on, and so on, and so on.

But mucus in your nose also has neuraminic acids all up and down it. Think of mucus as a long string of decoys to fool the flu virus. When a flu virus enters your nose, it latches onto the first thing it finds with a neuraminic acid on it, mucus. Then, you have the chance to get the mucus out of your nose, so the virus won’t infect you. Pretty neat defense, huh?

But the virus has a way around that defense.

The flu virus has an enzyme (a protein that does a job), called neuraminidase, which cuts its bond with the neuraminic acid if the virus can’t find a cell underneath the neuraminic acid. So, if you don’t blow your nose, the virus can cut itself free of the mucus, float into your lungs, and give you the flu.

Take home message: Blow your nose and wash your hands after you’ve been around someone who is sick.

Thursday, October 26, 2006

Sometimes, Grey's Anatomy Makes Me Crazy

You know, I like Grey’s Anatomy. It’s an interesting show with some astonishingly good writing about character and complex issues, not to mention some lovely, funny zingers. However, I’m getting a little tired of them screwing up the science and the medicine in service to the story.

On last night’s rerun on the season opener of Grey’s Anatomy, McDreamy and Whats-his-face are quarantined in the locker room because they might have been exposed to the Bubonic Plague. This is unrealistic for a variety of reasons.

First, Bubonic Plague is only moderately transmissible. Rather than having the index case (patient) present with enlarged lymph nodes (buboes,) they should have given him Pneumonic Plague, which is spread by aerosolized droplets by coughing or sneezing. That’s much scarier.

Second, the plague’s etiologic agent is a bacteria, specifically, by Yersinia pestis, a gram-negative rod-shaped bacteria. It can be easily cured by an antibiotic. They wouldn’t have quarantined them; they would have prescribed a broad-spectrum antibiotic like Zithromax (azithromycin, also “Z-Pac,”) or Gentamycin. There was no reason to lock them in a little room until unspecified “tests” were performed to clear them, except for storyline reasons.

Even better: monkeypox, a zoonosis that is a monkey analog of smallpox, which has been rarely transmitted between humans. Or Ebola. Because viruses can’t be cured by antibiotics, they’re much scarier.

Wednesday, October 25, 2006

Films And Books Magazine Interviews TK Kenyon has posted an interview in which I discuss the religion and science in RABID, my forthcoming novel. It's pretty controversial stuff, and they did an excellent job of making it clear. Thanks to!'s interview with TK Kenyon:

Tuesday, October 24, 2006

TK Kenyon's novel RABID to be reviewed by
Publisher's Weekly and Kirkus Reviews

My forthcoming novel RABID will be reviewed by Publisher's Weekly on November 1st and Kirkus Reviews on November 15th. I thank these two prestigious journals for noticing RABID.

RABID is the next evolution of the religious thriller novel, where science and the Church clash, and nothing is sacred. Read more at TK Kenyon's website.

TK Kenyon

Monday, October 23, 2006

The Spectrum of Autism Research: From Brilliant to Just Plain Stupid

This week, several research papers on autism spectrum disorders were published by press conference, a practice universally acknowledged as hiding one’s research.

One was a brilliant but extremely short paper pre-published in the prestigious Proceedings of the National Academy of Sciences (PNAS) by a team of molecular biologists researching genes associated with autism spectrum disorders. This paper may very well explain why some people are predisposed to developing autism, and the gene in question (MET, a tyrosine kinase receptor) explains the range of neurological, behavioral, and digestive symptoms associated with autism spectrum disorders. It’s a lovely piece of science. More on this paper below.

The other paper was produced by a triumvirate of rogue economists who tried to apply economic statistical theory to autism, a subtle biological condition, and made some of the most astoundingly stupid conclusions that I’ve ever seen. Because they did no empirical science (despite their claims in their paper, which I read, all 67 pages of it,) none of their findings can be disproved in the scientific sense of the word. These three men (Michael Waldman and Sean Nicholson of Cornell, and Nodir Adilov of Indiana University) wound through an amazingly vapid intellectual argument to arrive at what might be the exactly wrong conclusion.

Here’s what those idiots did: they selected a few counties (in California, Oregon, and Washington,) and looked at precipitation records for those areas between 1972 and 1989. That’s right, rain. They found that autism rates incrementally increased more in rainy counties than in less rainy counties.

They then inquired about cable television subscription rates in these counties and found that cable television subscription rates also increased, an astounding finding that one could have figured out by being alive and conscious. In a later test involving counties in California and Pennsylvania, they correlate those areas with the most cable TV subscriptions to county autism rates.

So, they blamed the increase on autism on increased TV viewing.

Here’s only a few of the problems with that data:

Autism rates increased substantially during the time period studied. If the authors had used any increasing variable, they would have found the same correlation.

The Dow Jones Industrial Index increased from 900 to 2300 in that time period, which positively correlates with the rise of autism rates.

The per capita income in the U.S. grew from around $15,000 to $23,000 in that time period. Autism thus correlates with increased income.

Childhood obesity increased from around 7% to about 11% in the same time period.

The feral and domestic cat population in the U.S. doubled from 30 million in 1970 to 60 million in 1990, which positively correlates with the increase in autism diagnoses.

In 1970, only 24% of mothers with children under the age of two worked even part-time. In 1984, that number had nearly doubled to 46.8%. Today, 55% of women with children under one year old work full-time. Consider that statistic. Now consider this line of reasoning:

In 1970, there were very few two-income families. Increase in working women correlates to an increase in two-income families. Two-income families can better afford to subscribe to cable television, which explains the increase in cable TV rates.

However, when women work, they do not stay home with their tots and watch TV. The tot goes to daycare, where most of the time the tot is engaged in structured play and activities, not television watching. Thus, TV-watching by tots may have decreased during the time that autism rates increased, suggesting that TV has a protective effect on autism.

That line of reasoning is every bit as well supported as the line of reasoning in the Cornell-Purdue paper. What’s more, it incorporates data that the three men never thought of: whether or not the televisions were actually watched.

In addition, the three men who wrote this article fail to account for excellent research that shows that the neurological damage associated with autism begins before birth. Their conclusions actually should state that pregnant women watching television causes autism.

This paper is an excellent example of non-scientists (they’re all economists!) trying to apply non-scientific principles (economic statistics) to science and then even forgetting to apply their own rules. Rarely in economics does one find monocausal patterns. There is almost never one cause that produces one effect. This specious attempt to blame autism on television viewing by infants is an example of using the wrong tools and doing the job badly.

The molecular biology paper, on the other hand, produced by Daniel B. Campbell, James S. Sutcliffe, Philip J. Ebert, Roberto Militerni, Carmela Bravaccio, Simona Trillo, Maurizio Elia, Cindy Schneider, Raun Melmed, Roberto Sacco, Antonio M. Persico, and Pat Levitt, is a exquisite piece of statistical modeling that explains nicely why some people are more prone to developing autism spectrum disorders. The candidate gene, MET, is a tyrosine kinase receptor, which means that it is a telephone for conducting signals inside a cell, and MET signaling can result in the cell reproducing, changing, or dying. MET participates in brain growth and maturation, immune function, and repair of the digestive system. Children with autism often have symptoms of disturbances in some or all of these systems. This research ties together these disparate symptoms and explains why children with neurological symptoms often have diarrhea or immunological problems.

There are two common alleles (forms of the gene) for the MET gene. In this case, the change in the gene results in more or less of the protein (and thus the tyrosine kinase receptor) being produced in the cells. Remember that each person has two copies of a gene (one from your mom and one from your dad,) so you have two flips of the proverbial gene coin.

The C allele is associated with an increased risk for autism. The C allele makes less of the MET protein. In this case, less is bad.

The G allele is protective against autism. The G allele means that more MET tyrosine kinase receptor protein is made and thus there is more met signaling.

The relative risk of being diagnosed with autism was 2.27 times higher if you have two copies of the C allele (the CC genotype) and 1.67 times higher if you have one of each allele (the CG genotype, heterozygous) compared with having two of the protective G alleles (the GG homozygous genotype).

There you have it: an excellent autism paper and piece of scientific-sounding poop. I desperately hope that people won’t go bonkers over restricting television viewing for their kids because they believe that, otherwise, the kids will get autism. There are a lot of reasons to moderate television viewing, but fear of autism isn’t one of them.

I also hope that parents of autistic kids won’t beat themselves up over their television viewing because they erroneously think that they caused their kids’ autism. That statistics paper should only be used for potty training.