In an Atlantic essay called "The Science of Success," David Dobbs writes about two types of children: "orchids" and "dandelions." Dandelion children tend to do pretty well no matter what environment they grow up in. Orchid children, meanwhile, may develop behavior or mood problems in abusive or neglectful homes — but in loving ones, they may thrive even more than dandelions. And according to new research, the difference between dandelions and orchids may be genetic. For instance, kids with a certain variant of a dopamine-processing gene are at greater risk of ADHD and "externalizing behavior" (i.e. "acting out") than other children. But in one study, these kids also improved much more in response to a video-based behavioral intervention than did kids who didn't have the at-risk variant. Similarly, rhesus monkeys with another gene variant (one associated with depression in humans) are worse at processing serotonin than their peers if they are raised as orphans. But when raised by a loving monkey mother, these seemingly at-risk animals process serotonin more efficiently than other monkeys, and are also more socially successful. These and other studies suggest that certain genes confer not risk per se, but a kind of openness to environmental stimuli, positive or negative. Dobbs writes,

At first glance, this idea, which I'll call the orchid hypothesis, may seem a simple amendment to the vulnerability hypothesis. It merely adds that environment and experience can steer a person up instead of down. Yet it's actually a completely new way to think about genetics and human behavior. Risk becomes possibility; vulnerability becomes plasticity and responsiveness. It's one of those simple ideas with big, spreading implications. Gene variants generally considered misfortunes (poor Jim, he got the "bad" gene) can instead now be understood as highly leveraged evolutionary bets, with both high risks and high potential rewards: gambles that help create a diversified-portfolio approach to survival, with selection favoring parents who happen to invest in both dandelions and orchids.

Dobbs spends a lot of time talking about the population-level implications of this new idea. He points out "that a genetic trait tremendously maladaptive in one situation can prove highly adaptive in another" and that "every society needs some individuals who are more aggressive, restless, stubborn, submissive, social, hyperactive, flexible, solitary, anxious, introspective, vigilant-and even more morose, irritable, or outright violent-than the norm." If the orchid hypothesis is true, then perhaps a certain number of people who react extremely strongly to their environment, even if these reactions seem negative to our modern eyes, may be important to the flexibility and survival of our species. But what I found most interesting about Dobbs's piece was its implications for the individual. Dobbs writes of his decision to get tested for a gene variant that increases depression risk but may also confer orchid-like properties. A depression sufferer himself, he turned out to have the variant. Dobbs writes,

[A]s I sat absorbing this information, the chill came to seem less the coldness of fear than a shiver of abrupt and inverted self-knowledge-of suddenly knowing with certainty something I had long suspected, and finding that it meant something other than I thought it would. The orchid hypothesis suggested that this particular allele, the rarest and riskiest of the serotonin-transporter gene's three variants, made me not just more vulnerable but more plastic. And that new way of thinking changed things. I felt no sense that I carried a handicap that would render my efforts futile should I again face deep trouble. In fact, I felt a heightened sense of agency. Anything and everything I did to improve my own environment and experience-every intervention I ran on myself, as it were-would have a magnified effect. In that light, my short/short allele now seems to me less like a trapdoor through which I might fall than like a springboard-slippery and somewhat fragile, perhaps, but a springboard all the same.

In this early age of genetic testing, it's easy to think of genes simplistically — and since most testing is still meant to predict disease, our genotypes sometimes begin to seem like maps full of danger signs. But human beings (and monkeys, too) are extraordinarily complicated, and what seems like a risk may also be a blessing. We still tend to see depression, anxiety, ADHD, and other mood and behavioral abnormalities as defects — if a child is "at risk" for one of these, she needs to be protected as though from a gathering storm. Yet to be at risk may also be to have a unique opportunity.

If the orchid hypothesis is true, then people like Dobbs may possess a plasticity that makes them more vulnerable to sorrow and yet also more capable of change. This would have enormous implications for those suffering from certain mental ailments. Perhaps along with their difficulties, their genes have granted them a tool for solving them — and beyond that, for reaching new heights of personal fulfillment. It would also have an impact on how we raise and teach kids. Some have already speculated that children with ADHD need something different from the one-size-fits-all American educational model. If it's true that some kids are uniquely influenced by environment, then maybe what we need is not to try to make them more like other kids — the current approach — but rather to construct the environment that will best help them thrive. This is likely to be difficult, and expensive, and for these reasons it may not catch on. But we might have much to gain, both as individuals and as a society, by seeing a springboard where we once saw a trapdoor.

The Science Of Success [Atlantic]

If you've ever read a word I've written, you've already guessed that I come down on the side of the second argument. Which is basically this, in the words of Jeffrey Friedman, who wrote the op-ed:

The heritability of obesity — a measure of how much obesity is due to genes versus other factors — is about the same as the heritability of height. It's even greater than that for many conditions that people accept as having a genetic basis, including heart disease, breast cancer, and schizophrenia. As nutrition has improved over the past 200 years, Americans have gotten much taller on average, but it is still the genes that determine who is tall or short today. The same is true for weight. Although our high-calorie, sedentary lifestyle contributes to the approximately 10-pound average weight gain of Americans compared to the recent past, some people are more severely affected by this lifestyle than others. That's because they have inherited genes that increase their predisposition for accumulating body fat. Our modern lifestyle is thus a necessary, but not a sufficient, condition for the high prevalence of obesity in our population.

But Friedman had already pissed me off before he even got to that. In an apparent effort to prove that he's a Serious Person and not just some delusional fatass with an axe to grind (hi!), he acknowledges that obesity is a risk factor for a bunch of diseases, claiming it has "consequences that include diabetes, heart disease, and cancer, and that cause nearly 300,000 deaths in the United States each year."

Y'ALL, THE 300,000 DEATHS THING WAS DEBUNKED IN 2005. By the CDC, not delusional fatties with axes to grind. Same folks who came up with the original stat, in fact. They just fucked up the first time:

According to the [second] study, obesity and extreme obesity cause about 112,000 deaths per year, but being overweight was found to prevent about 86,000 deaths annually. Based on those figures, the net U.S. death toll from excess weight is 26,000 per year. By contrast, researchers found that being underweight results in 34,000 deaths per year.

Emphasis added.

Seeing that error — four years after that crucial revision came out — automatically makes me think I can't take the person talking seriously. Which sucks, because in this particular debate, Friedman is, generally speaking, the one dealing in reality.

Ken Thorpe and Christine Ferguson, on the other hand, get it wrong from the headline: "We Have the Power to Change Our Weight" (And no, they probably didn't write the headline, but they wrote the op-ed that made that a logical summary.) Sure, most of us have the power to change our weight, temporarily. I was a champion dieter for a while there, losing 65 lbs. the first time I got serious about it, and 45 lbs. the second time. Haters will go to their graves believing that's because I gave up, both times, and started mainlining powdered sugar delivered to me via an elaborate pulley system constructed so I'd never have to leave the couch, but those who have even a passing interest in facts might consider looking at the research on long-term weight loss. Such as the 2007 UCLA study (PDF), in which researchers reviewed 31 earlier studies and concluded that on the whole:

[D]ieters were not able to maintain their weight losses in the long term, and there was not consistent evidence that the diets resulted in significant improvements in their health. In the few cases in which health benefits were shown, it could not be demonstrated that they resulted from dieting, rather than exercise, medication use, or other lifestyle changes. It appears that dieters who manage to sustain a weight loss are the rare exception, rather than the rule. Dieters who gain back more weight than they lost may very well be the norm, rather than an unlucky minority."

The part about not being able to identify which variables actually produced the (few demonstrated) health benefits is crucial. Thorpe and Ferguson write, "We know that as little as a 5 to 10 percent weight loss can significantly reduce risk factors for chronic disease, including lower blood-glucose levels, lower blood pressure, and reduced cholesterol levels," but they don't question how those studies proved it was the weight loss itself, as opposed to the lifestyle interventions that elicited it. In fact, other research suggests that a Health at Every Size approach — focusing on intuitive eating, exercise and (wonder of wonders) self-acceptance, all without regard to weight loss — delivers better health outcomes than dieting. No one disputes that a steady diet of junk food and a sedentary lifestyle are bad for your health. But A) Many fat people can and do eat balanced diets and exercise just as much as thin people without losing weight — that's where the whole genetic thing comes in — and B) plenty of thin people suffer from health issues related to lifestyle choices, but the default assumption is that they're "taking care of themselves" because they don't happen to have fat genes. Eating a balanced diet and exercising can be beneficial for all of us, but they will not cause permanent weight loss in most of us — and there's no real proof that we'd be markedly better off if they did. (Even if being thinner is theoretically advantageous — and again, "overweight" people win the longevity game — we must keep in mind that a fat person who's lost weight is not the same thing as a person who's always been thin.)

Friedman gets this mostly right:

There is no evidence that obese individuals need to "normalize" their weight to reap health benefits. In fact, it is not even clear whether there are enduring health benefits to weight loss among obese individuals who do not suffer from diabetes, heart disease, hypertension, or liver disease.

But then, once again, he blows it, basically reiterating Thorpe and Ferguson's point about losing 5-10% of your weight:

What is known is that the obese who do suffer from these conditions receive a disproportionately large benefit from even modest weight loss, which together with exercise and a heart-healthy diet can go a long way toward improving health.

Apart from what I've already said about the variables involved in weight loss and the fact that permanent weight loss is a pipe dream for all but a few statistical outliers, here's the obvious question about the "just lose 5-10%" thing: What happens when I do that and am still fat? Losing 10% of my weight (+/- 19 lbs.*) would leave me squarely in the obese category, not improving their statistics one little bit — so even if my health improved, would anyone actually quit bitching about the "obesity crisis"? Oh, but wait — enough people are on the cusp of BMI categories that if we all lost 5-10% of our weight, we'd see a dramatic drop in "obesity" and "overweight" population-wide, at which point we could all congratulate ourselves on no longer being a nation of embarrassing fatties who are going to die younger than our parents, even though individual losses would generally be quite small. The important thing is, on paper, that would look fantastic. At least until everyone gained it back.

Thorpe and Ferguson argue for many of the public health interventions I addressed in an inexplicably controversial post last week, and as always, I'm in favor of several of them, e.g., "lowering copays on preventive care... reinstating physical education and requiring school lunches to meet nutritional standards... ensuring that all Americans have access to a place to be physically active and purchase healthy foods." What I'm not in favor of are undefined "programs to help overweight Americans" (unless they mean programs to help us overcome the ill effects of relentless fat-hatred, see above about diets not working) and "tax credits to employers that offer wellness benefits and encourage health inside and outside of the workplace" — which sound fairly unobjectionable until you consider that this is what leads to demeaning "Biggest Loser" competitions at the office, employers badgering their workers to join specific commercial weight loss programs, and hysteria about a plate of cupcakes in the break room. If we're talking about tax credits for offering employees free or discounted gym memberships — and then leaving them the hell alone to work out as they please, or not — then great, have at it. But that's never all we're talking about. We're talking about diet culture invading the workplace even more than it already has, and a whole new layer of shame for fat people who aren't interested in joining Weight Watchers — probably because they've already been on it multiple times, and gained back everything they lost.

"[T]o win the fight against obesity," Thorpe and Ferguson write, "all of us need to be individually committed." Really? All of us? What role do people who aren't fat play in this, exactly? If you mean they need to be constantly reminding fat people that we're disgusting, unlovable, smelly, lazy, undisciplined, and above all, unhealtheeeeeee, then as a whole, they're doing a bang-up job already. (This does not, of course, apply to all thin people. Some of my best friends are thin!) So I'm pretty sure what you mean is "Fat people need to be individually committed" to fighting their own bodies. To which I'd point out: Most of us already are. Who the fuck do you think is keeping the $50 billion dollar weight loss industry afloat? Magic sprites?

Oh, and about that. You know that population-wide weight gain that happened in the last 30 years? (Friedman says the average is about 10 lbs.; I've heard anywhere from 7 to 20). Check out that last sentence from the UCLA researchers I quoted above: "Dieters who gain back more weight than they lost may very well be the norm, rather than an unlucky minority." Not only does dieting not work, but a lot of times it makes you fatter. And the weight loss industry has been growing right along with our asses all that time. Is that the only reason for the gain over that period? I have no idea, probably not. But it's something obesity alarmists never, ever factor in, even though common sense suggests somebody really ought to explore that correlation.

If you're a regular reader of mine and you feel like you've heard everything in this post a million, billion times, you have my apologies. I am so sick of making these arguments, I cannot even tell you. Unfortunately, people can't even get it through their heads that diets don't work — despite both a mountain of scientific evidence to that effect and a friggin' "results not typical" disclaimer on every ad — let alone that it is possible to be fat and healthy, that it is equally possible to be thin and unhealthy, that correlation does not equal causation, that there is strong evidence that obesity is highly heritable, that calories in/calories out is a ludicrously simplistic equation unless you think human beings are Bunsen burners, and that, above all, fat people are human beings. Which means we can hear you. And our continued fatness is not a personal attack on you or our country or our healthcare system, but the result of complex factors science is only beginning to understand, and in very many cases, something we have already tried our damnedest to change.

Or, as Friedman puts it:

While research into the biologic system that controls weight is moving toward the development of effective therapies for obesity, we are not there yet. In the meantime we must change our attitudes toward the obese and focus less on appearance and more on health. In their efforts to lose weight they are fighting against their biology. But they also are fighting against a society that wrongly believes that obesity is a personal failing.

I've stopped fighting against my biology, but I am still fighting against that society every goddamned day. And I don't just mean the trolls who swing by to tell me things like,

My fear that a woman with the legal power to take half of my possessions might some day become so fat and sexually unappealing that I'd sooner cut my own penis off than have sex with the manatee that used to be my wife is unfortunately all too common and blogs like this one that dangerously suggest to naive future fatties that it's ok are only leading your victims down the primrose path to a battle they can't win."

Or:

I personally dislike most fat people for their lack of will power or mental strength. If fat people would just have a strong mental will power, then they would either be able to deal with the jokes, or become skinny by actually sticking to their dieting and exercise plan without giving up.

Or:

FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS FATTIES ARE GROSS

(I truncated that one. By a lot.)

It's not just those shitheads, who are incredibly easy to dismiss. I'm talking about the people who swear they are really only concerned for my health, without ever having heard of Health at Every Size. The people who write screeds on how much obesity (theoretically) costs our healthcare system, and exhort individuals to fix that problem, without acknowledging that pile of research showing permanent weight loss is virtually impossible. I'm talking about the people who try to sell good ideas for improving public health as cures for childhood obesity, making fat kids feel like enemies of their entire communities, and yet not making them noticeably thinner. I'm talking even about people like Friedman, who are starting to get the message about the basic intractability of fat — and kudos to him for spreading it — but still repeat debunked, alarmist statistics in an effort to boost their own credibility before daring to suggest that fat people might not be a bunch of lazy slobs. I'm talking about everyone who's ever said, "I don't think we should treat fat people badly, but..."

Because that right there? Is treating fat people badly. It's still treating us as a problem to be solved, not as human beings.

To win the fight against fat hatred and discrimination, we all must be individually committed.

*I've said many times that I weigh around 200 lbs., though I haven't weighed myself since I jumped on a dog scale at the vet's office to prove a point 2 years ago. I weighed 185 then, after which I gained a pants size, which probably represents 10-15 lbs. But as it happens, I have recently dropped a pants size, so am probably somewhere around 190. Yes, the Queen of the Fat-o-Sphere has lost weight! And because I love you, I will share the secret of how I did it: I went off the pill.

The Real Cause of Obesity [Newsweek]
We Have the Power to Change Our Weight[Newsweek]

Not exactly. By comparing the DNA of echidnas and platypi (obviously the coolest part of the experiment was just looking at these Aussie critters) with that of other animals, scientists determined that the Y chromosome was evolving much faster than all the others. That means it is shedding genes at a faster rate. All this hard living by the Y chromosome began when it split from the X (a sort of DNA midlife crisis?), and can only end in tears. National Science Foundation Graduate Research Fellow Melissa Wilson says,

Today, the human Y chromosome contains less than 200 genes, while the human X chromosome contains around 1,100 genes. We know that a few of the genes on the Y chromosome are important, such as the ones involved in the formation of sperm, but we also know that most of the genes were not important for survival because they were lost, which led to the very different numbers of genes we observe between the once-identical X and Y. Although there is evidence that the Y chromosome is still degrading, some of the surviving genes on the Y chromosome may be essential, which can be inferred because these genes have been maintained for so long.

But watch out! Those magical sperminating gene may be on the way out too. According to study leader Kateryna Makova, "Even though some of the genes appear to be important, we still think there is a chance that the Y chromosome eventually could disappear." Will this lead to a Sapphic universe devoid of males? Nope, says Makova: "If this happens, it won't be the end of males. Instead, a new pair of non-sex chromosomes likely will start on the path to becoming sex chromosomes." So dudes are safe, but in a million years or so, lame trend pieces will have a different chromosome to blame for why men can't ask for directions. Then again, we'll probably be robots by then anyway.

Image via exitmundi.

Male Sex Chromosome Losing Genes By Rapid Evolution, Study Reveals [EurekAlert]

The blog Hit & Run quotes h+ magazine, as follows:

A January 2009 study by researchers at NYU Langone Medical Center found that an overwhelming 75% of parents would be in favor of trait selection using PGD [pre-implantation genetic diagnosis] – as long as that trait is the absence of mental retardation. A further 54% would screen their embryos for deafness, 56% for blindness, 52% for a propensity to heart disease, and 51% for a propensity to cancer. Only 10% would be willing to select embryos for better athletic ability, and 12.6% would select for greater intelligence. 52.2% of respondents said that there were no conditions for which genetic testing should never be offered, indicating widespread support for [pre-implantation genetic diagnosis]-as long as it's for averting disease and not engineering human enhancement.

Despite these figures, the Fertility Institutes announced in February that it would start allowing parents to choose their babies' hair and eye color. Institutes director Jeff Steinberg said, "I would not say this is a dangerous road. It's an uncharted road." h+ quotes a few advocates of Steinberg's position, including George Dvorsky, who says, "What we're talking about here is endowing our children with all the tools we can give them so that they may live an enriched, open-ended and fulfilling life. By denying them these benefits we are closing doors and potentially reducing the quality of their lives." Most people, though, seem to agree with geneticist William Kearns, who says, "My goal is to screen embryos to help couples have healthy babies free of genetic diseases. Traits are not diseases."

But is the distinction so easy to maintain? What about something like autism, which some advocates say is more trait than disease? It seems cruel to deny parents the right to prevent serious illnesses in their children, but we do need to codify what constitutes a serious illness — and we need to consider the fact that pre-implantation genetic diagnosis, as a component of in vitro fertilization, is currently only available to those with money. What will happen to research into treatments for genetic diseases if these diseases become exclusively a problem of the poor? These are all important issues, which Katherine Mangu-Ward of Hit & Run chooses to wrap up with these lines:

Of course, people are also getting used to selecting traits like eye color on their Miis. It's only a matter of time before they come around on doing the same for flesh and blood babies.

Thanks for the insight! I'm off to get myself implanted with a two-dimensional child with a huge head and spherical hands. (I'm making his shirt green!)

Let's Make A Baby [Hit & Run]
The Great Designer Baby Controversy Of '09 [h+]

Researchers at the University of Parana, Brazil, studied 90 married couples' DNA and compared them to 152 randomly-generated control couples, EurekAlert explains. They looked for differences in couples' major histocompatibility complex (MHC), a genetic region found in most vertebrates that is related to the immune system. After comparing the couples MHC dissimilarities, scientists found that there were greater differences in the real couples than the virtual couples. "If MHC genes did not influence mate selection," said Professor Maria da Graca Bicalho, "we would have expected to see similar results from both sets of couples. But we found that the real partners had significantly more MHC dissimilarities than we could have expected to find simply by chance."

Other studies have shown that in humans and other vertebrates females prefer mates with dissimilar MHC. The genetic region is known to influence mating selection by creating a preference for certain body odors, like those found in sweat. Other research suggests that face structure may be influenced by MHC as well.

Scientists believe their findings, which were presented yesterday at the European Society of Human Genetics, reveal an evolutionary strategy to produce healthy offspring. According to the Telegraph people with more MHC variations in their immune system can recognize and cope with infections more easily. It may also be related to the evolutionary impulse to avoid incest. Previous studies have shown that couples with similar MHC genes had longer intervals between births, which may mean that they suffered undetected early miscarriages.

Professor Bicalho said that while people like to think that they chose their partner based on their similarities, "our research has shown clearly that it is differences that make for successful reproduction, and that the subconscious drive to have healthy children is important when choosing a mate."

Another scientist who conducted similar research on human leukocyte antigens, which also influence the immune system, turned her findings into a dating service that matches people based on their DNA. The Times of London reports that last fall Croatian geneticist Dr. Tamara Brown created GenePartner, a dating service that matches couples by analyzing their DNA samples. Brown says that people can't be matched solely on their genetic compatibility, but a good biological match means a greater likelihood of "forming an enduring and successful relationship; having a satisfying sex life; higher fertility rates and healthier children."

Opposites Attract — How Genetics Influences Humans To Choose Their Mates [EurekAlert]
Sexual Chemistry Found In Genes Causes 'Opposites To Attract' [The Telegraph]
DNA Dating: Has Science Unlocked The Secret Of A Perfect Match? [The Times of London]

Prasad argues that a virgin could give birth to a child, but no woman could produce a boy without the donation of a Y chromosome. In order for Mary to have given birth to Jesus, she would have had to have a condition called testicular feminisation, which would make her genetically male, but with the genitals of a woman. Unlike pythons, hammerhead sharks, and Komodo dragons, there has never been a documented example of a virgin birth in humans.

Virgin Conception Would Be More Plausible If Mary Was A Man [Guardian]

According to the Journal, "Parker survived and is now 20 months old. He has poor language and motor skills and may never walk. Already hospitalized three times, Parker's medical odyssey has stretched the Cardens' finances and put a huge strain on their relationship." It got to the point where the Cardens had to get help from their parents to buy groceries for their family, which included three other children in addition to Parker.

A piece in the Washington Post outlines the pros and cons of increasingly advanced fetal DNA testing. Proponents of the test, which "use 'gene chips' to detect much subtler chromosomal variations than standard prenatal testing can," like Baylor's Arthur L. Beaudet, argue that for people who want maximum information, they deserve to know. "Some of these disorders are quite burdensome. They require lifelong nursing care. In some cases these children never walk, never talk, never feed themselves," Beaudet tells the Washington Post. "It can have a major impact on the family. People say, 'I wish you had given me the opportunity to know ahead of time. It's really destroyed our lives.' That's why women want to know."

Opponents say that not only is the test not accurate enough, but that its use could lead to eugenics. "The question is, what is the information used for?" David Prentice of the pro-life Family Research Council asks the Post. "If it's for informing the parents so they can be prepared for what might come, that's great. But if it's being used for eugenics purposes — for abortion — we would be against it." Where I think this could add a new wrinkle in the abortion debate is that perhaps some pro-choicers will believe that aborting a special needs child is morally wrong. This is pure speculation based on anecdotal evidence, but possibly it hews too close to eugenics for some, even considering the dire emotional and fiscal costs to the family involved.

But let's get back to Trig, the public face of special needs. Unfortunately, his mother, for all her purported caring about other children with Down syndrome, does not support the raising of taxes to fund special needs programs. She came out against Colorado's Prop 51, which according to the Guardian, "would provide thousands of children and adults with autism, Down's syndrome, cerebral palsy and other disabilities with critically needed care, through a phased-in sales tax of 0.2%." The proposition has been championed by a McCain/Palin supporter, former Colorado first lady Frances Owens. Palin is against the ballot measure because, "There's got to be an alternative to raising taxes. It's a matter of prioritizing the dollars that are already there in government. What I did as governor of the state of Alaska was prioritize for a great increase in funding for our students with special needs up there. And I think that Colorado can do that also."

But, as the Guardian points out, "It's hard to see how this could become a reality. McCain has sworn to an immediate government spending freeze. And Palin, in Colorado Springs, promised to cut taxes and balance the budget in one year. If past experience is any guide, all that means is cutting programmes affecting children with special needs." Again, as with Bristol's pregnancy, and the Alaska Governor's history of non-support for pregnant teens, it seems that the only children Palin cares about supporting are her own.

The Toughest Test [WSJ]
Fresh Hopes And Concerns As Fetal DNA Tests Advance [Washington Post]
Special Needs And Conservative Creeds [Guardian]

Earlier: Ask Not What Bristol Palin Can Do For You, Ask What Sarah Palin Can Do For Your Pregnant Daughter

Men with the gene, which, as the Washington Post notes, regulates the hormone vasopressin, are more likely to live with women without marrying them; if they are married, these men are more likely to fight with their spouses and consider divorce. Their female partners (the study only looked at heterosexual couples) also "reported lower levels of satisfaction, affection, cohesion and consensus in the relationship" than partners of men without the variant.

"No one is saying biology is destiny," says anthropologist Helen Fisher, who studies romantic love. She might marry a man with the "love-rat gene" — "but," she says, "I might not start a joint bank account with them for the first few years."

Kidding aside, this study looks at first glance like another great way to reduce human relationships to biological imperatives. As if comparisons between men and male animals weren't popular enough, the Post cites an earlier study in which the same gene variant was found in mountain voles, who are apparently more caddish than their prairie cousins. (Interestingly, Ayelet Waldman got the jump on this years ago, calling her faithful husband Michael Chabon a "prairie vole.")

People seem to find it comforting to believe that their behavior is predetermined. Fisher says a man with the variant "might be able to use the knowledge to ignore tugs of restlessness he might feel in his marriage: "You can say, 'Oh, it is just my DNA, and I am going to ignore it.'" Certainly better than the alternative — "oh, it is just my DNA, and I can't do anything about it" — but still kind of disturbing. The danger in putting too much stock in this kind of research is that we'll use it as yet another proxy for actual communication in relationships. In the last five years, the science sections of newspapers have started to read a little like Cosmo — they tell us how to learn all about our men without ever actually asking.

On the other hand, the study does counter a spate of recent books and articles that blame women for male inability to commit. In addition to Dante Moore, there's psychotherapist Gary Neuman, whose The Truth About Cheating: Why Men Stray and What You Can Do to Prevent It says "Men will eventually find their way into the arms of another if they are not getting enough sex at home." And of course there's Elroy Riggs at the Central Kentucky News-Journal, who blames divorce on modern women's unwillingness to whip up homemade biscuits.

If the love-rat gene makes people realize that infidelity is often more about the cheater than the cheat-ee, then more power to the Karolinska Institute. The most interesting research, however, has yet to be done. The Institute plans to study whether oxytocin, another hormone, affects women's ability to commit. This study might take some of the annoying stereotypical sting out of sex research. Thus far, much of it has been about why men "can't commit," with the assumption that women want them to. Corresponding research into women's predispositions might underscore the fact that we're not all sad little lady voles who sit around waiting for our man vole to come home. Nor are we slaves to biology. Some men and some women want to commit, and some don't, and our goal should be to avoid a mismatch of the two, not to pore over our genes for predictors of our happiness.

The love-rat gene: Why some men are born to cause trouble and strife
Study Links Gene Variant in Men to Marital Discord
Monogamy gene found in people
Author risks fury of millions of women with a claim that THEY are to blame when husbands stray