One of the big sources of dissension among people trying to place human behavior and social organization in the context of biological evolution is understanding the nature of heredity. It is only hereditary causes that are involved in evolution (and for the purposes of this post, that means genes) and hence play a role in the nature of organisms over the long haul. What you are depends on your environment, but your reactions to that are constrained by the patrimony built up over 4+ billion years of heritable ancestry.
There are countless examples of casual views of what makes us what we are. One of us (Ken) has been reading the satires written by the Roman author Juvenal, writing about 125 AD. Satire 14 seemed relevant to these ideas. Here's one translation.
Satire 14 is called "The influence of vicious parents" in at least one translation (though it's "No teaching like that of example" in another). In any case, Juvenal notes the strong influence of parents. Some children learn from their "wastrel father... to enjoy such things as peeled truffles and seasoned mushrooms, and warblers steeped til they drown in the mushrooms' sauce."
"So Nature ordains," writes Juvenal, that "no evil example corrupts us so soon and so rapidly as one that has been set at home, since it comes into the mind on high authority." [this quote from a different translation] Juvenal is being cynically satirical about bad, selfish, or debauched human behavior, but his point is cogent: to a great extent we are what we pick up at home.
The point here, with respect to modern genetics, and MT, is that if one has a belief that this or that trait is inherited in the genetic sense, one can make up stories of how the trait got that way, by virtue of a long history of natural selection. But what evidence do we need before we should be taken seriously in such arguments of inherency?
The essential evidence must include that there are family resemblances. Factors like recessiveness can obscure patterns, but so can what are called 'incomplete penetrance' or 'phenocopies' or 'sporadic' instances of a trait. This means that even if there is a gene 'for' a trait--that is, whose variation confers the trait on its inheritor--the trait may not always be present, or, it can arise for other reasons. Family environment is another factor that influences presence/absence of a trait.
Rigorous genetic inference should have to show that traits are not just familial, but obey Mendel's laws of inheritance. However, the problem is that such patterns are almost impossible to prove, because there are so many possible causal factors ('parameters' in the statistical tests of inheritance patterns), that almost any trait, or any hypothesis, can be given support. This is made all the more complicated by the obvious and undoubted fact that many if not the vast majority of genetic effects are context-dependent, in that they are affected by the environment. And environment begins at home.
The difficulty of showing that a trait that aggregates in families actually 'segregates' as Mendel's laws would have it, has led to a general abandonment of rigorous segregation analysis, replaced by the assumption that traits simply must be importantly genetic and all we need to do is scan the whole genome to find the responsible genes. How much greed, vice, or seasoned mushrooms is needed to show that the child is the likeness and image of the parent? See all our previous posts on GWAS if you want to know what the issues are (and what we think of them, whether you agree with us or not!).
In this very sloppy epistemological environment, that is, we face fluid and largely unconstrained criteria for making inferences about what is genetic and what isn't, and how something that you assume 'must be' genetic can be explained by some sort of adaptive scenario that you can invent. This makes assumption into truth in a rather untestable way. And when evidence is gathered, there are so many ways to interpret it that it is almost always possible to find one that fits your prior expectations.
Each of us is, to a great extent, what we are. Clearly everything about us has some genetic under-pinnings, or we would not so clearly resemble our parents to an obvious extent. But just as clearly, much of what we are comes from our surroundings. In that sense, it is not inherent in us.
Social politics is complex but there are many reasons why it is convenient to view the sins of the sons as having been visited on them by their fathers. But if "young people readily copy most of our vices," as Juvenal wrote, selfishness and greed and other sins may reflect the nature of society as much as they do the nature of our genes. Sorting this out is a major challenge, because there are so many social consequences when those in power use convenient assumptions to manipulate others to their own advantage. Science is built on assumptions, but assumptions are not science.
Wednesday, February 9, 2011
Tuesday, February 8, 2011
Are we too clean? The hygiene hypothesis and asthma
Cleanliness is next to wheeziness?
An article in The New Yorker last week says that physicians have it all wrong when it comes to childhood allergies (also called atopy). The recommendation of the American Pediatric Association since 2000 has been that, to prevent food allergies, infants should be breastfed exclusively for 6 months, with solid foods introduced one by one for the next 6 months, to monitor effects of each food, but avoiding eggs and peanuts, because they are the foods to which kids are most likely to develop allergies.
But peanut, egg and dairy allergies are now skyrocketing! So, some people are starting to think that prevention by avoidance may actually be causing the disease and suggesting that perhaps infants should be exposed to these foods in small quantities much earlier than current recommendations. And some studies are beginning to show that such exposure might in fact eliminate even an existing allergy. Perhaps, according to the article, medicine has erred on the side of excessive cleanliness once again. Cleanliness reduces serious infectious disease exposures, perhaps, but one shouldn't overdo it because we've evolved to be commensal with microorganisms, both viruses and bacteria--we've coevolved with them, are absolutely covered inside and out with them, and in many ways our lives literally depend on them.
By the way, it's worth pointing out that while there is undoubtedly some genetic variation, overall genes have little if anything to do with the spike in allergy incidence--genomes haven't changed in the last 50 years!
An inverse relationship between allergy and helminth infection has been recognized since the 1960s, despite the fact that both induce a similar immunological response, but the reasoning that allergy may be a side effect of excessive cleanliness starts with a hypothesis first proposed in 1989 in a paper published in the British Medical Journal in 1989. This paper was the first to propose that the 'post industrial revolution epidemic' of hay fever and eczema in Britain could be due to what has come to be called the 'hygiene hypothesis'. The author looked at a handful of factors that could be associated with risk of hay fever, in a study sample of 18,000 children. "Of the 16 perinatal, social, and environmental factors studied the most striking associations with hay fever were those for family size and position in the household in childhood."
The author concludes,
A much-cited paper in Science in 2002 is worth quoting at length.
As the worm turns!
The helminth connection led to some interesting work in the fine tradition of self-experimentation, with researchers infecting themselves with helminths and monitoring what happened to their own allergies or asthma, with some positive effect. Some people now propose worm therapy, in fact, but the pathogen load has to be a heavy one.
But, as usual, the story is not so simple. An article in last week's Scientific American discusses a paper in Pediatric Allergy and Immunology reporting that Ugandan kids of mothers treated for helminth infection when they were pregnant were more likely to have eczema than kids whose mothers weren't treated. The paper is subscription only, so we don't have access to the full text, but it looks like the story is more complicated than Scientific American would have it. Mothers were treated with 1 of 2 different anti-helminthic drugs (albendazole or praziquantel) or placebo, and, from what we can tell from the abstract, the effects seem to differ depending on which drug the mother received and which pathogens she was carrying.
And, the same Science paper we've quoted at length suggests that TH1/ TH2 balance may not in fact be the explanation for the inverse correlation between helminth infection and allergy, but instead the protective effect of infection may have to do with the anti-inflammatory response it triggers. Other severe infections such as measles or tuberculosis are also inversely correlated with allergy. The authors propose an alternative protective pathway to explain the hygiene hypothesis:
So, does the 'hygiene hypothesis' explain the significant rise in asthma, allergies and autoimmune diseases in the industrialized world? The evidence is building, but the relationship is still more of a correlation, based on epidemiological associations, than demonstrated causation and there are still many unanswered questions. If nothing else, you can be sure that the complexity of the immune response, and how much is still not understood, are limiting factors when it comes to answering those questions.
But it is possible that one day the apparent protective mechanism will be demonstrated and understood, and therapeutic approaches will be designed based on this mechanism so you won't have to infect yourself with helminths to treat your asthma.
And, we'd like to point out that the mechanisms will involve genetic pathways, undoubtedly, and the approaches will involve molecular technology. But the therapies won't depend on personalized medicine, nor on the sequencing of the human genome -- whose 10th anniversary is being so heavily feted this month in Science.
An article in The New Yorker last week says that physicians have it all wrong when it comes to childhood allergies (also called atopy). The recommendation of the American Pediatric Association since 2000 has been that, to prevent food allergies, infants should be breastfed exclusively for 6 months, with solid foods introduced one by one for the next 6 months, to monitor effects of each food, but avoiding eggs and peanuts, because they are the foods to which kids are most likely to develop allergies.But peanut, egg and dairy allergies are now skyrocketing! So, some people are starting to think that prevention by avoidance may actually be causing the disease and suggesting that perhaps infants should be exposed to these foods in small quantities much earlier than current recommendations. And some studies are beginning to show that such exposure might in fact eliminate even an existing allergy. Perhaps, according to the article, medicine has erred on the side of excessive cleanliness once again. Cleanliness reduces serious infectious disease exposures, perhaps, but one shouldn't overdo it because we've evolved to be commensal with microorganisms, both viruses and bacteria--we've coevolved with them, are absolutely covered inside and out with them, and in many ways our lives literally depend on them.
By the way, it's worth pointing out that while there is undoubtedly some genetic variation, overall genes have little if anything to do with the spike in allergy incidence--genomes haven't changed in the last 50 years!
An inverse relationship between allergy and helminth infection has been recognized since the 1960s, despite the fact that both induce a similar immunological response, but the reasoning that allergy may be a side effect of excessive cleanliness starts with a hypothesis first proposed in 1989 in a paper published in the British Medical Journal in 1989. This paper was the first to propose that the 'post industrial revolution epidemic' of hay fever and eczema in Britain could be due to what has come to be called the 'hygiene hypothesis'. The author looked at a handful of factors that could be associated with risk of hay fever, in a study sample of 18,000 children. "Of the 16 perinatal, social, and environmental factors studied the most striking associations with hay fever were those for family size and position in the household in childhood."
The author concludes,
These observations do not support suggestions that viral infections, particularly of the respiratory tract, are important precipitants of the expression of atopy. They could, however, be explained if allergic diseases were prevented by infection in early childhood, transmitted by unhygienic contact with older siblings, or acquired prenatally from a mother infected by contact with her older children. Later infection or reinfection by younger siblings might confer additional protection against hay fever.
Over the past century declining family size, improvements in household amenities, and higher standards of personal cleanliness have reduced the opportunity for cross infection in young families. This may have resulted in more widespread clinical expression of atopic disease, emerging earlier in wealthier people, as seems to have occurred for hay fever.The idea was soon fleshed out to suggest that reduced exposure to pathogens, such as hepatitis A, Toxoplasma gondii or helicobacter pylori, changes the balance between two types of immune response, type 1 (TH1, triggered by bacterial and viral infections and autoimmune diseases), and type 2 (TH2, associated with helminth infections and allergic diseases). An extension of the hygiene hypothesis to include autoimmune diseases was proposed in 2002 (cited here), and has subsequently been demonstrated in animals. E.g., in lab mice, the incidence of type 1 diabetes rises with cage cleanliness. (Type 1 diabetes is another disease whose incidence has risen in the industrialized world, along with asthma.)
A much-cited paper in Science in 2002 is worth quoting at length.
There has been a significant increase in the prevalence of allergic diseases over the past 2 to 3 decades. Currently, more than 130 million people suffer from asthma, and the numbers are increasing ; nevertheless, there is a considerably lower prevalence of allergic diseases in developing countries. There are also clear differences in the prevalence of allergies between rural and urban areas within one country. For example, in Ethiopia, asthma is more prevalent in urban areas than in rural villages, and asthma is more common in residents of urban Germany than in farmers living in rural Bavaria. To explain these observations, environmental factors associated with more industrialized and urban living have been studied intensively, but there is little consistent evidence to suggest that obvious risk factors, such as increased exposure to indoor allergens, pollution, or changes in diet and breastfeeding, could account for the rise in atopic diseases. However, another category of environmental factors, childhood infections, shows an overwhelming and consistent negative association with atopy and allergic diseases. Allergic sensitization is overrepresented among first-born but is less frequent in children from large families and those attending day care, suggesting that a frequent exchange of infections may have a protective effect.
Divergent outcome of TH2 responses in industrialized (low pathogen exposure) and developing countries (high pathogen exposure). It has been argued that improved hygiene, frequent use of antibiotics, and vaccination has led to reduced bacterial and viral infections in industrialized countries and therefore to insufficient stimulation of TH1 responses, which in turn allows the expansion of TH2 cells. TH2 responses are characterized by increased IgE to allergens, mastocytosis, and eosinophilia. Mast cell degranulation and release of inflammatory mediators leads to mucus production and smooth muscle cell contraction, precipitating allergic diseases of the airways. Helminths are prevalent in developing countries and lead to strong TH2 responses. Nevertheless, helminth-infected populations show little signs of allergic disorders. This difference may be explained by the differences in exposure to pathogens. A high prevalence of chronic infections in developing countries results in persistent immune challenge, with cycles of infection and inflammation, which is followed by the triggering of anti-inflammatory molecules to restrict immunopathology. This dynamic interaction educates the immune system to establish a robust regulatory network, possibly the key to controlling allergic diseases. Such a network would be weakly developed in industrialized countries with a low pathogen load, allowing inappropriate immunopathological reactions to develop more readily.
As the worm turns!
The helminth connection led to some interesting work in the fine tradition of self-experimentation, with researchers infecting themselves with helminths and monitoring what happened to their own allergies or asthma, with some positive effect. Some people now propose worm therapy, in fact, but the pathogen load has to be a heavy one.
But, as usual, the story is not so simple. An article in last week's Scientific American discusses a paper in Pediatric Allergy and Immunology reporting that Ugandan kids of mothers treated for helminth infection when they were pregnant were more likely to have eczema than kids whose mothers weren't treated. The paper is subscription only, so we don't have access to the full text, but it looks like the story is more complicated than Scientific American would have it. Mothers were treated with 1 of 2 different anti-helminthic drugs (albendazole or praziquantel) or placebo, and, from what we can tell from the abstract, the effects seem to differ depending on which drug the mother received and which pathogens she was carrying.
Results: Worms were detected in 68% of women before treatment. Doctor-diagnosed infantile eczema incidence was 10.4/100 infant years. Maternal albendazole treatment was associated with a significantly increased risk of eczema [Cox HR (95% CI), p: 1.82 (1.26–2.64), 0.002]; this effect was slightly stronger among infants whose mothers had no albendazole-susceptible worms than among infants whose mothers had such worms, although this difference was not statistically significant. Praziquantel showed no effect overall but was associated with increased risk among infants of mothers with Schistosoma mansoni [2.65 (1.16–6.08), interaction p = 0.02]. In a sample of infants, skin prick test reactivity and allergen-specific IgE were both associated with doctor-diagnosed eczema, indicating atopic aetiology. Albendazole was also strongly associated with reported recurrent wheeze [1.58 (1.13–2.22), 0.008]; praziquantel showed no effect.It's impossible to know from the abstract whether the authors considered the alternative explanation, that any atopy and asthma was the result the drug of eliminating the infection, or in fact of the drug--as Holly pointed out here.
And, the same Science paper we've quoted at length suggests that TH1/ TH2 balance may not in fact be the explanation for the inverse correlation between helminth infection and allergy, but instead the protective effect of infection may have to do with the anti-inflammatory response it triggers. Other severe infections such as measles or tuberculosis are also inversely correlated with allergy. The authors propose an alternative protective pathway to explain the hygiene hypothesis:
Education of the immune system by pathogens. Dendritic cells can develop into distinct subpopulations, depending on the nature of the signals they receive from the microenvironment, and then direct T cell differentiation into polarized subsets. Viruses, bacteria, and helminths carry distinct signature molecules that interact with dendritic cells to stimulate TH1-type and TH2-type immune responses. When uncontrolled, strong TH1 and TH2 responses lead to autoimmunity and allergy. High pathogen burden may either change the physiology of the microenvironment or result in the accumulation of novel signature molecules that together endow dendritic cells with the ability to induce regulatory T cells. Regulatory T cells produce suppressory cytokines and are part of an anti-inflammatory network that ensures that inflammatory T cells (both TH1 and TH2) and their downstream effectors are kept under control.
So, does the 'hygiene hypothesis' explain the significant rise in asthma, allergies and autoimmune diseases in the industrialized world? The evidence is building, but the relationship is still more of a correlation, based on epidemiological associations, than demonstrated causation and there are still many unanswered questions. If nothing else, you can be sure that the complexity of the immune response, and how much is still not understood, are limiting factors when it comes to answering those questions.
But it is possible that one day the apparent protective mechanism will be demonstrated and understood, and therapeutic approaches will be designed based on this mechanism so you won't have to infect yourself with helminths to treat your asthma.
And, we'd like to point out that the mechanisms will involve genetic pathways, undoubtedly, and the approaches will involve molecular technology. But the therapies won't depend on personalized medicine, nor on the sequencing of the human genome -- whose 10th anniversary is being so heavily feted this month in Science.
Friday, February 4, 2011
Laws of nature? Can social science find them?
Nature has published a list of the 10 most pressing questions in social science, as determined by a symposium of social scientists who met last April to collect ideas and propose the list. These questions will, they hope, drive social science research for decades to come.
So here's the social science road map.
We can't say that we actually understand all of these -- number 6, for example. What is it that we don't understand about how humans create knowledge? The anatomy and physiology of creativity, learning and speech? The role of cultural context in inspiration? Not sure.
But, we'd say that a lot is already known about some of the others. Number 1, how to induce people to look after their health. You know what they are talking about here -- not how to get rich people to be more careful when they ski to avoid breaking their legs, or how to prevent their yachts from capsizing. Yes, effective health education is a problem. But really, which segments of society are most likely to smoke and be overweight? Not the rich. The obvious solution is to give more money to the poor. Improve their standard of living, and their health will follow.
And number 2, how do societies create effective and resilient institutions, such as governments? Aren't repressive regimes effective at what they do? Wasn't Saddam's government effective in many ways? Electricity was on more hours of the day, a lot more oil got pumped out of the ground than the post-Saddam government has managed to do. But we're pretty sure that's not what the list-makers had in mind.
And number 4, how to reduce the skill gap between whites and blacks. Better funding for schools in poor neighborhoods would be one way. Unless the unstated assumption is that whites are genetically predisposed to be better skilled.
This list strikes us as largely about what might be called 'bourgeois' concerns of the here and now (and upper-middle class) in a way that the list of mathematics challenges can't be, or a list of, say, unanswered questions in biology wouldn't be. That doesn't make these questions irrelevant by any means, but they are a kind of we-they list of current issues, reflecting assumptions and perspectives of the people asking them.
These applied social engineering questions are analogous to pharma or agribusiness objectives of using genetics to make drugs or crops that work, or, by their sales, satisfy the companies, or whatever. If social science is to actually make progress in understanding human nature, rather than simply re-inventing the questions whenever something crops up, we think more attention should be paid to the basics. For example, does life follow tractable 'laws' and if so how they are to be understood and applied to specific questions, across the spectrum of life, like the nature of thistle burrs or the nature of lipid metabolism? If there are such laws, do we know them? can we know them? can they help us account for societal structures?
The social sciences should be at the core of our understanding of ourselves. But they need to come up with a better list of questions before that can happen.
The 'top ten' approach was inspired by a list of 23 major unsolved questions compiled by the mathematician David Hilbert in 1900. The Hilbert problems helped to focus the attention of mathematicians throughout the following century. "He laid out the road map for twentieth-century math," says Nick Nash, a vice-president at General Atlantic, an investment firm based in Greenwich, Connecticut. "What if we had a road map for other disciplines?"
So here's the social science road map.
Social science lines up its biggest challenges
Top ten social-science questions:
1. How can we induce people to look after their health?
2. How do societies create effective and resilient institutions, such as governments?
3. How can humanity increase its collective wisdom?
4. How do we reduce the ‘skill gap’ between black and white people in America?
5. How can we aggregate information possessed by individuals to make the best decisions?
6. How can we understand the human capacity to create and articulate knowledge?
7. Why do so many female workers still earn less than male workers?
8. How and why does the ‘social’ become ‘biological’?
9. How can we be robust against ‘black swans’ — rare events that have extreme consequences?
10. Why do social processes, in particular civil violence, either persist over time or suddenly change?
We can't say that we actually understand all of these -- number 6, for example. What is it that we don't understand about how humans create knowledge? The anatomy and physiology of creativity, learning and speech? The role of cultural context in inspiration? Not sure.
But, we'd say that a lot is already known about some of the others. Number 1, how to induce people to look after their health. You know what they are talking about here -- not how to get rich people to be more careful when they ski to avoid breaking their legs, or how to prevent their yachts from capsizing. Yes, effective health education is a problem. But really, which segments of society are most likely to smoke and be overweight? Not the rich. The obvious solution is to give more money to the poor. Improve their standard of living, and their health will follow.
And number 2, how do societies create effective and resilient institutions, such as governments? Aren't repressive regimes effective at what they do? Wasn't Saddam's government effective in many ways? Electricity was on more hours of the day, a lot more oil got pumped out of the ground than the post-Saddam government has managed to do. But we're pretty sure that's not what the list-makers had in mind.
And number 4, how to reduce the skill gap between whites and blacks. Better funding for schools in poor neighborhoods would be one way. Unless the unstated assumption is that whites are genetically predisposed to be better skilled.
This list strikes us as largely about what might be called 'bourgeois' concerns of the here and now (and upper-middle class) in a way that the list of mathematics challenges can't be, or a list of, say, unanswered questions in biology wouldn't be. That doesn't make these questions irrelevant by any means, but they are a kind of we-they list of current issues, reflecting assumptions and perspectives of the people asking them.
These applied social engineering questions are analogous to pharma or agribusiness objectives of using genetics to make drugs or crops that work, or, by their sales, satisfy the companies, or whatever. If social science is to actually make progress in understanding human nature, rather than simply re-inventing the questions whenever something crops up, we think more attention should be paid to the basics. For example, does life follow tractable 'laws' and if so how they are to be understood and applied to specific questions, across the spectrum of life, like the nature of thistle burrs or the nature of lipid metabolism? If there are such laws, do we know them? can we know them? can they help us account for societal structures?
The social sciences should be at the core of our understanding of ourselves. But they need to come up with a better list of questions before that can happen.
Thursday, February 3, 2011
Whence minority rule?
Well, no science post today. We're spending too much time watching live footage from Egypt. Not only do we, as Americans and people fortunate enough to live in a democracy, sympathize with the protestors, but our daughter is now living and teaching music in a conservatory in Palestine, amidst people for whom occupation is a constant fact of life (and we sit here smugly, the occupiers of North America, who put its prior indigenous inhabitants essentially in permanent refugee camps).
But in addition to the sense of unfairness about human politics in so many places, this leads us to muse about how it is that human societies manage to establish minority rule, often cruel minority rule. How is it that a small number of people can control the lives of a much larger number?
The evolutionary basis of inequality is perhaps interesting but not the answer. Social hierarchies cannot be put down to the leaders' better intelligence or belligerence genes. Even if dominance were genetic, its evolution over countless generations in small demes would largely have fixed the responsible genes, so that most positions in the dominance hierarchy would be due to chance or something other than genes.
Social pyramids are something different. One person leverages several others by dint of personality or resources or something, and they in turn leverage a larger number. Those at the top control information, resources, education, and so on. They then control acculturation, beliefs (including the belief that the boss deserves to be boss because of some religious or political ideology), and so on.
But these are descriptions of what happens, even in democracies. Yet it seems inevitable regardless of ideology, as communist countries surely and clearly showed. Hierarchies are of all sorts, some more rigid than others, but they are found at all levels of society. It's easy, one might say, to see why organizations from families to teams to clubs to governments function only when they have leaders and followers, but again description is not what's interesting to us from a biological point of view.
From that point of view, how do minorities manage to control majorities? Is the answer to be found in physiology or genetics in any useful sense? Or is it, as the founders of modern (and hence pre-postmodern) social scientists argued, something that must be explained in terms of social, rather than biological facts--that is, that society's structures may be manned by biological organisms, but the nature and evolution of those structures has its own properties independent of the biological details: hierarchies can exist in any population with any set of genotypes. Are there some properties or principles by which such social facts can be explained, and if so are they like 'laws of Nature'? Could it be otherwise, and if not, why?
These are thoughts that come to us as we watch the struggles now going on in the Middle East.
But in addition to the sense of unfairness about human politics in so many places, this leads us to muse about how it is that human societies manage to establish minority rule, often cruel minority rule. How is it that a small number of people can control the lives of a much larger number?
The evolutionary basis of inequality is perhaps interesting but not the answer. Social hierarchies cannot be put down to the leaders' better intelligence or belligerence genes. Even if dominance were genetic, its evolution over countless generations in small demes would largely have fixed the responsible genes, so that most positions in the dominance hierarchy would be due to chance or something other than genes.
Social pyramids are something different. One person leverages several others by dint of personality or resources or something, and they in turn leverage a larger number. Those at the top control information, resources, education, and so on. They then control acculturation, beliefs (including the belief that the boss deserves to be boss because of some religious or political ideology), and so on.
But these are descriptions of what happens, even in democracies. Yet it seems inevitable regardless of ideology, as communist countries surely and clearly showed. Hierarchies are of all sorts, some more rigid than others, but they are found at all levels of society. It's easy, one might say, to see why organizations from families to teams to clubs to governments function only when they have leaders and followers, but again description is not what's interesting to us from a biological point of view.
From that point of view, how do minorities manage to control majorities? Is the answer to be found in physiology or genetics in any useful sense? Or is it, as the founders of modern (and hence pre-postmodern) social scientists argued, something that must be explained in terms of social, rather than biological facts--that is, that society's structures may be manned by biological organisms, but the nature and evolution of those structures has its own properties independent of the biological details: hierarchies can exist in any population with any set of genotypes. Are there some properties or principles by which such social facts can be explained, and if so are they like 'laws of Nature'? Could it be otherwise, and if not, why?
These are thoughts that come to us as we watch the struggles now going on in the Middle East.
Wednesday, February 2, 2011
Causes of aggressive behavior found?
Here's an interesting juxtaposition of stories about causes of aggressive behavior in mice. A story on the BBC web site, reporting on a paper in the Proceedings of the National Academy of Sciences, suggests that the microbiome in the gut of some lab mice is responsible for their adventurousness.
In contrast, a paper in Nature, as reported in the New York Times, suggests that altering a specific gene boosts aggressive behavior in mice. The Times says
On the other hand, either or both results might well be no more than speculation, as many science stories these days. The amount of basically wild speculation, picked up by the media as if substantial or well-anchored scientifically, continues to be high. With 24/7 media, and a public (and scientists) hungry for simple stories, reinforces this.
Of course, there is no reason to doubt that anything might affect anything else, so the main point of responsible science is to balance what is found so far with might be found or might be true or correlated with what is found. If that were more predominant, stories like these, that are certainly interesting, might be more likely to be viewed as science rather than stories.
The teeming trillions of bacteria in the digestive tracts of mice have been shown to affect the animals' brain development and behaviour.
Mice bred in sterile environments without these "gut flora" were seen to be more adventurous and less anxious than mice with normal gut flora.The authors compared gene expression profiles in the brains of mice raised in the germ free environment with those in the non-sterile environment and found consistent differences in the levels of expression of 50 genes. The authors conclude "our results suggest that the microbial colonization process initiates signaling mechanisms that affect neuronal circuits involved in motor control and anxiety behavior."
 |
| In situ hybridization results showing Grb10 inactivated in mouse on right. |
For some genes, either the father’s version or the mother’s version is active, but not both. Which version of the gene works is determined before conception, as the sperm and egg are developing, in a process called imprinting. By mimicking that process in the lab, and turning off a gene in mice, scientists have produced a change in social dominance behavior. In laboratory tests, mice with the paternal version of the gene known as Grb10 inactivated were more aggressive in their behavior...These papers don't necessarily contradict each other, although it doesn't look like Grb10 is one of the 50 genes whose expression level is affected by microbes in the gut. If both results are real, this suggests that, like many traits, there may be multiple paths to aggressive behavior. And that there is no single allele 'for' a trait like this. That wouldn't be a surprise.
On the other hand, either or both results might well be no more than speculation, as many science stories these days. The amount of basically wild speculation, picked up by the media as if substantial or well-anchored scientifically, continues to be high. With 24/7 media, and a public (and scientists) hungry for simple stories, reinforces this.
Of course, there is no reason to doubt that anything might affect anything else, so the main point of responsible science is to balance what is found so far with might be found or might be true or correlated with what is found. If that were more predominant, stories like these, that are certainly interesting, might be more likely to be viewed as science rather than stories.
Tuesday, February 1, 2011
Lost and found -- Breaking Dollo's Law
It has long been thought that once a species loses a trait, that trait is gone forever. The loss can't be reversed. This is so well-accepted that it's risen to the status of a law of nature, Dollo's Law. Dollo was a Belgian paleontologist working around the turn of the last century, and as he put it, "An organism is unable to return, even partially, to a previous stage already realized in the ranks of its ancestors." So, for example, according to Dollo's Law, we have lost the tail our ancestors had, and we won't regain it, reptiles that have made the transition from egg-laying to giving birth to live offspring can't go back, and so on.
But laws are made to be broken, and the idea that life follows 'laws' the way gravity and chemistry do is tenuous at best. In this case, Dollo's 'Law' is currently under challenge. A paper published online in Evolution on Jan 27, and discussed on the BBC website, describes the re-evolution of mandibular teeth in frogs after more than 200 million years. Recent reports of exceptions to the irreversibility principle -- wings lost and regained in stick insects, the re-evolution of coiling in snail shells, re-evolved ocelli in cave crickets, wings in water spiders, and so forth -- have been called into question for methodological reasons, but the re-evolution of frogs teeth and other examples look pretty solid. As Wiens concludes,
Another example of an exception to Dollo's Law is described by Lynch and Wagner in the Jan 2010 issue of Evolution. They present evidence for the re-evolution of oviparity, or egg laying, in "Old World sand boas in the genus Eryx nearly 60 million years after the initial boid transition to viviparity" based on a phylogenetic analysis of genetic data from boid snakes and other related groups. In addition to the statistical support for re-evolution, they note that morphological evidence includes the fact that, like live born boas, the hatchlings of the "oviparous Eryx lack an egg-tooth providing independent evidence that oviparity is a derived state in these species." And, the shells of the boas that have re-evolved oviparity are extremely thin compared with the shells of other boas, suggesting that the structure of the eggshell re-evolved as well.
The argument over whether Dollo's Law can be violated may primarily reflect the way we classify species and think about phylogenies. As Wiens says,
Indeed, the normal tissue is not required. There are mouse and human examples in which hair or teeth grow where the other normally does. Ovarian teratomas are disorganized tumor-like structures of disorganized embryos that, as was known even in the early 1800's (and cited by Darwin), developed hair and teeth (even chicks do not have enamel genes, but teeth can be induced to form by genetically similar processes as hair or feathers, and transgenic expression of some environment-preparing genes in embryonic chick jaws can lead to tooth-like structures).
Dental formulas (numbers and shapes of teeth in upper and lower jaws) and hair or coloration patterns can come and go for similar reasons. In many cases, the genetic change can be a modification of existing genes and tissues. Similar dental formulas have evolved numerous times in vertebrates. In others, there are different pathways to similar outcomes. This is what happens in some selection experiments, and seems, if we recall correctly, to be the case with ocelli in insects. But the overall pathways are presumably rather simple, or the different activations activate similar pathways that are conserved because they are still doing something. In the frogs, they're making teeth in the upper jaw, a tissue histologically similar to lower jaws.
The point here is not that reversals are trivial or uninteresting, but they are explicable when they occur. However, highly organized or complex structures are unlikely to recur after too long of divergence. If we re-evolved, say, swimming anatomy it would not likely be the same as what is found in fish. Indeed, that is what whales did, and they swim by up and down motion rather than the side to side motion of fish, because their mechanism is anatomically different.
Again, these instances are interesting, and perhaps most interesting is that even before the genetic age anyone should have suggested, much less canonized, 'laws' about how evolution works. At most they are statistical generalizations that, in genetic terms, relate to the likelihood of the same genetic mechanism re-evolving.
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| From the BBC |
The results presented here offer an incontrovertible phylogenetic example of trait re-evolution, showing that mandibular teeth were lost in the ancestor of all living frogs and then re-evolved in the hemiphractid species G. guentheri. The alternate hypothesis, that mandibular teeth were lost independently in each of the dozens of lineages leading up to G. guentheri, is statistically unsupported and seems incredibly unlikely. Although the hypothesis that G. guentheri re-evolved mandibular teeth may be unsurprising to experts in amphibian anatomy, this compelling example has been ignored in the recent literature on Dollo's law. Further, this example is made remarkable by the application of a time scale for this event: mandibular teeth were absent for at least 225 million years (and likely much longer) before being regained.
The argument over whether Dollo's Law can be violated may primarily reflect the way we classify species and think about phylogenies. As Wiens says,
...the observation that most well-documented cases of trait re-evolution occur after a period of trait loss of greater than 15 million years (Table 2) may also reflect methodological bias. A complex structure that re-evolves may need to be absent for tens of millions of years before its re-acquisition can be confidently distinguished from multiple losses (e.g., given typical diversification rates, this period of time may be needed for a group to diversify enough to have species nested deep in the phylogeny). Yet, if the gain of lost traits is possible, a consideration of the underlying genetics suggests that it should be much more likely soon after the trait is lost (Marshall et al. 1994). Thus, trait re-evolution may actually be hardest to detect under the conditions when it is most likely to occur, raising the question of whether trait re-evolution might be more widespread but frequently undetected due to methodological biases.So, how is the re-evolution of a trait explained genetically? Weins suggests that the fact that G. Guentheri still have teeth in their upper jaw facilitates the repositioning of teeth to the lower jaw. The structural genes are there, they just need to be recruited for expression in a different place. Generally, this is not very perplexing. Single gene expression changes can lead to signaling environments that, in relevant tissues, can induce cascades of patterning-gene interactions that produce structures like teeth.
Indeed, the normal tissue is not required. There are mouse and human examples in which hair or teeth grow where the other normally does. Ovarian teratomas are disorganized tumor-like structures of disorganized embryos that, as was known even in the early 1800's (and cited by Darwin), developed hair and teeth (even chicks do not have enamel genes, but teeth can be induced to form by genetically similar processes as hair or feathers, and transgenic expression of some environment-preparing genes in embryonic chick jaws can lead to tooth-like structures).
Dental formulas (numbers and shapes of teeth in upper and lower jaws) and hair or coloration patterns can come and go for similar reasons. In many cases, the genetic change can be a modification of existing genes and tissues. Similar dental formulas have evolved numerous times in vertebrates. In others, there are different pathways to similar outcomes. This is what happens in some selection experiments, and seems, if we recall correctly, to be the case with ocelli in insects. But the overall pathways are presumably rather simple, or the different activations activate similar pathways that are conserved because they are still doing something. In the frogs, they're making teeth in the upper jaw, a tissue histologically similar to lower jaws.
The point here is not that reversals are trivial or uninteresting, but they are explicable when they occur. However, highly organized or complex structures are unlikely to recur after too long of divergence. If we re-evolved, say, swimming anatomy it would not likely be the same as what is found in fish. Indeed, that is what whales did, and they swim by up and down motion rather than the side to side motion of fish, because their mechanism is anatomically different.
Again, these instances are interesting, and perhaps most interesting is that even before the genetic age anyone should have suggested, much less canonized, 'laws' about how evolution works. At most they are statistical generalizations that, in genetic terms, relate to the likelihood of the same genetic mechanism re-evolving.
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