What is inheritance?

The original meaning of a gene was simply a heritable unit. This was long before the discovery of DNA. The theory was based on phenotype, i.e., observable characteristics. What they didn’t know and what still doesn’t often get acknowledged is that much gets inherited from parents, especially from the mother. This includes everything from epigenetics to microbiome, the former determining which genes express and how they express while the latter consists of the majority of genetics in the human body. The fetus will also inherit health conditions from the mother, such as malnutrition and stress, viruses and parasites — all of those surely having epigenetic effects and microbiome changes that could get passed on for generations.

Even more interestingly, DNA itself gets passed on in diverse ways. Viruses will snip out sections of DNA and then put them into the DNA of new hosts. Mothers, including surrogate mothers, can gain DNA from the fetuses they carry. And then those mothers can pass that DNA to any fetus she carries after that, which could cause a fetus to have DNA from two fathers. Fetuses can also absorb the DNA from fraternal twins or even entirely absorb the other fetus, forming what is called a chimera. Bone marrow transplantees also become chimeras because they inherit the stem cells for blood cells from the donor, along with inheriting epigentics from the donor. These chimeras could pass this on during a transplantee’s pregnancy.

We hardly know what all that might mean. There is no single heritable unit that by itself does anything. That is not the direct source of causation. A gene only acts as part of DNA within a specific cell and all of that within the entire biological system existing within specific environmental conditions. The most important causal factors are various. What is in DNA only matters to the degree it is expressed, but what determines its expression will also determine how it expresses. Evelyn Keller Fox writes that, “the causal interactions between DNA, proteins, and trait development are so entangled, so dynamic, and so dependent on context that the very question of what genes do no longer makes much sense. Indeed, biologists are no longer confident that it is possible to provide an unambiguous answer to the question of what a gene is. The particulate gene is a concept that has become increasingly ambiguous and unstable, and some scientists have begun to argue that the concept has outlived its productive prime” (The Mirage of a Space between Nature and Nurture, p. 50). Gene expression as seen in phenotype is determined by a complex system of overlapping factors. Talk of genes doesn’t help us much, if at all. And heritability rates tells us absolutely nothing about the details, such as distinguishing what exactly is a gene as a heritable unit and causal factor, much less differentiating that from everything else. As Fox further explains:

“It is true that many authors continue to refer to genes, but I suspect that this is largely due to the lack of a better terminology. In any case, continuing reference to “genes” does not obscure the fact that the early notion of clearly identifiable, particulate units of inheritance— which not only can be associated with particular traits, but also serve as agents whose actions produce those traits— has become hopelessly confounded by what we have learned about the intricacies of genetic processes. Furthermore, recent experimental focus has shifted away from the structural composition of DNA to the variety of sequences on DNA that can be made available for (or blocked from) transcription— in other words, the focus is now on gene expression. Finally, and relatedly, it has become evident that nucleotide sequences are used not only to provide transcripts for protein synthesis, but also for multilevel systems of regulation at the level of transcription, translation, and posttranslational dynamics. None of this need impede our ability to correlate differences in sequence with phenotypic differences, but it does give us a picture of such an immensely complex causal dynamic between DNA, RNA, and protein molecules as to definitely put to rest all hopes of a simple parsing of causal factors. Because of this, today’s biologists are far less likely than their predecessors were to attribute causal agency either to genes or to DNA itself— recognizing that, however crucial the role of DNA in development and evolution, by itself, DNA doesn’t do anything. It does not make a trait; it does not even encode a program for development. Rather, it is more accurate to think of DNA as a standing resource on which a cell can draw for survival and reproduction, a resource it can deploy in many different ways, a resource so rich as to enable the cell to respond to its changing environment with immense subtlety and variety. As a resource, DNA is indispensable; it can even be said to be a primary resource. But a cell’s DNA is always and necessarily embedded in an immensely complex and entangled system of interacting resources that are, collectively, what give rise to the development of traits. Not surprisingly, the causal dynamics of the process by which development unfolds are also complex and entangled, involving causal influences that extend upward, downward, and sideways.” (pp. 50-52)

Even something seemingly as simple as gender is far from simple. Claire Ainsworth has a fascinating piece, Sex redefined (nature.com), where she describes the new understanding that has developed. She writes that, “Sex can be much more complicated than it at first seems. According to the simple scenario, the presence or absence of a Y chromosome is what counts: with it, you are male, and without it, you are female. But doctors have long known that some people straddle the boundary — their sex chromosomes say one thing, but their gonads (ovaries or testes) or sexual anatomy say another. Parents of children with these kinds of conditions — known as intersex conditions, or differences or disorders of sex development (DSDs) — often face difficult decisions about whether to bring up their child as a boy or a girl.”

This isn’t all that rare considering that, “Some researchers now say that as many as 1 person in 100 has some form of DSD.” And, “What’s more, new technologies in DNA sequencing and cell biology are revealing that almost everyone is, to varying degrees, a patchwork of genetically distinct cells, some with a sex that might not match that of the rest of their body. Some studies even suggest that the sex of each cell drives its behaviour, through a complicated network of molecular interactions. Gender should be one of the most obvious areas to prove genetic determinism, if it could be proven. But clearly there is more going on here. The inheritance and expression of traits is a messy process. And we are barely scratching the surface. I haven’t seen any research that explores how epigenetics, microbiome, etc could influence gender or similar developmental results.

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Clusters and Confluences

A favorite topic in my family is the personality differences, psychological issues, behavioral traits, and other idiosyncracies among family members. In the immediate family and on both sides of the extended family, there are patterns that can be seen. Some of this might be genetic in origin, but no doubt there is much involving epigenetics, shared environmental conditions, parenting style, learned behavior, etc. Besides, nature and nurture are inseparable, in terms of actual people in the real world.

One example of a familial pattern is learning disabilities. I was diagnosed with learning disabilities when younger, but before my generation such diagnoses weren’t common. There appears to be some learning disabilities or rather learning style differences among some of my mother’s family. Another example is a dislike of physicality that was passed down from my paternal grandmother to my father and then to my older brother.

That latter one is interesting. My older brother has always been physically sensitive, like my dad. This to some extent goes along with an emotional sensitivity and, at least in the case of my brother, the physical sensitivity of allergies. His daughter has also taken on these psychological and physiological traits. All of these family members also have a hypersensitivity to social conditions, specifically in seeking positive responses from others.

I, on the other hand, have had an opposite cluster of factors. I was socially oblivious as a child and still maintain some degree of social indifference as an adult. My psychological and social insensitivity, although compensated for in other ways, goes hand in hand with a physical hardiness.

Unlike my paternal grandmother, father, brother, and niece, I am big-boned and more physical like my mother’s family. I even look more like my mother’s family with thicker hair, big feet, a bump on my nose, an underbite, and hazel eyes. About my physicality, it goes beyond just my body type, features, and activity level. I have such a high pain tolerance that I commonly don’t notice when I get a cut. I also don’t worry about cuts when I get them because I’m not prone to infections. I’ve always had a strong immune system and rarely get sick, but neither do I have an over-active immune system that leads to allergies.

All of this is the opposite of my older brother. He and his family are constantly getting sick, even as they constantly worry about germs and try to protect themselves. I played in filthy creeks as a child with exposed cuts and was far healthier than my cleanliness-obsessed brother who, when younger, panicked if his new shoes got scuffed.

It’s strange how these kinds of things tend to group together. It indicates a possible common cause or set of causes. That would likely be some particular combination of nature and nurture. I not only take more after my mother’s family for I also spent more time with my mother as a child than did my brothers, since she took time off from work when I was born (I was the third and last child, although fourth pregnancy following a miscarriage). My brothers didn’t get the same opportunity. So, I was also more likely to pick up behaviors from her. Between my brothers and I, only I am able to relate well with my mother. In particular, my older brother’s sensitivity is in constant conflict with my mother’s insensitivity. But I’m used to my mother’s way of relating, allowing me to better understand and sympathize, not to mention be more forgiving, partly because I share some of her tendencies.

Why is one kind of high sensitivity often related to other high sensitivities: emotional, social, pain, immune system, allergies, etc? And why is the opposite pattern seen with low sensitivities? What causes these clustered differences? And how can two such distinct clusters be found among siblings, sometimes even identical twins, who shared many factors?

It makes me curious.

It’s not just conditions like allergies and intolerances. There are similar clusters of neurocognitive, behavioral, and health conditions observed in various immune system disorders, the autism spectrum, fragile x syndrome, irritable bowel syndrome and other nutritional/dietary/intestinal issues, migraines, ADHD, toxoplasmosis and parasite load, heavy metal toxicity such as lead and mercury, etc. When there is one abnormal symptom or developmental issue, there are often others that show up at the same time or later on. This can involve such things as depression, anxiety, IQ, learning disabilities, irritability, impulse control issues, emotional instability, suicidal tendencies, accident proneness, etc along with more basic issues like asthma, diabetes, obesity, and much else.

In some cases, such as lead toxicity, the causal mechanisms are known as the toxin impacts every part of the body, especially the brain and nervous system. Or consider toxoplasmosis which apparently can alter the rates of personality traits in a population, along with differences in health consequences and social results, whatever is the exact chain of causation. But sometimes the correlations are far less clear and certain in their causal relationship. For example, what is the possible connection(s) between depressive tendencies, anger issues, addictive behaviors, learning difficulties, and physical hardiness among my maternal family?

There was a particular conversation that inspired this line of thought. My parents and I were discussing many of the above issues. But a major focus was on sleep patterns. My brother, like my dad, has a difficulty getting up and moving in the morning. They both tend to feel groggy when first waking up and prefer to remain physically inactive for a long period after. They also both find it hard to fall asleep and, in the case of my dad, a problem of waking up in the middle of the night. My mom and I, however, don’t have any of these issues. We fall asleep easily, typically stay asleep throughout the night, and wake up quickly. So, the difference between sensitivity and insensitivity impacts every aspect of life, even sleeping and waking.

Oftentimes, in our society, we blame individuals for the way they are. We act like people have a choice about how they feel and what motivates them. But it’s not as if because of moral superiority and strength of will that I’ve chosen to sleep well, have a strong immune system, feel physically energetic, and generally be insensitive. No more than I chose to have a learning disability and severe depression. It’s simply the way I’ve always been.

There is obviously much more going on here than mere genetics. And so genetic determinism is intellectually unsatisfying, even as some might find it personally convenient as a way of rationalizing differences. We have too much data proving environmental and epigenetic causes. A recent study could only find a few percentage of genes correlated to intelligence and, even then, they couldn’t prove a causal connection. The same thing is seen with so much other correlation research. The way various clusters form, as I argue, implies a complex web of factors that as of yet we don’t come close to understanding.

One intriguing connection that has been found is that between the brain and the gut. There are more neurons in the lining of the gastrointestinal system (the enteric nervous system) than in either the spinal cord or the peripheral nervous system. This is often called the “second brain,” but in evolutionary terms it was the earliest part of the brain. This is why there has been proven such a close relationship between intestinal health, diet, nutrition, microbiome, neurotransmitters, and mood. The human brain isn’t limited to the skull. The importance of this is demonstrated by introducing a new microbiome into the gut which can lead to physiological and pyschological changes.

Much else, however, remains a mystery. Seemingly minor changes in initial conditions, even epigenetic changes from prior generations, can lead to major changes in results. There can be a cascade of effects that follow. As I’ve previously stated, “This is because of the cumulative effect of initial conditions. One thing leads to another. Lowered nutrition or increased toxicity has its impact which gets magnified by such things as school tracking. Each effect becoming a cause and all the causal factors combining to form significant differences in end results.”

Later conditions can either lessen or exacerbate these results. Even epigenetics, by way of altered environmental conditions, can be switched back the opposite direction in a single generation with results that we know little about. Now consider the complexity of reality where there are millions of factors involved, with only a tiny fraction of those factors having been discovered and studied in scientific research. Those multitudinous factors act in combined ways that couldn’t be predicted by any single factor. All of this has to be kept in mind at the very moment in history when humans are ignorantly and carelessly throwing in further factors with unknown consequences such as the diversity of largely untested chemicals in our food and other products, not to mention large-scale environmental changes.

We don’t live at a society ruled by the precautionary principle. Instead, our collective ignorance makes us even more brazen in our actions and more indifferent to the results. The measured increase in certain physical and mental health conditions could be partly just an increase in diagnosis, but it’s more probable that at least some of the increase is actual. We are progressing in some ways as a society such as seen with the Moral Flynn Effect, but this is balanced by an Amoral Flynn Effect along with many other unintended consequences.

Along with this, our society has a lack of appreciation for the larger context such as historical legacies and a lack of respect for the power of larger forces such as environmental conditions. We are born into a world created by others, each generation forming a new layer upon the ground below. We are facing some tough issues here. And we aren’t prepared to deal with them.

As individuals, the consequences are laid upon our shoulders, without our realizing all that we have inherited and have had externalized onto our lives, as we grow up internalizing these realities and coming to identify with them. Each of us does the best we can with the hand we’ve been dealt, but in the process we get more praise and blame than we deserve. The individual, as the product of collective forces, is the ultimate scapegoat of society. The lives we find ourselves in are a confluence of currents and undercurrents, the interference pattern of waves. Yet, in our shared ignorance and incomprehension, we are simply who we are.

* * * *

The Ending of the Nature vs Nurture Debate
Heritability & Inheritance, Genetics & Epigenetics, Etc
What Genetics Does And Doesn’t Tell Us
Weak Evidence, Weak Argument: Race, IQ, Adoption
Identically Different: A Scientist Changes His Mind
What do we inherit? And from whom?
To Put the Rat Back in the Rat Park
Rationalizing the Rat Race, Imagining the Rat Park
Social Conditions of an Individual’s Condition
On Welfare: Poverty, Unemployment, Health, Etc
From Bad to Worse: Trends Across Generations
The Desperate Acting Desperately
It’s All Your Fault, You Fat Loser!
Facing Shared Trauma and Seeking Hope
Society: Precarious or Persistent?
Plowing the Furrows of the Mind
Union Membership, Free Labor, and the Legacy of Slavery.
Uncomfortable Questions About Ideology

What Genetics Does And Doesn’t Tell Us

I was looking at various articles and blogs on genetics, race, and IQ. I was also looking at the comments. It got me thinking about the quality of the public debate.

Much of the analysis and discussion is high quality. There are many people involved who are intelligent and well-read. But there still is a lot of misunderstanding and confusion about the issues of heritability, genetic inheritance, and shared environment. Without understanding these issues, there is no way to tackle all the related issues of race, IQ, etc.

This is a topic that I’ve posted about before. In that post, I offered many different perspectives from both online sources and books. If you check out some of the info from that post, you’ll realize how many complex factors are involved in a trait getting passed on and how difficult it is to determine causal relationships, specifically determining genetic influence.

This post is a continuation of what I shared there. I feel compelled to return to the topic because of its importance.

I’ll keep this post simpler, though. I’m only going to offer four articles for consideration, all of them from the website Science 2.0. There is no particular reason I’m offering these articles from this website other than that they caught my attention as I was browsing the web. The authors explain the issues well and I want to use this opportunity to promote their explanations.

* * * *

What Is Heritability?
By Gerhard Adam

“Heritability” is a term used in many articles and through much of the scientific literature and invariably promotes the idea that it relates specifically to inherited traits. As a result, it is often assumed that the heritability of a particular trait relates to how much influence genetics has on the trait manifesting in an individual.

However, that isn’t what it means.

Heritability attempts to address the relationship between nature (genetics) and nurture (environment), so that as each changes, the variation between individuals within a population can be estimated based on these influences. In this context, “environment” simply represents everything external to the genome that could effect expression.

Therefore the first significant aspect of heritability that must be understood is that it tells us nothing about individuals. It is strictly an estimate of the variations that occur within populations. If heritability is applied to an individual it is a meaningless concept [since an individual cannot be said to vary with anything].

It also doesn’t tell us anything about the specific influence of genes on any particular trait, since that would be the result of inheritance. We also need to understand that a trait is something that is “selectable”. In other words, there exists a possibility that outcomes can vary in the expression of a particular trait. This follows from the Mendelian view of inheritance where genes are represented as two alleles [dominant and recessive], so that particular combinations would produce certain outcomes. Therefore if there is no variation in the alleles, then everyone has the same genes and heritability would be zero. Adaptations like having a heart or a stomach are not selectable (too many genes and interactions) and therefore tell us nothing about heritability. The primary difference is that adaptations represent the cumulative effect of changes over time that have gone to fixation in a population. As a result, there is no “selection” that would determine “heart or no heart”. Therefore we can consider that the heart is an adaptation, while the risk of heart disease is a trait.

[ . . . . ]

One difficulty that arises with heritability is that any considered trait must be demonstrably linked to genetic transmission. This can become problematic when heritability is used to evaluate behavioral traits where the genetic link may be tenuous. In an effort to measure heritability, there is often a reliance on twin studies under the assumption that variances between them must be accountable to environment since they are effectively genetically identical. However, as previously mentioned, this can result in difficult interpretations when the traits in question are purely behavioral. Until such time as behavioral traits can be explicitly linked to genes, any statement regarding heritability must be considered suspect.

Heritability: A Primer
By Josh Witten

RED FLAG: If someone says the heritability of X is Y, then they probably don’t know what they are talking about.

Folks in the know, know that there are two kinds of heritability, broad sense and narrow sense. Those knowledgeable folks in the know are aware that it is extremely important to clearly state which heritability one is using, as the interpretation of each is different.

[ . . . . ]

Broad sense heritability tells us what proportion of the phenotypic variation is due to the genotypes of the individuals of the population. It tells us nothing about how similar the phenotype of a child will be to its parent. For that, we need the narrow sense heritability.

[ . . . . ]

Human behavioral studies, such as on IQ, have it much more difficult. Environmental variance is very difficult to control experimentally. Statistical methods can be used to correct for the effects of known environmental variables, but one cannot be certain that all variables have been accounted for. Without knowledge of the environmental variance, one cannot determine the value of Cov(G,E). Underestimating environmental variance and assuming, without evidence, that Cov(G,E)=0, will lead to an overestimation of Var(G), Var(A), and both broad and narrow sense heritability.

In this context, it becomes impossible to interpret either broad sense or narrow sense heritability rigorously. It is even questionable whether these metrics have any validity at all.

For a more thorough examination of the issue of heritability of IQ along these lines, I recommend dusting off a Science paper from 1974 by Layzer entitled “Heritability analyses of IQ scores: science or numerology?”.

What Our Genes Tell Us About Race
By Michael White

The debate over race and intelligence has a long and tarnished history, although that doesn’t mean it’s not a legitimate scientific question to address. However, the debate has taken place almost entirely outside modern genetics, falling instead within the realm of psychology (such as work done by Arthur Jensen). Some writers would have you believe that science is converging on a consensus that the ‘IQ’ gap between various races is genetic (and that liberal conspirators are trying to cover it up). That claim is false. Researchers have not identified a single genetic variant with an impact on intelligence that falls along population lines. In fact several studies have recently tested variants in genes that appear to be involved in controlling brain size. No correlation with intelligence was found. Yes, genetics does play a significant role in intelligence, and many other traits. But there is simply no genetic evidence (and I mean real genetics, not psychology) for genetic differences in intelligence between human populations.

Why is this so? Other traits, like skin color, obviously fall along population lines. While skin color is obviously not a 100% reliable predictor, skin color is a major indicator of race. Irish, Kenyans, Pakistanis, and Chinese populations all have clearly different skin tones.

It turns out, not surprisingly, that the genetic variation for some (but not all) skin color genes does in fact follow population divisions, in contrast with most other genetic variation. This is most likely because skin color differences end up being relatively simple – a single variant of a gene (causing lighter skin, for example) can easily become common in a population through natural selection. The result is that you have different human populations with dramatic differences in skin color.

Other traits, however, are much more complex than skin color. Physical differences which are determined not by one, but many different genetic variants, are unlikely to split neatly by population. Intelligence is probably one of the most complex traits humans possess. It is almost certainly affected by variants in many different genes, and many of those genes have other important functions in the body. That means this: two different human populations could have easily developed differences in skin color between them, but differences in intelligence would have been extremely hard to develop, by chance or by natural selection.

Racial conflict has long been a part of human societies. Along with that conflict has come frequent speculation (most famously, but not exclusively among whites with European ancestry) that one race is inferior to another. Some have been worried that modern genetics would substantiate that belief, but our best genetic evidence to date shows those worries unfounded. Genetics does play a large role in the diversity we find among human beings. That diversity, in spite of some dramatic but superficial exceptions like skin color, is shared in common among all races.

Why Race Is Pseudo-Science
By Gerhard Adam

However, the premise is quite simple. If you can’t actually define it in scientific terms, then it cannot be science. Therefore any claims that derive from it are not science. Similarly, we cannot claim that “race” is valid by simply engaging in arm-waving arguments based on the fact that there are genetic differences between various population groups. “Race” must be fully quantifiable as specific heritable trait(s) that serves to identify the group in question.

[ . . . . ]

If the concept of race is to be scientific, then it would need to specifically identify the genetic criteria that is to be used for that differentiation. Merely claiming some external trait isn’t going to do it.

Such simplistic thinking is insufficient to raise the idea of “race” beyond anything except another convenient [or inconvenient as the case may be] cultural grouping.

[ . . . . ]

So, if we really want to pursue the topic of “race” or designating subspecies of humans, then lets do so on a scientific basis, and not some arbitrary socio-cultural designation. If “race” is going to be based on genetics, then it should be intuitively obvious that people will have their “racial” classification changed based solely on their personal family history. As a result, the designation of any particular “race” could actually change from generation to generation. Therefore any claim at racial knowledge that is based on arbitrary external traits rather than the specific genetic traits, is, by definition, wrong 7.

Show me the genes.

http://www.ncbi.nlm.nih.gov/pubmed/15508004

http://www.ncbi.nlm.nih.gov/pubmed/15510170

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1446406/pdf/11076233.pdf

Identically Different: A Scientist Changes His Mind

Another book I picked up from the public library is Identically Different by Tim Spector.

I read the introduction and skimmed the rest of the book. It is about genetic and environmental influences, about the interaction between them, and about heritability and epigenetics. I already have a bunch of books about all of this, and so it is mostly data and ideas I’ve come across before. Still, it is always interesting to read about this subject.

What makes this book somewhat unique is the author himself. He is a research scientist who has been heavily involved in the popularizing of this field. According to the book, he has changed his views in recent years. A revolutionary paradigm shift is happening right now, largely because of new research that is challenging old theories. It’s nice to see that established scientists can and do change their minds, rather than merely old scientists dying and younger scientists replacing them with new perspectives.

Here is from the introduction to this book:

“Until three years ago I was one of the many scientists who took the gene-centric view of the universe for granted. I had spent the last 17 years producing hundreds of twin studies trying to convince a sceptical public and scientific world that virtually every trait and disease had a major genetic influence. My colleagues and I around the world were largely successful in this, and the prospect of finding the genes underlying most diseases looked increasingly certain. But I had a nagging doubt that we were missing something. [ . . . ]

“However, despite the extensive list of successes, a few signs were emerging that the paradigm was wrong. Most of the gene discoveries for common diseases turned out to be interesting in terms of biology, but the more we discovered the less useful each new gene became in accounting for the disease, since each gene is of tiny individual effect. For example, the 30 or so genes discovered for obesity, even when combined, account for only 2 per cent of the disease.

“This was frustrating to all of us working in the field, as it meant that each common disease was contolled not by one gene but by hundreds or even thousands of genes. This would require teams from many countries to combine forces and perform studies of tens, and sometimes hundreds of thousands, of subjects in order to find these tiny effects. Another consequence was that for common diseases (unlike rare monogenic diseases) these gene tests were pretty useless for prediction [ . . . ]

“While hundreds of recent gene discoveries have given us great insights into new disease mechanisms and possible drug targets, the common genes found to date usually account only for less than 5 per cent of the genetic influence. Exactly where the missing 95 per cent comes from is a mystery that is perplexing the field. Most scientists agree that we simply aren’t smart enough to realize what we don’t know. [ . . . ]

“There are few if any examples of environmental factors without a genetic component, and conversely genes don’t work alone and are usually dependent on the cells they live in and their environments. So in a world where hundreds of genes are working together to influence a trait or disease, the old distinction between nature and nurture is simply no longer relevant.”

The introduction is worthy of being read on its own. It could easily be read as a stand-alone essay.

The rest of the book deals with specific issues about traits and diseases. It is all standard analysis for this type of book, but it is useful as a fairly recent review of the research as it was published in 2012. The research is constantly changing which means books quickly become less relevant. As the author points out, “Most scientists agree that we simply aren’t smart enough to realize what we don’t know.” There are more questions than answers at this point. So, any theory is largely speculation, to varying degrees of probability not easily calculated.

I did have one problem with the book. The author seems to still be trapped within the terminological constraints of the old paradigm of nature versus nurture. He constantly refers to percentages of influences being genetic or environmental. Such claims are meaningless. The author speaks of the problem, but doesn’t get to the core issue.

He argues that the research shows that only a tiny percentage of influence is genetics alone and that only a tiny percentage is environment alone. I suspect, to be most accurate, absolutely zero percent of genetics and environment ever acts alone. They are inseparable. Genetics never exists or acts outside of an environment. And an environment that exists without genetics would be an environment that is irrelevant to human biology and behavior.

As David Shenk explains, in The Genius in All of Us, “heritability estimates are statistical phantoms; they detect something in populations that simply does not exist in actual biology.” The larger context of that quote can be found in a previous post of mine, along with quoted material from a bunch of other books. Also, scientific commentary can be found in another of my posts as well.

The paradigm that needs to change isn’t just about data and theory, but also about the terminological and conceptual framework we use to discuss data and theory.

Heritability & Inheritance, Genetics & Epigenetics, Etc

There is so much misinformation and misunderstanding about genetics, inheritance and heritability; also the emerging field of epigenetics. Few discussions online about race, IQ, etc seem worthy of taking seriously. I admit that I don’t understand much about this field of science, but I at least acknowledge its complexity. Some others, however, wish to assert more certainty than the scientific evidence strictly allows.

I have little desire to try to summarize, much less analyze, all of the complexities, even if I did comprehend it well enough to do so. Besides, that is more than is possible in a single blog post. Instead, I’ll offer more than a few helpful resources. Below are some articles and, following that, some passages from books I’ve been reading. If you wish to actually understand these issues or at least not appear absolutely stupid in a discussion, reading these sources might be a good place to start in order to give yourself at least a basic grasp of the diverse research and the key distinctions to keep in mind.

I’ve been slowly working my way through a bunch of dense books (a few of them are found below). I’m trying my best to make sense of this difficult area of knowledge. My only purpose in spending my time in this fashion is to create a groundwork for discussion of the more social and cultural issues that I’m interested in. I want to be able to articulate what the data does and doesn’t show us, maybe even according to present limits of science what it can and can’t show us. I want to get past all the ideological biases and assumptions, on all sides, so as to get to the heart of the matter.

My hope is, in my own small way, to further discussion. To do so, I need to inform myself and in the process maybe others will be better informed as well. The following is some small part of the results of my ongoing studies. It is information to be considered.

* * * * *

Genetic vs. heritable trait
By Razib Khan
Discover Magazine

Rethinking The Genetic Theory Of Inheritance: Heritability May Not Be Limited To DNA
Science Daily

Missing Heritability — Or Whole-Organism Inheritance?
Stephen L. Talbott
The Nature Institute

Rethinking inheritance
Cell Press Discussions

We Still Don’t Know Why We Look Like Our Parents
Genetics? Sure, but it’s not that simple.
By Michael White
Pacific Standard Magazine

Schizophrenia is (arguably*) 80% heritable; it is not 80% genetic
Manchester Psychiatry Society Blog

No Genes for Intelligence
Institute of Science in Society

* * * * *

What’s the Use of Race?: Modern Governance and the Biology of Difference
By Ian Whitmarsh and David S. Jones
pp. 52-3

As critics stress (McCabe and McCabe 2006), the relationship between genotype and phenotype is complex. It is well understood only in exceptional cases, such as single gene diseases like Huntington’s disease or cystic fibrosis, where the presence of a specific, single, changed gene predicts the disease, virtually without exception. Historically, scientists assumed that more conditions would mirror the single gene model and that scientific advances would proceed by identifying a limited set of disease genes with treatments targeted at the associated phenotypes. But these assumptions are increasingly being proved wrong. Instead, researchers are discovering complex, highly contingent relationships between genotype and phenotype that challenge ready explanation. Some are associated with epigenetic events, which are heritable changes in phenotype or gene expression that result from influences external to changes in the underlying DNA (Riddihough and Pennisi 2001). Others remain unexplained, and in many fields, understanding of the genotype-phenotype relationship seems to recede, rather than advance, despite intensive study (Gaedigk et al. 2005; McCabe and McCabe 2006).

* * * * *

What Is Intelligence?
By James Flynn
pp. 39-40

In other words, genetic advantages that may have been quite modest at birth have a huge effect on eventual basketball skills by getting matched with better environments – and genes thereby get credit for the potency of powerful environmental factors, such as more practice, team play, professional coaching. It is not difficult to apply the analogy to IQ. One child is born with a slightly better brain than another. Which of them will tend to like school, be encouraged, start haunting the library, get into top-stream classes, and attend university? And if that child has a separated identical twin that has much the same academic history, what will account for their similar adult IQs? Not identical genes alone – the ability of those identical genes to co-opt environments of similar quality will be the missing piece of the puzzle.

Note that genes have profited from seizing control of a powerful instrument that multiplies causal potency, namely, feedback loops that operate between performance and its environment. A gene-caused performance advantage causes a more-homework-done environment, the latter magnifies the academic performance advantage, which upgrades the environment further by entry into a top stream, which magnifies the performance advantage once again, which gets access to a good university environment. Since these feedback loops so much influence the fate of individuals throughout their life histories, the Dickens/Flynn model calls them “individual multipliers.”

Understanding how genes gain dominance over environment in kinship studies provides the key to how environment emerges with huge potency between generations. There must be persistent environmental factors that bridge the generations; and those factors must seize control of a powerful instrument that multiplies their causal potency.

* * * * *

Ungifted: Intelligence Redefined
By Scott Barry Kaufman
pp. 6-9

In 1990 the behavioral geneticist Thomas J. Bouchard Jr. and his colleagues at the University of Minnesota published a striking finding: about 70 percent of the differences in IQ found among twins and triplets living apart were associated with genetic variation. 8 What’s more, the identical twins (whose genes were assumed to be 100 percent identical * ) were remarkably similar to identical twins reared together on various measures of personality, occupational and leisure-time interests, and social attitudes, despite spending most of their lives apart.

This study, and the hundreds of twin and adoption studies that have been conducted since then, have painted a consistent picture: genetic variation matters. 9 The studies say nothing about how they matter, or which genes matter, but they show quite convincingly that biological variation does matter. Genes vary within any group of people (even among the inhabitants of middle-class Western society), and this variation contributes to variations in these people’s behaviors. The twin findings shouldn’t be understated; it counters many a prevailing belief that we are born into this world as blank slates, completely at the mercy of external forces. 10

The most important lesson researchers have learned from over twenty-five years’ worth of twin studies is that virtually every single psychological trait you can measure— including IQ, personality, artistic ability, mathematical ability, musical ability, writing, humor styles, creative dancing, sports, happiness, persistence, marital status, television viewing, female orgasm rates, aggression, empathy, altruism, leadership, risk taking, novelty seeking, political preferences, television viewing, and even rates of Australian teens talking on their cell phones— has a heritable basis. * Because our psychological characteristics reflect the physical structures of our brains and because our genes contribute to those physical structures, it is unlikely that there are any psychological characteristics that are completely unaffected by our DNA. 11

Unfortunately there is frequent confusion about the meaning of heritability. The most frequent misunderstanding is the purpose of twin studies. Heritability estimates are about understanding sources of similarities and differences in traits between members of a particular population. The results apply only to that population. The purpose is not to determine how much any particular individual’s traits are due to his or her genes or his or her environment. Behavioral geneticists are well aware that all of our traits develop through a combination of both nature and nurture. Heritability estimates are about explaining differences among people, not explaining individual development. The question on the table for them is this: In a particular population of individuals, what factors make those individuals the same as each other, and which factors make them different?

Therefore, twin studies aren’t designed to investigate human development. In recent years developmental psychologists, including L. Todd Rose, Kurt Fischer, Peter Molenaar, and Cynthia Campbell, have been developing exciting new techniques to study intraindividual variation. 12 Intraindividual variation focuses on a single person and looks at how an integrated dynamic system of behavioral, emotional, cognitive, and other psychological processes change across time and situations. New intraindividual techniques allow researchers to focus on a single twin pair and see how nature and nurture interact in nonlinear ways to explain both their similarities and their differences. 13 Both levels of analysis— twin studies and developmental analysis— are informative, but the results from the one do not apply to the other. 14

Many people also confuse heritability with immutability. They hear the word “heritable” and immediately think of “genes,” which then conjures up pictures of a fixed trait that can’t be altered by external forces. In contrast, many people hear the word “environment” and breathe a sigh of relief, thinking the trait is easily modifiable. This requires quite a strong faith in social engineering!

Just because a trait is heritable (and virtually all of our psychological traits are heritable) doesn’t necessarily mean that the trait is fixed or can’t be developed. Virtually all of our traits are substantially genetically influenced and are influenced by environmental conditions. Even though television viewing has a heritable basis, 15 most people don’t think of the activity as being outside our personal control. Indeed, parents frequently control (or try to control) the length of time their children spend sitting in front of the tube.

Another source of confusion is the role of parenting in the development of traits. A common finding in twin studies is that the environments experienced by twins (or any two siblings) do little to create differences in intelligence and personality as adults. In other words, the heritability of traits tends to increase as one ages and escapes the influence of parents. 16 Judith Rich Harris showed that peers exert a greater influence in creating differences in personality among adolescents than parents. 17 But do these findings mean that parents cannot effectively help their child develop their unique traits? Absolutely not. That’s like saying that water has no influence on a fish’s development because all fish live in water. A nurturing family environment is a necessity to help the child flourish, just as a fish needs water to swim and survive.

Just because a variable doesn’t vary doesn’t mean it has no causal impact on a particular outcome. Genes could “account for” 100 percent of the variability in a trait in a particular twin study, but this does not mean that environmental factors, including parental quality, are therefore unimportant in the development of the trait. Instead it turns out that parenting matters in a way that is different from what was originally assumed: Parents matter to the extent that they affect the expression of genes. Parents can exert important influence in the child’s development by nurturing productive interests and helping the child channel destructive inclinations into more productive outlets.

The importance of parenting becomes more salient when we look at a wider range of environments. Only a few of the twins in Bouchard’s original study were reared in real poverty or were raised by illiterate parents, and none were mentally disabled. This matters. Consider a recent study by Eric Turkheimer and colleagues. They looked at 750 pairs of American twins who were given a test of mental ability when they were 10 months old and again when they were 2 years. 18 When looking at the group of kids aged just 10 months, the home environment appeared to be the key variable across different levels of socioeconomic status. The story changed considerably as the children got a bit older and differences in education became more pronounced. For the 2-year-olds living in poorer households, the home environment mattered the most, accounting for about 80 percent of the variation in mental ability. For these kids, genetics played little role in explaining differences in cognitive ability. In wealthy households, on the other hand, genetics explained more of the differences in performance, accounting for nearly 50 percent of all the variation in mental ability.

Prominent behavioral geneticists, including Bouchard, eventually realized that it was time to move on from simply calculating heritability estimates . In a 2009 paper entitled “Beyond Heritability,” researchers Wendy Johnson, Eric Turkheimer, Irving I. Gottesman, and Bouchard concluded that “given that genetic influences are routinely involved in behavior,” “little can be gleaned from any particular heritability estimate and there is little need for further twin studies investigating the presence and magnitude of genetic influences on behavior.” 19

* * * * *

The Mismeasure of Man (Revised & Expanded)
By Stephen Jay Gould
Kindle Locations 463-486

Errors of reductionism and biodeterminism take over in such silly statements as “Intelligence is 60 percent genetic and 40 percent environmental.” A 60 percent (or whatever) “heritability” for intelligence means no such thing. We shall not get this issue straight until we realize that the “interactionism” we all accept does not permit such statements as “Trait x is 29 percent environmental and 71 percent genetic.” When causative factors (more than two, by the way) interact so complexly, and throughout growth, to produce an intricate adult being, we cannot , in principle, parse that being’s behavior into quantitative percentages of remote root causes. The adult being is an emergent entity who must be understood at his own level and in his own totality. The truly salient issues are malleability and flexibility, not fallacious parsing by percentages. A trait may be 90 percent heritable, yet entirely malleable. A twenty-dollar pair of eyeglasses from the local pharmacy may fully correct a defect of vision that is 100 percent heritable. A “60 percent ” biodeterminist is not a subtle interactionist , but a determinist on the “little bit pregnant” model.

Thus, for example, Mr. Murray, in high dudgeon about my review of The Bell Curve (reprinted here as the first essay in the concluding section), writes in the Wall Street Journal ( December 2, 1994), excoriating my supposed unfairness to him:

Gould goes on to say that “Herrnstein and Murray violate fairness by converting a complex case that can yield only agnosticism into a biased brief for permanent and heritable differences.” Now compare Mr. Gould’s words with what Richard Herrnstein and I wrote in the crucial paragraph summarizing our views on genes and race: “If the reader is now convinced that either the genetic or environmental explanations have won out to the exclusion of the other, we have not done a sufficiently good job of presenting one side or the other. It seems highly likely to us that both genes and the environment have something to do with racial differences. What might the mix be?”

Don’t you get it yet, Mr. Murray? I did not state that you attribute all difference to genetics— no person with an iota of knowledge would say such a foolish thing. My quoted line does not so charge you; my sentence states accurately that you advocate “permanent and heritable differences”— not that you attribute all disparity to genetics. Your own defense shows that you don’t grasp the major point. Your statement still portrays the issue as a battle of two sides, with exclusive victory potentially available to one. No one believes such a thing; everyone accepts interaction. You then portray yourself as a brave apostle of modernity and scholarly caution for proclaiming it “highly likely … that both genes and the environment have something to do with racial differences.” You have only stated a truism entirely outside the real issue. When you make the proper distinction between heritability and flexibility of behavioral expression, then we might have a real debate beyond the rhetoric of phrasing.

Kindle Locations 2937-2939

Within- and between-group heredity are not tied by rising degrees of probability as heritability increases within groups and differences enlarge between them. The two phenomena are simply separate . Few arguments are more dangerous than the ones that “feel” right but can’t be justified.

Kindle Locations 6022-6041

The central fallacy in using the substantial heritability of w.thin-group IQ (among whites, for example) as an explanation for average differences between groups (whites vs. blacks, for example) is now well known and acknowledged by all, including Herrnstein and Murray, but deserves a restatement by example. Take a trait far more heritable than anyone has ever claimed for IQ, but politically uncontroversial— body height. Suppose that I measure adult male height in a poor Indian village beset with pervasive nutritional deprivation. Suppose the average height of adult males is 5 feet 6 inches, well below the current American mean of about 5 feet 9 inches. Heritability within the village will be high— meaning that tall fathers (they may average 5 feet 8 inches) tend to have tall sons , while short fathers (5 feet 4 inches on average) tend to have short sons. But high heritability within the village does not mean that better nutrition might not raise average height to 5 feet 10 inches (above the American mean) in a few generations. Similarly the well-documented 15-point average difference in IQ between blacks and whites in America, with substantial heritability of IQ in family lines within each group, permits no conclusion that truly equal opportunity might not raise the black average to equal or surpass the white mean.

Since Herrnstein and Murray know and acknowledge this critique, they must construct an admittedly circumstantial case for attributing most of the black-white mean difference to irrevocable genetics— while properly stressing that the average difference doesn’t help at all in judging any particular person because so many individual blacks score above the white mean in IQ. Quite apart from the rhetorical dubriety of this old ploy in a shopworn genre—“ some-of-my-best-friends-are-group-x”—Herrnstein and Murray violate fairness by converting a complex case that can only yield agnosticism into a biased brief for permanent and heritable difference. They impose this spin by turning every straw on their side into an oak, while mentioning but downplaying the strong circumstantial case for substantial malleability and little average genetic difference (impressive IQ gains for poor black children adopted into affluent and intellectual homes; average IQ increases in some nations since World War II equal to the entire 15-point difference now separating blacks and whites in America; failure to find any cognitive differences between two cohorts of children born out of wedlock to German women, and raised in Germany as Germans, but fathered by black and white American soldiers).

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The Emperor’s New Clothes: Biological Theories of Race at the Millennium
Joseph L. Graves Jr.
Kindle Locations 2115-2146

Such inconsistencies also demonstrate that the psychometricians have only an amateurish grasp of evolutionary genetics. Numerous errors flow from this lack of scientific perspective. The vast majority of Herrnstein and Murray’s evidence is based on phenotypic information; that is, the reputed difference between races is based on some indirect measure of cognitive function, usually a standardized test. The reliance on such tests is made worse by the fact that they have not been conclusively shown to properly measure intellectual function. From these tests, psychometricians infer an underlying genetic difference, despite the fact that standard quantitative genetic protocols are premised on the extensively corroborated demonstration that procedures such as theirs are scientifically invalid. The flaws in their research program are best illustrated in their obsession with the false association between “group heritability” and the necessity of racial differences in IQ. They presume they can show that IQ is inherited genetically and that there must be substantial genetically based differences between the races. Their focus on genetic predestination of intellectual ability is thus their rationale for supporting the status quo because, in their rather limited view, genes cannot be easily altered.

Heritability in the Psychometric Worldview

Much of the argument concerning racial differences in intelligence has focused on an inappropriate assumption, that is, the heritability of IQ. Throughout the debate on race and intelligence, the methodologies used to establish heritability have been fraught with error and fraud. Psychometricians often ignore basic difficulties in estimating quantitative genetic formulas for variation. The fact that IQ test scores have a continuous distribution indicates that whatever cognitive functions are related to these tests must be influenced by many genetic and environmental factors. The formal expression for heritability in the broad sense is simply the ratio of variance in the character due to genetic sources, over all sources of variance. Direct estimates of heritability in laboratory studies can be tedious. They require rigorous control of confounding environmental factors and careful measurements of the phenotype in question.

Consider the equation for VP, the variance in the phenotype:

VP = Vg + Ve + Vg X e + Cov(g,e) + Verroo

where Vg = variance of genetic origin, Ve = variance of environmental origin, Vg X e = variance due to gene X environment interaction, Cov(g,e) = the covariance of genes and environment, and Verror = variance due to errors in measurement. This equation illustrates that one cannot infer that a phenotypic difference between two groups automatically indicates a genetic difference. Under laboratory conditions we can control the environment such that we can eliminate the third and fourth terms of the equation. For example, if we measure the longevity of fruit flies from two different populations and hold all environmental conditions the same for both groups, then we can safely assume that the third and fourth terms are close to zero. This leaves

VP =Vg + Ve + Verror’

If we have carefully measured the longevity phenotype, then we can assume that the difference between the two populations is indeed due to genetic sources. However, there is an additional caveat: before we can make these measurements we must rear the flies under identical conditions for at least two generations because complex phenotypes are strongly influenced by maternal environmental effects. The environmental conditions experienced during development can influence the expression of genes in the adult. It should be clear that none of the rigorous controls that are required to identify genetic effects in the laboratory exist under the conditions in which attempts to measure human IQ have been made.

Psychometricians emphasize the heritability of intelligence. But the particular estimate of the heritability of intelligence, however defined, has little to do with the question of cognitive differences between races because the estimates used to calculate the heritability of intelligence result from studies of close relatives. We already know that most of the genetic variability in the human species is at the level of individuals or families. But family-level variation does not therefore translate directly into racial variation. Data from an experiment in my laboratory examining the effect of a known genetic substitution on the complex trait of longevity revealed significant variation in families within populations but no significant variation between the populations. That is, both populations had family genetic backgrounds that responded differentially to the genetic substitution when measured under rigorously controlled environmental conditions. This is another way of saying that if genes do influence intelligence, then we should expect that all races will have families that run the range of the genetic variability for intelligence. Thus, given the large genetic overlap of human populations, our expectation should be that there is no significant racial difference in intelligence or other behavioral traits.

To this prediction the racists will howl, How then do you explain the persistent IQ differential reported by twentieth-century studies? The answer is elementary; let us look at the conditions under which the tests were given. Do they really adhere to the requirements of a valid test of genetic differentiation? Absolutely not. The problems of the psychometric program do not improve when it attempts to look at specific “genetic” systems reputedly associated with intelligence. After all, Arthur Jensen even admitted that there should be many genes that impact the expression of intelligence, precisely because it is a polygenic trait. It is significant that the psychometricians have been unable to properly define the physiological traits that are purportedly responsible for intelligence and that are differentiated among the racial groups. This lack of precision makes attempts at localizing the genes involved very difficult.

* * * * *

The Bell Curve Wars: Race, Intelligence, and the Future of America
By Steven Fraser
Kindle Locations 163-174

Herrnstein and Murray’s second claim, the lightning rod for most commentary, extends the argument for innate cognitive stratification to a claim that racial differences in IQ are mostly determined by genetic causes-small difference for Asian superiority over Caucasian, but large for Caucasians over people of African descent. This argument is as old as the study of race, and is most surely fallacious. The last generation’s discussion centered on Arthur Jensen’s 1980 book Bias in Mental Testing (far more elaborate and varied than anything presented in The Bell Curve, and therefore still a better source for grasping the argument and its problems), and on the cranky advocacy of William Shockley, a Nobel Prize-winning physicist. The central fallacy in using the substantial heritability of within-group IQ (among whites, for example) as an explanation of average differences between groups (whites versus blacks, for example) is now well known and acknowledged by all, including Herrnstein and Murray, but deserves a restatement by example. Take a trait that is far more heritable than anyone has ever claimed IQ to be but is politically uncontroversial-body height. Suppose that I measured the heights of adult males in a poor Indian village beset with nutritional deprivation, and suppose the average height of adult males is five feet six inches. Heritability within the village is high, which is to say that tall fathers (they may average five feet eight inches) tend to have tall sons, while short fathers (five feet four inches on average) tend to have short sons. But this high heritability within the village does not mean that better nutrition might not raise average height to five feet ten inches in a few generations. Similarly, the well-documented fifteen-point average difference in IQ between blacks and whites in America, with substantial heritability of IQ in family lines within each group, permits no automatic conclusion that truly equal opportunity might not raise the black average enough to equal or surpass the white mean.

Kindle Locations 2281-2307

Ironically, one of the best arguments against the hereditarian approach comes from the genetics of heredity itself.

Heritability (h2), it will be recalled, is technically defined as the percentage of total phenotypic variance in a given trait which is explained by the genes in question, for a given population. More technically, it is the ratio of the additive genetic variance to the phenotypic variance of the trait or character being considered: h2= Vg/Vp. The fact that it is only the additive variance (Va) which enters the equation must be emphasized, since an important additional fact usually goes unmentioned, especially by psychologists, in discussions of heredity. This is the fact that total genetic variance actually contains two other elements, namely, dominance variance (Vd) and epistatic or genetic interaction variance (Vi). Hence complete genetic variance is properly given by the additive equation: Vg = Va + Vd + Vi. Further, taking environment (e) into account, total phenotypic variance on a given trait is Vp = Vg + Ve.

Now, recall that, throughout The Bell Curve, and indeed among all hereditarian psychologists, it is claimed that intelligence, as measured by IQ tests, is highly hereditary: ranging between .40 and .80, and taken to be .60 by Herrnstein and Murray. If we return to the equation for heredity which is commonly employed-and the one used throughout The Bell Curve-(h2= Vg/Vp) in the light of one well established principle of genetic selection, we are immediately faced with what Vale calls a “nice irony.” The selection principle in question is the fact that any trait which has been under strong selection for a long evolutionary period will demonstrate very little additive genetic variance and should consist mainly of dominance and possibly epistatic variance, the reason being that almost all the additive genetic variance-which is the only component of the three elements of total genetic variance that responds to evolutionary selection-will have been “used up,” so to speak. This being so, the hereditarians are faced with an embarrassing, because inexplicable, dilemma. To quote Vale:

It is true of fitness characters that the proportion of additive genetic variance is small. It is therefore noteworthy that not only the total genetic component of variance (heredity in the broad sense or the degree of genetic determination) of IQ has been found to be so large, but that the proportion of additive variance within that component has been found to contribute the most to it…. The question is: If IQ is fitness character, why should the additive variance be anywhere near .71?

Or .60 or .40 or for that matter anywhere other than hovering close to zero, which is where one expects to find the additive genetic variance of a trait that, as the hereditarian psychologists claim, and we fully agree, has been highly selected as an essential factor in the survival and fitness of the human species to its environment.

The problem which Herrnstein, Jensen, and all hereditarian psychologists face then, from the discipline on which they have so heavily drawn, is that IQ scores are too hereditary if they are to sustain the claim that these tests have any significance beyond the test center and classroom. Whatever it is that IQ tests are measuring, whatever it is that g is-whether it be some Platonic ideal, or g for ghost, a pun which Ryle might not have intended when he dismissed the whole thing in his Concept of Mind as “the ghost of the machine”-it could have nothing whatever to do with those vitally important behavioral qualities that meaningfully account for our survival in both broad evolutionary and narrower sociological terms.

I return, then, to my more familiar sociological terrain with this understanding of the problem. Intelligence is not an essence but a process, not some operationally inferred static entity, indicated by IQ tests-and the much beloved analogies with the discovery of gravity and electricity are as pretentious and silly as the tautology that intelligence is whatever it is that IQ tests are testing’-but that mode of thinking, symbolizing, acting, and interacting which, in their totality, facilitates survival in, and/or mastery of, its environment by an individual or group. It is acknowledged that cognitive functioning is central to this behavioral configuration, and further, that genetic factors are important in its determination-that, indeed, intelligence was a major factor in our evolution as a species-but that there is absolutely no way in which we can meaningfully separate genetic and environmental effects, and that, given the impossibility of conducting experiments on human populations, it is practically impossible, theoretically misguided, sociologically reprehensible, and morally obtuse to attempt to separate or even talk about the two as distinct processes.

* * * * *

Race and the Genetic Revolution: Science, Myth, and Culture
“Intelligence, Race, and Genetics”
By Robert J. Sternberg, Elena L Grigorenko, Kenneth K. Kidd, and Steven E. Stemler
pp. 216-220

Most recently, Deary et al. found that “there is still almost no replicated evidence concerning the individual genes, which have variants that contribute to intelligence differences.”89 Of course, the future may bring conclusive identifications: we just do not know yet.

As a result, virtually all attempts to study genes related to intelligence have been indirect, through studies of heritability. But heritability is itself a troubled concept. Are differences in intelligence between so-called races heritable? The question is difficult to answer in part because it is difficult even to say what can be concluded from the heritability statistic commonly used. Consider some facts about heritability.90

What Heritability Tells Us

Heritability (also referred to as h2) is the ratio of genetic variation to total variation in an attribute within a population. Thus, the coefficient of heritability tells us nothing about sources of between-population variation. Moreover, the coefficient of heritability does not tell us the proportion of a trait that is genetic in absolute terms, but rather, the proportion of variation in a trait that is attributable to genetic variation within a specific population.

Trait variation in a population is referred to as phenotypic variation, whereas genetic variation in a population is referred to as genotypic variation. Thus, heritability is a ratio of genotypic variation to phenotypic variation. Heritability has a complementary concept, that of environmentality. Environmentality is a ratio of environmental variation to phenotypical variation. Note that both heritability and environmentality apply to populations, not to individuals. There is no way of estimating heritability for an individual, nor is the concept meaningful for individuals. Consider a trait that has a heritability statistic equaling 70 percent; it is nonsense to say that the development of the trait in an individual is 70 percent genetic.

Heritability is typically expressed on a 0 to 1 scale, with a value of 0 indicating no heritability whatsoever (i.e., no genetic variation in the trait) and a value of 1 indicating complete heritability (i.e., only genetic variation in the trait). Heritability and environmentality add to unity (assuming that the error variance related to measurement of the trait is blended into the environmental component). Heritability tells us the proportion of individual-difference variation in an attribute that appears to be attributable to genetic differences (variation) within a population. Thus, if IQ has a heritability of .50 within a certain population, then 50 percent of the variation in scores on the attribute within that population is due (in theory) to genetic influences. This statement is completely different from the statement that 50 percent of the attribute is inherited.

An important implication of these facts is that heritability is not tantamount to genetic influence. An attribute could be highly genetically influenced and have little or no heritability. The reason is that heritability depends on the existence of individual differences. If there are no individual differences, there is no heritability (because there is a 0 in the denominator of the ratio of genetic to total trait variation in a given population). For example, being born with two eyes is 100 percent under genetic control (except in the exceedingly rare case of severe dismorphologies, with which we will not deal here). Regardless of the environment into which one is born, a human being will have two eyes. But it is not meaningful to speak of the heritability of having two eyes, because there are no individual differences. Heritability is not 1: it is meaningless (because there is a 0 in the denominator of the ratio) and cannot be sensibly calculated.

Consider a second complementary example, occupational status. It has a statistically significant heritability coefficient associated with it,91 but certainly it is not under direct genetic control. Clearly there is no gene or set of genes for occupational status. How could it be heritable, then? Heredity can affect certain factors that in turn lead people to occupations of higher or lower status. Thus, if things like intelligence, personality, and interpersonal attractiveness are under some degree of genetic control, then they may lead in turn to differences in occupational status. The effects of genes are at best indirect.92 Other attributes, such as divorce, may ran in families, that is, show familiality, but again, they are not under direct genetic control; in fact, the familiality may be because they are culturally “inherited.”

Heritability Can Vary Within a Given Population

Heritability is not a fixed value for a given attribute. Although we may read about “the heritability of IQ,”93 there really is no single fixed value that represents any true, constant value for the heritability of IQ or anything else, as Herrnstein and Murray and most others in the field recognize.94 Heritability depends on many factors, but the most important one is the range of environments. Because heritability represents a proportion of variation, its value will depend on the amount of variation. As Herrnstein pointed out, if there were no variation in environments, heritability would be perfect, because there would be no other source of variation.95 If there is wide variation in environments, however, heritability is likely to decrease.

When one speaks of heritability, one needs to remember that genes always operate within environment contexts. All genetic effects occur within a reaction range, so that, inevitably, environment will be able to have differential effects on the same genetic structure. The reaction range is the range of phenotypes (observable effects of genes) that a given genotype (latent structure of genes) for any particular attribute can produce, given the interaction of environment with that genotype. For example, genotype sets a reaction range for the possible heights a person can attain, but childhood nutrition, diseases, and many other factors affect the adult height realized. Moreover, if different genotypes react differently to the environmental variation, heritability will show differences depending on the mean and variance in relevant environments.96 Thus, the statistic is not a fixed value. There are no pure genetic effects on behavior, as would be shown dramatically if a child were raised in a small closet with no stimulation. Genes express themselves through covariation and interaction with the environment, as discussed further later.

Heritability and Modifiability

Because the value of the heritability statistic is relevant only to existing circumstances, it does not and cannot address a trait’s modifiability. A trait could have zero, moderate, or even total heritability and, in any of these conditions, be not at all, partially, or fully modifiable. The heritability statistic deals with correlations, whereas modifiability deals with mean effects. Correlations, however, are independent of score levels. For example, adding a constant to a set of scores will not affect the correlation of that set with another set of scores. Consider height as an example of the limitation of the heritability statistic in addressing modifiability. Height is highly heritable, with a heritability of over .90. Yet height also is highly modifiable, as shown by the fact that average heights have risen dramatically throughout the past several generations.

As an even more extreme example, consider phenylketonuria (PKU). PKU is a genetically determined, recessive condition that arises due to a mutation (or, rather, a number of various rare mutations resulting in similar functional damages to the coded protein, see below) in a single gene, the PAH gene, on chromosome 12 (with a heritability of 1), and yet its effects are highly modifiable. Feeding an infant with PKU a diet free of phenylalanine prevents the mental retardation that otherwise would become manifest. Note also that a type of intellectual disability that once incorrectly was thought to be purely genetic is not. Rather, the intellectual disability associated with PKU is the result of the interaction with an environment (a “normal” diet) in which the infant ingests phenylalanine. Take away the phenylalanine and you reduce level of, or, in optimal cases, eliminate intellectual disability. Note that the genetic endowment does not change: the infant still has a mutant gene causing phenylketonuria. What changes is the manifestation of its associated symptoms in the environment. Similarly, with intelligence or any other trait, we cannot change (at least with our knowledge today) the genetic structure underlying manifestations of intelligence, but we can change those manifestations, or expressions of genes in the environment. Thus, knowing the heritability of a trait does not tell us anything about its modifiability.

* * * * *

The Genius in All of Us: New Insights into Genetics, Talent, and IQ
By David Shenk
Kindle Locations 1003-1031

But the nature of that genetic influence is easily— and perilously— misinterpreted. If we are to take the word “heritability” at face value, genetic influence is a powerful direct force that leaves individuals rather little wiggle room. Through the lens of this word, twin studies reveal that intelligence is 60 percent “heritable,” which implies that 60 percent of each person’s intelligence comes preset from genes while the remaining 40 percent gets shaped by the environment. This appears to prove that our genes control much of our intelligence; there’s no escaping it.

In fact, that’s not what these studies are saying at all.

Instead, twin studies report, on average, a statistically detectable genetic influence of 60 percent. Some studies report more, some a lot less . In 2003, examining only poor families, University of Virginia psychologist Eric Turkheimer found that intelligence was not 60 percent heritable, nor 40 percent, nor 20 percent, but near 0 percent —demonstrating once and for all that there is no set portion of genetic influence on intelligence. “These findings,” wrote Turkheimer , “suggest that a model of [genes plus environment] is too simple for the dynamic interaction of genes and real-world environments during development.”

How could the number vary so much from group to group? This is how statistics work. Every group is different; every heritability study is a snapshot from a specific time and place, and reflects only the limited data being measured (and how it is measured).

More important, though, is that all of these numbers pertain only to groups— not to individuals. Heritability, explains author Matt Ridley , “is a population average, meaningless for any individual person : you cannot say that Hermia has more heritable intelligence than Helena. When somebody says that heritability of height is 90 percent, he does not and cannot mean that 90 percent of my inches come from genes and 10 percent from my food. He means that variation in a particular sample is attributable to 90 percent genes and 10 percent environment . There is no heritability in height for the individual.”

This distinction between group and individual is night and day. No marathon runner would calculate her own race time by averaging the race times of ten thousand other runners; knowing the average lifespan doesn’t tell me how long my life will be; no one can know how many kids you will have based on the national average. Averages are averages— they are very useful in some ways and utterly useless in others. It’s useful to know that genes matter, but it’s just as important to realize that twin studies tell us nothing about you and your individual potential. No group average will ever offer any guidance about individual capability.

In other words, there’s nothing wrong with the twin studies themselves. What’s wrong is associating them with the word “heritability,” which, as Patrick Bateson says, conveys “the extraordinary assumption that genetic and environmental influences are independent of one another and do not interact. That assumption is clearly wrong.” In the end, by parroting a strict “nature vs. nurture” sensibility, heritability estimates are statistical phantoms; they detect something in populations that simply does not exist in actual biology. It’s as if someone tried to determine what percentage of the brilliance of King Lear comes from adjectives. Just because there are fancy methods available for inferring distinct numbers doesn’t mean that those numbers have the meaning that some would wish for.

Kindle Locations 3551-3554

“The models suggest,” Turkheimer wrote, “that in impoverished families, 60% of the variance in IQ is accounted for by the shared environment, and the contributions of genes is close to zero; in affluent families, the result is almost exactly the reverse.” (Italics mine.) (Turkheimer et al., “Socioeconomic status modifies heritability of IQ in young children,” p. 632.)

Kindle Locations 2013-2074

These histones protect the DNA and keep it compact . They also serve as a mediator for gene expression, telling genes when to turn on and off. It’s been known for many years that this epigenome ( “epi-” is a Latin prefix for “above” or “outside”) can be altered by the environment and is therefore an important mechanism for gene-environment interaction.

What scientists didn’t realize, though, was that changes to the epigenome can be inherited. Prior to 1999, everyone thought that the epigenome was always wiped clean like a blackboard with each new generation.

Not so, discovered Enrico Coen. In the case of the Peloria toadflax flower, a clear alteration to the epigenome had subsequently been passed down through many generations.

And it wasn’t just flowers. That same year, Australian geneticists Daniel Morgan and Emma Whitelaw made a very similar discovery in mice. They observed that their batch of genetically identical mice were turning up with a range of different fur colors —differences traced back to epigenetic alterations and passed on to subsequent generations. What’s more, they and other researchers discovered that these fur-color epigenes could be manipulated by something as basic as food. A pregnant yellow mouse eating a diet rich in folic acid or soy milk would be prone to experience an epigenetic mutation producing brown-fur offspring, and even with the pups returning to a normal diet, that brown fur would be passed to future generations .

After that, more epigenetic discoveries piled in one after another:

  • In 2004, Washington State University’s Michael Skinner discovered that exposure to a pesticide in one generation of rats spurred an epigenetic change that led to low sperm counts lasting at least four generations.
  • In 2005, New York University’s Dolores Malaspina and colleagues discovered age-related epigenetic changes in human males that can lead to lower intelligence and a higher risk of schizophrenia in children.
  • In 2006, London geneticist Marcus Pembrey presented data from Swedish medical records to show that nutritional deficiencies and cigarette smoking in one generation of humans had effects across several generations .
  • In 2007, the Institute of Child Health’s Megan Hitchins and colleagues reported a link between inherited epigenetic changes and human colon cancer .

Welcome back, Monsieur Lamarck! “Epigenetics is proving we have some responsibility for the integrity of our genome,” says the Director of Epigenetics and Imprinting at Duke University, Randy Jirtle . “Before, [we thought that] genes predetermined outcomes. Now [we realize that] everything we do—everything we eat or smoke— can affect our gene expression and that of future generations. Epigenetics introduces the concept of free will into our idea of genetics.”

And that of future generations. This is big, big stuff— perhaps the most important discovery in the science of heredity since the gene.

No one can yet measure the precise implications of these discoveries, because so little is known. But it is already clear that epigenetics is going to radically alter our understanding of disease, human abilities, and evolution. It begins with this simple but utterly breathtaking concept:

Lifestyle can alter heredity.

Lamarck was probably not correct about the giraffe in particular, and he was certainly wrong about inherited characteristics being the primary vehicle of evolution. But in its most basic form, his idea that what an individual does in his/ her life before having children can change the biological inheritance of those children and their descendants— on this he turns out to have been correct. (And two hundred years ahead of everyone else.) Quietly, biologists have come to accept in recent years that biological heredity and evolution is a lot more intricate than we once thought. The concept of inherited epigenetic changes certainly does not invalidate the theory of natural selection, but it makes it a lot more complicated. It offers not just another mechanism by which species can adapt to changing environments, but also the prospect of an evolutionary process that is more interactive, less random, and runs along several different parallel tracks at the same time. “DNA is not the be all and end all of heredity,” write geneticists Eva Jablonka and Marion Lamb . “Information is transferred from one generation to the next by many interacting inheritance systems . Moreover, contrary to current dogma, the variation on which natural selection acts is not always random … new heritable variation can arise in response to the conditions of life.”

How do these recent findings impact our understanding of talent and intelligence? We can’t yet exactly be sure. But the door of possibility is wide-open. If a geneticist had suggested as recently as the 1990s that a twelve-year-old kid could improve the intellectual nimbleness of his or her future children by studying harder now, that scientist would have been laughed right out of the conference hall. Today, that preposterous scenario looks downright likely:

Washington, D.C.— New animal research in the February 4 [2009] issue of The Journal of Neuroscience shows that a stimulating environment improved the memory of young mice with a memory-impairing genetic defect and also improved the memory of their eventual offspring . The findings suggest that parental behaviors that occur long before pregnancy may influence an offspring’s well-being. “While it has been shown in humans and in animal models that enriched experience can enhance brain function and plasticity, this study is a step forward, suggesting that the enhanced learning behavior and plasticity can be transmitted to offspring long before the pregnancy of the mother,” said Li-Huei Tsai, PhD, at Massachusetts Institute of Technology and an investigator of the Howard Hughes Medical Institute, an expert unaffiliated with the current study.

In other words, we may well be able to improve the conditions for our grandchildren by putting our young children through intellectual calisthenics now.
What else is possible? Could a family’s dedication to athletics in one or more generations induce biological advantages in subsequent generations?
Could a teenager’s musical training improve the “musical ear” of his great-grandchildren?
Could our individual actions be affecting evolution in all sorts of unseen ways?

“People used to think that once your epigenetic code was laid down in early development, that was it for life,” says McGill University epigenetics pioneer Moshe Szyf. “But life is changing all the time, and the epigenetic code that controls your DNA is turning out to be the mechanism through which we change along with it. Epigenetics tells us that little things in life can have an effect of great magnitude.”

Everything we know about epigenetics so far fits perfectly with the dynamic systems model of human ability. Genes do not dictate what we are to become, but instead are actors in a dynamic process. Genetic expression is modulated by outside forces. “Inheritance” comes in many different forms: we inherit stable genes, but also alterable epigenes; we inherit languages, ideas, attitudes, but can also change them. We inherit an ecosystem, but can also change it.

Everything shapes us and everything can be shaped by us. The genius in all of us is our built-in ability to improve ourselves and our world.

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To say that there is much we don’t control in our lives is a dramatic understatement, roughly on the order of saying that the universe is a somewhat large place. To begin with, there are many influences we can’t even detect. In 1999 , Oregon neuroscientist John C . Crabbe led a study on how mice reacted to alcohol and cocaine. Crabbe was already an expert on the subject and had run many similar studies, but this one had a special twist: he conducted the exact same study at the same time in three different locations (Portland , Oregon; Albany, New York; and Edmonton, Alberta) in order to gauge the reliability of the results. The researchers went to “extraordinary lengths” to standardize equipment, methods, and lab environment: identical genetic mouse strains, identical food, identical bedding, identical cages, identical light schedule, etc. They did virtually everything they could think of to make the environments of the mice the same in all three labs.

Somehow, though, invisible influences intervened. With the scientists controlling for nearly everything they could control, mice with the exact same genes behaved differently depending on where they lived. And even more surprising: the differences were not consistent, but zigged and zagged across different genetic strains and different locations. In Portland, one strain was especially sensitive to cocaine and one especially insensitive , compared to the same strains in other cities. In Albany, one particular strain— just the one— was especially lazy. In Edmonton , the genetically altered mice tended to be just as active as the wild mice, whereas they were more active than the wild mice in Portland and less active than the wild mice in Albany. It was a major hodgepodge.

There were also predictable results. Crabbe did see many expected similarities across each genetic strain and consistent differences between the strains. These were, after all, perfect genetic copies being raised in painstakingly identical environments. But it was the unpredicted differences that caught everyone’s attention. “Despite our efforts to equate laboratory environments, significant and, in some cases, large effects of site were found for nearly all variables,” Crabbe concluded. “Furthermore, the pattern of strain differences varied substantially among the sites for several tests.”

Wow. This was unforeseen, and it turned heads . Modern science is built on standardization; new experiments change one tiny variable from a previous study or a control group, and any changes in outcome point crisply to cause and effect. The notion of hidden, undetectable differences throws all of that into disarray. How many assumptions of environmental sameness have been built right into conclusions over the decades?

What if there really is no such thing? What if the environment turns out to be less like a snowball that one can examine all around and more like the tip of an iceberg with lurking unknowables? How does that alter the way we think about biological causes and effects?

Something else stood out in Crabbe’s three-city experiment : gene-environment interplay . It wasn’t just that hidden environmental differences had significantly affected the results. It was also clear that these hidden environments had affected different mouse strains in different ways— clear evidence of genes interacting dynamically with environmental forces.

But the biggest lesson of all was how much complexity emerged from such a simple model. These were genetically pure mice in standard lab cages. Only a handful of known variables existed between groups. Imagine the implications for vastly more complex animals— animals with highly developed reasoning capability, complex syntax, elaborate tools, living in vastly intricate and starkly distinct cultures and jumbled genetically into billions of unique identities. You’d have a degree of GxE volatility that would boggle any scientific mind— a world where, from the very first hours of life, young ones experienced so many hidden and unpredictable influences from genes, environment, and culture that there’d be simply no telling what they would turn out like.

Such is our world. Each human child is his/ her own unique genetic entity conceived in his/ her own distinctive environment , immediately spinning out his/ her own unique interactions and behaviors. Who among these children born today will become great pianists, novelists, botanists , or marathoners? Who will live a life of utter mediocrity? Who will struggle to get by? We do not know.

Response to ‘Why are zealots so happy?’

Response to ‘Why are zealots so happy?’

Posted on May 29th, 2008 by Marmalade : Gaia Child Marmalade
I came across a recent blog post by C4Chaos titled Why are zealots so happy?

Basically, I do believe such presently uncontrollable factors as genetics do have a disproportionate influence on human experience and behavior, but I’m not sure how disproportionate it is.  This is something I’ve thought about a lot over the years and I did enjoy Seligman’s book even though I’m uncertain about his optimistic conclusions.  I want to look further into the happiness research to see what the latest evidence is showing.

C4Chaos touches upon how happiness fits into religion.  Here is the statistics(from the link in C4Chaos‘ blog) that relate to happy zealots(ie extremists):

SurveySource: 2004 General Social Survey

I would add the morality angle.  What has troubled me over the years is how the ideal of The Good is inextricably tangled with feeling good.  And, yet, I sense they aren’t identical even though there may be an influence.  If there is an influence, does the influence go both ways?  I can imagine how feeling out The Good may help one to feel good.  But by seeking to feel good can we feel out The Good?

Here is an insightful paper that relates:
http://www.ksharpe.com/Word/EP20.htm
The Sense of Happiness:
Biological Explanations and Ultimate Reality and Meaning
Kevin Sharpe

Here is my response to C4Chaos:

I do think there is a connection between discontentment and questioning, and also between discontentment and creatively seeing possibilities.  This translates as unhappy people are more motivated to ask new questions and to seek new answers.  Of course, there is a point of too much discontentment and unhappiness that shuts the mind down.

Here is a nice dialogue between Steven Pinker and Martin Seligman.
http://www.slate.com/?id=2072079&entry=2072402

I’ve read one of Seligman’s books.  His view is that human choice is greater than genetics.  The limitation of his writing is that its basically pop psychology and its only moderately backed up by research.  One thing I remember is that pessimists have a more realistic perception of reality, but optimists have more ability to create a different future.  Its funny that the optimists delusion is what makes them effective, but you don’t want to ask them for objective understanding.  On the other hand, the pessimist knows precisely what is going on, but doesn’t know how or feel capable of changing it.  (Interestingly, I’m a depressed person and I value the straight truth more than anything including happiness… which conforms to this view.)

However, despite the pessimist’s useful ability to see reality clearly, Seligman believes that everyone should strive to be optimistic.  He does concede that society needs a few pessimists to ground the optimists’ vision. But, as I remember, he seems to optimistically think that the strengths of pessimism can be carried over into a more optimistic attitude.

Steven Pinker comes at it from a pure scientific perspective.  He limits himself to what the research says.  And his book isn’t meant as inspirational writing.  I haven’t read his book, but I have recently come across some of the research done on happiness.  Here is an interesting one:
http://www.psych.umn.edu/psylabs/happness/happy.htm
Happiness is a Stochastic Phenomenon
David Lykken and Auke Tellegen
University of Minnesota
Psychological Science Vol.7, No. 3, May 1996

Abstract
“Happiness or subjective wellbeing was measured on a birth-record based sample of several thousand middle-aged twins using the Well Being (WB) scale of the Multidimensional Personality Questionnaire (MPQ). Neither socioeconomic status (SES), educational attainment, family income, marital status, nor an indicant of religious commitment could account for more than about 3% of the variance in WB. From 44% to 53% of the variance in WB, however, is associated with genetic variation. Based on the retest of smaller samples of twins after intervals of 4.5 and 10 years, we estimate that the heritability of the stable component of subjective wellbeing approaches 80%.”

Access_public Access: Public 6 Comments Print Post this!views (266)
 

Nicole : wakingdreamer 

about 10 hours later

Nicole said

wow. very interesting. i wonder why people think zealots are happy? the ones i know are a pretty miserable lot actually…

 

Marmalade : Gaia Child 

about 22 hours later

Marmalade said

Good question.  There is a lot of research out there, but I’m not a scientist.  Here is one paper that looked particularly interesting.

Religious orientation, religious Coping and happiness among UK adults

Christopher Alan Lewis, John Maltby and Liz Day
“In general, no significant associations were found between religiosity scores and happiness scores. However, both higher intrinsic orientation scores and positive religious coping were significantly associated with higher scores on the Oxford Happiness Questionnaire Short-Form. It is proposed that these differential findings are consistent with the theoretical distinction between subjective and psychological well-being. It is suggested that when religiosity is related to happiness, it is related to psychological well-being, which is thought to reflect human development, positive functioning and existential life challenges.”

Here is from the link in C4Chaos’ blog:
http://freakonomics.blogs.nytimes.com/2008/05/14/the-politics-of-happiness-part-4/

“In the 2004 General Social Survey, 35 percent of people who said they were extremely liberal were very happy (versus 22 percent of people who were just liberal). At the same time, a whopping 48 percent of people who were “extremely conservative” gave this response (compared with 43 percent of non-extreme conservatives). Twenty-eight percent of people squarely in the middle – “slightly liberal” to “slightly conservative” – were very happy.”

“A happiness edge enjoyed by the extremes persists even if we control for the other relevant forces like income, education, race, religion, and so on.”

The conclusion of this author is based on 3 factors: evidence showing extremists as more happy than moderates, evidence showing conservatives as more happy than liberals, and evidence showing the religious as more happy than the non-religious.  He notes that conservative extremists are the happiest of any political sector and implies the connection with how vocally religious this group of people are.  Hence, religious zealots are happier.

The conclusion is fairly straightforward.  Any disagreements would be with the research he uses as evidence.  Is it accurate?

 

Marmalade : Gaia Child 

about 22 hours later

Marmalade said

Here are some comments from this section in the series that C4Chaos was linking to:
http://freakonomics.blogs.nytimes.com/2008/05/14/the-politics-of-happiness-part-4/

1. May 14th,
2008
11:43 am

I haven’t read all 4 parts completely but I wonder if this is true all the time. In other words, could the extreme be happy right now because of current conditions in our country? Extreme left: “Change is coming, yoo-hoo!” Extreme right: “We have beaten off terrorists and liberals for 7 years, who would have thought?!”

– Posted by Marcus Lynn
4. May 14th,
2008
11:55 am

Interesting… but isn’t it likely that anyone who rates themselves as “extremely” anything is likely to have strong views in general, and therefore more likely to put “very happy” rather than just “happy”. It would be interesting to see the above graph with numbers of people who are “very UNhappy”

– Posted by Charles
17. May 14th,
2008
2:15 pm

To follow on what frankenduf(14) said:
Psychological studies have shown that when people believe they have control over their lives and actions, they are happier; whether or not they ever exercise that control. Could it be that extremists, because they are more likely to be “acting out”, feel that they are in greater control? Moderates, on the other hand, “moderate” their views to accomodate multiple other points-of-view; in essence, ceding control, and increasing their discomfort.

A second, not necessarily contradictory, explanation would be that cognitive dissonance causes most frustration. Other psychological studies have shown that the more extreme our beliefs, the more likely we are to attribute facts that belie our worldview to chicanery, and the more likely we are to become emotional rather than analytical in response to statements that contradict our ideas. Byt this theory, extremists will become angry, per frankenduf, release anger, and thus avoid unpleasant cognitive dissonance by avoiding considering inconvenient truths.

– Posted by misterb
33. May 16th,
2008
7:04 am

This analysis misses one significant point.

Combined with those in the “moderate” camps, left and right, are those who can’t bother to have strong political opinions. Among these are those who are depressed, clinically or otherwise.

This subset of depressed people can completely skew the numbers when it comes to associating happiness with political fervor.

– Posted by Greta
36. May 18th,
2008
11:47 am

2 comments:
#1: Depressed people tend to have a more accurate self-assessment of their abilities and performance. (I really hate to say “studies show…”, but they do. It’s a simply psychological experiment: give people a task to do, then ask them to rate their own performance.)
It’s certainly been my experience as well….

#2: Well, duh! The message of the study is not that conservatives are happier, it is that IN THE USA, conservatives are happier. It’s an easy bet that in a liberal society, the happiness distribution would be reversed. Anyway you cut it, compared to other nations, the US is politically & religiously conservative society.

So, yeah, you analyze the data controlling for income, education, race, religion, etc, so that you can conclude that conservatives are happier folks, but the results are only valid in the USA!

– Posted by Dennis

 

Nicole : wakingdreamer 

2 days later

Nicole said

interesting… i think there is some amount of truth in each comment… so who can say really what it all means?

 

Marmalade : Gaia Child 

2 days later

Marmalade said

Yes, interesting… but what to make of it?!  I find research about this very intriguing, but I don’t have the capacity to really understand it.  Statistics are so easily interpreted with one’s bias.  Seligman interprets it one way but there is no objective reason for him to interpret it that way.  He gives it an optimistic slant and he is probably the happier for it whether or not he is correct.  🙂

 

Nicole : wakingdreamer 

3 days later

Nicole said

i have similar reservations to you about this whole optimism thing…

and yes, like archaeology where “rocks are plastic” or in other words, diggings can “reveal” many things depending on the assumptions of the scientist or interpreter, statistics can mean pretty much anything. So, IMO are often meaningless