Monthly Archives: October 2015

Nature, Nurture, and the Folly of “Holistic Interactionism.”

[Notable New Media]

by Kenneth W. Krause.

Kenneth W. Krause is a contributing editor and “Science Watch” columnist for the Skeptical Inquirer.  Formerly a contributing editor and books columnist for the Humanist, Kenneth contributes regularly to Skeptic as well.  He may be contacted at krausekc@msn.com.

Most contemporary scientists, according to Harvard University experimental psychologist, Steven Pinker, have abandoned both the nineteenth-century belief in biology as destiny and the twentieth-century doctrine that the human mind begins as a “blank slate.”  In his new anthology, Language, Cognition, and Human Nature: Selected Articles (Oxford 2015), Pinker first reminds us of the now-defunct blank slate’s political and moral appeal:  “If nothing in the mind is innate,” he chides, “then differences among races, sexes, and classes can never be innate, making the blank slate the ultimate safeguard against racism, sexism, and class prejudice.”

Pinker15

Even so, certain angry ideologues, for example, continue to wallow in blank slate dogma.  Gender differences in STEM professions, for example, are often attributed entirely to prejudice and hidden barriers.  The mere possibility that women, on average, are less interested than men in people-free pursuits remains oddly “unspeakable,” says Pinker (but see a recent exception here).  The point, he clarifies, is not that we know for certain that evolution and genetics are relevant to explaining so-called “underrepresentation” in high-end science and math, but that “the mere possibility is often treated as an unmentionable taboo, rather than as a testable hypothesis.”

A similar exception to the general rule centers around parenting and the behavior of children.  It may be true that parents who spank raise more violent children, and that more conversant parents produce children with better language skills.  But why does “virtually everyone” conclude from such facts that the parent’s behavior causes that of the child?  “The possibility that the correlations may rise from shared genes is usually not even mentioned, let alone tested,” says Pinker.

Equally untenable for the author is the now-popular academic doctrine he dubs “holistic interactionism” (HI).  Carrying a “veneer of moderation [and] conceptual sophistication,” says Pinker, HI is based on a few “unexceptional points,” including the facts that nature and nurture are not mutually exclusive and that genes cannot cause behavior directly.  But we should confront this doctrine with heightened scrutiny, according to Pinker, because “no matter how complex the interaction is, it can be understood only by identifying the components and how they interact.”  HI “can stand in the way of such an understanding,” he warns, “by dismissing any attempt to disentangle heredity and environment as uncouth.”

HI mistakenly assumes, for example, that hereditary cannot constrain behavior because genes depend critically on the environment.  “To begin with,” says Pinker, “it is simply not true that any gene can have any effect in some environment, with the implication that we can always design an environment to produce whatever outcome we value.”  And even if some extreme “gene-reversing” environment can be imagined, it simply doesn’t follow that “the ordinary range of environments will [even] modulate that trait, [or that] the environment can explain the nature of the trait.”  The mere existence of environmental mitigations, in other words, does not render the effects of genes inconsequential.  To the contrary, Pinker insists, “genes specify what kinds of environmental manipulations will have what kinds of effects and with what costs.”

Although the postmodernists and social constructionists who tend to dominate humanities departments in American Universities especially, continue to tout HI as a supposedly nuanced means of comprehending the nature-nurture debate, it is in truth little more than a pseudo-intellectual “dodge,” Pinker concludes: a convenient means to “evade fundamental scientific problems because of their moral, emotional, and political baggage.”

Among intellectually honest, truly curious, and consistently rational thinkers (a diminutive demographic indeed), Pinker’s reputation is and has long stood as something perhaps just short of heroic, in no small part due to his defense of politically incorrect but nonetheless scientifically viable hypotheses.  What a shame it is that only academics of similar status (and tenure) can safely rise and demand the freedom required to mount such defenses.  And what a tragedy that so few in such privileged company actually do.

 

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“Race” in 2015: Myth or Reality? (part 2)

[Notable New Media]

by Kenneth W. Krause.

Kenneth W. Krause is a contributing editor and “Science Watch” columnist for the Skeptical Inquirer.  Formerly a contributing editor and books columnist for the Humanist, Kenneth contributes regularly to Skeptic as well.  He may be contacted at krausekc@msn.com.

If we inherit from our parents traits typically associated with “race,” including skin, hair, and eye color, why do most scientists insist that race is more social construct than biological reality?  Are they suffering from an acute case of political correctness, perhaps, or a misplaced paternalistic desire to deceive the irresponsible and short-sighted masses for the greater good of humanity?  More ignoble things have happened, of course, even within scientific communities.  But according to geneticist Daniel J. Fairbanks, the denial of biological “race” is all about the evidence.

In Everyone is African: How Science Explodes the Myth of Race (Prometheus 2015), Fairbanks points out that, although large-scale analyses of human DNA have recently unleashed a deluge of detailed genetic information, such analyses have so far failed to reveal discrete genetic boundaries along traditional lines of racial classification.  “What they do reveal,” he argues, “are complex and fascinating ancestral backgrounds that mirror known historical immigration, both ancient and modern.”

Fairbanks

In 1972, Harvard geneticist Richard Lewontin analyzed seventeen different genes among seven groups classified by geographic origin.  He famously discovered that subjects within racial groups varied more among themselves than their overall group varied from other groups, and concluded that there exists virtually no genetic or taxonomic significance to racial classifications.  Later characterizing that conclusion as “Lewontin’s Fallacy” in 2003, Cambridge geneticist A.W.F. Edwards reminded us how easy it is to predict race simply by looking at people’s genes.

So who was right?  Both of them were, according to Lynn Jorde and Stephen Wooding at the University of Utah School of Medicine.  Summarizing several large-scale studies on the topic in 2004, they confirmed Lewontin’s finding that about 85-90% of all human genetic variation exists within continental groups, while only 10-15% between them.  Even so, as Edwards had insisted, they were also able to assign all native European, east Asian, and sub-Saharan African subjects to their continent of origin using DNA alone.  In the end, however, Jorde and Wooding revealed that geographically intermediate populations–South Indians, for example–did not fit neatly into commonly conceived racial categories.  “Ancestry,” they concluded, was “a more subtle and complex description” of one’s genetic makeup than “race.”

Fairbanks concurs.  Humans have been highly mobile for thousands of years, he notes.  As a result, our biological variation “is complex, overlapping, and more continuous than discreet.”  When one analyzes DNA from a geographically broad and truly representative sample, the author surmises, “the notion of discrete racial boundaries disappears.”

Nor are the genetic signatures of typically conceived racial traits always consistent between populations native to different geographic regions.  Take skin color, for example.  We know, of course, that the first Homo sapiens inherited dark skin previously evolved in Africa to protect against sun exposure and folate degradation, which negatively affects fetal development.  Even today, the ancestral variant of the MC1R gene, conferring high skin pigmentation, is carried uniformly among native Africans.

But around 30,000 years ago, long after our species had first ventured out of Africa into the Caucasus region, a new variant appeared.  KITLG evolved in this population prior to the European-Asian split to reduce pigmentation and facilitate vitamin D absorption in regions of diminished sunlight.  Some 15,000 years later, however, another variant, SLC24A5, evolved by selective sweep as one group migrated west into Europe.  Extremely rare in other native populations, nearly 100% of modern native Europeans carry this variant.  On the other hand, as their varied skin tones demonstrate, African and Caribbean Americans carry either two copies of an ancestral variant, two copies of the SLC24A5 variant, or one of each.  Asians, by contrast, developed their own pigment-reducing variants–of the OCA2 gene, for example–via convergent evolution, a process where similar external traits result independently among different populations due to similar environmental pressures.

So how can biology support traditional notions of race when the genetic signatures of those notions’ most relied upon trait–that is, skin color–are so diverse among people sharing the same or similar degree of skin pigmentation?  Fairbanks finds such ideas utterly bankrupt “in light of the obvious fact that actual variation for skin color in humans does not fall into discrete classes,” but rather “ranges from intense to little pigmentation in continuously varying gradations.”

To long-time science journalist, Nicholas Wade, who, in his recent book, A Troublesome Inheritance, judged that biological races are real and can be distinguished genetically at the continental level, Fairbanks offers the following reply: “Traditional racial classifications constitute an oversimplified way to represent the distribution of genetic variation among the people of the world.  Mutations have been creating new DNA variants throughout human history, and the notion that a small proportion of them define human races fails to recognize the complex nature of their distribution.”

Mom, Dad, and the Epigenetics of Childhood Obesity.

[Notable New Media]

by Kenneth W. Krause.

Kenneth W. Krause is a contributing editor and “Science Watch” columnist for the Skeptical Inquirer.  Formerly a contributing editor and books columnist for the Humanist, Kenneth contributes regularly to Skeptic as well.  He may be contacted at krausekc@msn.com.

A relatively new field of inquiry, epigenetics (literally, “above the genes”) contemplate how heritable and stable changes in gene expression can occur without altering underlying DNA sequences.  It’s also one form of “developmental programming,” where, during critical periods of child development, environmental stimuli can have persistent, even lifelong, impacts on gene expression, metabolism, and disease risk.  As such, parents’ pre-pregnancy and, in the mother’s case, prenatal and postnatal lifestyle choices and environments can affect their children’s risk of subsequent obesity and associated chronic diseases, for example.

Perhaps the clearest instance of epigenetic dysregulation was discovered in an animal study.  Genetically identical agouti mice developed into either the lean brown or obese yellow phenotype depending on the degree of DNA “methylation” (one epigenetic mechanism) at the Avy gene locus.  In humans, however, the classic example occurred during the Dutch Hunger Winter of 1944-1945 when food shortages resulted in dramatic decreases in daily energy intakes.  Here, it was shown that children born to mothers exposed to famine during pregnancy suffered an increased risk of obesity, heart disease, and diabetes later in life–indeed, 60 years after the famine.

To explain this strange effect, the “mismatch hypothesis” is frequently invoked.  Poor maternal nutrition, some researchers argue, might signal to the fetus that food is scarce and cause the fetus to adapt its metabolism epigenetically by reducing energy demands and increasing its propensity to store fat.  It has been further suggested that such a mechanism might also account for the rapid rise in obesity rates in still-developing nations where populations continue to migrate from rural to urban areas and begin to experience a novel abundance of energy-rich foods.

But what about parental over-nutrition–can moms and dads unwittingly predispose their developing fetuses to obesity and its related diseases because of their excessive eating (and inadequate exercise) habits?  In Examining a Developmental Approach to Childhood Obesity: the Fetal and Early Childhood Years, the Institute of Medicine gathered a diverse group of scientists to explore how the risk of childhood obesity can be affected by (1) maternal and paternal nutrition prior to conception, (2) maternal and placental nutrition during pregnancy, and (3) maternal and infant nutrition following delivery.

Epigenetics of Childhood Obesity

Although the precise means of such changes remain obscure, much evidence now suggests that parental over-consumption behaviors do indeed affect their unborn and newborn children’s risks of overweight and its associated complications.  According to Jacob Friedman, professor of pediatrics at the University of Colorado, Denver, “obesity begets obesity.”  Both animal and human studies, he reports, demonstrate that prenatal and postnatal exposures to maternal obesity predispose infants to early-onset metabolic disease and childhood obesity.

For example, Friedman continued, the pre-pregnancy BMI of mothers can predict higher newborn liver fat at two weeks of age, which continues to increase during lactation.  During breastfeeding, maternal diet and obesity can also affect the child’s immune system along with infant behavior, weight gain, and risk of obesity.  Epidemiological evidence also suggests that, independent of lifestyle factors, the effect of maternal obesity can haunt children over their entire life spans.

So understood, the fact that overweight and obesity rates among women of childbearing age have “increased fairly dramatically” in recent years–with the largest increases found in the Americas, Oceania, and the Caribbean–seems to demand our immediate attention.  Sixty percent of all women aged 20 to 39, and nearly 80 percent of black and Hispanic women in the same age range, are now overweight or obese.  Predictably, the fastest-growing rates of childhood obesity are found among low-income populations.

Although mothers certainly possess a greater capacity to shape their children’s phenotypes, fathers are not necessarily off the hook.  Their sperm can also be exposed to harmful (as well as beneficial) behaviors and other environmental influences, and some researchers believe that epigenetic mechanisms may affect certain RNA molecules–previously implicated as having an early developmental role in obesity–delivered to the oocyte via the male gamete.

The authors are careful, of course, to caution us that epigenetic causation has yet to be firmly established.  Nevertheless, they argue, “Increasing evidence suggests that a number of environmental factors, including nutrition, can affect the epigenome and that the epigenome seems most susceptible to those environmental factors during the prenatal, neonatal, and pubertal periods.”

Why would nature provide such a mechanism?  The epigenome, unlike its “host” genome, can respond to rapidly changing environments that are likely to change again.  Its effects are not necessarily permanent.  So the good news is that parents might save their children a great deal of trouble and suffering simply by substituting good nutritional behaviors and environments for bad.

 

Reference:

Institute of Medicine. 2015. Examining a developmental approach to childhood obesity: The fetal and early childhood years: Workshop summary. Washington D.C.: The National Academies Press. 159 pp.