The Genius in All of Us: New Insights Into Genetics, Talent, and IQ (25 page)

   In a 2009 essay for the
New York Times Magazine
, Steven Pinker writes: “For most … traits, any influence of the genes will be
probabilistic
. Having a version of a gene may change the odds, making you more or less likely to have a trait, all things being equal, but as we shall see, the actual outcome depends on a tangle of other circumstances as well.” (Italics mine.)

While this is important acknowledgment that most genes do not determine traits directly, the use of the word “probabilistic” is crude and troublesome in two ways: First, it gives a
new
wrong impression about how genes work—making them sound like dice. Second, it misses a critical opportunity to help the general public understand genetic expression and gene-environment interaction.

The term “probabilistic” is meant to convey the understanding that most specific gene variants (alleles) do not guarantee certain outcomes. That much is true.

But the term goes much further. It also conveys the strong sense that a certain gene creates a specific probability that a person will develop a certain trait. That is very misleading—as Pinker himself demonstrates.

To explore the current state of genetics, Pinker had his own DNA analyzed. Among other things, it was revealed that he had the T version of a gene called
rs2180439 SNP
. As it turns out, 80 percent of men with the T version of this gene are bald. Pinker has a head full of curly gray hair. “Something strange happens when you take a number representing the proportion of people in a sample and apply it to a single individual,” he writes. “The first use of the number is perfectly respectable as an input into a policy that will optimize the costs and benefits of treating a large similar group in a particular way. But the second use of the number is just plain weird.”

Exactly. And that is also, in my opinion, why it is a bad idea to use the word “probabilistic” to describe the nature of genes. Genes don’t always lead to certain outcomes, because they are involved in a complex gene-environment dynamic. For the exact same reason, genes also don’t create a specific probability of an outcome.

My argument with the term “probabilistic” is not an argument against population genetics research. Such studies can be darn useful in setting medical policy, as Pinker suggests. But such studies should not drive our descriptive terminology for genes and how they work. (Quotes from Pinker, “My Genome, My Self.”)

    
Proteins are large, specialized molecules that help create cells, transport vital elements, and produce necessary chemical reactions
.

From the online Genetics Home Reference guide:

What are proteins and what do they do?

Proteins are large, complex molecules that play many critical roles in the body. They do most of the work in cells and are required for the structure, function, and regulation of the body’s tissues and organs. Proteins are made up of hundreds or thousands of smaller units called amino acids, which are attached to one another in long chains. There are 20 different types of amino acids that can be combined to make a protein. The sequence of amino acids determines each protein’s unique 3-dimensional structure and its specific function. Proteins can be described according to their large range of functions in the body, listed in alphabetical order:

Examples of protein functions

Antibody:
Antibodies bind to specific foreign particles, such as viruses and bacteria, to help protect the body.

Enzyme:
Enzymes carry out almost all of the thousands of chemical reactions that take place in cells. They also assist with the formation of new molecules by reading the genetic information stored in DNA.

Messenger:
Messenger proteins, such as some types of hormones, transmit signals to coordinate biological processes between different cells, tissues, and organs.

Structural component:
These proteins provide structure and support for cells. On a larger scale, they also allow the body to move.

Transport/storage:
These proteins bind and carry atoms and small molecules within cells and throughout the body.

    
This explains how every brain cell and hair cell and heart cell in your body can contain
all
of your DNA but still perform very specialized functions
.

Lawrence Harper writes:

Every cell inherits a full nuclear complement of DNA. That is, all cells in the organism have the same potential. In the presence of appropriate external conditions, what underlies the development of multicellular organisms is a progressive, differential production (
expression
) of certain subsets of this genetic potential in different tissues … The features of each tissue type are thus determined by the pattern of gene expression, the genes in the cells that are “turned on” or “off” or show distinctive rates of production of gene products. (Harper, “Epigenetic inheritance and the intergenerational transfer of experience,” p. 344.)

    
“Development is chemistry
”:
Brockman, “Design for a Life: A Talk with Patrick Bateson.”

    
All of this means that, on their own, most genes cannot be counted on to directly produce specific traits
.
They are active participants in the developmental process and are built for flexibility. Anyone seeking to describe them as passive instruction manuals is actually minimizing the beauty and power of the genetic design.

Lawrence Harper writes:

Of particular relevance to the understanding of behavioral ontogeny is the fact that, in the process of development, cellular gene expression can be stably altered in response to conditions outside the organism to permit it to adapt to its environment. That is, not only do cells differentiate (specialize in function) in response to external signals, but once so differentiated, their subsequent functional activity as, for example, nerves or glandular tissue, also can be modified at the molecular level. Probably the most obvious example of such altered activity of specialized cells is the development of immunity to pathogens. (Harper, “Epigenetic inheritance and the intergenerational transfer of experience,” p. 345.)

    
“Even in the case of eye color,” says Patrick Bateson, “the notion that the relevant gene is
the
[only] cause is misconceived, because [of] all the other genetic and environmental ingredients
.
” (Italics mine). Bateson, “Behavioral Development and Darwinian Evolution,” p. 149.

   A taste of the complexities behind eye color, from three different sources:

Iris color was one of the first human traits used in investigating Mendelian inheritance in humans. Davenport and Davenport (1907) outlined what was long taught in schools as a beginner’s guide to genetics, that brown eye color is always dominant to blue, with 2 blue-eyed parents always producing a blue-eyed child, never one with brown eyes. As with many physical traits, the simplistic model does not convey the fact that eye color is inherited as a polygenic, not as a monogenic, trait (Sturm and Frudakis, 2004). Although not common, 2 blue-eyed parents can produce children with brown eyes. (McKusick, “Eye Color 1.”)

Human iris color is a quantitative, multifactorial phenotype that exhibits quasi-Mendelian inheritance … To identify genetic features for best-predicting iris color, we selected sets of SNPs by parsing P values among possible combinations … These results confirm that OCA2 is the major human iris color gene and suggest that using an empirical database-driven system, genotypes from a modest number of SNPs within this gene can be used to accurately predict iris melanin content from DNA. (Frudakis, Terravainen, and Thomas, “Multilocus OCA2 genotypes specify human iris colors,” pp. 3311–26.)

The highest association for blue/nonblue eye color was found with three OCA2 SNPs … The TGT/TGT diplotype found in 62.2% of samples was the major genotype seen to modify eye color, with a frequency of 0.905 in blue or green compared with only 0.095 in brown eye color. This genotype was also at highest frequency in subjects with light brown hair and was more frequent in fair and medium skin types, consistent with the TGT haplotype acting as a recessive modifier of lighter pigmentary phenotypes. (Duffy et al., “A three-single-nucleotide polymorphism haplotype in intron 1 of OCA2 explains most human eye-color variation,” p. 241.)

    
Single-gene diseases do exist and account for roughly 5 percent of the total disease burden in developed countries
:
Khoury, Yang, Gwinn, Little, and Flanders, “An epidemiological assessment of genomic profiling for measuring susceptibility to common diseases and targeting interventions,” Hall, Morley, and Lucke, “The prediction of disease risk in genomic medicine.”

Susan Brooks Thistlethwaite adds:

Genetics is not merely a matter of single gene disorders or single gene traits, such as flower color and pod shape in Mendel’s pea plants. Mendelian genetics is about single gene disorders [that] occur in only 3 percent of all individuals born alive …

Human inheritance is much more complicated. Most conditions are polygenic (involve many genes), and their expression depends on gene-gene and environment-gene interactions. (Thistlethwaite,
Adam, Eve, and the Genome
, p. 70.)

    
“A disconnected wire can cause a car to break down
”:
Oyama, Griffiths, and Gray,
Cycles of Contingency
, p. 157.

    
“Genes store information coding for the amino acid sequences of proteins,” explains Bateson
.
“That is all”: Bateson,
Design for a Life
, p. 66.

Similar statement: “All the genes can code for, if they code for anything, is the primary structure (amino acid sequence) of a protein.” (Godfrey-Smith, “Genes and Codes,”. p. 328)

    
One of the most striking early hints of the new understanding of development as a dynamic process emerged in 1957
.