The Survival of Genes for Stupidity:

Consistency of Fitness and Heritability

To appear: Personality and Individual Differences

Abstract

Elsewhere, it is argued that intelligence could not be both a heritable trait and one that has made an important contribution to fitness because fitness related traits usually show low heritability. However, pleitropy and balancing selection could maintain such traits. The currently observed smaller families of the more intelligent is a too recent effect to explain the survival of genes for low intelligence. The recently reported mitochondrial DNA allele (15,925 bp in the region coding for threonine tRNA) adversely affecting intelligence in whites (but absent in blacks) affecting intelligence may be an example of an intelligence raising gene with adverse effects through decreased maximal oxygen consumption. An alternative location (13,365 bp, affecting energy metabolism) for the intelligence affecting mutation is proposed. The apparent slower ageing in the better educated and the more intelligent may be due to less free radical oxidative damage. However, intelligence is an unique trait in that it requires an observer who is himself intelligent to be observed. Thus, at the time in human evolutionary history when the concept of intelligence is first developed by the most intelligent, it is to be expected that alleles for low intelligence will still be being eliminated.

High Heritability Is Not Inconsistent with Intelligence Being Fitness Related

A question frequently posed is, if high intelligence is beneficial and under genetic control, how come the genes for low intelligence are still so common?

This is not the place for a long discussion on what is intelligence. Briefly , what is meant by intelligence here is g, or the common factor that can be extracted when a battery of cognitive tests are given (Jensen, 1980). In modern societies this correlates with virtually all known tests of mental ability, and with brain size (Rushton & Ankney, 1996). It is plausible (but not proven) that in prehistoric times g was also a fitness characteristic which helped in solving social, economic, and survival problems (Miller 1991), including ones of choosing and monitoring mates (Miller 1995). While intelligence is a phenotypic trait there is strong evidence from behavioral genetic studies that much of the variability in it is genetic in origin, and there are standard behavior genetic methods for estimating the percentage of the observed phenotypic variability that is genetic in origin, a number that is referred to as the heritability. This heritability is usually found to be at least .5 (Jensen, 1980; Herrnstein & Murray, 1994; Rushton, 1995).

Traits that are subject to strong selection normally show little genetic variability (i.e. low heritability). Usually such variables reach their equilibrium values quickly, and are not observed in the process of reaching equilibrium. This is predicted by theory (Falconer,1989) and it has been found empirically that in non-human species that the traits that appear closest related to fitness tend to have lower heritabilities (Gustafsson, 1986; Mousseau & Roff, 1987; Roff &Mousseau, 1987).

As an example of this critique, Patterson (1995, p. 210) gives great weight to Vale's (1980, p. 435) rhetorical question, "If IQ is a fitness character, why should the additive variance be anywhere near.71?". Vale goes on to argue, "The answer of course is that it should not, if indeed IQ is closely related to fitness. If it is not so related, then presumably it has not been selected for throughout human evolution. If it has not been selected for, then it evidently has not played a very great role in that evolution."

One answer to the problem is provided by Whitney, (1976) who points out that the prediction of low genetic variability in a fitness characteristic applies only if the environment remains unchanged for a large number of generations, and it is unlikely that the human environment has been unchanged for enough generations (remembering humans are very long lived, and that many environmental changes can be documented from the historical, archaeological, and climatic records).Another possibility for explaining the survival of genes for other than the highest intelligence (which at first glance do appear to be more widespread than would be predicted if mental capacity were indeed a fitness characteristic) is that there could be disadvantages to the genes for intelligence that offset the fitness advantages of these genes. In such a case, the net effect of the gene on fitness would be neutral, and the gene would be not selected against. In another paper, the author (Miller, 1994) has speculated that thicker myelin contributes to intelligence. If there is no disadvantage to genes in the brain to the genes for superior intelligence, one may wish to look to the rest of the body to find an offsetting disadvantage. Perhaps these genes divert essential fatty acids to the brain at the expense of the rest of the body, creating an offsetting disadvantage for these genes in the functioning of organs that also use the same fatty acids.

Offsetting Effects for the New Mitochondrial Allele

One way of answering this question is to look for some disadvantage to the genes for high intelligence such that they would not be selected for. One possibility is the well known tendency for the more intelligent to have fewer children (see the summary by Lynn, 1996, of the many papers on this, or Herrnstein & Murray, 1994; Rethford, &Sewell, 1988; Van Court & Bean, 1985). If this tendency has existed throughout prehistory, one could imagine greater survival due to higher intelligence offsetting the less intelligent's greater number of children, with the net effect being to keep the genes for low intelligence in the population. However, the evidence is that the smaller families of the intelligent is a relatively recent phenomenon due to the less intelligent's frequent contraceptive failure, and the more intelligent women consciously choosing careers over children. The dysgenic trend has emerged too recently to explain the survival of gene sfor low intelligence (Lynn, 1996).

Recently, evidence has been presented (Skuder, Plomin, McClearn,Smith, Vignetti, Chorney, Chorney, Kasarda, Thompson, Detterman, Petrill, Daniels, Owen, & McGuffin, 1995) that a mitochondrial mutation(at 15,925 base pairs, in the region coding for threonine tRNA) is a quantitative trait loci for intelligence. In this study intelligence was defined as "the first unrotated principal component scores derived from a battery of psychometric tests, which included the Wechsler Intelligence Scale for Children Revised (WISC-R) subtests and correlated.95 with full -scale IQ scores from the WISC-R."

The paper reported that in several populations the frequencies "of the two alleles (called MspI-morph 1 and Msp-morph) were similar to the frequencies of 86% and 14% in the present study." All of the populations mentioned were Eurasian ones. Interestingly, "Africans, on the other hand, lack MspI-morph4, which is instead common in Caucasians and Orientals." (Scozzari et al, 1988, p. 543). It is perhaps fortunate that the first possibly intelligence lowering allele identified should be virtually absent in blacks, while present in whites. Of course, this frequency difference alone is insufficient to refute the strong evidence for blacks, on average, being less intelligent than whites. (Herrnstein& Murray, 1994; Rushton, 1995).

In Caucasians, this polymorphism could be maintained by balancing selection arising from the relevant allele having positive effects on intelligence and negative effects on muscle performance. Thesame morph has been claimed to increase maximal oxygen consumption in humans (Dionne, Turcotte, Thibault, Boulay, Skinner, & Bouchard, 1993).However, the claim is based on the same subjects that are also used to support a claim of increased oxygen consumption for another morph at a different location. The second location (13,365 bp) more plausibly could affect oxygen consumption since it codes for one of the five subunit enzyme complexes (complex I in which reduced nicotinamide adeninedinucleotide is oxidized) on the mitochondrial inner membrane which through oxidative phosphorylation provide the energy for all cells(Wallace, 1992), including the neurons in the brain. For at least one mitochondrial mutation, the effects of at least one mitochondrial mutation have been shown to have similar effects on energy metabolism in both the brain and the muscles (Barbiroli, Montagna, Cortelli, Iotti,Lodi, Barboni, Monari, Lugaresi, Frassineti, & Zaniol, 1995). Thus the morph reported as affecting intelligence at a point that codes for threonine tRNA may be serving as a marker for a genetic variation that directly affects the brain's energy use.

Haier has presented evidence derived from positron emission tomography that the brains of high IQ individuals use less energy than the brains of low IQ individuals (Haier, Siegel, Nuechterlein, Hazlett,Wu, Paek, Browing, & Buchsbaum, 1988; also see Haier, Siegel, Tang,Abel, & Buchsbaum, 1992; Haier, Chueh, Touchette, Lott, Buchsbaum, MacMillan, Sandman, LaCasse, & Sosa, 1995; and Larson, Haier, LaCasse, &Hazen, 1995). The case for mitochondrial genes affecting oxygen consumption is increased by the knowledge that the mitochondria are responsible for much of the body's energy production, and by the observation that human offspring resemble their mothers more than their fathers in this respect (Lesage, Simoneau, Jobin, Leblanc, & Bouchard,1985). It is known that long distance running performance is related to maximum aerobic performance as measured by oxygen consumption (Morgan,Baldini, Martin, & Kohrt, 1987). Thus, a high maximal oxygen consumption when exercising at peak capacity would probably have been an asset for primitive man. If the gene that produces such high muscle output also lower the individual's intelligence, the two effects could offset each other, making the gene close to neutral for fitness, even though low intelligence alone would have reduced fitness.

There is one more reason for looking at the possibility that a mitochondrial mutation (or mutations) that lower IQ may raises oxygen consumption.

One theory of ageing is that much of it occurs as a result of cumulative oxidative damage to the cells from free radicals, including the neurons, with oxidative reactions in mitochondria being a major source of free radicals (Holliday, 1995). The higher the rate at which a cell uses oxygen during its lifetime, the shorter its life should be. Thus, if some individuals have mitochondrial mutations that raise IQ, but lower oxygen consumption, it would be predicted that they would live longer. It would also be predicted that this longer life would be especially apparent in the cells (such as neurons) that are not replaced during the individuals life. Indeed, there is evidence (Joseph, 1992)suggesting oxidative damage may play a role in senescence of neurons.

It has been known for a good while that the higher socio-economic parts of the population lived longer than the lower socio-economic parts. This has usually be attributed to the depressing effects of poverty on life span through poorer medical care, nutrition, housing, etc. However, studies of nuns living in a common environment showed that college graduates lived longer (89.4 years for sisters with bachelor's degree, 82.2 years for sisters with some high school or college, and 82.0 years for sisters with only a grade school education)and maintained their ability to care for themselves longer thann on-college graduates (Snowdon, Ostwald, & Kane, 1989).

Recently, part of the same study showed that a measure of verbal ability predicted Alzheimers fifty years later (Snowdon, Kemper,Mortimer, Greiner, Wekstein, & Markesbery, 1996) among these nuns livingin a common environment. Evidence also showed that the decrease in Mini-Mental State Exam scores with age was less in sisters with bachelor's degrees (which is here interpreted as a surrogate for IQ)than in sisters without bachelor's degrees (Snowdon, Butler, & Ashford,1996).

The highly-educated had better mobility and hand coordination, stronger handgrip, better distant and near visual acuity, and fewer mental impairments than the low-educated group (Snowdon, Ostwald, Kane, & Keenan, 1989). While the longer retention of mental functioning might merely indicate that those that started with more mental abilities retained enough ability to function adequately longer, the mobility, handgrip, and visual acuity data indicates that the rate of ageing did indeed appear to be slower in the more educated, suggesting that there was something fundamental that affected both intellectual functioning at the time people are going to college (or deciding not to), and fifty years later when they are old and retired. The Nun Study investigated the relationship of plasma antioxidants to reduced functional capacity in the elderly, and found that higher levels of the anti-oxidant lycopene had a strong negative association with dependence in self-care(Snowdon, Gross, & Butler, 1996)

One of the factors that makes for the wide variability in intelligence is assortative mating in which people choose mates who have intelligence resembling their own. This significantly widens the range of observed intelligence (Jensen, 1978). However, since assortative mating does not change gene frequencies, this observation makes no contribution to explaining the genes for low intelligence's survival.

Why Humans Intelligence is Unique

However, even leaving aside the possibility of pleiotropic genes, there is a good reason for rejecting the argument about the inconsistency of genetic variability for intelligence and high heritability for human intelligence, even while accepting the validity of the argument for most traits in most species.

Intelligence, since it is needed to discover its own existence, occupies a special position among all traits. As intelligence gradually increases, it is to be expected that a few individuals with sufficient intelligence to do psychometrics, and discover the concept of g will emerge. When the distribution of intelligence has risen to the point where some individuals do psychometrics, others will be of much lower intelligence. Because natural selection requires variability to operate on, any trait will show variability while selection is occurring. At this time, only a small fraction of the population is likely to have sufficient intelligence to do psychometrics and to understand the concept of g. Thus, soon (in evolutionary time) after the development of the concept of intelligence, a finding of a wide range in intelligence is to be expected. Thus, even if intelligence contributes to fitness, a wide range in the heritable aspects of intelligence is not as surprising as it might appear to those trained on non-humans, or human traits other than intelligence.

Thus, Patterson's (1995, p. 196) argument "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" is wrong. This would be a much more powerful argument if applied to any trait other than intelligence.

In general, a trait can be contributing to fitness and be selected for without the trait having reached its genetic limit, although powerful selection makes it more likely that the limit will be rapidly approached, making it harder to observe the organism in the process of being selected. For a trait subject to the type of selection in which one animal having the trait increases the benefit of an even higher level of the trait in another individual (the so called arms race or Red Queen effect, see Ridley, 1994), the period of adaptation is increased. If intelligence is subject to unidirectional selection in which the more intelligent benefit reproductively from being able to outwit those of lower intelligence, it is likely that at any given time there will be some of higher intelligence than others, thus solving the problem in another way.

The same argument can be extended to populations. Because of the wide geographical area Homo sapiens occupy, its long generations, and the obstacles to gene flow across tribes (Rouhani, 1989), there are likely to be differences in the intelligence of different populations a tany time. When some populations have reached the point of having the technology to explore the world, they are likely to discover that other populations have not yet developed to this point, and they can be expected to conclude that there are differences between the world's various populations in intelligence.

Conclusions

The process of intelligence raising natural selection will inevitably produce a dispersion in intelligence while it is raising intelligence. Psychometrics and the concept of intelligence will likely be developed when there are enough highly intelligent individuals to do so. When this happens there will still be many less intelligent individuals. It follows that there is no problem in intelligence being a highly heritable trait which also makes a difference to the fitness of the individuals carrying it, at least not within the first few thousand years of this potential difficulty first being raised.

References

Barbiroli, B., Montagna, P., Cortelli, P., Iotti, S., Lodi, R., Barboni, P., Monari, L., Lugaresi, E., Frassineti, C., & Zaniol, P., (1995). Defective brain and muscle energy metabolism shown by in vivo 31P magnetic resonance spectroscopy in nonaffected carriers of 11778 mtDNA mutation. Neurology, 45, 1364 -1369

Butler, S. A., Ashford, J. W., & Snowdon, D. A., (1996). Age, education and changes in the Mini-Mental State Exam scores of older women: Findings from the Nun Study, Journal of the American Geriatrics Society, 44, 675-681.

Dionne, F.T., Turcotte, L., Thibault, M., Boulay, M. R., Skinner, J.S., & Bouchard, C, (1993). Mitochondrial DNA sequence polymorphism, VO2max, and response to endurance training. Medicine & Science in Sports & Exercise, 25, 766-774.

Falconer, D. S. (1989). Introduction to Quantitative Genetics. New York: John Wiley & Sons.

Gustafsson, L., (1986). Lifetime reproductive success and heretability: Empirical support for Fisher's Fundamental Theorem. The American Naturalist, 128, 761-764.

Haier, R. J., Siegel, B. V., Nuechterlein, K. H., Hazlett, E., Wu, J. C., Paek, J., Browing, H. L., & Buchsbaum, M. S. (1988). Cortical glucose metabolic rate: correlates of abstract reasoning and attention studied with positron emission tomography. Intelligence, 12, 199-217.

Haier, R. J., Siegel, B., Tang, C., Abel, L., & Buchsbaum, M. S. (1992). Intelligence and changes in regional cerebral glucose metabolic rate following learning. Intelligence, 16, 415-426.

Haier, R. J., Chueh, D., Touchette, P., Lott, I., Buchsbaum, M. S., MacMillan, D., Sandman, C., LaCasse, L., & Sosa, E. (1995). Brain size and cerebral glucose metabolic rate in non-specific mental retardation and Down syndrome. Intelligence, 29, 191-210.

Herrnstein, R. J. & Murray, C. (1994). The Bell Curve: Intelligence and Class Structure in American Life. New York: The Free Press.

Holliday, R. (1995). Understanding Ageing. Cambridge: Cambridge University Press.

Jensen, A. R. (1978). Genetic and behavioral effects of nonrandom mating. In R. T. Osborne, C. E. Noble, & N. Weyl (eds), Human Variation: the Biopsychology of Age, Race, and Sex (pp. 51-105). New York: Academic Press.

Jensen, A. R. (1980). Bias In Mental Testing. New York: The Free Press.

Joseph, J. A. (1992). The putative role of free radicals in the loss of neuronal functioning in senescence. Integrative Physiological and Behavioral Science, 27, 216-227.

Larson, G. E., Haier, R. J., LaCasse, L., & Hazen, K. (1995). Evaluation of a "mental effort" hypothesis for correlations between cortical metabolism and intelligence. Intelligence, 21, 267-278.

Lesage, R., Simoneau, J., Jobin, J., Leblanc, J. & Bouchard, C. (1985). Familial resemblance in maximal heart rate, blood lactate, and aerobic power, Human Heriditary, 35, 182-289.

Lynn, R. (1996). The Case for Dysgenics: Genetic Deterioration in Modern Populations. Manuscript.

Miller, E. M. (1991). Climate and Intelligence, Mankind Quarterly, XXXII 127-132.

Miller, E. M. (1994). Intelligence and brain myelination: A hypothesis. Personality and Individual Differences, 17, 803-833.

Miller, E. M. (1995). Environmental Variability Selects for Large Families only in Special Circumstances: Another Objection to Differential K Theory. Personality and Individual Differences, 19 , 903-918.

Morgan, D. W., Baldini, F. D., Martin, P. E., & Kohrt, W. M. (1987). Ten kilometer performance and predicted velocity at VO2max among well-trained male runners. Medicine and Science in Sports and Exercise, 21, 78-83.

Mousseau, T. A. & Roff, D. A. (1987). Natural selection and the heritability of fitness components. Heredity, 58, 181-197.

Patterson, O. (1995). For whom the bell curves. In Fraser, S. (Ed.) The Bell Curve Wars. New York: Basic Books.

Rethford, R. D. & Sewell, W. H. (1988). Intelligence and family size reconsidered. Social Biology, 35, 1-40.

Ridley, M. (1994). The Red Queen: Sex and the Evolution of Human Nature. New York: Macmillan.

Roff, D. A. & Mousseau, T. A. (1987). Quantitative genetics and fitness: Lessons from Drosophila. Heredity, 58, 103-118.

Rouhani, S. (1989). Molecular genetics and the pattern of human evolution: plausible and implausible models. In Mellars, P. & Stringer, C. (Eds.), The human revolution.. Princeton: Princeton University Press.

Rushton, J. P. (1995) Race, Evolution and Behavior: A Life History Perspective, New Brunswick: Transaction Publishers.

Rushton, J.P. & Ankney, C.D. (1996). Brain size and cognitive ability: Correlations with age, sex, social class, and race", Psychonomic Bulletin and Review, 3, 21-36.

Scozzari, R., Torroni, A. Semino, O, Sirugo, G., Brega, A. & Santachiara-Benerecetti, A. S. (1988). Genetic studies on the Sengal population. I. mitochondrial DNA polymorphisms. American Journal of Human Genetics, 43, 534-544.

Skuder, P., Plomin, R., McClearn, G., Smith, D., Vignetti, S., Chorney, M., Chorney, K., Kasarda, S., Thompson, L., Detterman, D., Petrill, S., Daniels J., Owen, M., & McGuffin, P. (1995). A polymorphism in mitochondrial DNA associated with IQ? Intelligence, 21, 1-12.

Snowdon, D. A., Gross, M. D., & Butler, S. M. (1996). Antioxidants and reduced functional capacity in the elderly: Findings from the Nun Study. Journals of Gerontology: Medical Sciences, 51A(1), M10-M16.

Snowdon, D. A. , Kemper, S. J., Mortimer, J. A., Greiner, L. H., Wekstein, D. R. & Markesbery, W. R. (1996). Linguistic ability in early life and cognitive function and Alzheimer's disease in late life: Findings From the Nun Study. Journal of the American Medical Association (JAMA), 275, 528-532.

Snowdon, D. A., Ostwald, S. K., & Kane, R L.(1989). Education, survival, and independence in elderly Catholic sisters, 1936-1988. American Journal of Epidemiology,130, 999-1012

Snowdon, D. A., Ostwald, S. K. , Kane, R L.& Keenan, N. L. (1989) Years of life with good and poor mental and physical function in the elderly. Journal of Clinical Epidemiology, 42, 1055-1066.

Vale, J. R. (1980). Genes, Environment, and Behavior: An Interactionist Approach. Cambridge, Harper and Rowe.

Van Court, M. & Bean, F. D. (1985) Intelligence and fertility in the United States: 1912-1982. Intelligence, 9, 23-32.

Wallace, D. C. (1992). Mitochondrial genetics: A paradigm for aging and degenerative diseases. Science, 256, 628-632.

Whitney, G. (l976) Genetic considerations in studies of the evolution of the nervous system and behavior. In: Masterton, R.B., W. Hodos, & H. Jerison (Eds.), Evolution, Brain, and Behavior: Persistent Problems. Hillsdale, NJ, Lawrence Erlbaum Associates, Pubs., pp79-106.