Our Fragile Intellect

Last updated

"Our Fragile Intellect" is a 2012 article by American biochemist Gerald Crabtree, published in the journal Trends in Genetics . Crabtree's speculative and controversial thesis argues that human intelligence peaked sometime between 2,000 and 6,000 years ago and has been in steady decline since the advent of agriculture and increasing urbanization. Modern humans, according to Crabtree, have been losing their intellectual and emotional abilities due to accumulating gene mutations that are not being selected against as they once were in our hunter-gatherer past. [1] [2] This theory is sometimes referred to as the "Idiocracy hypothesis". [3]

Contents

Thesis

Crabtree argues that advancements in modern science allow new predictions to be made about both the past and the future of humanity and we can predict "that our intellectual and emotional abilities are genetically surprisingly fragile". [4] Recent studies of genes correlated with human intelligence on the X chromosome indicate typical intellectual and emotional activity depends on 10% of genes. Intelligence-dependent (ID) genes appear to be widely distributed throughout the entire genome, leading to a figure of 2,000 and 5,000 genes responsible for our cognitive abilities. Deleterious mutations in these genes can impact normal intellectual and emotional functioning in humans. It is thought that in just the last 120 generations (3000 years), humans have received two or more harmful mutations to these genes, or one every 20-50 generations. [4] [5] Crabtree points out that he loves our society's supportive institutions and wishes that they could be extended to include more of our population. The data that support the theory that our intellectual abilities are particularly susceptible to the accumulation of mutations begins with determinations of the human intergenerational mutation rate. This rate has been determined in several human populations to be about 1.20 x10-8 per position per haploid genome [6] [7] [8] [9] with an average father's age of 29.7 years. This rate doubles every 16.5 years with the father's age and ascribes most of the new mutations to the father during the production of sperm. [10] In contrast to popular opinion, this figure indicates that the biological clock (in terms of accumulation of deleterious mutations with time) is ticking faster for men than for women. This figure of 1.20 x10-8 mutations per nucleotide per generation predicts that about 45 to 60 new mutations will appear in each generation. These mutations might accumulate or be removed by natural selection. The speculation that the nervous system and the brain would be more sensitive than other cell types and organs to the accumulation of these new mutations was based on the estimate of the fraction of genes necessary for normal development of the nervous system. The data quantifying the number of genes required for normal intellectual development comes from thousands of published studies (about 23,000 on PubMed from the National Library of Medicine) in which scientists have identified a mutated gene or a region of DNA associated with or causing human intellectual disability. These genes may not even be expressed in the brain. For example, the phenylalanine hydroxylase gene is expressed only in the liver, yet its mutation leads to severe intellectual disability due to the accumulation of metabolites. [11] [12] Many of these genes operate like links on a chain rather than a robust network underlining the fragility of our intellectual abilities. For example, mutations of a single nucleotide out of the 3 billion human nucleotides in our genomes in one copy of the ARID1B gene are a common cause of intellectual disability. [13] Estimates of the total number of genes that when mutated give rise to intellectual disability is thought to be several thousand, perhaps 10-20% of all human genes, which produces a very large target for random mutations. In addition, neuronal genes tend to be large [14] [15] and hence increase the size of the genomic target region for random mutations. The simple combination of the number and size of genes required for normal brain development (>1000) and the fact that each new human generation has 45-60 new mutations per genome led Crabtree to suggest that our intellectual abilities are particularly genetically fragile over many generations. Seemingly the only practical implication of this theory is that perhaps men should have their children when they are young and that women should prefer younger men for mates.

Several counterarguments are presented. The Flynn effect, for example, shows an apparent increase in IQ around the world since 1930. Crabtree attributes the rise in IQ to advancements in environmental and public health measures as well as improved education and other factors. The Flynn effect also shows, argues Crabtree, not an increase in intelligence, but more intelligent test taking. [4] [16]

Reception

Kevin Mitchell, associate professor at the Smurfit Institute of Genetics at Trinity College Dublin agreed that genetic mutations could harm the development of the brain in humans and diminish intelligence; new mutations would become apparent in new generations. However, Mitchell criticizes Crabtree for failing to acknowledge the role of natural selection. According to Mitchell, natural selection "definitely has the ability to weed out new mutations that significantly impair intellectual ability". Mitchell describes Crabtree's argument as a conceptual fallacy and says Crabtree is "thinking about things in a wrong way". [2]

Biologist Steve Jones, Emeritus Professor of Genetics at University College London questioned the journal's decision to publish the paper, calling the study "a classic case of Arts Faculty science. Never mind the hypothesis, give me the data, and there aren't any". [17] Crabtree acknowledges that the data isn't there because a slow genetic deterioration in intelligence can't be detected by comparing it to people today. Instead, Crabtree argues that he is synthesizing already existing data and making a purely mathematical argument that estimates the probability of the number of new mutations that could result in cognitive deficits in future generations. [18]

Anthropologist Robin Dunbar at Oxford University argues against Crabtree's position that brain size was driven by tool use. Instead, Dunbar argues that the social environment drives intelligence. "In reality what has driven human and primate brain evolution is the complexity of our social world", says Dunbar. "That complex world is not going to go away. Doing things like deciding who to have as a mate or how best to rear your children will be with us forever." [19]

Cultural trope

Writer Andrew Brown notes that Crabtree's paper represents a familiar, reoccurring notion in both fiction and evolutionary biology. "The idea that civilized man is a degenerate and self-domesticated variation on the wild type is partly a cultural trope, a result of the anxieties of industrialized life", writes Brown. The idea, Brown observes, was popular in the early 20th century fiction of E. M. Forster ("The Machine Stops") and Jack London ( The Scarlet Plague ). It could also be found in the work of biologists such as Ronald Fisher, who espoused similar concepts in The Genetical Theory of Natural Selection (1930). The most important parts of Fisher's book, Brown writes, expounds on the theme that "civilization is dreadfully threatened by the way the lower classes outbreed the aristocracy." Brown finds related sentiments expressed in the work of W. D. Hamilton, who believed that the "life-saving efforts of modern medicine" threatened the human genome. [20]

See also

Related Research Articles

<span class="mw-page-title-main">Mutation</span> Alteration in the nucleotide sequence of a genome

In biology, a mutation is an alteration in the nucleic acid sequence of the genome of an organism, virus, or extrachromosomal DNA. Viral genomes contain either DNA or RNA. Mutations result from errors during DNA or viral replication, mitosis, or meiosis or other types of damage to DNA, which then may undergo error-prone repair, cause an error during other forms of repair, or cause an error during replication. Mutations may also result from substitution, insertion or deletion of segments of DNA due to mobile genetic elements.

<span class="mw-page-title-main">Human genome</span> Complete set of nucleic acid sequences for humans

The human genome is a complete set of nucleic acid sequences for humans, encoded as the DNA within each of the 24 distinct chromosomes in the cell nucleus. A small DNA molecule is found within individual mitochondria. These are usually treated separately as the nuclear genome and the mitochondrial genome. Human genomes include both protein-coding DNA sequences and various types of DNA that does not encode proteins. The latter is a diverse category that includes DNA coding for non-translated RNA, such as that for ribosomal RNA, transfer RNA, ribozymes, small nuclear RNAs, and several types of regulatory RNAs. It also includes promoters and their associated gene-regulatory elements, DNA playing structural and replicatory roles, such as scaffolding regions, telomeres, centromeres, and origins of replication, plus large numbers of transposable elements, inserted viral DNA, non-functional pseudogenes and simple, highly repetitive sequences. Introns make up a large percentage of non-coding DNA. Some of this non-coding DNA is non-functional junk DNA, such as pseudogenes, but there is no firm consensus on the total amount of junk DNA.

A microsatellite is a tract of repetitive DNA in which certain DNA motifs are repeated, typically 5–50 times. Microsatellites occur at thousands of locations within an organism's genome. They have a higher mutation rate than other areas of DNA leading to high genetic diversity. Microsatellites are often referred to as short tandem repeats (STRs) by forensic geneticists and in genetic genealogy, or as simple sequence repeats (SSRs) by plant geneticists.

<span class="mw-page-title-main">Fragile X syndrome</span> X-linked dominant genetic disorder

Fragile X syndrome (FXS) is a genetic neurodevelopmental disorder characterized by mild-to-moderate intellectual disability. The average IQ in males with FXS is under 55, while about two thirds of affected females are intellectually disabled. Physical features may include a long and narrow face, large ears, flexible fingers, and large testicles. About a third of those affected have features of autism such as problems with social interactions and delayed speech. Hyperactivity is common, and seizures occur in about 10%. Males are usually more affected than females.

<span class="mw-page-title-main">FOXP2</span> Transcription factor gene of the forkhead box family

Forkhead box protein P2 (FOXP2) is a protein that, in humans, is encoded by the FOXP2 gene. FOXP2 is a member of the forkhead box family of transcription factors, proteins that regulate gene expression by binding to DNA. It is expressed in the brain, heart, lungs and digestive system.

Gene duplication is a major mechanism through which new genetic material is generated during molecular evolution. It can be defined as any duplication of a region of DNA that contains a gene. Gene duplications can arise as products of several types of errors in DNA replication and repair machinery as well as through fortuitous capture by selfish genetic elements. Common sources of gene duplications include ectopic recombination, retrotransposition event, aneuploidy, polyploidy, and replication slippage.

<span class="mw-page-title-main">Single-nucleotide polymorphism</span> Single nucleotide in genomic DNA at which different sequence alternatives exist

In genetics and bioinformatics, a single-nucleotide polymorphism is a germline substitution of a single nucleotide at a specific position in the genome. Although certain definitions require the substitution to be present in a sufficiently large fraction of the population, many publications do not apply such a frequency threshold.

<span class="mw-page-title-main">Human genetic enhancement</span> Technologies to genetically improve human bodies

Human genetic enhancement or human genetic engineering refers to human enhancement by means of a genetic modification. This could be done in order to cure diseases, prevent the possibility of getting a particular disease, to improve athlete performance in sporting events, or to change physical appearance, metabolism, and even improve physical capabilities and mental faculties such as memory and intelligence. These genetic enhancements may or may not be done in such a way that the change is heritable.

Genetic genealogy is the use of genealogical DNA tests, i.e., DNA profiling and DNA testing, in combination with traditional genealogical methods, to infer genetic relationships between individuals. This application of genetics came to be used by family historians in the 21st century, as DNA tests became affordable. The tests have been promoted by amateur groups, such as surname study groups or regional genealogical groups, as well as research projects such as the Genographic Project.

<span class="mw-page-title-main">Mutation rate</span> Rate at which mutations occur during some unit of time

In genetics, the mutation rate is the frequency of new mutations in a single gene, nucleotide sequence, or organism over time. Mutation rates are not constant and are not limited to a single type of mutation; there are many different types of mutations. Mutation rates are given for specific classes of mutations. Point mutations are a class of mutations which are changes to a single base. Missense, nonsense, and synonymous mutations are three subtypes of point mutations. The rate of these types of substitutions can be further subdivided into a mutation spectrum which describes the influence of the genetic context on the mutation rate.

<span class="mw-page-title-main">Identity by descent</span> Identical nucleotide sequence due to inheritance without recombination from a common ancestor

A DNA segment is identical by state (IBS) in two or more individuals if they have identical nucleotide sequences in this segment. An IBS segment is identical by descent (IBD) in two or more individuals if they have inherited it from a common ancestor without recombination, that is, the segment has the same ancestral origin in these individuals. DNA segments that are IBD are IBS per definition, but segments that are not IBD can still be IBS due to the same mutations in different individuals or recombinations that do not alter the segment.

<span class="mw-page-title-main">Mutant</span> Phenotypically-different organism resulting from a mutation

In biology, and especially in genetics, a mutant is an organism or a new genetic character arising or resulting from an instance of mutation, which is generally an alteration of the DNA sequence of the genome or chromosome of an organism. It is a characteristic that would not be observed naturally in a specimen. The term mutant is also applied to a virus with an alteration in its nucleotide sequence whose genome is in the nuclear genome. The natural occurrence of genetic mutations is integral to the process of evolution. The study of mutants is an integral part of biology; by understanding the effect that a mutation in a gene has, it is possible to establish the normal function of that gene.

<span class="mw-page-title-main">MT-ND6</span> Mitochondrial gene coding for a protein involved in the respiratory chain

MT-ND6 is a gene of the mitochondrial genome coding for the NADH-ubiquinone oxidoreductase chain 6 protein (ND6). The ND6 protein is a subunit of NADH dehydrogenase (ubiquinone), which is located in the mitochondrial inner membrane and is the largest of the five complexes of the electron transport chain. Variations in the human MT-ND6 gene are associated with Leigh's syndrome, Leber's hereditary optic neuropathy (LHON) and dystonia.

<span class="mw-page-title-main">Cat genetics</span> Study of inheritance in domestic cats

Cat genetics describes the study of inheritance as it occurs in domestic cats. In feline husbandry it can predict established traits (phenotypes) of the offspring of particular crosses. In medical genetics, cat models are occasionally used to discover the function of homologous human disease genes.

<span class="mw-page-title-main">Neurogenetics</span> Study of role of genetics in the nervous system

Neurogenetics studies the role of genetics in the development and function of the nervous system. It considers neural characteristics as phenotypes, and is mainly based on the observation that the nervous systems of individuals, even of those belonging to the same species, may not be identical. As the name implies, it draws aspects from both the studies of neuroscience and genetics, focusing in particular how the genetic code an organism carries affects its expressed traits. Mutations in this genetic sequence can have a wide range of effects on the quality of life of the individual. Neurological diseases, behavior and personality are all studied in the context of neurogenetics. The field of neurogenetics emerged in the mid to late 20th century with advances closely following advancements made in available technology. Currently, neurogenetics is the center of much research utilizing cutting edge techniques.

<span class="mw-page-title-main">Gene redundancy</span>

Gene redundancy is the existence of multiple genes in the genome of an organism that perform the same function. Gene redundancy can result from gene duplication. Such duplication events are responsible for many sets of paralogous genes. When an individual gene in such a set is disrupted by mutation or targeted knockout, there can be little effect on phenotype as a result of gene redundancy, whereas the effect is large for the knockout of a gene with only one copy. Gene knockout is a method utilized in some studies aiming to characterize the maintenance and fitness effects functional overlap.

<span class="mw-page-title-main">Genome evolution</span> Process by which a genome changes in structure or size over time

Genome evolution is the process by which a genome changes in structure (sequence) or size over time. The study of genome evolution involves multiple fields such as structural analysis of the genome, the study of genomic parasites, gene and ancient genome duplications, polyploidy, and comparative genomics. Genome evolution is a constantly changing and evolving field due to the steadily growing number of sequenced genomes, both prokaryotic and eukaryotic, available to the scientific community and the public at large.

Genome instability refers to a high frequency of mutations within the genome of a cellular lineage. These mutations can include changes in nucleic acid sequences, chromosomal rearrangements or aneuploidy. Genome instability does occur in bacteria. In multicellular organisms genome instability is central to carcinogenesis, and in humans it is also a factor in some neurodegenerative diseases such as amyotrophic lateral sclerosis or the neuromuscular disease myotonic dystrophy.

Cognitive genomics is the sub-field of genomics pertaining to cognitive function in which the genes and non-coding sequences of an organism's genome related to the health and activity of the brain are studied. By applying comparative genomics, the genomes of multiple species are compared in order to identify genetic and phenotypical differences between species. Observed phenotypical characteristics related to the neurological function include behavior, personality, neuroanatomy, and neuropathology. The theory behind cognitive genomics is based on elements of genetics, evolutionary biology, molecular biology, cognitive psychology, behavioral psychology, and neurophysiology.

Gerald R. Crabtree is the David Korn Professor at Stanford University and an Investigator in the Howard Hughes Medical Institute. He is known for defining the Ca2+-calcineurin-NFAT signaling pathway, pioneering the development of synthetic ligands for regulation of biologic processes and discovering chromatin regulatory mechanisms involved in cancer and brain development. He is a founder of Ariad Pharmaceuticals, Amplyx Pharmaceuticals, Foghorn Therapeutics, and Shenandoah Therapeutics (Shenandoah Therapeutics was mentioned in a July 26, 2023 New York Times online article by Gina Kolata).

References

  1. ↑ Kim, JuJu. (2012, November 15). "Human Beings Are Getting Dumber, Says Study ". Time.
  2. 1 2 Boyle, Rebecca. (2012, November 19). "Are People Getting Dumber? One Geneticist Thinks So Archived 2012-12-02 at the Wayback Machine ". PopSci. Retrieved December 6, 2012.
  3. ↑ Adee, Sally. (2013, April 1). Stupidity: What makes people do dumb things Archived 2015-04-02 at the Wayback Machine . New Scientist. 216(2910): 30-33. Retrieved December 20, 2013.
  4. 1 2 3 Crabtree, Gerald R. (2013). "Our fragile intellect. Part I". Trends in Genetics. 29: 1–3. doi:10.1016/j.tig.2012.10.002.
  5. ↑ Brooks, Rob. (2012, November 19). "Is human intellect on the downward slide? Archived 2012-11-30 at the Wayback Machine ". The Conversation. Retrieved December 7, 2012.
  6. ↑ Roach, J. C.; Glusman, G.; Smit, A. F.; Huff, C. D.; Hubley, R.; Shannon, P. T.; Rowen, L.; Pant, K. P.; Goodman, N.; Bamshad, M.; Shendure, J.; Drmanac, R.; Jorde, L. B.; Hood, L.; Galas, D. J. (2010). "Analysis of genetic inheritance in a family quartet by whole-genome sequencing". Science. 328 (5978): 636–639. Bibcode:2010Sci...328..636R. doi:10.1126/science.1186802. PMC   3037280 . PMID   20220176.
  7. ↑ Kondrashov, A. (2012). "Genetics: The rate of human mutation". Nature. 488 (7412): 467–468. Bibcode:2012Natur.488..467K. doi:10.1038/488467a. PMID   22914161.
  8. ↑ Campbell, C. D.; Eichler, E. E. (2013). "Properties and rates of germline mutations in humans". Trends in Genetics. 29 (10): 575–584. doi:10.1016/j.tig.2013.04.005. PMC   3785239 . PMID   23684843.
  9. ↑ Michaelson, J. J.; Shi, Y.; Gujral, M.; Zheng, H.; Malhotra, D.; Jin, X.; Jian, M.; Liu, G.; Greer, D.; Bhandari, A.; Wu, W.; Corominas, R.; Peoples, A.; Koren, A.; Gore, A.; Kang, S.; Lin, G. N.; Estabillo, J.; Gadomski, T.; Singh, B.; Zhang, K.; Akshoomoff, N.; Corsello, C.; McCarroll, S.; Iakoucheva, L. M.; Li, Y.; Wang, J.; Sebat, J. (2012). "Whole-genome sequencing in autism identifies hot spots for de novo germline mutation". Cell. 151 (7): 1431–1442. doi:10.1016/j.cell.2012.11.019. PMC   3712641 . PMID   23260136.
  10. ↑ Kong, A.; Frigge, M. L.; Masson, G.; Besenbacher, S.; Sulem, P.; Magnusson, G.; Gudjonsson, S. A.; Sigurdsson, A.; Jonasdottir, A.; Jonasdottir, A.; Wong, W. S.; Sigurdsson, G.; Walters, G. B.; Steinberg, S.; Helgason, H.; Thorleifsson, G.; Gudbjartsson, D. F.; Helgason, A.; Magnusson, O. T.; Thorsteinsdottir, U.; Stefansson, K. (2012). "Rate of de novo mutations and the importance of father's age to disease risk". Nature. 488 (7412): 471–475. Bibcode:2012Natur.488..471K. doi:10.1038/nature11396. PMC   3548427 . PMID   22914163.
  11. ↑ Fini, M. A.; Monks, J.; Farabaugh, S. M.; Wright, R. M. (2011). "Contribution of xanthine oxidoreductase to mammary epithelial and breast cancer cell differentiation in part modulates inhibitor of differentiation-1". Molecular Cancer Research : MCR. 9 (9): 1242–1254. doi:10.1158/1541-7786.MCR-11-0176. PMC   3175308 . PMID   21775420.
  12. ↑ Woo, S. L.; Lidsky, A. S.; Güttler, F.; Chandra, T.; Robson, K. J. (1983). "Cloned human phenylalanine hydroxylase gene allows prenatal diagnosis and carrier detection of classical phenylketonuria". Nature. 306 (5939): 151–155. Bibcode:1983Natur.306..151W. doi:10.1038/306151a0. PMID   6316140.
  13. ↑ Deciphering Developmental Disorders Study; et al. (2017). "Prevalence and architecture of de novo mutations in developmental disorders". Nature. 542 (7642): 433–438. Bibcode:2017Natur.542..433M. doi:10.1038/nature21062. PMC   6016744 . PMID   28135719.
  14. ↑ McCoy, M. J.; Fire, A. Z. (2024). "Parallel gene size and isoform expansion of ancient neuronal genes". Current Biology. 34 (8): 1635–1645.e3. Bibcode:2024CBio...34.1635M. doi:10.1016/j.cub.2024.02.021. PMC  11043017. PMID   38460513.
  15. ↑ King, I. F.; Yandava, C. N.; Mabb, A. M.; Hsiao, J. S.; Huang, H. S.; Pearson, B. L.; Calabrese, J. M.; Starmer, J.; Parker, J. S.; Magnuson, T.; Chamberlain, S. J.; Philpot, B. D.; Zylka, M. J. (2013). "Topoisomerases facilitate transcription of long genes linked to autism". Nature. 501 (7465): 58–62. Bibcode:2013Natur.501...58K. doi:10.1038/nature12504. PMC   3767287 . PMID   23995680.
  16. ↑ Ghose, Tia. (2012, November 12). "Are humans becoming less intelligent? It could very well be Archived 2012-11-17 at the Wayback Machine ". LiveScience . NBCNews.com. Retrieved December 6, 2012.
  17. ↑ Connor, Steve. (2012, November 12). "Human intelligence 'peaked thousands of years ago and we've been on an intellectual and emotional decline ever since'". The Independent. Retrieved December 6, 2012.
  18. ↑ Flatow, Ira. (2012, November 16). "Are We Getting Dumber? Maybe, Scientist Says". National Public Radio. Science Friday. (audio Archived 2013-01-16 at the Wayback Machine ). Retrieved December 20, 2012.
  19. ↑ Collins, Nick (2012, November 12). "Civilisation is making humanity less intelligent, study claims". Telegraph Online. Retrieved December 21, 2012.
  20. ↑ Brown, Andrew. (2012, November 13). "Why it's unlikely we are more stupid than our hunter-gatherer ancestors Archived 2020-01-21 at the Wayback Machine . The Guardian. Retrieved December 20, 2013.

Further reading

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.