The 10,000 Year Explosion

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https://en.wikipedia.org/wiki/The_10,000_Year_Explosion 

 

The 10,000 Year Explosion: How Civilization Accelerated Human Evolution

Authors	Gregory Cochran Henry Harpending
Language	English
Subject	Recent human evolution
Genre	Non-fiction
Publisher	Basic Books
Publication date	2009
Media type	Print
Pages	304
ISBN	0-465-00221-8
Dewey Decimal	599.93'8-dc22
LC Class	GN281.4.c632 2009

The 10,000 Year Explosion: How Civilization Accelerated Human Evolution is a 2009 book by anthropologists Gregory Cochran and Henry Harpending. Starting with their own take on the conventional wisdom that the evolutionary process stopped when modern humans appeared, the authors explain the genetic basis of their view that human evolution is accelerating, illustrating it with some examples.

Reviewers considered that while the book raised valuable questions, some assumptions also relied on discredited views. It has been criticized for history oversimplification, not allowing to make predictions about future human evolution and for racialism reification.

Opinions in book

Cochran and Harpending put forward the idea that the development of agriculture has caused an enormous increase in the rate of human evolution, including numerous evolutionary adaptations to the different challenges and lifestyles that resulted. Moreover, they argue that these adaptations have varied across different human populations, depending on factors such as when the various groups developed agriculture, and the extent to which they mixed genetically with other population groups.

Such changes, they argue, include not just well-known physical and biological adaptations such as skin colour, disease resistance, and lactose tolerance, but also personality and cognitive adaptations that are starting to emerge from genetic research. These may include tendencies towards (for example) reduced physical strength, enhanced long-term planning, or increased docility, all of which may have been counter-productive in hunter-gatherer societies, but become favoured adaptations in a world of agriculture and its resulting trade, governments and urbanization. These adaptations are even more important in the modern world, and have helped shape today's nation states. The authors speculate that the scientific and Industrial Revolutions came about in part due to genetic changes in Europe over the past millennium, the absence of which had limited the progress of science in Ancient Greece. The authors suggest we would expect to see fewer adaptive changes among the Amerindians and sub-Saharan Africans, who have farmed for the shortest times and were genetically isolated from older civilizations by geographical barriers. In groups that had remained foragers, such as the Australian Aborigines, there would presumably be no such adaptations at all. This may explain why Indigenous Australians and many Native Americans have characteristic health problems when exposed to modern Western diets. Similarly, Amerindians, Aboriginals, and Polynesians, for example, had experienced very little infectious disease. They had not evolved immunities as did many Old World dwellers, and were decimated upon contact with the wider world.

Summary

The book's main thesis is that human civilisation greatly accelerated increases in the rates of evolution. The authors begin their discussion by providing two quotes they feel portray the conventional wisdom on this topic. First, they quote Ernst Mayr as stating in 1963: "Something must have happened to weaken the selective pressure drastically. We cannot escape the conclusion that man's evolution towards manness suddenly came to a halt." Second, they quote Stephen J. Gould as stating in 2000: "There's been no biological change in humans in 40,000 or 50,000 years. Everything we call culture and civilization we've built with the same body and brain."

This had become the established viewpoint—when modern humans appeared, evolution was essentially over. The received wisdom is based on the doctrine that human minds are the same, everywhere: Bastian's Psychic Unity of Mankind. Unfortunately, the authors find, this is no more than wishful thinking. Were it true, human bodies would also be the same worldwide, which clearly they are not. Finns cannot be mistaken for Zulus, nor Zulus for Finns. Not only are there strong reasons to believe that significant human evolution is theoretically possible, or even likely; it is completely obvious that it has taken place, since people are different from one another.

The first four of the book's seven chapters serve as a preamble to the final three. First, Cochran and Harpending present evidence for recent, accelerated human evolution after the invention of agriculture. In itself, this argument represents a paradigm shift, albeit one that now has clear data to back it up. The International HapMap Project and other studies have shown that selection is ongoing and has accelerated over time. This has been a key discovery in human biology, and Cochran and Harpending, building on their own work and that of others such as John Hawks of the University of Wisconsin-Madison, tie the advent of agriculture—and the selection pressures resulting from the new diets, new modes of habitation, new animal neighbors, and new modes of living that agriculture made possible—to this accelerating evolution.

Neanderthals

Wolpoff writes that Cochran and Harpending continue to refute conventional wisdom in their discussion of the Neanderthals. For natural selection to have a chance, they argue, there need to be favourable mutations, or favourable combinations of existing alleles such as genes for blue eyes or pale skin. Cochran and Harpending concentrate on the Neolithic farming revolution as the beginning of major population expansions that provided enough mutations to accelerate genetic change. Infectious diseases were another consequence of the early urban populations and soon became a new source of selection pressures. The origins of many recently adapted genes have now been traced to this period, creating effects such as regional differences in skin colour and skeletal gracility. Adaptations may have sacrificed muscle strength for higher intelligence and less aggressive human behaviours. By 5000 years ago, the authors estimate that adaptive alleles were coming into existence at a rate about 100 times faster than during the Pleistocene. This is the ‘‘explosion’’ of the book’s title.

Research cited by Cochran and Harpending provides evidence of genetic mixing between modern humans and an ancient Homo lineage such as the Neanderthals. According to Cochran and Harpending, it supports the idea that modern humans could have benefited by acquiring adaptive alleles evolved by our Neanderthal relatives - in this case, microcephalin, an adaptive allele associated with brain development. Microcephalin (MCPH1) regulates brain size, and has evolved under strong positive selection in the human evolutionary lineage. One genetic variant of Microcephalin, which arose about 37,000 years ago, increased its frequency in modern humans too rapidly, they argue, to be compatible with neutral genetic drift. As anatomically modern humans emerged from Africa and spread across the globe, the "indigenous" Homo populations they encountered had already inhabited their respective regions for long periods of time and might have been better adapted to the local environments than the colonizers. It follows, it is argued, that modern humans, although probably superior in their own way, could have benefited from adaptive alleles gained by interbreeding with the populations they replaced, as was proposed to be the case for the brain-size-determining gene microcephalin. However, analysis of the genomes of neanderthals did not find the microcephalin gene variant in question to be present, and later studies have not found the gene variant to be associated with mental ability.

Agriculture

Farming, which, the authors note, produces 10 to 100 times more calories per acre than foraging, carried this trend further. Over the period from 10,000 BC to AD 1, the world population increased about a hundredfold - estimates range from 40 to 170 times. An accelerated rate of evolution is a direct result of the larger human population. More people will have more mutations, thereby increasing opportunity for evolutionary change under natural selection. The spread of rapidly expanding populations eventually outpaced the spread of favourable mutations under selection in those populations, so for the first time in human history favourable mutations could not fully disperse throughout the human species. In addition, of course, selection pressures changed once farming was adopted, favouring distinctive adaptations in different geographic areas.

Gene flow

About halfway through the book, Cochran and Harpending pause to consider two different ways of looking at the information found in gene variants. Researchers commonly see them merely as markers of human migration, ignoring their functions. The authors support such research, but argue for a more complete understanding of the geographic distributions of genes. Where the usual geographical analysis treats the distribution of genes as an effect of history, in the authors' view, the genes themselves are a major cause: Two variants in the same gene do not necessarily have the same effect, and their relative, selective benefits will control the spread of genes through populations in both space and time.

Expansions

From that platform the authors discuss ideas that range from the possible origins of the Arthurian legend in Britain to the Spanish colonization of the Americas. Others have attempted this, for example in Jared Diamond's Guns, Germs, and Steel. But, according to Kelleher, Cochran and Harpending go one better than Diamond. He goes on to state that where Diamond was content with environmental determinism, at times opposing the roles of human biology and population differences, Cochran and Harpending embrace them both. Their discussion of gene flow becomes the core of an argument for biology as central to history, and the backdrop for the book's two major hypotheses.

The first seeks to resolve a longstanding debate in historical linguistics by making a case for the Kurgan hypothesis on the origins of the Indo-European language group. The Kurgan theory holds that Indo-European speakers came from lands between the Black and Caspian seas before spreading their language by conquest. The authors suggest that dairy farming and a complementary adaptation - the ability to digest lactose in adulthood - lie behind their conquests. With a walking food source, the milk-drinking warriors defeated their plant-growing neighbours. Drinking milk, from cows, horses, or camels, is a behavior shared by many of history's greatest conquering peoples, whether Kurgans, Scythians, Arabs, or Mongols. Without continuing evolution, the ability to digest milk could never have arisen. In fact, it has done so several times, in different ways, in various places, and it has helped shape human history. Kelleher comments that the authors’ argument makes it difficult to imagine the language in which their book would have been written, were it not for the ability to digest milk.

Ashkenazi Jews

The second major argument, which takes up the final chapter, sets out to explain why Ashkenazi Jews have a mean IQ so much higher than that of the population in general, as well as a higher rate of some genetic disorders such as Tay-Sachs disease. This argument had been published previously in an earlier paper. This hypothesis proposes that from A.D. 800 until around 1700, Askhenazi Jews were restricted to professions that required high intelligence, and that this produced a selective pressure in favor of intelligence. When faced with a sudden threat, evolution may favor any change that offers protection, and Cochran and Harpending propose that selection for genes promoting high intelligence thus had the side effect of also selecting for these genetic disorders. The hypothesis has drawn a mixed reaction from scientists, with some arguing the hypothesis is highly implausible, and others regarding it as worth considering. According to cognitive psychologist Steven Pinker, this theory "meets the standards of a good scientific theory, though it is tentative and could turn out to be mistaken." According to the Southern Poverty Law Center, these claims were based on the work of discredited psychologist Kevin MacDonald.

Reception

The paleoanthropologist Milford H. Wolpoff praised the book's central thesis as being insightful and worthy of further research, while also criticizing the book for its reification of biological race, and its dubious or oversimplified view of history.

In New Scientist, Christopher Willis wrote that the "evidence the authors present an overwhelming case that natural selection has recently acted strongly on us". However, Willis criticizes the authors for not discussing what the "recent and continuing evolution means for our species as a whole". Willis concludes by saying that "the book offers a limited and biased interpretation of some very exciting research".

In Evolutionary Psychology, Gregory Gorelik and Todd K. Shackelford wrote, "Although many of their arguments need more fleshing out and some may not withstand the assault of further scientific analysis, the authors are stunningly creative when considering human history. If even a handful of their arguments survive the onslaught of rigorous scientific scrutiny, Cochran and Harpending will have offered a valuable and novel approach to addressing questions of recent human evolution."

In Evolution and Human Behavior, anthropologist Edward Hagen wrote that the book makes "many unsupported and often questionable assertions", but it is nevertheless valuable in raising "bold questions about major historical encounters between populations — Neanderthal and modern humans, German tribes and Romans, Europeans and Native Americans — in light of formidable (but not unassailable) arguments from population genetics". Hagen considered that it "should also be on the summer reading list of all evolutionary social scientists".

Anthropologist Cadell Last wrote that by using race as a natural fact, the book "undermines the attempt to find a legitimate scientific approach to understanding recent human evolution and conceptualizing human genetic diversity" and that it was "unfortunate" that it had received "praise from prominent, influential well-established biological anthropologists" such as John D. Hawks.

Evolutionary anthropologist Keith Hunley, writing for the Journal of Anthropological Research, described the book's thesis as interesting, but said the list of behavioral adaptations supposedly favored by agricultural lifeways was "bizarre". Per Hunley, the authors "provide no evidence whatsoever that there is any genetic basis to the specific behaviors in their list." Hunley specifically criticizes the last chapter on Ashkenazim for being based on shoddy or fabricated data, and for failing to mention the human suffering caused by pseudoscientific racism. Hunley says the book "fails utterly" to meet the stringent scientific standards of behavioral genetic research.

According to a review in the Financial Times, "Interestingly, the authors make no predictions for our future. And accordingly, biologists – as opposed to social scientists – may not find their thesis all that novel. But it is an engaging book with valuable information about how advantageous genes spread through a population."

In Seed, T.J. Kelleher wrote that "The strength and sheer number of the book’s best sections, however, more than overshadow the wanness and paucity of its worst. Even with its flaws, Cochran and Harpending’s book has provided the best example to date of what E.O. Wilson would recognize as consilient history".

Reporter Ben Schreckinger, writing for Politico in 2017, listed the book among the canon of works which influenced the alt-right's worldview.

Senescence

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Senescence 

Supercentenarian Ann Pouder (8 April 1807 – 10 July 1917) photographed on her 110th birthday. A heavily lined face is common in human senescence.

Senescence (/sɪˈnɛsəns/) or biological aging is the gradual deterioration of functional characteristics. The word senescence can refer either to cellular senescence or to senescence of the whole organism. Organismal senescence involves an increase in death rates and/or a decrease in fecundity with increasing age, at least in the latter part of an organism's life cycle.

Senescence is the inevitable fate of all multicellular organisms with germ-soma separation, but it can be delayed. The discovery, in 1934, that calorie restriction can extend lifespan by 50% in rats, and the existence of species having negligible senescence and potentially immortal organisms such as Hydra, have motivated research into delaying senescence and thus age-related diseases. Rare human mutations can cause accelerated aging diseases.

Environmental factors may affect aging, for example, overexposure to ultraviolet radiation accelerates skin aging. Different parts of the body may age at different rates. Two organisms of the same species can also age at different rates, making biological aging and chronological aging distinct concepts.

Definition and characteristics

Organismal senescence is the aging of whole organisms. Actuarial senescence can be defined as an increase in mortality and/or a decrease in fecundity with age. The Gompertz–Makeham law of mortality says that the age-dependent component of the mortality rate increases exponentially with age.

In 2013, a group of scientists defined nine hallmarks of aging that are common between organisms with emphasis on mammals:

• genomic instability,
• telomere attrition,
• epigenetic alterations,
• loss of proteostasis,
• deregulated nutrient sensing,
• mitochondrial dysfunction,
• cellular senescence,
• stem cell exhaustion,
• altered intercellular communication.

Aging is characterized by the declining ability to respond to stress, increased homeostatic imbalance, and increased risk of aging-associated diseases including cancer and heart disease. Aging has been defined as "a progressive deterioration of physiological function, an intrinsic age-related process of loss of viability and increase in vulnerability."

The environment induces damage at various levels, e.g. damage to DNA, and damage to tissues and cells by oxygen radicals (widely known as free radicals), and some of this damage is not repaired and thus accumulates with time. Cloning from somatic cells rather than germ cells may begin life with a higher initial load of damage. Dolly the sheep died young from a contagious lung disease, but data on an entire population of cloned individuals would be necessary to measure mortality rates and quantify aging.

The evolutionary theorist George Williams wrote, "It is remarkable that after a seemingly miraculous feat of morphogenesis, a complex metazoan should be unable to perform the much simpler task of merely maintaining what is already formed."

Variation among species

Different speeds with which mortality increases with age correspond to different maximum life span among species. For example, a mouse is elderly at 3 years, a human is elderly at 80 years, and gingko trees show little effect of age even at 667 years.

Almost all organisms senesce, including bacteria which have asymmetries between "mother" and "daughter" cells upon cell division, with the mother cell experiencing aging, while the daughter is rejuvenated. There is negligible senescence in some groups, such as the genus Hydra. Planarian flatworms have "apparently limitless telomere regenerative capacity fueled by a population of highly proliferative adult stem cells." These planarians are not biologically immortal, but rather their death rate slowly increases with age. Organisms that are thought be biologically immortal would, in one instance, be the Turritopsis dohrnii, also known as the immortal jellyfish. The Turritopsis dohrnii received such a title by having the ability to revert to its youth when it undergoes stress during adulthood. The reproductive system is observed to remain intact, and even the gonads of the Turritopsis dohrnii are existing.

Some species exhibit "negative senescence", in which reproduction capability increases or is stable, and mortality falls with age, resulting from the advantages of increased body size during aging.

Evolutionary theories of aging

Mutation accumulation

Natural selection can support lethal and harmful alleles, if their effects are felt after reproduction. The geneticist J. B. S. Haldane wondered why the dominant mutation that causes Huntington's disease remained in the population, and why natural selection had not eliminated it. The onset of this neurological disease is (on average) at age 45 and is invariably fatal within 10–20 years. Haldane assumed that, in human prehistory, few survived until age 45. Since few were alive at older ages and their contribution to the next generation was therefore small relative to the large cohorts of younger age groups, the force of selection against such late-acting deleterious mutations was correspondingly small. Therefore, a genetic load of late-acting deleterious mutations could be substantial at mutation–selection balance. This concept came to be known as the selection shadow.

Peter Medawar formalised this observation in his mutation accumulation theory of aging. "The force of natural selection weakens with increasing age—even in a theoretically immortal population, provided only that it is exposed to real hazards of mortality. If a genetic disaster... happens late enough in individual life, its consequences may be completely unimportant". The 'real hazards of mortality' such as predation, disease, and accidents, are known 'extrinsic mortality', and mean that even a population with negligible senescence will have fewer individuals alive in older age groups.

Antagonistic pleiotropy

Another evolutionary theory of aging was proposed by George C. Williams and involves antagonistic pleiotropy. A single gene may affect multiple traits. Some traits that increase fitness early in life may also have negative effects later in life. But, because many more individuals are alive at young ages than at old ages, even small positive effects early can be strongly selected for, and large negative effects later may be very weakly selected against. Williams suggested the following example: Perhaps a gene codes for calcium deposition in bones, which promotes juvenile survival and will therefore be favored by natural selection; however, this same gene promotes calcium deposition in the arteries, causing negative atherosclerotic effects in old age. Thus, harmful biological changes in old age may result from selection for pleiotropic genes that are beneficial early in life but harmful later on. In this case, selection pressure is relatively high when Fisher's reproductive value is high and relatively low when Fisher's reproductive value is low.

Adaptive aging

Programmed theories of aging posit that aging is adaptive, normally invoking selection for evolvability or group selection.

The reproductive-cell cycle theory suggests that aging is regulated by changes in hormonal signaling over the lifespan.

Disposable soma

The disposable soma theory of aging was proposed by Thomas Kirkwood in 1977. The theory suggests that aging occurs due to a strategy in which an individual only invests in maintenance of the soma for as long as it has a realistic chance of survival. A species that uses resources more efficiently will live longer, and therefore be able to pass on genetic information to the next generation. The demands of reproduction are high, so less effort is invested in repair and maintenance of somatic cells, compared to germline cells, in order to focus on reproduction and species survival.

Cellular senescence

Cellular senescence
(upper) Primary mouse embryonic fibroblast cells (MEFs) before senescence. Spindle-shaped. (lower) MEFs became senescent after passages. Cells grow larger, flatten shape and expressed senescence-associated β-galactosidase (SABG, blue areas), a marker of cellular senescence.

Cells accumulate damage over time. In particular DNA damage, e.g. due to reactive oxygen species, leads to the accumulation of harmful somatic mutations.

The cellular senescence theory of aging posits that organismal aging is a consequence of the accumulation of less physiologically useful, i.e. senescent cells. In agreement with this, the experimental elimination of senescent cells from transgenic progeroid mice and non-progeroid, naturally-aged mice led to greater resistance against aging-associated diseases. Ectopic expression of the embryonic transcription factor, NANOG, is shown to reverse senescence and restore the proliferation and differentiation potential of senescent stem cells.

In many organisms, there is asymmetric cell division, e.g. a stem cell dividing to produce one stem cell and one non-stem cell. The cellular debris that cells accumulate is not evenly divided between the new cells when they divide. Instead more of the damage is passed to one of the cells, leaving the other cell rejuvenated. One lineage then undergoes cellular senescence faster than the other.

Natural selection can remove damaged cells and prevent their proliferation, counterbalancing the natural tendency for damaged cells to accumulate. However, some cells mutate in ways that escape these control mechanisms. Cancer cells avoid replicative senescence to become immortal. In about 85% of tumors, this evasion of cellular senescence is the result of up-activation of their telomerase genes.

In most multicellular species, somatic cells eventually experience replicative senescence and are unable to divide. This can prevent highly mutated cells from becoming cancerous. In culture, fibroblasts can reach a maximum of 50 cell divisions; this maximum is known as the Hayflick limit. Replicative senescence is the result of telomere shortening that ultimately triggers a DNA damage response. Cells can also be induced to senesce via DNA damage in response to elevated reactive oxygen species (ROS), activation of oncogenes and cell-cell fusion, independent of telomere length.

Cancer versus cellular senescence tradeoff theory of aging

Senescent cells within a multicellular organism can be purged by competition between cells, but this increases the risk of cancer. This leads to an inescapable dilemma between two possibilities—the accumulation of physiologically useless senescent cells, and cancer—both of which lead to increasing rates of mortality with age.

Chemical damage

Elderly Klamath woman photographed by Edward S. Curtis in 1924

One of the earliest aging theories was the Rate of Living Hypothesis described by Raymond Pearl in 1928 (based on earlier work by Max Rubner), which states that fast basal metabolic rate corresponds to short maximum life span.

While there may be some validity to the idea that for various types of specific damage detailed below that are by-products of metabolism, all other things being equal, a fast metabolism may reduce lifespan, in general this theory does not adequately explain the differences in lifespan either within, or between, species. Calorically restricted animals process as much, or more, calories per gram of body mass, as their ad libitum fed counterparts, yet exhibit substantially longer lifespans. Similarly, metabolic rate is a poor predictor of lifespan for birds, bats and other species that, it is presumed, have reduced mortality from predation, and therefore have evolved long lifespans even in the presence of very high metabolic rates. In a 2007 analysis it was shown that, when modern statistical methods for correcting for the effects of body size and phylogeny are employed, metabolic rate does not correlate with longevity in mammals or birds. (For a critique of the Rate of Living Hypothesis see Living fast, dying when?)

With respect to specific types of chemical damage caused by metabolism, it is suggested that damage to long-lived biopolymers, such as structural proteins or DNA, caused by ubiquitous chemical agents in the body such as oxygen and sugars, are in part responsible for aging. The damage can include breakage of biopolymer chains, cross-linking of biopolymers, or chemical attachment of unnatural substituents (haptens) to biopolymers. Under normal aerobic conditions, approximately 4% of the oxygen metabolized by mitochondria is converted to superoxide ion, which can subsequently be converted to hydrogen peroxide, hydroxyl radical and eventually other reactive species including other peroxides and singlet oxygen, which can, in turn, generate free radicals capable of damaging structural proteins and DNA. Certain metal ions found in the body, such as copper and iron, may participate in the process. (In Wilson's disease, a hereditary defect that causes the body to retain copper, some of the symptoms resemble accelerated senescence.) These processes termed oxidative stress are linked to the potential benefits of dietary polyphenol antioxidants, for example in coffee, red wine and tea.

Sugars such as glucose and fructose can react with certain amino acids such as lysine and arginine and certain DNA bases such as guanine to produce sugar adducts, in a process called glycation. These adducts can further rearrange to form reactive species, which can then cross-link the structural proteins or DNA to similar biopolymers or other biomolecules such as non-structural proteins. People with diabetes, who have elevated blood sugar, develop senescence-associated disorders much earlier than the general population, but can delay such disorders by rigorous control of their blood sugar levels. There is evidence that sugar damage is linked to oxidant damage in a process termed glycoxidation.

Free radicals can damage proteins, lipids or DNA. Glycation mainly damages proteins. Damaged proteins and lipids accumulate in lysosomes as lipofuscin. Chemical damage to structural proteins can lead to loss of function; for example, damage to collagen of blood vessel walls can lead to vessel-wall stiffness and, thus, hypertension, and vessel wall thickening and reactive tissue formation (atherosclerosis); similar processes in the kidney can lead to kidney failure. Damage to enzymes reduces cellular functionality. Lipid peroxidation of the inner mitochondrial membrane reduces the electric potential and the ability to generate energy. It is probably no accident that nearly all of the so-called "accelerated aging diseases" are due to defective DNA repair enzymes.

It is believed that the impact of alcohol on aging can be partly explained by alcohol's activation of the HPA axis, which stimulates glucocorticoid secretion, long-term exposure to which produces symptoms of aging.

Biomarkers of aging

If different individuals age at different rates, then fecundity, mortality, and functional capacity might be better predicted by biomarkers than by chronological age. However, graying of hair, skin wrinkles and other common changes seen with aging are not better indicators of future functionality than chronological age. Biogerontologists have continued efforts to find and validate biomarkers of aging, but success thus far has been limited. Levels of CD4 and CD8 memory T cells and naive T cells have been used to give good predictions of the expected lifespan of middle-aged mice.

There is interest in an epigenetic clock as a biomarker of aging, based on its ability to predict human chronological age. Basic blood biochemistry and cell counts can also be used to accurately predict the chronological age. It is also possible to predict the human chronological age using the transcriptomic aging clocks.

Genetic determinants of aging

A number of genetic components of aging have been identified using model organisms, ranging from the simple budding yeast Saccharomyces cerevisiae to worms such as Caenorhabditis elegans and fruit flies (Drosophila melanogaster). Study of these organisms has revealed the presence of at least two conserved aging pathways.

Gene expression is imperfectly controlled, and it is possible that random fluctuations in the expression levels of many genes contribute to the aging process as suggested by a study of such genes in yeast. Individual cells, which are genetically identical, nonetheless can have substantially different responses to outside stimuli, and markedly different lifespans, indicating that epigenetic factors play an important role in gene expression and aging as well as genetic factors.

The ability to repair DNA double-strand breaks declines with aging in mice and humans.

A set of rare hereditary (genetics) disorders, each called progeria, has been known for some time. Sufferers exhibit symptoms resembling accelerated aging, including wrinkled skin. The cause of Hutchinson–Gilford progeria syndrome was reported in the journal Nature in May 2003. This report suggests that DNA damage, not oxidative stress, is the cause of this form of accelerated aging.

Evolutionary medicine

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Evolutionary_medicine 

Evolutionary biology
Darwin's finches by John Gould

The bacterium Mycobacterium tuberculosis can evolve to subvert the protection offered by immune defenses

Evolutionary medicine or Darwinian medicine is the application of modern evolutionary theory to understanding health and disease. Modern medical research and practice have focused on the molecular and physiological mechanisms underlying health and disease, while evolutionary medicine focuses on the question of why evolution has shaped these mechanisms in ways that may leave us susceptible to disease. The evolutionary approach has driven important advances in the understanding of cancer, autoimmune disease, and anatomy. Medical schools have been slower to integrate evolutionary approaches because of limitations on what can be added to existing medical curricula.

Core principles

Utilizing the Delphi method, 56 experts from a variety of disciplines, including anthropology, medicine, and biology agreed upon 14 core principles intrinsic to the education and practice of evolutionary medicine. These 14 principles can be further grouped into five general categories: question framing, evolution I and II (with II involving a higher level of complexity), evolutionary trade-offs, reasons for vulnerability, and culture. Additional information regarding these principles may be found in the table below.

Human adaptations

Adaptation works within constraints, makes compromises and trade-offs, and occurs in the context of different forms of competition.

Constraints

Adaptations can only occur if they are evolvable. Some adaptations which would prevent ill health are therefore not possible.

• DNA cannot be totally prevented from undergoing somatic replication corruption; this has meant that cancer, which is caused by somatic mutations, has not (so far) been completely eliminated by natural selection.
• Humans cannot biosynthesize vitamin C, and so risk scurvy, vitamin C deficiency disease, if dietary intake of the vitamin is insufficient.
• Retinal neurons and their axon output have evolved to be inside the layer of retinal pigment cells. This creates a constraint on the evolution of the visual system such that the optic nerve is forced to exit the retina through a point called the optic disc. This, in turn, creates a blind spot. More importantly, it makes vision vulnerable to increased pressure within the eye (glaucoma) since this cups and damages the optic nerve at this point, resulting in impaired vision.

Other constraints occur as the byproduct of adaptive innovations.

Trade-offs and conflicts

One constraint upon selection is that different adaptations can conflict, which requires a compromise between them to ensure an optimal cost-benefit tradeoff.

• Running efficiency in women, and birth canal size
• Encephalization, and gut size
• Skin pigmentation protection from UV, and the skin synthesis of vitamin D
• Speech and its use of a descended larynx, and increased risk of choking

Competition effects

Different forms of competition exist and these can shape the processes of genetic change.

• mate choice and disease susceptibility
• genomic conflict between mother and fetus that results in pre-eclampsia

"Diseases of civilization"

Humans evolved to live as simple hunter-gatherers in small tribal bands. Contemporary humans now have a very different environment and way of life. This change makes present humans vulnerable to a number of health problems, termed "diseases of civilization" and "diseases of affluence". Stone-age humans evolved to live off the land, taking advantage of the resources that were readily available to them. Evolution is slow, and the rapid change from stone-age environments and practices to the world of today is problematic because we are still adapted to stone-age circumstances that no longer apply. This misfit has serious implications for our health. "Modern environments may cause many diseases such as deficiency syndromes like scurvy and rickets".)

Diet

In contrast to the diet of early hunter-gatherers, the modern Western diet often contains high quantities of fat, salt, and simple carbohydrates, such as refined sugars and flours. These relatively sudden dietary changes create health problems.

• Trans fat health risks
• Dental caries
• High GI foods
• Modern diet based on "common wisdom" regarding diets in the paleolithic era

Life expectancy

Examples of aging-associated diseases are atherosclerosis and cardiovascular disease, cancer, arthritis, cataracts, osteoporosis, type 2 diabetes, hypertension and Alzheimer's disease. The incidence of all of these diseases increases rapidly with aging (increases exponentially with age, in the case of cancer).

Age-Specific SEER Incidence Rates, 2003-2007

Of the roughly 150,000 people who die each day across the globe, about two thirds—100,000 per day—die of age-related causes. In industrialized nations, the proportion is much higher, reaching 90%.

Exercise

Many contemporary humans engage in little physical exercise compared to the physically active lifestyles of ancestral hunter-gatherers. Prolonged periods of inactivity may have only occurred in early humans following illness or injury, so a modern sedentary lifestyle may continuously cue the body to trigger life preserving metabolic and stress-related responses such as inflammation, and some theorize that this causes chronic diseases.

Cleanliness

Contemporary humans in developed countries are mostly free of parasites, particularly intestinal ones. This is largely due to frequent washing of clothing and the body, and improved sanitation. Although such hygiene can be very important when it comes to maintaining good health, it can be problematic for the proper development of the immune system. The hygiene hypothesis is that humans evolved to be dependent on certain microorganisms that help establish the immune system, and modern hygiene practices can prevent necessary exposure to these microorganisms. "Microorganisms and macroorganisms such as helminths from mud, animals, and feces play a critical role in driving immunoregulation" (Rook, 2012). Essential microorganisms play a crucial role in building and training immune functions that fight off and repel some diseases, and protect against excessive inflammation, which has been implicated in several diseases. For instance, recent studies have found evidence supporting inflammation as a contributing factor in Alzheimer's Disease.

Evolutionary approaches to depression

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Evolutionary_approaches_to_depression 

Evolutionary approaches to depression are attempts by evolutionary psychologists to use the theory of evolution to shed light on the problem of mood disorders. Depression is generally thought of as dysfunction or a mental disorder, but its prevalence does not increase with age the way dementia and other organic dysfunction commonly does. Some researchers have surmised that the disorder may have evolutionary roots, in the same way that others suggest evolutionary contributions to schizophrenia, sickle cell anemia, psychopathy and other disorders. Psychology and psychiatry have not generally embraced evolutionary explanations for behaviors, and the proposed explanations for the evolution of depression remain controversial.

Background

Major depression (also called "major depressive disorder", "clinical depression" or often simply "depression") is a leading cause of disability worldwide, and in 2000 was the fourth leading contributor to the global burden of disease (measured in DALYs); it is also an important risk factor for suicide. It is understandable, then, that clinical depression is thought to be a pathology—a major dysfunction of the brain.

In most cases, rates of organ dysfunction increase with age, with low rates in adolescents and young adults, and the highest rates in the elderly. These patterns are consistent with evolutionary theories of aging which posit that selection against dysfunctional traits decreases with age (because there is a decreasing probability of surviving to later ages).

In contrast to these patterns, prevalence of clinical depression is high in all age categories, including otherwise healthy adolescents and young adults. In one study of the US population, for example, the 12 month prevalence for a major depression episode was highest in the youngest age category (15- to 24-year-olds). The high prevalence of unipolar depression (excluding depression associated bipolar disorder) is also an outlier when compared to the prevalence of other mental disorders such as major mental retardation, autism, schizophrenia and even the aforementioned bipolar disorder, all with prevalence rates about one tenth that of depression, or less. As of 2017, the only mental disorders with a higher prevalence than depression are anxiety disorders. 

The common occurrence and persistence of a trait like clinical depression with such negative effects early in life is difficult to explain. (Rates of infectious disease are high in young people, of course, but clinical depression is not thought to be caused by an infection.) Evolutionary psychology and its application in evolutionary medicine suggest how behaviour and mental states, including seemingly harmful states such as depression, may have been beneficial adaptations of human ancestors which improved the fitness of individuals or their relatives. It has been argued, for example, that Abraham Lincoln's lifelong depression was a source of insight and strength. Some even suggest that "we aren't designed to have happiness as our natural default" and so a state of depression is the evolutionary norm.

The following hypotheses attempt to identify a benefit of depression that outweighs its obvious costs.

Such hypotheses are not necessarily incompatible with one another and may explain different aspects, causes, and symptoms of depression.

Psychic pain hypothesis

One reason depression is thought to be a pathology is that it causes so much psychic pain and distress. However, physical pain is also very distressful, yet it has an evolved function: to inform the organism that it is suffering damage, to motivate it to withdraw from the source of damage, and to learn to avoid such damage-causing circumstances in the future. Sadness is also distressing, yet is widely believed to be an evolved adaptation. In fact, perhaps the most influential evolutionary view is that most cases of depression are simply particularly intense cases of sadness in response to adversity, such as the loss of a loved one.

According to the psychic pain hypothesis, depression is analogous to physical pain in that it informs the sufferer that current circumstances, such as the loss of a friend, are imposing a threat to biological fitness. It motivates the sufferer to cease activities that led to the costly situation, if possible, and it causes him or her to learn to avoid similar circumstances in the future. Proponents of this view tend to focus on low mood, and regard clinical depression as a dysfunctional extreme of low mood—and not as a unique set of characteristics that are physiologically distanced from regular depressed mood.

Alongside the absence of pleasure, other noticeable changes include psychomotor retardation, disrupted patterns of sleeping and feeding, a loss of sex drive and motivation—which are all also characteristics of the body's reaction to actual physical pain. In depressed people there is an increased activity in the regions of the cortex involved with the perception of pain, such as the anterior cingulate cortex and the left prefrontal cortex. This activity allows the cortex to manifest an abstract negative thought as a true physical stressor to the rest of the brain.

Behavioral shutdown model

The behavioral shutdown model states that if an organism faces more risk or expenditure than reward from activities, the best evolutionary strategy may be to withdraw from them. This model proposes that emotional pain, like physical pain, serves a useful adaptive purpose. Negative emotions like disappointment, sadness, grief, fear, anxiety, anger, and guilt are described as "evolved strategies that allow for the identification and avoidance of specific problems, especially in the social domain." Depression is characteristically associated with anhedonia and lack of energy, and those experiencing it are risk-aversive and perceive more negative and pessimistic outcomes because they are focused on preventing further loss. Although the model views depression as an adaptive response, it does not suggest that it is beneficial by the standards of current society; but it does suggest that many approaches to depression treat symptoms rather than causes, and underlying social problems need to be addressed.

A related phenomenon to the behavioral shutdown model is learned helplessness. In animal subjects, a loss of control or predictability in the subject's experiences results in a condition similar to clinical depression in humans. That is to say, if uncontrollable and unstoppable stressors are repeated for long enough, a rat subject will adopt a learned helplessness, which shares a number of behavioral and psychological features with human depression. The subject will not attempt to cope with problems, even when placed in a stressor-free novel environment. Should their rare attempts at coping prove successful in a new environment, a long lasting cognitive block prevents them from perceiving their action as useful and their coping strategy does not last long. From an evolutionary perspective, learned helplessness also allows a conservation of energy for an extended period of time should people find themselves in a predicament that is outside of their control, such as an illness or a dry season. However, for today's humans whose depression resembles learned helplessness, this phenomenon usually manifests as a loss of motivation and the distortion of one uncontrollable aspect of a person's life being viewed as representative of all aspects of their life – suggesting a mismatch between ultimate cause and modern manifestation.

Analytical rumination hypothesis

This hypothesis suggests that depression is an adaptation that causes the affected individual to concentrate his or her attention and focus on a complex problem in order to analyze and solve it.

One way depression increases the individual's focus on a problem is by inducing rumination. Depression activates the left ventrolateral prefrontal cortex, which increases attention control and maintains problem-related information in an "active, accessible state" referred to as "working memory", or WM. As a result, depressed individuals have been shown to ruminate, reflecting on the reasons for their current problems. Feelings of regret associated with depression also cause individuals to reflect and analyze past events in order to determine why they happened and how they could have been prevented. The rumination hypothesis has come under criticism. Evolutionary fitness is increased by ruminating before rather than after bad outcomes. A situation that resulted in a child being in danger but unharmed should lead the parent to ruminate on how to avoid the dangerous situation in the future. Waiting until the child dies and then ruminating in a state of depression is too late.

Some cognitive psychologists argue that ruminative tendency itself increases the likelihood of the onset of depression.

Another way depression increases an individual's ability to concentrate on a problem is by reducing distraction from the problem. For example, anhedonia, which is often associated with depression, decreases an individual's desire to participate in activities that provide short-term rewards, and instead, allows the individual to concentrate on long-term goals. In addition, "psychomotoric changes", such as solitariness, decreased appetite, and insomnia also reduce distractions. For instance, insomnia enables conscious analysis of the problem to be maintained by preventing sleep from disrupting such processes. Likewise, solitariness, lack of physical activity, and lack of appetite all eliminate sources of distraction, such as social interactions, navigation through the environment, and "oral activity", which disrupt stimuli from being processed.

Possibilities of depression as a dysregulated adaptation

Depression, especially in the modern context, may not necessarily be adaptive. The ability to feel pain and experience depression, are adaptive defense mechanisms, but when they are "too easily triggered, too intense, or long lasting", they can become "dysregulated". In such a case, defense mechanisms, too, can become diseases, such as "chronic pain or dehydration from diarrhea". Depression, which may be a similar kind of defense mechanism, may have become dysregulated as well.

Thus, unlike other evolutionary theories this one sees depression as a maladaptive extreme of something that is beneficial in smaller amounts. In particular, one theory focuses on the personality trait neuroticism. Low amounts of neuroticism may increase a person's fitness through various processes, but too much may reduce fitness by, for example, recurring depressions. Thus, evolution will select for an optimal amount and most people will have neuroticism near this amount. However, genetic variation continually occurs, and some people will have high neuroticism which increases the risk of depressions.

Rank theory

Rank theory is the hypothesis that, if an individual is involved in a lengthy fight for dominance in a social group and is clearly losing, then depression causes the individual to back down and accept the submissive role. In doing so, the individual is protected from unnecessary harm. In this way, depression helps maintain a social hierarchy. This theory is a special case of a more general theory derived from the psychic pain hypothesis: that the cognitive response that produces modern-day depression evolved as a mechanism that allows people to assess whether they are in pursuit of an unreachable goal, and if they are, to motivate them to desist.

Social risk hypothesis

This hypothesis is similar to the social rank hypothesis but focuses more on the importance of avoiding exclusion from social groups, rather than direct dominance contests. The fitness benefits of forming cooperative bonds with others have long been recognised—during the Pleistocene period, for instance, social ties were vital for food foraging and finding protection from predators.

As such, depression is seen to represent an adaptive, risk-averse response to the threat of exclusion from social relationships that would have had a critical impact on the survival and reproductive success of our ancestors. Multiple lines of evidence on the mechanisms and phenomenology of depression suggest that mild to moderate (or "normative") depressed states preserve an individual's inclusion in key social contexts via three intersecting features: a cognitive sensitivity to social risks and situations (e.g., "depressive realism"); it inhibits confident and competitive behaviours that are likely to put the individual at further risk of conflict or exclusion (as indicated by symptoms such as low self-esteem and social withdrawal); and it results in signalling behaviours directed toward significant others to elicit more of their support (e.g., the so-called "cry for help"). According to this view, the severe cases of depression captured by clinical diagnoses reflect the maladaptive, dysregulation of this mechanism, which may partly be due to the uncertainty and competitiveness of the modern, globalised world.

Honest signaling theory

Another reason depression is thought to be a pathology is that key symptoms, such as loss of interest in virtually all activities, are extremely costly to the sufferer. Biologists and economists have proposed, however, that signals with inherent costs can credibly signal information when there are conflicts of interest. In the wake of a serious negative life event, such as those that have been implicated in depression (e.g., death, divorce), "cheap" signals of need, such as crying, might not be believed when social partners have conflicts of interest. The symptoms of major depression, such as loss of interest in virtually all activities and suicidality, are inherently costly, but, as costly signaling theory requires, the costs differ for individuals in different states. For individuals who are not genuinely in need, the fitness cost of major depression is very high because it threatens the flow of fitness benefits. For individuals who are in genuine need, however, the fitness cost of major depression is low, because the individual is not generating many fitness benefits. Thus, only an individual in genuine need can afford to suffer major depression. Major depression therefore serves as an honest, or credible, signal of need.

For example, individuals suffering a severe loss such as the death of a spouse are often in need of help and assistance from others. Such individuals who have few conflicts with their social partners are predicted to experience grief—a means, in part, to signal need to others. Such individuals who have many conflicts with their social partners, in contrast, are predicted to experience depression—a means, in part, to credibly signal need to others who might be skeptical that the need is genuine.

Bargaining theory

Depression is not only costly to the sufferer, it also imposes a significant burden on family, friends, and society at large—yet another reason it is thought to be pathological. Yet if sufferers of depression have real but unmet needs, they might have to provide an incentive to others to address those needs.

The bargaining theory of depression is similar to the honest signaling, niche change, and social navigation theories of depression described below. It draws on theories of labor strikes developed by economists to basically add one additional element to honest signaling theory: The fitness of social partners is generally correlated. When a wife suffers depression and reduces her investment in offspring, for example, the husband's fitness is also put at risk. Thus, not only do the symptoms of major depression serve as costly and therefore honest signals of need, they also compel reluctant social partners to respond to that need in order to prevent their own fitness from being reduced. This explanation for depression has been challenged. Depression decreases the joint product of the family or group as the husband or helper only partially compensates for the loss of productivity by the depressed person. Instead of being depressed the person could break their own leg and gain help from the social group, but this obviously is a counterproductive strategy. And the lack of a sex drive certainly does not improve marital relations or fitness.

Social navigation or niche change theory

The social navigation or niche change hypothesis proposes that depression is a social navigation adaptation of last resort, designed especially to help individuals overcome costly, complex contractual constraints on their social niche. The hypothesis combines the analytical rumination and bargaining hypotheses and suggests that depression, operationally defined as a combination of prolonged anhedonia and psychomotor retardation or agitation, provides a focused sober perspective on socially imposed constraints hindering a person's pursuit of major fitness enhancing projects. Simultaneously, publicly displayed symptoms, which reduce the depressive's ability to conduct basic life activities, serve as a social signal of need; the signal's costliness for the depressive certifies its honesty. Finally, for social partners who find it uneconomical to respond helpfully to an honest signal of need, the same depressive symptoms also have the potential to extort relevant concessions and compromises. Depression's extortionary power comes from the fact that it retards the flow of just those goods and services such partners have come to expect from the depressive under status quo socioeconomic arrangements.

Thus depression may be a social adaptation especially useful in motivating a variety of social partners, all at once, to help the depressive initiate major fitness-enhancing changes in their socioeconomic life. There are diverse circumstances under which this may become necessary in human social life, ranging from loss of rank or a key social ally which makes the current social niche uneconomic to having a set of creative new ideas about how to make a livelihood which begs for a new niche. The social navigation hypothesis emphasizes that an individual can become tightly ensnared in an overly restrictive matrix of social exchange contracts, and that this situation sometimes necessitates a radical contractual upheaval that is beyond conventional methods of negotiation. Regarding the treatment of depression, this hypothesis calls into question any assumptions by the clinician that the typical cause of depression is related to maladaptive perverted thinking processes or other purely endogenous sources. The social navigation hypothesis calls instead for analysis of the depressive's talents and dreams, identification of relevant social constraints (especially those with a relatively diffuse non-point source within the social network of the depressive), and practical social problem-solving therapy designed to relax those constraints enough to allow the depressive to move forward with their life under an improved set of social contracts. This theory has been the subject of criticism.

Depression as an incentive device

This approach argues that being in a depressed state is not adaptive (indeed quite the opposite), but the threat of depression for bad outcomes and the promise of pleasure for good outcomes are adaptive because they motivate the individual toward undertaking effort that increase fitness. The reason for not relying on pleasure alone as an incentive device is because happiness is costly in terms of fitness as the individual becomes less cautious. This is most readily seen when an individual is manic and undertakes very risky behavior. The physiological manifestation of the incentives are most noticeable when an individual is bipolar with bouts of extreme elation and extreme depression as anxiety which is about the (possibly immediate) future is highly correlated with being bipolar. As noted earlier, bipolar disorder and clinical depression, as opposed to event depression, are viewed as dysregulation just as persistently high (or low) blood pressure are viewed as dysregulation even though at times high or low blood pressure is fitness enhancing.

Prevention of infection

It has been hypothesized that depression is an evolutionary adaptation because it helps prevent infection in both the affected individual and his/her kin.

First, the associated symptoms of depression, such as inactivity and lethargy, encourage the affected individual to rest. Energy conserved through such methods is highly crucial, as immune activation against infections is relatively costly; there must be, for instance, a 10% increase in metabolic activity for even a 1℃ change in body temperature. Therefore, depression allows one to conserve and allocate energy to the immune system more efficiently.

Depression further prevents infection by discouraging social interactions and activities that may result in exchange of infections. For example, the loss of interest discourages one from engaging in sexual activity, which, in turn, prevents the exchange of sexually transmitted diseases. Similarly, depressed mothers may interact less with their children, reducing the probability of the mother infecting her kin. Lastly, the lack of appetite associated with depression may also reduce exposure to food-borne parasites.

However, it should also be noted that chronic illness itself may be involved in causing depression. In animal models, the prolonged overreaction of the immune system, in response to the strain of chronic disease, results in an increased production of cytokines (a diverse group of hormonal regulators and signaling molecules). Cytokines interact with neurotransmitter systems—mainly norepinephrine, dopamine, and serotonin, and induce depressive characteristics. The onset of depression may help an individual recover from their illness by allowing them a more reserved, safe and energetically efficient lifestyle. The overproduction of these cytokines, beyond optimal levels due to the repeated demands of dealing with a chronic disease, may result in clinical depression and its accompanying behavioral manifestations that promote extreme energy reservation.

The third ventricle hypothesis

Third ventricle

The third ventricle hypothesis of depression proposes that the behavioural cluster associated with depression (hunched posture, avoidance of eye contact, reduced appetites for food and sex plus social withdrawal and sleep disturbance) serves to reduce an individual's attack-provoking stimuli within the context of a chronically hostile social environment. It further proposes that this response is mediated by the acute release of an unknown (probably cytokine) inflammatory agent into the third ventricular space. In support of this suggestion imaging studies reveal that the third ventricle is enlarged in depressives.

Reception

Clinical psychology and psychiatry have historically been relatively isolated from the field of evolutionary psychology. Some psychiatrists raise the concern that evolutionary psychologists seek to explain hidden adaptive advantages without engaging the rigorous empirical testing required to back up such claims. While there is strong research to suggest a genetic link to bipolar disorder and schizophrenia, there is significant debate within clinical psychology about the relative influence and the mediating role of cultural or environmental factors. For example, epidemiological research suggests that different cultural groups may have divergent rates of diagnosis, symptomatology, and expression of mental illnesses. There has also been increasing acknowledgment of culture-bound disorders, which may be viewed as an argument for an environmental versus genetic psychological adaptation. While certain mental disorders may have psychological traits that can be explained as 'adaptive' on an evolutionary scale, these disorders cause afflicted individuals significant emotional and psychological distress and negatively influence the stability of interpersonal relationships and day-to-day adaptive functioning.