Genetic Variation Quotes

With the capacity to represent the world in signs and symbols comes the capacity to change it, which, as it happens, is also the capacity to destroy it. A tiny set of genetic variations divides us from the Neanderthals, but that has made all the difference.

...the characters in my books all resemble each other. They live, with minor variations, the same moments, the same perils, and when I speak of them, my language, which is inspired by them, repeats the same poems in the same tone.

I’ve always felt there’s something genetically instilled and inbred in Californians—that California is a place of death, a place people are drawn to because they don’t realize deep down they’re actually afraid of what they want. It’s new, and they’re escaping their histories while at the same time moving headlong toward their own extinctions. Desire and death are all mixed up with the thrill and the risk of the unknown. It’s a variation of what Freud called the “death instinct.

the genes of modern-day Africans are a treasure house for all humanity. They possess our species’ greatest reservoir of genetic diversity, of which further study will shed new light on the heredity of the human body and mind. Perhaps the time has come, in light of this and other advances in human genetics, to adopt a new ethic of racial and hereditary variation, one that places value on the whole of diversity rather than on the differences composing the diversity. It would give proper measure to our species’ genetic variation as an asset, prized for the adaptability it provides all of us during an increasingly uncertain future. Humanity is strengthened by a broad portfolio of genes that can generate new talents, additional resistance to diseases, and perhaps even new ways of seeing reality. For scientific as well as for moral reasons, we should learn to promote human biological diversity for its own sake instead of using it to justify prejudice and conflict.

More than any other single trait, it is the apple’s genetic variability—its ineluctable wildness—that accounts for its ability to make itself at home in places as different from one another as New England and New Zealand, Kazakhstan and California. Wherever the apple tree goes, its offspring propose so many different variations on what it means to be an apple—at least five per apple, several thousand per tree—that a couple of these novelties are almost bound to have whatever qualities it takes to prosper in the tree’s adopted home.

They tell us race is an invention, that there is no genetic variation between two black people than there is between a black person and a white person. Then they tell us black people have a worse kind of breast cancer and get more fibroid. And white folk get cystic fibrosis and osteoporosis. So what’s the deal, is race an invention or not?

Bailey had profoundly changed the conversation around sexual identity away from the 1960s rhetoric of “choice” and “personal preference” toward biology, genetics, and inheritance. If we did not think of variations in height or the development of dyslexia or type 1 diabetes as choices, then we could not think of sexual identity as a choice. But

There is less genetic variation in the entire human race than in a typical wild population of chimpanzees.

If anyone imagines that scientists are dispassionate and impartial people, discussing theories and ideas unemotionally in the cool clear light of reason, they have been seriously misled.

Cultural variation in morality can be explained in part by noting that cultures can shrink or expand the current triggers of any module. For example, in the past fifty years people in many Western societies have come to feel compassion in response to many more kinds of animal suffering, and they’ve come to feel disgust in response to many fewer kinds of sexual activity. The current triggers can change in a single generation, even though it would take many generations for genetic evolution to alter the design of the module and its original triggers.

McKusick's belief in this paradigm-the focus on disability rather than abnormalcy-was actualized in the treatment of patients in his clinic. Patients with dwarfism, for instance, were treated by an interdisciplinary team of genetic counselors, neurologists, orthopedic surgeons, nurses, and psychiatrists trained to focus on specific disabilities of persons with short stature. Surgical interventions were reserved to correct specific deformities as they arose. The goal was not to restore "normalcy"-but vitality, joy, and function. McKusic had rediscovered the founding principles of modern genetics in the realm of human pathology. In humans as in wild flies, genetic variations abounded. Here too genetic variants, environments, and gene-environment interactions ultimately collaborated to cause phenotypes-except in this case, the "phenotype" in question was disease. Here too some genes had partial penetrance and widely variable expressivity. One gene could cause many diseases, and one disease could be caused by many genes. And here too "fitness" could not be judged in absolutes. Rather the lack of fitness-illness [italicized, sic] in colloquial terms- was defined by the relative mismatch between an organism and environment.

we need to try to make progress beyond the situation we are facing right now, in which many researchers are reluctant to undertake any studies of Native American genetic variation for fear of criticism, and because of the extraordinary time commitment that would be required

According to Dr. Bruce Lipton, gene activity can change on a daily basis. If the perception in your mind is reflected in the chemistry of your body, and if your nervous system reads and interprets the environment and then controls the blood’s chemistry, then you can literally change the fate of your cells by altering your thoughts. In fact, Dr. Lipton’s research illustrates that by changing your perception, your mind can alter the activity of your genes and create over thirty thousand variations of products from each gene. He gives more detail by saying that the gene programs are contained within the nucleus of the cell, and you can rewrite those genetic programs through changing your blood chemistry.

The thing that always impresses me about human beings is our diversity. Even when we are brought up in similar environments, we still somehow gravitate toward very different careers, hobbies. politics, manners of speaking and acting, aesthetic preferences, and so forth. Maybe this diversity is due to genetic variation. Or maybe, being naturally curious and adaptive creatures, we invariably tend to scatter all over the place, exploiting every niche we can possibly find. Either way, it's fairly obvious that we also end up all over the map when it comes to gender and sexuality.

The double-helix has solved all three of the major challenges of genetic physiology using ingenious variations on the same theme. Mirror-image chemicals are used to generate mirror-image chemicals, reflections used to reconstruct the orginal. Pairs used to maintain the fidelity and fixity of information. "Monet is but an eye," Cezanne once said of his friend, "but, God, what an eye." DNA, by the same logic, is but a chemical-but, God, what a chemical.

When most people had to hunt, a minor genetic variation in your ability to focus attention was hardly a problem, and may even have been an advantage [enabling a hunter to maintain his focus on multiple and simultaneous targets, for instance]. When most people have to make it through high school, the same variation can become a life-altering disease.

Africans carried more genetic diversity within their genomes than non-Africans, as a simple result of the fact that humanity had originated on that continent and spread outward. Non-African races had been founded by isolated groups of adventurers. Breeding among themselves, they had created gene pools that were necessarily limited to what they had brought with them: only a subset of what was to be found in Africa. This idea had been used to explain, for example, why Africa contained both the tallest and the most diminutive people in the world, and why so many top athletes were African. It wasn’t because they were naturally better athletes but because the bell-shaped curve of random genetic variation was wider.

Without this variation—without deep genetic diversity—an organism might ultimately lose its capacity to evolve.

The only answer that I can give to this problem is based on Darwin’s principle of natural selection. The idea is that in any population of self-reproducing organisms, there will be variations in the genetic material and upbringing that different individuals have. These differences will mean that some individuals are better able than others to draw the right conclusions about the world around them and to act accordingly. These individuals will be more likely to survive and reproduce and so their pattern of behavior and thought will come to dominate. It

There are three major genetic observations that have been made about the diversity of people living on the African continent. First, Africa shows more genetic diversity than the other continents. Second, most of the genetic variation outside of Africa is a subset of the variation found within Africa. Finally, genetic diversity decreases with increasing distance from Africa.

In 1905, still struggling for an alternative, Bateson coined a word of his own. Genetics, he called it: the study of heredity and variation-the word ultimately derived from the Greek genno, "to give birth.

That is why urban evolution can proceed so rapidly: the animals and plants that need to adapt to whatever new feature humans release in their urban environment do not need to wait for the right mutations to come along. Mostly, the necessary gene variants are already there, waiting in the wings of the standing genetic variation. It only takes natural selection to bring them out into the limelight, and give them a chance to shine.

When nobody read,” the psychologist Alison Gopnik writes, “dyslexia wasn’t a problem. When most people had to hunt, a minor genetic variation in your ability to focus attention was hardly a problem, and may even have been an advantage [enabling a hunter to maintain his focus on multiple and simultaneous targets, for instance]. When most people have to make it through high school, the same variation can become a life-altering disease.

The problem with racial discrimination, though, is not the inference of a person's race from their genetic characteristics. It is quite the opposite: it is the inference of a person's characteristics from their race. The question is not, can you, given an individual's skin color, hair texture, or language, infer something about their ancestry or origin. That is a question of biological systematics -- of lineage, taxonomy, of racial geography, of biological discrimination. Of course you can -- and genomics as vastly refined that inference. You can scan any individual genome and infer rather deep insights about a person's ancestry, or place of origin. But the vastly more controversial question is the converse: Given a racial identity -- African or Asian, say -- can you infer anything about an individual's characteristics: not just skin or hair color, but more complex features, such as intelligence, habits, personality, and aptitude? /I/ Genes can certainly tell us about race, but can race tell us anything about genes? /i/ To answer this question, we need to measure how genetic variation is distributed across various racial categories. Is there more diversity _within_ races or _between_ races? Does knowing that someone is of African versus European descent, say, allow us to refine our understanding of their genetic traits, or their personal, physical, or intellectual attributes in a meaningful manner? Or is there so much variation within Africans and Europeans that _intraracial_ diversity dominates the comparison, thereby making the category "African" or "European" moot? We now know precise and quantitative answers to these questions. A number of studies have tried to quantify the level of genetic diversity of the human genome. The most recent estimates suggest that the vast proportion of genetic diversity (85 to 90 percent) occurs _within_ so-called races (i.e., within Asians or Africans) and only a minor proportion (7 percent) within racial groups (the geneticist Richard Lewontin had estimated a similar distribution as early as 1972). Some genes certainly vary sharply between racial or ethnic groups -- sickle-cell anemia is an Afro-Caribbean and Indian disease, and Tay-Sachs disease has a much higher frequency in Ashkenazi Jews -- but for the most part, the genetic diversity within any racial group dominates the diversity between racial groups -- not marginally, but by an enormous amount. The degree of interracial variability makes "race" a poor surrogate for nearly any feature: in a genetic sense, an African man from Nigria is so "different" from another man from Namibia that it makes little sense to lump them into the same category.

Nature isn’t benign,” Lederberg said at the meeting’s opening. “The bottom lines: the units of natural selection—DNA, sometimes RNA elements—are by no means neatly packaged in discrete organisms. They all share the entire biosphere. The survival of the human species is not a preordained evolutionary program. Abundant sources of genetic variation exist for viruses to learn new tricks, not necessarily confined to what happens routinely, or even frequently.

Twin, family, and population studies have all conclusively shown that psychological traits are at least partly, and sometimes largely, heritable—that is, a sizable portion of the variation that we see in these traits across the population is attributable to genetic variation. However, as we have seen in the preceding chapters, the relationship between genes and traits is far from simple. The fact that a given trait is heritable seems to suggest that there must be genes for that trait. But phrasing it in that way is a serious conceptual trap. It implies that genes exist that are dedicated to that function—that there are genes for intelligence or sociability or visual perception. But this risks confusing the two meanings of the word gene: one, from the study of heredity, refers to genetic variants that affect a trait; the other, from molecular biology, refers to the stretches of DNA that encode proteins with various biochemical or cellular functions.

the multidimensionality of human traits, the great variation that exists among individuals, and the extent to which hard work and upbringing can compensate for genetic endowment, the only sensible approach is to celebrate every person and every population as an extraordinary realization of our human genius and to give each person every chance to succeed, regardless of the particular average combination of genetic propensities he or she happens to display. For me, the natural response to the

In the United States both scholars and the general public have been conditioned to viewing human races as natural and separate divisions within the human species based on visible physical differences. With the vast expansion of scientific knowledge in this century, however, it has become clear that human populations are not unambiguous, clearly demarcated, biologically distinct groups. Evidence from the analysis of genetics (e.g. DNA) indicates that most physical variation, about 94%, lies within so-called racial groups. Conventional geographic "racial" groupings differ from one another only in about 6% of their genes. This means that there is greater variation within "racial" groups than between them. In neighboring populations there is much overlapping of genes and their phenotypic (physical) expressions. Throughout history whenever different groups have come into contact, they have interbred. The continued sharing of genetic materials has maintained all of humankind as a single species.

compiling the information on the number of years of education for over four hundred thousand people of European ancestry whose genomes have been surveyed in the course of various disease studies, Daniel Benjamin and colleagues identified seventy-four genetic variations each of which has overwhelming evidence of being more common in people with more years of education than in people with fewer years even after controlling for such possibly confounding factors as heterogeneity in the study population.25

Much of contemporary "realism" turns out to be just a variation on good old fashioned fatalism: people feel relieved of responsibility by recourse to the concept of 'nature'. By nature, however, we are born ignorant. Therefore should we try not to learn? Some people produce more than the usual amount of androgens and therefore become excessively aggressive. Does that mean we should freely express violence? We cannot. Submission to genetic programming can become dangerous, because it leaves us helpless.

When changes in one genetic trait are the source of selection for changes in a second, the rate of response in the latter depends in parts on the rate of change in the former, which, as a rule, is not fast. In comparison, if a cultural practice modifies selection acting on human genetic variation, then the greater the proportion of individuals in the population that exhibit the cultural trait, the stronger the selection on the gene. As a consequence, the rapid spread of a cultural practice often leads quickly to the maximally strong selection of the advantageous genetic variant, which rapidly increases in frequency. Cultural practices typically spread more quickly than genetic mutations, simply because cultural learning typically operates at faster rates than biological evolution. What does the speed with which a culturla trait spreads depend upon? Answer: the fidelity of cultural transmission. The very factor that is critical to the emergence of complex cumulative culture in humans is also a major determinant of evolutionary responses to that culture.

EVOLUTION RESTS ON three steps: (a) certain biological traits are inherited by genetic means; (b) mutations and gene recombination produce variation in those traits; (c) some of those variants confer more “fitness” than others. Given those conditions, over time the frequency of more “fit” gene variants increases in a population.

a result, the most efficient way for evolutionary forces to spread beneficial mutations has often been to invent mutations anew rather than to import them from other populations.44 The limited migration rates between some regions of Africa over the last few thousand years has resulted in what Ralph and Coop have described as a “tessellated” pattern of population structure in Africa. Tessellation is a mathematical term for a landscape of tiles—regions of genetic homogeneity demarcated by sharp boundaries—that is expected to form when the process of homogenization due to gene exchanges among neighbors competes with the process of generating new advantageous variations in each region.

In Darwin's time no serious attempt had been made to examine the manifestations of variability. A vast assemblage of miscellaneous facts could formerly be adduced as seemingly comparable illustrations of the phenomenon "Variation." Time has shown this mass of evidence to be capable of analysis. When first promulgated it produced the impression that variability was a phenomenon generally distributed amongst living things in such a way that the specific divisions must be arbitrary. When this variability is sorted out, and is seen to be in part a result of hybridisation, in part a consequence of the persistence of hybrids by parthenogenetic reproduction, a polymorphism due to the continued presence of individuals representing various combinations of Mendelian allelomorphs, partly also the transient effect of alteration in external circumstances, we see how cautious we must be in drawing inferences as to the indefiniteness of specific limits from a bare knowledge that intermediates exist.

Let's look at one more quick example of modern evolution at work. In the early 1800s, light-colored lichens covered many of the trees in the English countryside. The peppered moth was a light-colored insect that blended in unnoticeably with the lichens. Predators had great difficulty distinguishing the peppered moth from its background environment, so the moths easily survived and reproduced. Then the Industrial Revolution came to the English country- side. Coal-burning factories turned the lichens a sooty black. The light-colored peppered moth became clearly visible. Most of them were eaten. But because of genetic variation and mutation, a few peppered moths displayed a slightly darker color. These darker moths were better able to blend in with the sooty lichens, and so lived to produce other darker-colored moths. In little over a hun- dred years, successive generations of peppered moths evolved from almost completely white to completely black. Natural selec- tion, rather than "random accident," guided the moth's evolution- ary progress.

Elms are dying all over the place, it's Dutch elm disease. [...] It came from America on a load of logs, and it's a fungal disease. That makes it sound even more as if it might be possible to do something. The elms are all one elm, they are clones, that's why they are all succumbing. No natural resistance among the population, because no variation. Twins are clones, too. If you looked at an elm tree you'd never think it was part of all the others. You'd see an elm tree. Same when people look at me now: they see a person, not half a set of twins.

The single genetic variant identified that most powerfully predicted height explained all of 0.4 percent—four tenths of one percent—of the variation in height, and all those hundreds of variants put together explained only about 10 percent of the variation. Meanwhile, an equally acclaimed study did a GWAS regarding body mass index (BMI). Similar amazingness—almost a quarter million genomes examined, even more authors than the height study. And in this case the single most explanatory genetic variant identified accounted for only 0.3 percent of the variation in BMI.

The idea is that in any population of self-reproducing organisms, there will be variations in the genetic material and upbringing that different individuals have. These differences will mean that some individuals are better able than others to draw the right conclusions about the world around them and to act accordingly. These individuals will be more likely to survive and reproduce and so their pattern of behavior and thought will come to dominate. It has certainly been true in the past that what we call intelligence and scientific discovery have conveyed a survival advantage.

In fact, the entire range of human variation for some genetic traits can be found on the African continent.77 A person from the Congo, a person from South Africa, and a person from Ethiopia are more genetically different from each other than from a person from France.78 This seems astonishing because we are so used to focusing on a tiny set of physical features, especially skin color, to assign people to racial categories. It turns out that the genes contributing to these phenotypic differences represent a minute and relatively insignificant fraction of our genotypes and do not reflect the total picture of genetic variation among groups.79 What’s more, these phenotypic differences do not even fall neatly into the categories known as races. Rather, the physical features are “discordant” among groups—they are assorted randomly and do not come assembled in racial packages. “Sub-Saharan Africa is home to both the tallest (Maasai) and the shortest (pygmies) people, and dark skin is found in all equatorial populations, not just in the ‘Black race’ as defined in the United States,” writes Richard S. Cooper, a physician epidemiologist at Loyola University.80 And most genetic variation is found within any human population.81

First, given what is known about the chemical basis of biology and genetics, what is the likelihood that self-reproducing life forms should have come into existence spontaneously on the early earth, solely through the operation of the laws of physics and chemistry? The second question is about the sources of variation in the evolutionary process that was set in motion once life began: In the available geological time since the first life forms appeared on earth, what is the likelihood that, as a result of physical accident, a sequence of viable genetic mutations should have occurred that was sufficient to permit natural selection to produce the organisms that actually exist?

But what *is* "natural"? I wonder. On one hand: variation, mutation, change, inconstancy, divisibility, flux. And on the other: constancy, permanence, indivisibility, fidelity. Bhed. Abhed. It should hardly surprise us that DNA, the molecule of contradictions, encodes an organism of contradictions. We seek constancy in heredity—and find its opposite: variation. Mutants are necessary to maintain the essence of our selves. Our genome has negotiated a fragile balance between counterpoised forces, pairing strand with opposing strand, mixing past and future, pitting memory against desire. It is the most human of all things that we possess. Its stewardship may be the ultimate test of knowledge and discernment for our species. 

Genetic atomism is dead. Hereditary stability and hereditary change are both based, not on a mosaic of genes, but on the action of the gene-complex 'as a whole'. But this face-saving expression-which is now coming into increased use-is empty, like so many other holistic formulations, unless we interpolate between the gene-complex as a whole, and the individual gene, a hierarchy of genetic sub-assemblies-self-regulating holons of heredity, which control the development of organs, and also control their possible evolutionary modifications, by canalising the effects of random mutations. A hierarchy with its built-in, self-regulatory safeguards is a stable affair. It cannot be pulled in here, pulled out there, like Patou belabouring his model. It is capable of variation and change, but only in co-ordinated ways and only in limited directions.

They discovered that commonly used ethnic labels did not match the genetic clusters and were not reliable at predicting variation in the DME genes. One glaring lack of correspondence was the fact that 62 percent of Ethiopians, who would socially be labeled as black and grouped with the Bantu and Afro-Caribbeans, fell in the same genetic cluster as Ashkenazi Jews, Norwegians, and Armenians. A gene variant involved in metabolizing codeine and antidepressants “is found in 9%, 17%, and 34% of the Ethiopian, Tanzanian, and Zimbabwean populations, respectively.”41 The prevalence of an allele that predicts severe reactions to the HIV-drug abacavir is 13.6 percent among the Masai in Kenya, but only 3.3 percent among the Kenyan Luhya, and 0 percent among the Yoruba in Nigeria.42 Grouping all these people together on the basis of race for purposes of drug tailoring would be disastrous.

Perhaps it is unfair to expect such a high degree of scientific precision. But studies that conclude health disparities are caused by genetic difference do not even come close. These studies typically control for the socio-economic status (SES) of the research subjects in an attempt to compare subjects of different races who have the same SES. If there remains a difference in the prevalence or outcome of a disease, the researchers typically attribute the unexplained variation to genetic distinctions between racial groups. But this conclusion suffers from a basic methodological error. The researchers failed to account for many other unmeasured factors, such as the experience of racial discrimination or differences in wealth, not just income, that are related to health outcomes and differ by race. Any one of these unmeasured factors—and not genes—might explain why health outcomes vary by race.

Study a gene in only one environment and, by definition, you’ve eliminated the ability to see if it works differently in other environments (in other words, if other environments regulate the gene differently). And thus you’ve artificially inflated the importance of the genetic contribution. The more environments in which you study a genetic trait, the more novel environmental effects will be revealed, decreasing the heritability score. Scientists study things in controlled settings to minimize variation in extraneous factors and thus get cleaner, more interpretable results—for example, making sure that the plants all have their height measured around the same time of year. This inflates heritability scores, because you’ve prevented yourself from ever discovering that some extraneous environmental factor isn’t actually extraneous.fn22 Thus a heritability score tells how much variation in a trait is explained by genes in the environment(s) in which it’s been studied.

Modeling the evolution of modularity became significantly easier after a kind of genetic variation was discovered by quantitative trait locus (QTL) mapping in the lab of James Cheverud at Washington University called 'relationship QTL' or r-QTL for short. An r-QTL is a genetic locus that affects the correlations between two quantitative traits (i.e. their variational relationship, and therefore, 'relationship' loci). Surprisingly, a large fraction of these so-mapped loci are also neutral with respect to the character mean. This means one can select on these 'neutral' r-QTLs without simultaneously changing the character mean in a certain way. It was easy to show that differential directional selection on a character could easily lead a decrease in genetic correlation between characters. Of course, it is not guaranteed that each and every population has the right kind of r-QTL polymorphisms, nor is it yet clear what kind of genetic architecture allows for the existence of an r-QTL. Nevertheless, these findings make it plausible that differential directional selection can enhance the genetic/variational individuality of traits and, thus, may play a role in the origin of evolutionary novelties by selecting for variational individuality. It must be added, though, that there has been relatively little research in this area and that we will need to see more to determine whether we understand what is going on here, if anything. In particular, one difficulty is the mathematical modeling of gene interaction (epistasis), because the details of an epistasis model determine the outcome of the evolution by natural selection. One result shows that natural selection increases or decreases mutational variance, depending on whether the average epistatic effects are positive or negative. This means that the genetic architecture is more determined by the genetic architecture that we start with than by the nature of the selection forces that act upon it. In other words, the evolution of a genetic architecture could be arbitrary with respect to selection.

Human evolution is not over, but the chances of natural selection adapting our species in dramatic, major ways to common non-infectious mismatch diseases are remote unless conditions change dramatically. One reason is that many of these diseases have little to no effect on fertility. Type 2 diabetes, for example, generally develops after people have reproduced, and even then, it is highly manageable for many years.8 Another consideration is that natural selection can act only on variations that affect reproductive success and that are also genetically passed from parent to offspring. Some obesity-related illnesses can hinder reproductive function, but these problems have strong environmental causes.9 Finally, although culture sometimes spurs selection, it is also a powerful buffer. Every year new products and therapies are being developed that allow people with common mismatch diseases to cope better with their symptoms. Whatever selection is operating is probably occurring at a pace too slow to measure in our lifetimes.

With the rise of molecular genetics, it has become possible to search for possible changes (mutations, polymorphisms) in target genes. Much effort has gone into investigating variations in genes that contribute to serotonin transmission, because serotonin-related drugs have antidepressant and anxiolytic properties. This assumes, however, that the treatment mechanism is the same mechanism that gives rise to the disorder.53 Although this is consistent with the old chemical imbalance hypothesis, it is not a conclusion that should simply be accepted without careful assessment. Nevertheless, studies of the genetic control of serotonin have found interesting results. For example, people with a certain variant (polymorphism) of a gene controlling a protein involved in serotonin transmission are more reactive to threatening stimuli, and this hyperreactivity is associated with increased amygdala activity during the threat.54 Further, it has been reported that this variant of the gene can account for 7 percent to 9 percent of the inheritance of anxiety.55

By the end of this decade, permutations and combinations of genetic variants will be used to predict variations in human phenotype, illness, and destiny. Some diseases might never be amenable to such a genetic test, but perhaps the severest variants of schizophrenia or heart disease, or the most penetrant forms of familial cancer, say, will be predictable by the combined effect of a handful of mutations. And once an understanding of "process" has been built into predictive algorithms, the interactions between various gene variants could be used to compute ultimate effects on a whole host of physical and mental characteristics beyond disease alone. Computational algorithms could determine the probability of the development of heart disease or asthma or sexual orientation and assign a level of relative risk for various fates to each genome. The genome will thus be read not in absolutes, but in likelihoods-like a report card that does not contain grades but probabilities, or a resume that does not list past experiences but future propensities. It will become a manual for previvorship.

Lamarck’s Impact So, how could these "favorable variations" occur? Darwin tried to answer this question from the standpoint of the primitive understanding of science at that time. According to the French biologist Chevalier de Lamarck (1744-1829), who lived before Darwin, living creatures passed on the traits they acquired during their lifetime to the next generation. He asserted that these traits, which accumulated from one generation to another, caused new species to be formed. For instance, he claimed that giraffes evolved from antelopes; as they struggled to eat the leaves of high trees, their necks were extended from generation to generation. Darwin also gave similar examples. In his book The Origin of Species, for instance, he said that some bears going into water to find food transformed themselves into whales over time. However, the laws of inheritance discovered by Gregor Mendel (1822-84) and verified by the science of genetics, which flourished in the twentieth century, utterly demolished the legend that acquired traits were passed on to subsequent generations. Thus, natural selection fell out of favor as an evolutionary mechanism.

Hence the term “voluntary muscle” is in many ways a figure of speech. I can consciously command a movement, but I cannot consciously command the recruitment of every muscle fiber which must be used, nor the precise order of their contractions and lengthenings which actually produce the desired effect. This is to say that every consciously willed movement is always conditioned by two things: genetically established organization and habitual usage. Our genetic organization is quite plastic, open-ended, filled with potential variations in behavior; on the other hand, habitual usage can become just as limiting as it is convenient, and can become a tyrant to exactly the degree that it becomes practiced, automatic, unconscious. We are free to train ourselves to act differently, but it is very difficult to suddenly act differently than we have been trained. The tendencies in our motor behavior created by genetically determined patterns and by habitual usage do not lie within the muscle cells, nor even in the motor neurons that unite them into motor units. The search for the organizational factors of purposeful muscular control—whether it be action or relaxation—takes us deeper and deeper into the central nervous system, where we find that every muscular response is built up, selected, and colored by the totality of our neural activity, both conscious and unconscious.

In effect, we know from Darwin that there are only four characteristics necessary in order to get adaptive evolution, right? If you have reproduction, variation, differential success, and an environment of limited resources, you're going to get adaptive evolution. When we set up an economic system, or a political system...*it evolves*. Things evolve within it. And if we don't anticipate that what we write down in our documents about what we're trying to accomplish does not have the capacity to overwhelm whatever niche we have set up and that we will ultimately see the creatures that are supported by the environment that we created, then we will never get this right. Because we will always be fooled by our own intentions, and we will create structures that create predators of an arbitrary kind. So we need to start thinking evolutionarily, because that's the mechanism for shaping society into something of a desirable type rather than a monstrous type. [...] So let's say we're talking about a political structure...and we know we don't like corruption...and we're going to set a penalty for attempting to corrupt the system. OK, now what you've done is you've built a structure in which evolution is going to explore the questions, 'What kind of corruptions are invisible?' and 'What kinds of penalties are tolerable from the point of view of discovering how to alter policy in the direction of some private interest?' Once you've set that up, if you let it run, evolutionarily it will create a genius corruptor, right? It will generate something that is capable of altering the functioning of the system without being spotted, and with being only slightly penalized -- and then you'll have no hope of confronting it, because it's going to be better at shifting policy than you will be at shifting it back. So what you have to do is, you have to build a system in which there *is no selection* that allows for this process to explore mechanisms for corrupting the system, right? You may have to turn the penalties up much higher than you would think, so that any attempt to corrupt the system is ruinous to the thing that attempts it. So the thing never evolves to the next stage, because it keeps going extinct, right? That's a system that is resistant to the evolution of corruption, but you have to understand that it's an evolutionary puzzle in the first place in order to accomplish that goal. [...] We sort of have this idea that we inherited from the wisdom of the 50s that genes are these powerful things lurking inside of us that shift all of this stuff that we can't imagine they would have control over, and there's some truth in it. But the larger truth is that so much of what we are is built into the software layer, and the software layer is there because it is rapidly changeable. That's why evolution shifted things in that direction within humans. And we need to take advantage of that. We need to be responsible for altering things carefully in the software, intentionally, in order to solve problems and basically liberate people and make life better for as many people as possible, rather than basically throw up our hands because we are going to claim that these things live at the genetic layer and therefore what can we do?

Neo-Darwinism and Mutations In order to find a solution, Darwinists advanced the "Modern Synthetic Theory," or as it is more commonly known, Neo-Darwinism, at the end of the 1930s. Neo- Darwinism added mutations, which are distortions formed in the genes of living beings due to such external factors as radiation or replication errors, as the "cause of favorable variations" in addition to natural mutation. Today, the model that stands for evolution in the world is Neo-Darwinism. The theory maintains that millions of living beings formed as a result of a process whereby numerous complex organs of these organisms (e.g., ears, eyes, lungs, and wings) underwent "mutations," that is, genetic disorders. Yet, there is an outright scientific fact that totally undermines this theory: Mutations do not cause living beings to develop; on the contrary, they are always harmful. The reason for this is very simple: DNA has a very complex structure, and random effects can only harm it. The American geneticist B. G. Ranganathan explains this as follows: First, genuine mutations are very rare in nature. Secondly, most mutations are harmful since they are random, rather than orderly changes in the structure of genes; any random change in a highly ordered system will be for the worse, not for the better. For example, if an earthquake were to shake a highly ordered structure such as a building, there would be a random change in the framework of the building which, in all probability, would not be an improvement. Not surprisingly, no mutation example, which is useful, that is, which is observed to develop the genetic code, has been observed so far. All mutations have proved to be harmful. It was understood that mutation, which is presented as an "evolutionary mechanism," is actually a genetic occurrence that harms living things, and leaves them disabled. (The most common effect of mutation on human beings is cancer.) Of course, a destructive mechanism cannot be an "evolutionary mechanism." Natural selection, on the other hand, "can do nothing by itself," as Darwin also accepted. This fact shows us that there is no "evolutionary mechanism" in nature. Since no evolutionary mechanism exists, no such any imaginary process called "evolution" could have taken place.

A note of caution: epigenetics is also on the verge of transforming into a dangerous idea. Epigenetic modifications of genes can potentially superpose historical and environmental information on cells and genomes—but this capacity is speculative, limited, idiosyncratic, and unpredictable: a parent with an experience of starvation produces children with obesity and overnourishment, while a father with the experience of tuberculosis, say, does not produce a child with an altered response to tuberculosis. Most epigenetic “memories” are the consequence of ancient evolutionary pathways, and cannot be confused with our longing to affix desirable legacies on our children. As with genetics in the early twentieth century, epigenetics is now being used to justify junk science and enforce stifling definitions of normalcy. Diets, exposures, memories, and therapies that purport to alter heredity are eerily reminiscent of Lysenko’s attempt to “reeducate” wheat using shock therapy. Mothers are being asked to minimize anxiety during their pregnancy—lest they taint all their children, and their children, with traumatized mitochondria. Lamarck is being rehabilitated into the new Mendel. These glib notions about epigenetics should invite skepticism. Environmental information can certainly be etched on the genome. But most of these imprints are recorded as “genetic memories” in the cells and genomes of individual organisms—not carried forward across generations. A man who loses a leg in an accident bears the imprint of that accident in his cells, wounds, and scars—but does not bear children with shortened legs. Nor has the uprooted life of my family seem to have burdened me, or my children, with any wrenching sense of estrangement. Despite Menelaus’s admonitions, the blood of our fathers is lost in us—and so, fortunately, are their foibles and sins. It is an arrangement that we should celebrate more than rue. Genomes and epigenomes exist to record and transmit likeness, legacy, memory, and history across cells and generations. Mutations, the reassortment of genes, and the erasure of memories counterbalance these forces, enabling unlikeness, variation, monstrosity, genius, and reinvention—and the refulgent possibility of new beginnings, generation upon generation.

In a major study, researchers in Queensland collated the results of 2,748 papers and concluded the average variation across all human traits and diseases is caused by 49 per cent genetic factors and 51 per cent environmental factors.

Darwin’s point about variation often goes unappreciated today in philosophical discussions, even though it has been uncontroversial for well over a century. Recent discussions of natural kinds, prompted by the seminal ideas of Saul Kripke and Hilary Putnam, often assume that one can revive essentialism. Yet if species are natural kinds no such revival is in prospect. Kripke and Putnam largely restricted their discussions to the cases of elements and compounds, and with good reason. For, given the insights of neo-Darwinism, it’s clear that the search for some analogue of the microstructural essences can’t be found. No genetic or karyotypic property will play for species the role that atomic number does for the elements.

Non-African races had been founded by isolated groups of adventurers. Breeding among themselves, they had created gene pools that were necessarily limited to what they had brought with them: only a subset of what was to be found in Africa. This idea had been used to explain, for example, why Africa contained both the tallest and the most diminutive people in the world, and why so many top athletes were African. It wasn’t because they were naturally better athletes but because the bell-shaped curve of random genetic variation was wider.

Selection on one of two genetically correlated characters will lead to a change in the unselected character, a phenomenon called 'correlated selection response.' This means that selection on one character may lead to a loss of adaptation at a genetically correlated character. If these two characters often experience directional selection independently of each other, then a decrease in correlation will be beneficial. This seems to be a reasonably intuitive idea, although it turned out to be surprisingly difficult to model this process. One of the first successful attempts to simulate the evolution of variational modularity was the study by Kashtan and Alon (2005) in which they used logical circuits as model of the genotype. A logical circuit consists of elements that take two or more inputs and transform them into one output according to some rule. The inputs and outputs are binary, either 0 or 1 as in a digital computer, and the rule can be a logical (Boolean) function. A genome then consists of a number of these logical elements and the connections among them. Mutations change the connections among the elements and selection among mutant genotypes proceeds according to a given goal. The goal for the network is to produce a certain output for each possible input configuration. For example, their circuit had four inputs: x,y,z, and w. The network was selected to calculate the following logical function: G1 = ((x XOR y) AND (z XOR w)). When the authors selected for this goal, the network evolved many different possible solutions (i.e. networks that could calculate the function G1). In this experiment, the evolved networks were almost always non-modular. In another experiment, the authors periodically changed the goal function from G1 to G2 = ((x XOR y) or (z XOR w)). In this case, the networks always evolved modularity, in the sense that there were sub-circuits dedicated to calculating the functions shared between G1 and G2, (x XOR y) and (z XOR w), and another part that represented the variable part if the function: either the AND or the OR function connecting (x XOR y) and (z XOR w). Hence, if the fitness function was modular, that is, if there were aspects that remained the same and others that changed, then the system evolved different parts that represented the constant and the variable parts of the environment. This example was intriguing because it overcame some of the difficulties of earlier attempts to simulate the evolution of variational modularity, although it did use a fairly non-standard model of a genotype-phenotype map: logical circuits. In a second example, Kashtan and Alon (2005) used a neural network model with similar results. Hence, the questions arise, how generic are these results? And can one expect that similar processes occur in real life?

There are one or two variations to this rule: a post-reproductive animal or human can afford to be totally altruistic from a genetic point of view. Grandmas and elderly spinster aunts have great evolutionary value. (We shall return to the role of grandmothers in co-operative nurturing of children.) And the menopause gives a human mother more time to perform her child-rearing and educational role, freed from the duties of reproduction, which tend to limit her selfless streak.

You may be wondering why Mother Nature would program this variability across people. As a social species, should we not all be synchronized and therefore awake at the same time to promote maximal human interactions? Perhaps not. As we’ll discover later in this book, humans likely evolved to co-sleep as families or even whole tribes, not alone or as couples. Appreciating this evolutionary context, the benefits of such genetically programmed variation in sleep/wake timing preferences can be understood. The night owls in the group would not be going to sleep until one or two a.m., and not waking until nine or ten a.m. The morning larks, on the other hand, would have retired for the night at nine p.m. and woken at five a.m. Consequently, the group as a whole is only collectively vulnerable (i.e., every person asleep) for just four rather than eight hours, despite everyone still getting the chance for eight hours of sleep. That’s potentially a 50 percent increase in survival fitness. Mother Nature would never pass on a biological trait—here, the useful variability in when individuals within a collective tribe go to sleep and wake up—that could enhance the survival safety and thus fitness of a species by this amount. And so she hasn’t.

The proposition that business firms are entitled to patent protection when they have produced variations in the genetic structure of plants (GMOs) conveniently ignores the fact that the pre-existing plants had, themselves, arisen from modifications or adaptations provided by our ancient ancestors.

these creatures grow up with a peculiar knowledge. They know that they have been born in an infinite variety. They know, for instance, that in their genetic material they are born with hundreds of different chromosome formations at the point in each cell that we would say determines their "sex". These creatures don't just come in XX or XY; they also come in XXY and XYY and XXX plus a long list of "mosaic" variations in which some cells in a creature's body have one combination and other cells have another. Some of these creatures are born with chromosomes that aren't even quite X or Y because a little bit of one chromosome goes and gets joined to another. There are hundreds of different combinations, and though all are not fertile, quite a number of them are. The creatures in this world enjoy their individuality; they delight in the fact that they are not divisible into distinct categories. So when another newborn arrives with an esoterically rare chromosomal formation, there is a little celebration: "Aha," they say, "another sign that we are each unique." These creatures also live with the knowledge that they are born with a vast range of genital formations. Between their legs are tissue structures that vary along a continuum, from clitorises with a vulva through all possible combinations and gradations to penises with scrotal sac. These creatures live with an understanding that their genitals all developed prenatally from exactly the same little nub of embryonic tissue called a genital tubercle, which grew and developed under the influence of varying amounts of the hormone androgen. These creatures honor and respect everyone's natural-born genitalia –including what we would describe as a microphallus or a clitoris several inches long. What these creatures find amazing and precious is that because everyone's genitals stem from th same embryonic tissue, the nerves inside all their genitals got wired very much alike, so these nerves of touch just go crazy upon contact in a way that resonates completely between them. "My gosh," they think, "you must feel something in your genital tubercle that intensely resembles what I'm feeling in my genital tubercle." Well, they don't think that in so many words; they're actually quite heavy into their feelings at that point; but they do feel very connected –throughout all their wondrous variety. I could go on. I could tell you about the variety of hormones that course through their bodies in countless different patterns and proportions, both before birth and throughout their lives –the hormones that we call "sex hormones" but that they call "individuality inducers." I could tell you how these creatures think about reproduction: For part of their lives, some of these creatures are quite capable of gestation, delivery, and lactation; and for part of their lives, some of them are quite capable of insemination; and for part or all of their lives, some of them are not capable of any of those things – so these creatures conclude that it would be silly to lock anyone into a lifelong category based on a capability variable that may or may not be utilized and that in any case changes over each lifetime in a fairly uncertain and idiosyncratic way. These creatures are not oblivious to reproduction; but nor do they spend their lives constructing a self-definition around their variable reproductive capacities. They don't have to, because what is truly unique about those creatures is that they are capable of having a sense of personal identity without struggling to fit into a group identity based on how they were born. These creatures are quite happy, actually. They don't worry about sorting /other/ creatures into categories, so they don't have to worry about whether they are measuring up to some category they themselves are supposed to belong to.

The fewer carbohydrates we consume, the leaner we will be. This is clear. But there’s no guarantee that the leanest we can be will ever be as lean as we’d like. This is a reality to be faced. As I discussed, there are genetic variations in fatness and leanness that are independent of diet. Multiple hormones and enzymes affect our fat accumulation, and insulin happens to be the one hormone that we can consciously control through our dietary choices. Minimizing the carbohydrates we consume and eliminating the sugars will lower our insulin levels as low as is safe, but it won’t necessarily undo the effects of other hormones—the restraining effect of estrogen that’s lost as women pass through menopause, for instance, or of testosterone as men age—and it might not ultimately reverse all the damage done by a lifetime of eating carbohydrate- and sugar-rich foods. This means that there’s no one-size-fits-all prescription for the quantity of carbohydrates we can eat and still lose fat or remain lean. For some, staying lean or getting back to being lean might be a matter of merely avoiding sugars and eating the other carbohydrates in the diet, even the fattening ones, in moderation: pasta dinners once a week, say, instead of every other day. For others, moderation in carbohydrate consumption might not be sufficient, and far stricter adherence is necessary. And for some, weight will be lost only on a diet of virtually zero carbohydrates, and even this may not be sufficient to eliminate all our accumulated fat, or even most of it.

All told, the bdelloids appear to have adopted a Frankenstein collage of foreign DNA from more than five hundred different other species.Whether that’s through ingestion or not is up for debate, but these pilfered genes provide the bdelloids with much-needed genetic variation in the absence of sex.

Heritability is one of the trickiest concepts in modern biology. It describes variations only across an entire population. If the heritability of a trait in a group of people is 50 percent, that doesn’t mean that in any given person, genes and environment are each responsible for half of it. And if a trait has a heritability of zero, that doesn’t mean that genes have nothing to do with it. The heritability of the number of eyes is zero, because children are virtually all born with a pair of them. When we walk down the street, we don’t pass someone with five eyes, another with eight, and another with thirty-one. If someone has only one eye, it’s probably because they lost the other one in an accident or from an infection. Yet we all inherit a genetic program that guides the development of eyes.

As our ancestral populations spread across the globe, they encountered the same environments and selective forces that shaped the phenotypes of other populations endemic to these regions. The imprint of these regional selective forces is still evidenced by genetically determined differences in the characteristics of indigenous populations of humans, who often exhibit the same ecogeographic patterns described earlier for other native wildlife. In comparison to populations endemic to tropical regions of the continents, human populations native to lands in the higher latitudes tend to be larger and have relatively shorter limbs—following Bergmann’s and Allen’s rules, respectively. Our indigenous populations also exhibit latitudinal variation in skin color reminiscent of Gloger’s rule: darker skin (greater melanism) in the tropics, protecting native humans from the potentially destructive effects of intense solar radiation; lighter skin in high latitude populations of our species promoting absorption of the limited sunlight to levels sufficient to stimulate the production and storage of vital nutrients in the skin. On islands, the body size of primates (including insular populations of hominids) generally follows the island rule—exhibiting a graded trend toward more pronounced dwarfism in the larger species. The hominid of Flores Island (the “hobbit”) was only one-third to one-half the mass of its ancestor (most likely, Homo erectus). The island peoples of Indonesia, Melanesia, Micronesia, and the Philippines also tend to be relatively small in stature, again consistent with the island rule.

There is a continual turnover of theories as they are altered or replaced by new ones. So all the theories are being subjected to variation and selection, according to criteria which are themselves subject to variation and selection. The whole process resembles biological evolution. A problem is like an ecological niche, and a theory is like a gene or a species which is being tested for viability in that niche. Variants of theories, like genetic mutations, are continually being created, and less successful variants become extinct when more successful variants take over. ‘Success’ is the ability to survive repeatedly under the selective pressures – criticism – brought to bear in that niche, and the criteria for that criticism depend partly on the physical characteristics of the niche and partly on the attributes of other genes and species (i.e. other ideas) that are already present there.

Was it even genetically possible that one couple could create so many variations of magnificent?

PDGFR, or Bcr/Abl. Their strategy was to focus on the exact place on the kinase that bound phosphate on its way from ATP to the protein. The theory behind kinase inhibition was that each kinase had a particular notch or groove that made a tight fit with ATP, and that the shape of these notches varied from kinase to kinase. That variation was what made kinases viable drug targets. Zimmermann believed that this binding site—the exact spot where the kinase bound ATP to capture the phosphate that would be used to switch on another protein—seemed like the most likely location of each kinase’s unique fingerprint. That binding site was what allowed the kinase to serve its function on the cell, so it made sense to Zimmermann that this area would be distinct both from the binding site of other kinases and from other areas on the same kinase.

Even though these individuals had seemed perfectly healthy at birth, something that had happened during their development in the womb affected them for decades afterwards. And it wasn’t just the fact that something had happened that mattered, it was when it happened. Events that take place in the first three months of development, a stage when the foetus is really very small, can affect an individual for the rest of their life. This is completely consistent with the model of developmental programming, and the epigenetic basis to this. In the early stages of pregnancy, where different cell types are developing, epigenetic proteins are probably vital for stabilising gene expression patterns. But remember that our cells contain thousands of genes, spread over billions of base-pairs, and we have hundreds of epigenetic proteins. Even in normal development there are likely to be slight variations in the expression of some of these proteins, and the precise effects that they have at specific chromosomal regions. A little bit more DNA methylation here, a little bit less there. The epigenetic machinery reinforces and then maintains particular patterns of modifications, thus creating the levels of gene expression. Consequently, these initial small fluctuations in histone and DNA modifications may eventually become ‘set’ and get transmitted to daughter cells, or be maintained in long-lived cells such as neurons, that can last for decades. Because the epigenome gets ‘stuck’, so too may the patterns of gene expression in certain chromosomal regions. In the short term the consequences of this may be relatively minor. But over decades all these mild abnormalities in gene expression, resulting from a slightly inappropriate set of chromatin modifications, may lead to a gradually increasing functional impairment. Clinically, we don’t recognise this until it passes some invisible threshold and the patient begins to show symptoms.

In their important masterpiece entitled When the Earth Nearly Died, Allan and Delair write: In Europe immense herds of diverse animals utterly vanished off the face of the earth for no obvious biological reason Coincident with this dreadful slaughter upon the land was the deposition of myriads of contemporary marine shells, and the stranding at great elevations of marine mammals, porpoises, walruses and seals In Siberia, the picture is everywhere one of appalling disorder, carnage and wholesale destruction, with countless animals and plants frozen in positions of death ever since the day they perished. As a result, their remains are amazingly fresh-looking and are frequently indistinguishable from those of animals and plants that have died mere weeks ago The magnitude of the biological extinctions achieved by the Deluge almost transcends the imagination. It annihilated literally billions of biological units of both sexes and every age indiscriminately. Only incredibly powerful flood waters operating world-wide could have achieved such results, and only a flood produced by the means previously suggested could have operated globally They comment on the preposterous Ice Age theories of their predecessors. Although these theories hold little water, they are accepted by supposedly intelligent people. ...it is astonishing that such an unscientific explanation ever came to be formulated, yet in a short time both it and the concept of immense thick ice-sheets descending from a hypothetical northern mountain system, to cover all of northern and eastern North America and western and northern Eurasia, was enthusiastically embraced...as virtually established fact The evidence is perfectly unambiguous. Along with the removal of an “Ice Age” like that which has been hitherto commonly envisaged, the evidence suggests that there is something seriously amiss with the last phases of standard geological chronology Evidence thus converges from numerous directions to support the conclusion that, on the testimony of radio-carbon and other dating techniques, immense physical and climatic changes occurred on earth some 11,000 years or so ago – when an Ice Age that probably never existed came to an end, and an apparently uniformitarian regime was abruptly terminated The gigantic worldwide tectonic disturbances of the ‘late Pleistocene’ times occurred almost simultaneously on a nearly unimaginable scale – precisely what could be expected from a powerful external influence but not from the ‘Ice Age’ conditions conventionally believed to have existed then They note the change in the magnetic fields that occurred during the cataclysmic period of Earth’s recent history: Significantly, a drop in the strength of the earth’s magnetic field appears to have occurred sometime between 13,750 and 12,350 years ago...attended by various other important changes, including earthquakes, vulcanism, water table fluctuations and large scale climatic variations. Of these, severe earthquakes in particular may even induce axial wobble, and polarity reversals

In 2005 scientists published the results of a number of experiments that indicated that humans are still evolving. In one case, a team of geneticists led by Bruce Lahn at the University of Chicago offered proof that the human brain has been continuously evolving since Homo Sapiens first appeared. The scientists looked at two genes known as microcephalin and ASPM, both of which are known to contribute to brain growth. (They are also expressed in other tissue in the body.) The geneticists sequenced DNA from a collection of human cells that represents the variation in our species, and they found that one variation of each gene, called an allele, occurred with particularly high frequencey. The fact that the alleles seemed to occur more normal genetic drift would allow suggests that they have been actively selected over time. The scientists believe that the frequent allele of microcephalin appeared around thirty-seven thousand years ago and the frequent allele of ASPM appeared only fifty-eight hundred years ago. It's not known what effect these variations of these genes have, or why they were selected. They could have shaped cognition, as Lahn argues. Other scientists suggest the genes could have had some other effect on the brain that doesn't directly impact thought.

In 2005 scientists published the results of a number of experiments that indicated that humans are still evolving. In one case, a team of geneticists led by Bruce Lahn at the University of Chicago offered proof that the human brain has been continuously evolving since Homo Sapiens first appeared. The scientists looked at two genes known as microcephalin and ASPM, both of which are known to contribute to brain growth. (They are also expressed in other tissue in the body.) The geneticists sequenced DNA from a collection of human cells that represents the variation in our species, and they found that one variation of each gene, called an allele, occurred with particularly high frequencey. The fact that the alleles seemed to occur more than normal genetic drift would allow suggests that they have been actively selected over time. The scientists believe that the frequent allele of microcephalin appeared around thirty-seven thousand years ago and the frequent allele of ASPM appeared only fifty-eight hundred years ago. It's not known what effect these variations of these genes have, or why they were selected. They could have shaped cognition, as Lahn argues. Other scientists suggest the genes could have had some other effect on the brain that doesn't directly impact thought.

Language and material culture have greatly increased the mobility of the world's population, and some researchers believe that this will lead to an unhealthy and irreversible diminishing of variation in our genome. As more and more humans breed across the boundaries of genetic variation, we become a blander, more homogenous bunch than our diverse parent groups. This could be a problem because variation is important to the evolutionary health of a species, for the more we are the same, the easier it is for one single thing to make us extinct. Indeed, some genetic variants of the human species are disappearing altogether as small indigenous groups die out.

Perhaps, I thought, the dead god gets folded into the existence of the new god, the way a dormant genetic variation can exist within an organism’s DNA—hanging about like an actor’s understudy until the right environmental conditions give it expression and—hey presto—suddenly a bacteria is heat resistant, our Chloe gets her big break on Broadway and a sniper for hire gets an unexpected half a meter of cold steel through the chest. Perhaps

Eighty-five percent of human variation, according to the genetic differences in blood groups, was seen in the same racial groups. Of the remaining 15 percent, only 8 percent accounted for differences between one racial group and another.

So on the one hand you can have identical genes leading to very different phenotypes, and on the other you can have dissimilar genes producing exactly the same

It is only when you have average or low levels of cholesterol that being a carrier of "bad" allele 4 puts you at a greater risk than others with the same cholesterol level.

Given that dogs and wolves are virtually indistinguishable genetically, the enormous variation in body size and shape in the dog is truly remarkable.

There is no such limit with DNA replication. The DNA reproduction system is indifferent to the content or function of what is copied

When we learn something new and try to teach it to someone else, our success in both receiving and transmitting the information depends on what it is about.

Knowing what causes differentiation in human skin pigmentation, fascinating though that is, does not furnish a satisfactory explanation for the phenomenon of racism. Similarly, the biological explanation for why one person is right-handed whilst another is left-handed, is of less interest than why, even recently, being left-handed was considered such a stigma (…).Do we need to know what ‘causes’ homosexuality or heterosexuality? (…)Would the discovery of a genetic basis to sexual attraction finally undermine discrimination against non-heterosexual people by establishing that variations of sexual orientation are all equally rooted in nature? Or would it furnish powerful homophobic forces with a new weapon in their drive to undermine and remove the rights of non-heterosexual people, perhaps even the right to life itself? The infamous remarks of a senior religious leader (a former Chief Rabbi) in the UK a few years ago that, if a gay gene could be discovered, he would consider it morally acceptable to test pregnant women and offer them the option of aborting any foetus likely to develop into a non-heterosexual person - homophobic extermination in the womb - indicate that the huge moral and cultural debates around sexuality and human identity will not be solved either way by the biological sciences alone

Cultural evolution can proceed so quickly because it operates, as biological evolution does not, in the "Lamarckian" mode - by the inheritance of acquired characters. Whatever one generation learns, it can pass to the next by writing, instruction, inculcation, ritual, tradition, and a host of methods that humans have developed to assure continuity in culture. Darwinian evolution, on the other hand, is an indirect process: genetic variation must first be available to construct an advantageous feature, and natural selection must then preserve it. Since genetic variation arises at random, not preferentially directed toward advantageous features, the Darwinian process works slowly. Cultural evolution is not only rapid; it is also readily reversible because its products are not coded in our genes.

the popular conception of the gene as a simple causal agent is not valid. The idea that there is a gene for adventurousness, heart disease, obesity, religiosity, homosexuality, shyness, stupidity, or any other aspect of mind or body has no place on the platform of genetic discourse.

Americans may already have begun adapting genetically to the American environment in the several generations since their ancestors arrived in the United States. The malaria-protecting genetic variants common in Africans, such as the variation that causes sickle-cell anemia, are no longer a necessity of survival in the United States, so the pressure of natural selection to retain these variants would be relaxed.

Our basic understanding of evolutionary theory (how evolution works) in the early twenty-first century may be summed up as follows:   1. Mutation introduces genetic variation, which may introduce phenotypic variation. 2. Developmental processes can introduce broader phenotypic variation, which may be heritable. 3. Gene flow and genetic drift mix genetic variation (and potentially its phenotypic correlates) without regard to the function of those genes or traits. 4. Natural selection shapes genotypic and phenotypic variation in response to specific constraints and pressures in the environment. 5. At any given time one or more of the processes above can be affecting a population. 6. Dynamic organism-environment interaction can result in niche construction, changing pressures of natural selection and resulting in ecological inheritance. 7. Cultural patterns and contexts can impact gene flow and the pressures of natural selection, which in turn can affect genetic evolution (gene-culture coevolution). 8. Multiple inheritance systems (genetic, epigenetic, behavioral, and symbolic) can all provide information and contexts that enable populations to change over time or avoid certain changes.

Much of the human cerebral cortex is devoted to the complexities of language and tool-use. Humans are genetically adapted to learn to speak a natural language, but the differences among natural languages apparently are trivial compared with their fundamental similarities in structure and ontogeny. There is no evidence that variations in natural languages have any adaptive significance, hence the human capacity to learn a variety of languages is best considered an incidental byproduct of linguistic ability.

The probability of human cognitive faculties being reliable (producing mostly true beliefs), given that human beings have cognitive faculties (of the sort we have) and given that these faculties have been produced by evolution (Darwin's blind evolution, unguided by the hand of God or any other person), [is low]. If metaphysical naturalism and this evolutionary account are both true, then our cognitive faculties will have resulted from blind mechanisms like natural selection, working on such sources of genetic variation as random genetic mutation. Evolution is interested, not in true belief, but in survival or fitness. It is therefore unlikely that our cognitive faculties have the production of true belief as a proximate or any other function, and the probability of our faculties being reliable (given naturalistic evolution) would be fairly low.

If our origin involves random genetic variation, then we and our cognitive faculties would have developed by way of chance rather than by way of design, as would be required by our having been created by God in his image. But this is to import far too much into the biologist's term 'random'. Those random variations are random in the sense that they don't arise out of the organism's design plan and don't ordinarily play a role in its viability; perhaps they are also random in the sense that they are not predictable. But of course it doesn't follow that they are random in the much stronger sense of not being caused, orchestrated and arranged by God.

If our origin involves random genetic variation, then we and our cognitive faculties would have developed by way of chance rather than by way of design, as would be required by our having been created by God in his image. But this is to import far too much into the biologist's term 'random'. Those random variations are random in the sense that they don't arise out of the organism's design plan and don't ordinarily play a role in its viability; perhaps they are also random in the sense that they are not predictable. But of course it doesn't follow that they are random in the much stronger sense of not being caused, orchestrated and arranged by God.

Crops are typically grown in cultivars, or variations on a single species, bred with some specific trait in mind. Within a single cultivar, the plants tend to be genetically similar, though not identical. But individual altruistic tendencies may be more clearly distinguishable among them. To develop cultivars in crop breeding, farmers select for the most “vigorous”-looking individual plants in a field. But these are actually the most competitive individuals. The plants with more altruistic tendencies will be more reserved, in that they will tend not to grow aggressively into their neighbor’s sun space. So it seems the history of crop breeding has actually helped to reduce altruism, to its own peril, writes Dudley. If a farmer were to instead select altruistic plants early in the breeding process, it could steer the crop toward allocating fewer resources into competing for space, therefore presumably putting more energy into reproduction—that is, the development of the fruit the crop is prized for. On the flip side, aggressive plants are useful when the aggression is directed to plants outside the cultivar—non-kin plants, including weeds. Choosing the plants adept at helping their neighbors but fighting off intruders might ultimately result in a highly resilient cultivar. In this way, paying attention to individual plants’ social traits—might we say personalities?—could have a real benefit to the way we grow food.

Many years later, research by Keiko Hayashi, Ph.D., of the University of Tsukuba in Japan showed the same thing. 12 In Hayashi’s study, diabetic patients watching an hour-long comedy program upregulated a total of 39 genes, 14 of which were related to natural killer cell activity. While none of these genes were directly involved in blood-glucose regulation, the patients’ blood-glucose levels were better controlled than after they listened to a diabetes health lecture on a different day. Researchers surmised that laughter influences many genes involved with immune response, which in turn contributed to the improved glucose control. The elevated emotion, triggered by the patients’ brains, turned on the genetic variations, which activated the natural killer cells and also somehow improved their glucose response—probably in addition to many other beneficial effects. As Cousins said of placebos back in 1979, “The process works not because of any magic in the tablet, but because the human body is its own best apothecary and because the most successful prescriptions are filled by the body itself.

there was only a 15 per cent genetic variation across ‘racially’ and geographically classified populations.

Africa contains the most variation in the world in physical type due to the vast variety of genetic heritage. It has the shortest and tallest people, populations with the thickest and thinnest lips, and very wide differences in the widths of noses and skull dimensions. Populations thought to consist of a single ‘tribe’ show a continuous grading of gene frequencies, while populations thought to be biologically separate have much greater genetic similarity than previously thought. The genetic diversity of Africa is often regarded as analogous to the fact that its population speaks 2,000 different languages.

One of the many pernicious aspects of this research was the way it was used to classify human “races.” In biology and anthropology, race has long been abandoned as a meaningful category; indeed, although the term has been in use since the seventeenth century, it has never been precisely defined. There has never been any agreement about the number of human races, or what the definitive characteristics of a race might be: skin color, hair type, head shape, etc. Genetic research in the twentieth century has shown that there are no genes that correspond to racial types and that the range of variation within so-called races is greater than the variation across them. But scientists in the early 1920s were working with an essentialist model of race as something immutable, definitive, and grounded in biological reality.

alcohol can consume more longer (get higher) without falling down, getting sick, or passing out, and they are, as a result, more likely to drink alcoholically. Another study links a specific genetic variation affecting D2 dopamine receptors, which are part of the rewards center in the brain, to addiction. This genetic mutation, which essentially magnifies the pleasurable effects of addictive substances and behaviors, increases the risk not just for alcoholism, but for all other types of addiction.2 Genetic variations can also reduce the risk for addiction. For instance,

As strange as it sounds, it is no longer possible to determine how many human genomes have been sequenced. At present the strategy of choice is whole-genome re-sequencing (Chapter 3) whereby next-generation sequence data are mapped onto a reference genome. The results have been breathtaking. The recently concluded (and aptly named) 1000 Genomes Project Consortium catalogued ~85 million SNPs, 3.6 million short insertions/deletions, and 60,000 larger structural variants in a global sampling of human genetic diversity. These data are catalysing research in expected and unexpected ways. Beyond providing a rich source of data for GWA-type studies focused on disease, scientists are also using the 1000 Genomes Project data to learn about our basic biology, something that proved surprisingly difficult when only a pair of genomes was available. For example, a recent GWAS taking advantage of the 1000 Genomes Project data identified ten genes associated with kidney development and function, genes that had previously not been linked to this critical aspect of human physiology. In 2016, Craig Venter’s team reported the sequencing of 10,545 human genomes. Beyond the impressively low cost (US$1,000–2,000 per genome) and high quality (30–40× coverage), the study was significant in hinting at the depths of human genome diversity yet to be discovered. More than 150 million genetic variants were identified in both coding and non-coding regions of the genome; each sequenced genome had on average ~8,600 novel variants. Furthermore, each new genome was found to contain 0.7 Mbp of sequence that is not contained in the reference genome. This underscores the need for methods development in the area of structure variation detection in personal genome data. Overall, however, the authors concluded that ‘the data generated by deep genome sequencing is of the quality necessary for clinical use’.

work for everyone. Put differently, at the Collective, we have a saying: “Personality doesn’t scale. Biology scales.” What we mean is, in the field of peak performance, too often, someone figures out what works for them and then assumes it will work for others. It rarely does. More often, it backfires. The issue is that personality is extremely individual. Traits that play a critical role in peak performance—such as your risk tolerance or where you land on the introversion-to-extroversion scale—are genetically coded, neurobiologically hardwired, and difficult to change. Add in all the possible environmental influences that come from variations in cultural background, financial means, and social status, and the problem compounds. For all these reasons, what works for me is almost guaranteed not to work for you. Personality doesn’t scale. Biology, on the other hand, scales. It is the very thing designed by evolution to work for everyone. And this tells us something important about decoding the impossible: if we can get below the level of personality, beneath the squishy and often subjective psychology of peak performance, and decode the foundational neurobiology, then we unearth mechanism. Basic biological mechanism. Shaped by evolution, present in most mammals and all humans. And this leads us to the next question: What’s the biological formula for the impossible? The answer is flow. Flow is defined as “an optimal state of

Structures are never monolithic,” Prax said. “There’s more genetic variation within Belters or Martians or Earthers than there is between them. Evolution would predict some divisions within the group structures and alliances with out-members. You see the same thing in ferns.” “Ferns?” Naomi asked. “Ferns can be very aggressive,” Prax said.

There is perhaps no more heartening proof of the role of environment in human intelligence than the Flynn effect, the worldwide phenomenon of upwardly trending IQ, named for the New Zealand psychologist who first described it. Since the early years of the twentieth century, gains have ranged between nine and twenty points per generation in the United States, Britain, and other industrialized nations for which reliable data-sets are available. With our knowledge of evolutionary processes, we can be sure of one thing: we are not seeing wholesale genetic change in the global population. No, these changes must be recognized as largely the fruits of improvement in overall standards both of education and of health and nutrition. Other factors as yet not understood doubtless play a role, but the Flynn effect serves nicely to make the point that even a trait whose variation is largely determined by genetic differences is in the end significantly malleable. We are not mere puppets upon whose strings our genes alone tug.