In this post, we will do the following:

• Discuss historical and contextual aspects of the term “Natural Selection” in order to make clear exactly what it might mean (and not mean).
• Provide what I feel is the best exact set of terms to use for these “three conditions,” because the words one uses are very important (there are probably some wrong ways to do it one would like to avoid).
• Discuss why the terms should be put in a certain order (for pedagogical reasons, mainly) and how they relate and don’t related to each other.

When you are done reading this post you should be able to:

• Make erudite and opaque comments to creationists that will get you points with your web friends.
• Write really tricky Multiple Choice Exam Questions if you are a teacher.
• Evolve more efficiently towards your ultimate goal because you will be more in control of the Random Evolutionary Process (only kidding on this third one…)

Here are some definitions of Natural Selection I found on the web for your review:

• The differential survival and reproduction of organisms with genetic characteristics that enable them to better utilize environmental resources [source]
• Natural selection is the process in which some organisms live and reproduce and others die before reproducing. Some life forms survive and reproduce because they are better suited to environmental pressures, ensuring that their genes are perpetuated in the gene pool. [source]
• Process by which the genotypes in a population that are best adapted to the environment increase in frequency relative to less well-adapted genotypes over a number of generations. source
• The concept developed by Charles Darwin that genes which produce characteristics that are more favorable in a particular environment will be more abundant in the next generation. [source]
• the differential survival and/or reproduction of individuals within a population based on hereditary characteristics. [source]
• The process by which new species evolve when influenced by selective pressure (Martin et al, 2000). Natural selection occurs when the natural factors of environmental resistance tend to eliminate those members of a population that are least well adapted to cope and thus, in effect, select those best adapted for survival and reproduction (Nebel et al, 1998). [source]
• central thesis of the biologist Charles Darwin which suggests that within every population of living organisms there are random variations which have different survival value. Those which aid survival (or enhance reproductive capacity) are ‘selected’ by being genetically transmitted to succeeding generations. [source]

There are things I don’t like about most of these definitions. A definition may focus on environmental conditions and thus ignore many very important other things such as developmental processes and mating. Definitions may focus on the individual’s survival, etc., which works, but we may want to speak of traits as well as individuals. Some definitions use active verbs such as “ensuring that their genes are perpetuated in the gene pool.” This may not be linguistically wrong but it incorporates teleological concepts, which don’t need our help in creeping into our thinking (especially in the formal definition of a natural force!). There is often a direct link to Charles Darwin. This is good because it is true that this is his concept. However, a modern definition of Natural Selection needs to be Neo-Darwinian. So specifically referring in the definition to Darwin without more attention to the historical development is inadequate. Referring to Darwin’s concept as a concept about genes is jarringly wrong.

Check out our new science podcast, Ikonokast.
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As a whole these definitions are not terrible, but they are mostly flawed for one reason or another. The definition I want to lay out here will have specific reference to the same process these definitions are about. However, there is also one very large problem with many of these definitions that is a bit more subtle than most but that is, to me, critical, that relates to the object of study. It is probably best to not assume a one-to-one correspondence between the process of Natural Selection that we are going to describe here and the concept of “adaptation.” Ultimately, I would like to say that “adaptation” is the noun and “Natural Selection” is the verb in a key evolutionary process. But having said that, a useful and precise definition of Natural Selection may have to leave out processes that are nonetheless related to adaptations, both in terms of understanding the historical aspects of an adaptation and the functional aspects, but that do not fall under the process “Natural Selection” as it is best defined.

An adaptation may reach its particular form through the process of Natural Selection, but there are aspects to that form that have to do with, for instance, abiotic realities. You cannot have adaptations that involve swimming without bodies of water, for example. Our definition does not say “Oh, and there must be air, and water, and trees to climb in.”

I actually want to provide TWO different (linguistically) but identical (functional) definitions of natural selection. The first is the coolest one, the simplest one, the one that makes you think. The second is a better pedagogical tool and serves better as the basis for adaptationist analysis of biological systems. The second also links better to certain historical aspects of the development of the concept.

The first definition is conceptually related to the following definition of evolution:

Change in allele frequency over time.

Which is something of an oversimplification, but an allowable one. And in this context we can define Natural Selection as:

Nonrandom elimination of alleles.

I believe that this was suggested by Ernst Mayr.

This is a cool definition because it is short, sweet, and correct. Note the very important asymmetry that this definition implies. There is no non-random generation of novel alleles. Only elimination. This jibes with selection as a creative force, but neutral processes as providing the raw material. Neutral processes lay down the sediments that become the marble, Natural Selection is the sculptor. The adaptation is the sculpture.

The second definition, and the one I really want to get to, involves the so called “three necessary and sufficient conditions” and it goes something like this:

1. Variation in a trait
2. Heritability of the trait
3. Differential fitness conferred by the trait.

Just as important as these elements is the theoretical and logical framework in which they are placed. They are the THREE NECESSARY and SUFFICIENT conditions. Let’s parse that out more.

Three … That there are three is obviously because all important things happen in threes, sevens, or tens, for unknown cosmic reasons. Be that as it may, I want to point out that “three” implies “three different” things. If two of them could have been combined, then we would have only two. But there are three.

What this implies is the following: If there is a trait that varies, then it meets the first criterion. But “No,” you say, “what about hair color? If I see a bunch of people with different color hair, and I KNOW they dyed their hair to get that way, this is not trait related to selection. So it does not meet the first criterion.”

But you would be wrong. Remember, there are THREE DIFFERENT criteria. The first one is variation. If you see a bunch of dogs and they have different coats because they went to a very creative groomer, or a bunch of students standing around the cafeteria with blue, red, unnaturally black, and vivid yellow hair because they all went to Target and got dye and colored their hair, then in both cases you have met the first criterion because there is variation. By saying “these traits are not inherited” you have skipped ahead and cheated.

The second criterion is usually stated as “heritability” and that is a small problem, because the term “heritability” has a specific meaning in biostats that falls apart for our present use. It is the measured variance in the genotype divided by the measured variance in the phenotype, squared. (Thus indicating something like the proportion of measured phenotypic variance that is accountable by genetic variation.) What is meant in our definition, however, is this: Is the variation in the trait conferred by genes? The dyed hair and the clipped poodle do not meat this criterion.

The third criterion is often stated as “Differential Reproductive Success” and that is simply wrong. The correct term is “Differential fitness” and it has to be differential fitness that is conferred by the trait. Why fitness instead of Reproductive Success (RS)? That is an important matter, and I will not discuss it here. For now, let’s just go with it.

OK, back to the theoretical context: Necessary.

Why are these three necessary? By necessary it is meant that ALL of them have to be true or it is not Natural Selection. This is fairly obvious. If you are missing any one of these three then what you are observing may be an interesting phenomenon but it is not Natural Selection. This also speaks to the need to be Neo-Darwinian. Darwin was aware of inheritance, but lacking an understanding of the mechanism, the necessary requirement of “heritability” (remember, shorthand for “the trait is passed on by genes”), any Darwinian definition (and I’ve avoided using his specific words here) is not good enough.

I had said at the beginning that the ordering of the three conditions is important. This is because they interact with each other in order. Here is how.

First, you need a trait that shows variation. Second you need to show that that trait is heritable, AND that the inheritance pattern relates to that variation. Third you need to show that the variation that is heritable maps on to differential fitness. So there is a strong logic to the order, that is embedded in the functional meaning of Natural Selection and any test criteria that are set up to investigate possible cases of it.

So the ordering works both for the understanding of the concept (pedagogy) and the investigation of the phenomenon.

Sufficient. That is a really important part of the context for this definition. If these three conditions are true, then Natural Selection IS happening. There is no alternative. The force of Natural Selection is activated when these three conditions are met, no matter what.

Does this mean that the selective force will have an effect? It depends. Natural Selection is a force, but there are other forces, including other instances of Natural Selection that may be operative in a particular organism. Gravity is a force but a fly can still walk on the ceiling. The gravity is still acting on the fly, but so is another force (adhesion) that keeps it up there.

This is an important point that bears emphasis. When the Three N&S Conditions of N.S. are working, Natural Selection happens. Period. The absence of an EFFECT is due to countervailing forces (including chance, because within it’s operation there are still stochastic effect).

I believe it is incorrect and counterproductive to make “Sexual Selection” distinct from and parallel to “Natural Selection.” Darwin was puzzled by apparent inconsistencies, especially along the lines of exaggerated traits mostly in males, and came up with Sexual Selection as a process to explain this. Fine. But I think it is best to think of both Sexual and Artificial Selection as subsets of Natural Selection.

The term “Selection” by itself is often used interchangeably with “Darwinian Selection,” but often (usually?) as not really meaning the same thing as Natural Selection. Natural Selection works between generations on reproducing organisms and their genomes. Darwinian Selection, or selection in general can work on other things, like prospective students trying to get into law school, or neurons during culling, etc.

This has been an enhanced repost from a very long time ago. You might imagine that I’m about to write a post on Falsehoods related to Natural Selection, and needed this post nearby. You’d be right!

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Other posts of interest:

• How to get rid of spiders in your house
• Why is your poop green?
• How many cells are there in the human body?
• Is there really a plot hole in Harry Potter Goblet of Fire?
• How long is a human generation?
• Is blog ever really blue?
• How to not get caught plagiarizing
• The origin of the domestic chicken
• What are the three necessary and sufficient conditions of Natural Selection?
• How do I get rid of foot fungus?
• Which is better, Tap Water or Bottled Water?
• Has Global Warming stopped?

Also of interest: In Search of Sungudogo: A novel of adventure and mystery, which is also an alternative history of the Skeptics Movement.

That is probably true sometimes. But we have sequenced the entire human genome, so shouldn’t we know about all the genes? Well, yes and no. We may have a list of genes found in a sample of humans, but “The Human Genome” can consist of a single individual (though it does not) and miss variation between individuals, i.e., it may not be a record of all of the possible alleles (variants) of each gene. Also, beyond the scope of this discussion but worth mentioning, a “gene” is not a simple concept. Whether or not a gene is expressed, where, when, and exactly what product it produces is not entirely encoded in the gene itself, but rather, elsewhere in the genome, or not encoded at all, but rather, dependent on external, non-genetic factors. So that complicates things too. So, if there is a trait that you think must be genetic, but years of research have failed to find it, the existence of a human genome and the prior acquisition of a lot of genetic data does not necessarily mean that the genetic information that determines the trait in question is not there. You can continue to believe that the genetic code for the trait will eventually be found

Except when you can’t.

There are two separate ways in which people sort out which traits are assumed to be genetic from those that are assumed to be not genetic. Both are heuristic, one is valid, and one is not. Let’s start with the one that is valid.

Suppose, as before, there is a trait that is seemingly inherited in families in such a way that a genetic trait would be, in the time tested manner that with respect this trait “offspring resemble their parents” as Darwin noted. The next question you can ask is this: Is it biologically sensible that this trait is inherited genetically, or is there a better, obvious, non-genetic mode of inheritance? If the trait is a physical feature such as eye color, then we have a sensible biological explanation for the trait having to do with developmental process we know something about and a set of metabolic pathways that produce various molecules such as pigments. The idea that this trait is genetic is biologically sensible, so even if you can’t find any, or all, of the genetic determinants of this trait, you can figure they are out there somewhere. Suppose, though, that the trait is a behavioral one that we see people in real life learning. For example, what language a person speaks generally follows the same kind of inheritance pattern many clearly genetic traits follow. With respect to spoken language, most of the time, offspring resemble their parents. But, rather than there being a sensible biological explanation for this trait, there is a sensible cultural explanation for this trait, so we don’t even look for the genetic variants for “French” vs. “Mandarin” vs. “English.” We simply assume this is not genetic.

The second method, the incorrect one, is to work with an article of faith. Broadly speaking, and I oversimplify greatly here, there are two primary articles of faith that often inform people’s thinking, shaping their assumptions, about genetics. Both usually have to do with behavioral traits in humans, but this can apply to physical traits as well. One article of faith asserts that humans are born as a blank slate, and all of their behavioral characteristics, such as their personality, intelligence by one measure or another, and so on, are added by experience. The other is the inheritance assumption, that some or much of an individual’s personality, intelligence, etc is determined by genes. There is not necessarily a consistent logic behind either of these assumptions, though various schools of thinking will include, often, a logical framework. However, this method of coming to a conclusion about the genetics or lack thereof behind various traits relies on one important element regarding genetic systems: Ignorance. If you are a blank slatist, then the absence of a clear pathway from genes to behavior means that your hypothesis can’t be falsified. If you are a genetic determinist, then the lack of such a pathway can be attributed to ongoing ignorance about the genes. The former might then be expected to live in fear that a gene will be found for their favorite learned behavior, and the latter might be expected to to live in a state of hubris, firmly knowing and asserting a truth that is not yet known but someday will be.

My impression is that over time there are fewer and fewer pure genetic determinists out there, and few and fewer blank slatists. I think the reasons for that shift have little to do with increasing knowledge, and more to do with changes in how one plays the academic game of argument, but that is discussion for another time. There is a danger in that shift, though. In the absence of any useful research results, if blank slatists start to admit that there could be some sort of genetics behind behavior, and determinists start to admit that experience and learning can also play a role, then we are converging on an increasingly simplified view of what is really a very complicated process. We should be gaining more complex, nuanced, and better informed views of how behavior arises, not simpler ones. Probably.

Over the last few decades, there have been a few important changes in how we should view human behavior over generational time and variation in those behaviors within and across categories (gender, ethnicity, geography, etc.). In short, certain behavioral traits have shown, synchronically (lacking the perspective of change over time) patterns that look genetic. For example, some families seem to be extra smart. Some have suggested that some “races” are smarter than others (at another time we can discuss why there really are no races, but let’s use “race” here as a potentially valid sampling strategy, which it can be even if the underlying races are fictions). We also see assertions of behavioral differences between the primary sexes (male vs female).

These observations are really statements about variance. Two groups are different, but vary within. There is overlap in the trait (i.e., IQ) but the means vary. We can statistically test the validity of the asserted differences in means by examining the variance in each sample and seeing if the mean of one sample fall within the predicted range of the central tendency of the others. In other words, asserting that there is a statistical difference between two groups is a process that involves understanding the variance of the underlying population(s) and samples. So, the questions can all be reframed in this manner:

Is the variation we see in trait X across certain groups best explained by underlying corresponding variation in the genetic system, or by the variation found in some other cause?

People fight vigorously over the underlying cause of IQ differences between groups. Some say it is primarily genetic, some say it is primarily not genetic, but rather, related somehow to what has become known as “lived experience.” Over the last couple of decades, there have been many attempts to explain observed variation in IQ using socioeconomic status, diet, education, issues having to do with test making or testing procedures. All of these factors have been shown to explain differences between groups to a modest to large degree in several studies. In other words, if you want to explain variation in IQ using non-genetic explanations, you can have some real success.

The genetic explanation of variation in IQ has had success in one main area which is irrelevant. This is the fact that genetically determined developmental differences between people that affect function that are generally classified as disorders predict large IQ differences. But this set of effects is not related to the question being asked.

The strongest evidence for a genetic underpinning of IQ is probably the large scale racial model solidified years ago by J. Philippe Rushton. He demonstrated that there is a grouping of brain sizes by race, with Asians having the largest brains, Caucasians the second larges, and Blacks the smallest (these race terms are his). He then showed that these brain sizes correlated with IQ difference. The modern psychometric literature assumes a racial difference in IQs, and asserts that this difference is real, but does to by citing sources that then site sources that ultimately cite Rushton. Rushtons all the way down, as it were.

The problem with this is that Rushton’s analysis was bogus. The brain sizes were taken from such sources at hat sizes for army conscripts classified by race, with the hat sizes used to estimate brain size. The Black (African) brain got smaller because Rushton subtracted a factor from that estimate of brain size, using an archaic thick skulled African fossil to assume that Africans have very very thick skulls. Correspondingly, the Asians were assumed to have thin skulls, and thus, got larger brains. The IQ data is similarly adulterated. In one part of the study, Rushton needed an “African” (native) IQ value, so he used the results of a test administered by racist anthropologists commissioned by the Apartheid government of South Africa to prove the inferiority of Blacks. And so on. The bottom turtle in this edifice is a fake.

The range of variation across “racial” groups (or other groups) in modern IQ data is very small compared to the change in IQ measured or estimated over decades of time through the 20th century within a single large and diverse population (Americans). If IQ is genetically determined and a stable feature of behavior, then there has been more evolution of these genes over less than 100 years of time in the US than we see across any two groups of modern humans. That is impossible. Again, IQ does not behave nicely as a genetic trait.

The discovery of a gene or set of genes that would underly IQ has not happened. In some recent studies, IQ is assumed to be very complex and the result of many different genes, and there is some statistical evidence for this. But, there is a big problem there too. Any trait can be linked to a set of genetic variants if the set of genes is large enough. That is a statistical effect and it is not really a link. More like a party trick, or a con game. (In fact this method is a con you may have heard of. I send 10,000 people an email predicting that a certain stock will go up, another 10,000 people an email predicting it will go down. One or the other happens. I then send 5,000 of the people who got the “correct” prediction another prediction, and 5,000 of them the opposite prediction. Now, 2,500 people have gotten two correct predictions from me. I keep doing that until I’ve got several dozen people convinced I am a stock market genius, and I take their money.)

Generally speaking, many behavioral traits have been explained, in part and sometimes in large part, by factors that are not genetic, while at the same time, the hunt for the presumed underlying genes have come up empty. There was great optimism up through the 1990s that genetic underpinning of human behavior … genetic variation corresponding to behavioral variation … would be found. But even as early as 1993 this was being questioned. Here is a sidebar, reproduced in full, from a Scientific American article by John Horgan summarizing the work up to that time:

Behavioral Genetics: A lack of progress report (1993)

CRIME: Family, twin and adoption studies have suggested a heritability of 0 to more than 50 percent for predisposition to crime. … In the 1960s researchers reported an association between an extra Y chromosome and vio-lent crime in males. Follow-up studies found that association to be spurious. MANIC DEPRESSION: Twin and family studies indicate heritability of 60 to 80 percent for susceptibility to manic depression. In 1987 two groups reported locating different genes linked to manic depression, one in Amish families and the other in Israeli families. Both reports have been retracted. SCHIZOPHRENIA: Twin studies show heritability of 40 to 90 percent. In 1988 a group reported finding a gene linked to schizophrenia in British and Icelandic families. Other studies documented no linkage, and the initial claim has now been retracted. ALCOHOLISM: Twin and adoption studies suggest heritability ranging from 0 to 60 percent. In 1990 a group claimed to link a gene—one that produces a receptor for the neurotransmitter dopamine—with alcoholism. A recent re-view of the evidence concluded it does not support a link. INTELLIGENCE: Twin and adoption studies show a heritability of performance on intelligence tests of 20 to 80 percent. One group recently unveiled preliminary evidence for genetic markers for high intelligence (an IQ of 130 or higher). The study is unpublished. HOMOSEXUALITY: In 1991 a researcher cited anatomic differences be-tween the brains of heterosexual and homosexual males. Two recent twinstudies have found a heritability of roughly 50 percent for predisposition to male or female homosexuality. These reports have been disputed. Another group claims to have preliminary evidence fo genes linked to male homosexualty. The data have not been published.

This is from a study by Jay Joseph on the “Classical Twin Method in the Social and Behavioral Sciences”

The classical twin method assesses differences in behavioral trait resemblance between reared-together monozygotic and same-sex dizygotic twin pairs. Twin method proponents argue that the greater behavioral trait resemblance of the former supports an important role for genetic factors in causing the trait. Many critics, on the other hand, argue that non-genetic factors plausibly explain these results…. In 2012, a team of researchers in political science using behavioral genetic methods performed a study based on twin data in an attempt to test the critics’ position, and concluded in favor of the validity of the twin method and its underlying monozygotic–dizygotic “equal environment assumption.” The author argues that this conclusion is not supported, because the investigators (1) framed their study in a way that guaranteed validation of the twin method, (2) put forward untenable redefinitions of the equal environment assumption, (3) used inadequate methods to assess twin environmental similarity and political ideology, (4) reached several conclusions that argue against the twin method’s validity, (5) overlooked previous evidence showing that monozygotic twin pairs experience strong levels of identify confusion and attachment, (6) mistakenly counted environmental effects on twins’ behavioral resemblance as genetic effects, and (7) conflated the potential yet differing roles of biological and genetic influences on twin resemblance. The author concludes that the study failed to support the equal environment assumption, and that genetic interpretations of twin method data in political science and the behavioral science fields should be rejected outright.

With respect to psychiatric disorders, from the same author:

The psychiatric genetics ?eld is currently undergoing a crisis due to the decades-long failure to uncover the genes believed to cause the major psychiatric disorders. Since 2009, leading researchers have explained these negative results on the basis of the ‘‘missing heritability’’ argument, which holds that more effective research methods must be developed to uncover presumed missing genes. According to the author, problems with the missing heritability argument include genetic determinist beliefs, a reliance on twin research, the use of heritability estimates, and the failure to seriously consider the possibility that presumed genes do not exist. The author concludes that decades of negative results support a ?nding that genes for the major psychiatric disorders do not appear to exist, and that research attention should be directed away from attempts to uncover ‘‘missing heritability’’ and toward environmental factors and a reassessment of previous genetic interpretations of psychiatric family, twin, and adoption studies.

And from researcher Tim Crow:

A substantial body of research literature, identified by nine out of ten papers on genetics in the recent ISI research front on schizophrenia, claims to have established associations between aspects of the disease and sequence variation in specific candidate genes. These candidatures have proven unreplicated in large sibling pair linkage surveys and a targeted association study. Even if the case for an association be regarded as a lucky guess (assuming one gene in 30 000 was guessed right) the large linkage and association studies provide no evidence of sequence variation relating to psychosis at any of these gene loci. Thus this body of work must be regarded as an indicator of the extent to which the ‘eye of faith’ is able to discern meaning in complex data when none is present.

I could go on. There have been further criticisms of the twin studies, for example. The most interesting, potentially, of these studies was on twins reared apart, more or less separated at birth. Commonalities among such individuals would be strong evidence for a genetic underpinning, because these individuals were raised in completely different environments so there would be no chance of a learned or cultural component other than a general background effect of having been raised n the same planet, or in the same country. Right? Well, no. Twins separated at birth were mostly twins that were not all that separated. After all, where do researchers actually find twins truly and distantly separated at birth, especially in the days when people seeking birth parents had hardly become a thing yet? Many of these twins, probably the vast majority, were separated only in the sense that they were raised by different members of the same family, or separately by divorced parents. Many were raised in the same neighborhood or often, the same house. My brother and I are not twins, but we were “raised apart” by the criteria of the twin studies because my family was distributed among the rooms of a two family residence, so technically he and I had bedrooms at different addresses.

In sum, it is easier to find sociological, cultural, or environmental explanations for variation in human abilities, intelligence, or personality traits. The seeming inheritance by family of some of these traits may well be a combination of something genetic and something experiential or cultural, but when looking for the actual underlying causes, genetics has repeatedly come up wanting while environmental explanations do a good job of addressing a fairly large part of the variation we see. Models of race based differences are so poorly done, and are often highly politically motivated, that they should never be trusted. That scientific ship sailed a long time ago.

Maybe the blank slate theory isn’t so bad after all. It does not imply that just anything can happen when making a human being out of a sperm and an egg. After all, it is a blank slate and not a blank whatever. But it is probably not true that some people’s lived experiences are written on slate, while others on white boards, and still others on smart boards, even if there are some people who I’m sure assume that they were.

Selected references:

Horgan, John. 1992. Eugenics Revisited. Scientific American. June.
Joseph, J. (2011). The Crumbling Pillars of Behavioral Genetics. GeneWatch, 24 (6),4–7. Web page
Joseph, J. (2012). The “Missing Heritability” of Psychiatric Disorders: Elusive Genes or Non-Existent Genes? Applied Developmental Science, 16(2), 65–83. doi:10.1080/10888691.2012.667343
Joseph, J. (2013). The Use of the Classical Twin Method in the Social and Behavioral Sciences : The Fallacy Continues, 34(1), 1–40.
Lewontin, R. Human Diversity. 2000, Scientific American Library.
Marks, J. (2008) Race: Past, Present, and Future. In: Revisiting Race in a Genomic Age, edited by B. Koenig, S. Lee, and S. Richardson. New Brunswick, NJ: Rutgers University Press, pp. 21–38. PDF
Marks, J. (2008) Race across the physical-cultural divide in American anthropology. In: A New History of Anthropology, edited by H. Kuklick. New York: Blackwell, pp. 242–258. PDF
Tizard, B. (1974). IQ and Race. Nature, 247, (5349), 316.

Other posts of interest:

• How to get rid of spiders in your house
• Why is your poop green?
• How many cells are there in the human body?
• Is there really a plot hole in Harry Potter Goblet of Fire?
• How long is a human generation?
• Is blog ever really blue?
• How to not get caught plagiarizing
• The origin of the domestic chicken
• What are the three necessary and sufficient conditions of Natural Selection?
• How do I get rid of foot fungus?
• Which is better, Tap Water or Bottled Water?
• Has Global Warming stopped?

Also of interest: In Search of Sungudogo: A novel of adventure and mystery, which is also an alternative history of the Skeptics Movement.

Among the DNA sequences co-opted by bacteria is the famous gene-frag-family known as CRISPR. You’ve heard of it, and you probably know what it does. Briefly, genetic scientists can use the innate power of CRISPR to manipulate other DNA to “repair” or modify in situ DNA sequences in living organisms. Got a genetic disease? No problem. We get the good genetic sequence, and then use the CRISPR based technology to replace all your bad DNA with the good DNA.

Now, of course, that doesn’t really work this way, and CRISPR technology has had fairly limited success so far. But there have been successes, and CRISPR is generally regarded as the Next Great Hope in the future of genetic therapy.

But now there may be a problem. Among the bacteria that use a CRISPER sort of sequence are two that are fairly nasty and common human pathogens. These are Staphylococcus aureus and Streptococcus pyogenes. In fact, the specific CRISPER sequences that genetic scientists use to do the CRISPR thing, come from these specific bacteria.

So, think about this for a moment. If CRISPER is used by bacteria to do any of their dirty work, and the bacteria are common human pathogens, is it possible that some humans have built up an immunity to the CRISPER sequences, perhaps putting them off limits for future CRISPR therapy?

Yes.

From the abstract of a recent paper:

Based on the fact that these two bacterial
species cause infections in the human population at high frequencies, we looked for the presence of pre-existing adaptive immune responses to their respective Cas9 homologs, SaCas9 (S. aureus homolog of Cas9) and SpCas9 (S. pyogenes homolog of Cas9). To determine the presence of anti-Cas9 antibodies, we probed for the two homologs using human serum and were able to detect antibodies against both, with 79% of donors staining against SaCas9 and 65% of donors staining against SpCas9. Upon investigating the presence of antigen-specific T-cells against the two homologs in human peripheral blood, we found anti-SaCas9 T-cells in 46% of donors. Upon isolating, expanding, and conducting antigen re-stimulation experiments on several of these donors’ anti-SaCas9 T-cells, we observed an SaCas9-specific response confirming that these T-cells were antigen-specific. We were unable to detect antigen- specific T-cells against SpCas9, although the sensitivity of the assay precludes us from concluding that such T-cells do not exist. Together, this data demonstrates that there are pre-existing humoral and cell-mediated adaptive immune responses to Cas9 in humans, a factor which must be taken into account as the CRISPR-Cas9 system moves forward into clinical trials.

This could be a problem. Maybe it is time to look for CRISPR sequences in other more obscure bacteria.

This is all new, and the ultimate meaning of it all remains to be seen. Stay tuned!

A Fortunate Universe: Life in a Finely Tuned Cosmos

This is a concept that has always fascinated me, ever since reading some stuff about the Periodic Table of Elements. Check it out:

Over the last forty years, scientists have uncovered evidence that if the Universe had been forged with even slightly different properties, life as we know it – and life as we can imagine it – would be impossible. Join us on a journey through how we understand the Universe, from its most basic particles and forces, to planets, stars and galaxies, and back through cosmic history to the birth of the cosmos. Conflicting notions about our place in the Universe are defined, defended and critiqued from scientific, philosophical and religious viewpoints. The authors’ engaging and witty style addresses what fine-tuning might mean for the future of physics and the search for the ultimate laws of nature. Tackling difficult questions and providing thought-provoking answers, this volumes challenges us to consider our place in the cosmos, regardless of our initial convictions.

Getting Risk Right: Understanding the Science of Elusive Health Risks

Understanding risk, and misunderstanding it, became a major topic of discussion, initially in economics, about the time that I was working in a major think tank where much of this discussion was happening. Risk perception had been there as a topic for a while (the head risk-thinker where I worked had already won a Nobel on the topic) but it became a popular topic when a couple of economists figured out how to get the message out to the general public.

In my view, the modern analsyis of risk perception is deeply flawed in certain ways, but very valuable in other ways. This book is very relevant, and very current, and is the go to place to assess health related risk issues, and I think it is very good. I do not agree with everything in it, but smart people reading a smart book … that’s OK, right?

Do cell phones cause brain cancer? Does BPA threaten our health? How safe are certain dietary supplements, especially those containing exotic herbs or small amounts of toxic substances? Is the HPV vaccine safe? We depend on science and medicine as never before, yet there is widespread misinformation and confusion, amplified by the media, regarding what influences our health. In Getting Risk Right, Geoffrey C. Kabat shows how science works?and sometimes doesn’t?and what separates these two very different outcomes.

Kabat seeks to help us distinguish between claims that are supported by solid science and those that are the result of poorly designed or misinterpreted studies. By exploring different examples, he explains why certain risks are worth worrying about, while others are not. He emphasizes the variable quality of research in contested areas of health risks, as well as the professional, political, and methodological factors that can distort the research process. Drawing on recent systematic critiques of biomedical research and on insights from behavioral psychology, Getting Risk Right examines factors both internal and external to the science that can influence what results get attention and how questionable results can be used to support a particular narrative concerning an alleged public health threat. In this book, Kabat provides a much-needed antidote to what has been called “an epidemic of false claims.”

Feeding the World: Agricultural Research in the Twenty-First Century (Texas A&M AgriLife Research and Extension Service Series)

In the not too distant past, it was understood that we, the humans, were going to run out of food within a certain defined time range. This actually happened several times, this estaimte, followed by the drop-dead date coming and going, and the species continued. Kind of embarassing.

Historically, that estimate of when we would run out of food has been wrong for one, two, or all of three reasons. First, the rate of population increase can be misestimated. We now know a lot more about how that works, and still probably can’t get it right, but in the past, this has been difficult to guess. Second, it hasn’t always been about food production, but rather, distribution or other aspects of the food supply. Right now, the two big factors that need to be addressed in the future are probably commitment to meat and waste. Third, and this is the one factor that people usually think of first, is how much food is produced given the current agricultural technology. That third factor has changed, in the past, several times, usually increasing but sometimes decreasing, depending on the region or crop. Sadly, this is probably also the factor that will change least (in a positive direction) in the future, even given the supposed promise of GMOs, which have so far had almost no effect.

Anyway, this book is about this topic:

The astounding success of agricultural research has enabled farmers to produce increasingly more—and more kinds—of food throughout the world. But with a projected 9 billion people to feed by 2050, veteran researcher Gale Buchanan fears that human confidence in this ample supply, especially in the US, has created unrealistic expectations for the future. Without a working knowledge of what types and amounts of research produced the bounty we enjoy today, we will not be prepared to support the research necessary to face the challenges ahead, including population growth, climate change, and water and energy scarcity.

In this book, Buchanan describes the historical commitment to research and the phenomenal changes it brought to our ability to feed ourselves. He also prescribes a path for the future, pointing the way toward an adequately funded, more creative agricultural research system that involves scientists, administrators, educators, farmers, politicians, and consumers; resides in one “stand alone” agency; enjoys a consistent funding stream; and operates internationally.

Modern Prometheus: Editing the Human Genome with Crispr-Cas9

Gene editing and manipulation has come a long way. We may actually be coming to the point where methods have started to catch up with desire, and applications may start taking up more of the news cycle. We’ll see. Anyway:

Would you change your genes if you could? As we confront the ‘industrial revolution of the genome’, the recent discoveries of Crispr-Cas9 technologies are offering, for the first time, cheap and effective methods for editing the human genome. This opens up startling new opportunities as well as significant ethical uncertainty. Tracing events across a fifty-year period, from the first gene splicing techniques to the present day, this is the story of gene editing – the science, the impact and the potential. Kozubek weaves together the fascinating stories of many of the scientists involved in the development of gene editing technology. Along the way, he demystifies how the technology really works and provides vivid and thought-provoking reflections on the continuing ethical debate. Ultimately, Kozubek places the debate in its historical and scientific context to consider both what drives scientific discovery and the implications of the ‘commodification’ of life.

Nearly similar levels of climate change related pressure on agricultural systems elsewhere has led to very different outcomes, sometimes more adaptive outcomes that won’t (at least for now) lead to major geopolitical catastrophes as we have now in the Levant and elsewhere in West Asia. What’s the difference? The difference is how agriculture is done.

Are GMOs a solution? Are GMOs safe, and can the produce a small or medium size revolution in crop productivity? What about upgrading traditional agriculture to “industrial agriculture”?

And speaking of GMOs, what is the latest in GMO research? How should GMOs be regulated, by the method they are produced, or by the novel or altered traits they have? How do we communicate about GMO research and GMO crops? What about labeling?

These and many other questions are addressed ad Mike Haubrich, me, and Anastasia Bodnar talk about “Genetics and Food Security” on the latest installment of the Ikonokast Podcast. GO HERE to listen to the podcast. Also, if you go there, you can see a picture of Anastasia holding her latest GMO product, a corn plant that can see and talk!

Also, Iknokast has a Facebook Group. Please click here to go and joint it!

And, if you have not yet listened to our first podcast, with author and science advocate Shawn Otto, click here to catch up!

Here’s the press release for the paper:

Scientists know that temperature determines sex in certain reptiles—alligators, lizards, turtles, and possibly dinosaurs. In many turtles, warm temperatures during incubation create females. Cold temperatures, males. But no one understands why.

A recent study sheds further light on this question. The findings of researchers Kayla Bieser, assistant professor at Northland College, and Thane Wibbels, professor of reproductive biology at the University of Alabama at Birmingham, will be published this month in the primary research journal “Sexual Development,” and is now available online.

This study represents the most comprehensive, simultaneous evaluation of the chronology of how sex-determining genes express themselves during embryonic development and and looks at the impacts of estrogen.

Bieser and Wibbels followed five different genes and what was going on in the exact same turtle. To date, scientists have looked at a number of turtles and pooled the data but Bieser is the first to follow individual turtles. She wanted to know when and how they “express” themselves. For an example, Bieser describes expression as the physical manifestation of those genes such as blue or brown eye color.

She looked at turtle eggs incubated at male and female temperatures and documented what the genes were doing while sex is being determined. “Which genes ‘turn on’ and when, could be an indication of what is triggering sex,” Bieser said.

According to Bieser, temperature-dependent sex determination species may be unable to evolve rapidly enough to offset the increases in temperature, which may ultimately result in their extinction.

“It’s critical that we understand the genetic mechanisms for which temperature acts and incorporate this knowledge into management plans for the conservation of these vulnerable species.”

Secondly, Bieser applied estrogen to eggs at a male-producing temperature. The purpose she said is to help determine the triggers for sex determination and how hormones, such as estrogen, can override the temperature signal.

In other words, would temperature or estrogen win out in deciding sex? The answer: in short, neither. What she found — and this is new information — is when estrogen is applied to eggs incubating at a male temperature, gonads—or sexual parts—do not develop. Or, if they do, they barely develop.

Why? “We don’t know yet,” Bieser said.

Scientists have been doing this experiment for some time but never reported these results. She suspects the reason is because scientists did not dissect the gonadal area specifically and that they took the general area but may have not analyzed the gonads to the same detailed level. In fact, this was a sticking point for one of the reviewers of this study—so Bieser provided photos of her findings.

“This research provides a critical understanding of how temperature acts on and above the genes in species where temperature determines sex—this is particularly critical in light of global climate change,” Bieser said.

Here’s the video:

The original paper:
Bieser K.L. · Wibbels T. 2014. Chronology, Magnitude and Duration of Expression of Putative Sex-Determining/Differentiation Genes in a Turtle with Temperature-Dependent Sex Determination. Sexual Development 8(6).

The Coffea canephora Genome has been sequenced. This is probably more important than the Human Genome project because humans are completely useless first thing in the morning, but coffee is very important first thing in the morning.

Some important plant evolution involves wholesale duplication of large parts of the genome. This does not appear to be the case with coffee. Rather, diversification of single genes characterizes the genome, so, according to the paper reporting these results in Science, “…the genome includes several species-specific gene family expansions, among them N-methyltransferases (NMTs) involved in caffeine production, defense-related genes, and alkaloid and flavonoid enzymes involved in secondary compound synthesis.”

Also of great interest is the apparent fact that caffeine related genes either evolved separately from, or engaged in the important work of making caffeine separately from similarly functioning sets of genes in tea and cacao (chocolate). I had always suspected tea was … different.

So, not at all unexpectedly, the most important molecule on earth evolved more than once!

Elizabeth Pennisi also has a writeup here.

But wait, there is a way to get similar data without needing any permission from anyone and it is not illegal, and in fact, it could actually be cheaper and easier than your original proposal and, while it may not provide the same exact results, it could even provide BETTER results. Let’s call it Plan C.

Plan C involves looking at every iteration of every single Google Street View picture ever taken anywhere in the US at any time. All of them. The vast majority of these photographs will show you nothing, but every here and there, you will get some data. There will be a shot that shows a thing in an open window, or an open door, or an open garage, or being carried into our out of a person’s house, being delivered, thrown out on the curb, sold in a garage sale, sitting on the lawn after an explosion or fire, or in use (especially yard and garden implements). This is not the same thing as sampling hundreds of houses once each, looking at all contents. But it is sampling the homes lived in by hundreds of millions of people, and sampling them dozens of times over a few years. That could be some amazing data.

And nobody can stop you from studying this source of information or doing this research. If someone does try to stop you with silly regulations from a University or something, just change into a Journalist. Then you’re golden. It would be WRONG to stop a journalist from using this information!

Turns out that this works with genes, but even better. One might want to study the relationship between a putative genetic marker and a possible behavioral thing, like maybe a psychiatric disorder or something, in a genetically bottle necked tribal group somewhere. You can try to get permission to do this, and maybe you’ll get it. Maybe you won’t get permission but you can certainly steal the genetic data from some place and do the research anyway. But people will get mad at you and you’ll not get any more research money.

Or, you can go to Plan C.

Here’s how Plan C works with genes. We have a good idea of the distribution of many genetic markers that have to do with geographical patterns over time. (Some people would use the term “race” in that sentence but that’s incorrect and unnecessary.) So, something like “East Asian” or “Native South American” or “Central African” or whatever has a list of genetic markers that go with it. Genes are supposed to “independently assort” and act all random and all, but they don’t. At the finest level, on chromosomes, genetic markers that are near each other travel together because of “linkage.” More importantly, genes move in populations. So, those East Asian genetic markers are not going to get all mixed up with the Central African genetic markers too often. Also, if you have enough samples, some mixing up doesn’t matter all that much.

So, if you want to study a disease-related “gene” (allele, a variant of a gene, really), if you think such a thing exists, you can effectively study it in a small population of repressed brown people who, tired of repression and exploitation decided to be totally unfair to you and not give you their blood, by looking at the association of LBP (“little brown people”) markers and the alleles of interest. It does not even matter if many of those marker associations are found in totally non LBP people. They are still associated. Genetic lineages are the thing, not human lineages. Humans are merely reasonable approximations of genes, really. Or at least, you can make a case for the associations and get your research funded and published without asking anybody any permissions for anything, just using giant available genetic databases. OK, so, maybe this is not “any genetic research you want.” But it is without permission!

This all sounds very nefarious but may not be. Or maybe it is. I’ll leave that to the ethicists.

By the way, if you are interesting in a big fight on the Internet about genetic research, ethics, “IRB” permissions, LBP’s and science and so on and so forth, I recommend the following, in the order suggested.

First, read this blog post: Is the Havasupai Indian Case a Fairy Tale? by Ricki Lewis (and if you have time, along with it, this related blog post)

DON’T READ THE COMMENTS YET

Then, read this blog post: The Empire Strikes Back by Jonathan Marks

Then, go back to the first blog post (Is the Havasupai Indian Case a Fairy Tale?) and read the comments.

Then, report back here and tell me what you think. Especially about that last comment on the PLOS blog post.

Have a nice evening!

Photo Credit: tapasparida via Compfight cc

Regenesis: How Synthetic Biology Will Reinvent Nature and Ourselves by George Church and Ed Regis looks like a futurist tome on what could happen when technology finally catches up with human imagination and everything changes. Except it isn’t. Most futurists are people with some knowledge of technology, a fertile imagination, and a publicist. Regenesis is by a scientist (working with a writer) who is busy making a different future and who has been involved in every stage of development of the technology under discussion, and for this reason is one of the more important new science-related books you can read right now. Regis is a multiply published science author (his most recent book is What Is Life?: Investigating the Nature of Life in the Age of Synthetic Biology) and George Church is Professor of Genetics at Harvard Medical School who is one of the key players in the Personal Genome Project. He directs Personal Genomics.org, which curates the only OpenAccess human “Genomic, Environmental and Trait database. His work led to the first commercial genome sequence (for apathogen) and he has been involved in both genome sequencing (reading the genes) and synthesis (making new ones) in both the academic and private milieu. He is also director of the NIH “Center for Excellence in Genomic Science” which places him at the center of biosafety, gene privacy, and security policy development.

Church was finishing is PhD work at Harvard the same year that I started mine. We never met to my knowledge, but I remember the construction in those days of the new genetic research facility there. Cambridge, Massachusetts was the first and only city (and still maybe the only one) to write zoning and building regulations for genetic research facilities, and the building was right across from the museum I worked in. People were afraid of what might happen if some of the genes, or genetically modified organisms, they were working on in that building got out. That was a valid concern given the unknowns, but it would eventually happen that the details of what people needed to worry about shifted considerably over time. Had George Church been sent back in a time capsule and put in charge of that project, his understanding of and commitment to safety in genetic research would have been more than a little reassuring. Of course, this would have then affected his own future and thus … oh never mind, that damn Time Paradox is too confusing…

Regenesis covers the history and current status of some of the most innovative and interesting research in genetic engineering, and it is organized in a way that I really liked. The book is written as a time line. The chapters run as follows:

• -3,800 Myr, Late Hadan
• -3,500 Myr, Archean
• -500 Myr, Cambrian
• -360 Myr, Carboniferous
• -60 Myr, Paleocene
• -30,000 YR, Pleistocene Park
• -10,000 YR, Neolithic
• -100 Yr, Anthropocene
• -1 Yr, Holocene
• +1 Yr, The End of the Beginning, Transhumanis, and the Panspermia Era

See what they did there?

Each of these past eras represents a change in the genetics, cellular biology, evolutionary stage, or environmental context in which live existed, with the human role coming along in a big way near the end. This allows the authors to discuss the nature of life at each stage, and related the last 20 or so years of genomic and genetic research to different levels of organization of life. This causes this book to be different from the average run of the mill futurist book in two ways: 1) You learn stuff about how things are and have been, detailed stuff, interesting stuff; and 2) There is a solid road map imposed on the discussion of what is being done now and what could be done in the future, which allows the authors to avoid the messing around we see in a lot of futurist books. In other words, this is not futurist manifest; It is a history of life and a detailed discussion of what humans are actually doing with life these days and what we seem poised to be able to do based on a solid grounding in actual ongoing research.

One of the most interesting themes that helps underscore the nature of this discussion is left- vs right-handedness in biology. Most complex biological molecules could be built with the structure and symmetry organized in a left handed vs right handed way. It is quite possible that we could encounter a planet (if we could get there) rich in life that is all built on molecules that are the opposite in orientation from what we have here on Earth. Not only that, but it is possible to build such a life form now. We could construct a human that is left-handed, and thus, fundamentally different from all other humans. Such a human could not be infected by many, perhaps most, cell-level pathogens because those pathogens would not be able to interact with the left-handed body. Obviously, this is a complex issue and there is a lot too it…you’ll have to read the book to find out what the implications and complications of such a thing might be.

The most important theme in the book, and also very interesting, is the concept of synthetic biology. The goal of synthetic biology is to create an organism or set of organisms that use the standard biological machinery (proteins and enzymes and stuff building other molecules in a certain way) that will be instructed with their DNA to produce a certain product, such as oil, a house, a cute little furry organism that will replace your Roomba. Well, maybe not that last one. We use lots of synthetic biology now but we are at the chipped-stone tool phase. The basics are in place, the research is progressing, the market for the products is there. Synthetic biology is one of those “technologies” that many hope will come along and solve many of our problems. It should be relatively straight forward to create a thing that will make hydrocarbon based fuels, which one must admit are a very handy way of storing energy, from raw materials that do not include fossil carbon. My personal fantasy is to build large flat factories on the sea surface or in open arid regions that will produce a solid that we just pile up somewhere to contain carbon taken from the atmosphere, and a steady stream of a clean burning liquid. Down the street, I want to see a factory that consist of a giant, 30 acre leaf surface under which is constantly being built a layer of genetically engineered wood, with whatever properties are needed. Imagine 2X4s of just the right strength and flexibility, but indurated with anti-fungicidal and other preservative chemicals. A combination of balsa, ebony, maple, cedar and hickory. Left-handed, of course. Who needs plastic and concrete when we have Frankewood! Bwahahaha!

I interviewed George Church a couple of weeks ago on the radio. The podcast of that interview is located hare on iTunes
, or you can find out other ways to get it or listen to it directly here.

From the official description of the book:

Imagine a future in which human beings have become immune to all viruses, in which bacteria can custom-produce everyday items, like a drinking cup, or generate enough electricity to end oil dependency. Building a house would entail no more work than planting a seed in the ground. These scenarios may seem far-fetched, but pioneering geneticist George Church and science writer Ed Regis show that synthetic biology is bringing us ever closer to making such visions a reality.

In Regenesis, Church and Regis explorethe possibilities—and perils—of the emerging field of synthetic biology. Synthetic biology, in which living organisms are selectively altered by modifying substantial portions of their genomes, allows for the creation of entirely new species of organisms. Until now, nature has been the exclusive arbiter of life, death, and evolution; with synthetic biology, we now have the potential to write our own biological future. Indeed, as Church and Regis show, it even enables us to revisit crucial points in the evolution of life and, through synthetic biological techniques, choose different paths from those nature originally took.