Human Behavioral Biology

Process that results in the adaptation of an organism to its environment by means of selectively reproducing changes in its genotype source

Evolution of certain conspicuous physical traits—such as pronounced coloration, increased size, or striking adornments—in animals may grant the possessors of these traits greater success in obtaining mates. From the perspective of natural selection, such increases in mating opportunities outweigh the risks associated with the animal’s increased visibility in its environment. source

Animals does not behave for the good of species. Animals behave for passing on as many genes as possible. Sometimes, a chicken is an egg's way of making another egg

Natural selection favours a trait due to its positive effects on the reproductive success of an organism's relatives, even when at a cost to the organism's own survival and reproduction. Kin selection can lead to the evolution of altruistic behaviour

• Animals can keep track of kinship
• Evolution selects for organisms cooperating with their relatives

Each organism has the potential to harm one of the others but doesn't do so because the overall impact of those actions would hurt the original organism.

Behaviour whereby an organism acts in a manner that temporarily reduces its fitness while increasing another organism's fitness, with the expectation that the other organism will act in a similar manner at a later time. The concept was initially developed by Robert Trivers to explain the evolution of cooperation as instances of mutually altruistic acts. The concept is close to the strategy of "tit for tat" used in game theory.

• We are more attuned to picking up cheating than a random act of kindness.
• Until you're not putting more into i than what you're getting
• Nash equilibrium

Branch of applied mathematics that provides tools for analyzing situations in which parties, called players, make decisions that are interdependent. This interdependence causes each player to consider the other player’s possible decisions, or strategies, in formulating strategy. A solution to a game describes the optimal decisions of the players, who may have similar, opposed, or mixed interests, and the outcomes that may result from these decisions.

Studies have shown that brain centers responsible for pleasure light up during times of stabbing the other guy in the back and during times of cooperation. There is a pronounced gender difference as to when these areas are activated.

Humans are right in the middle.

In essence, having males is a "risky strategy" in a tournament species because 5% of the males get to produce 95% of the future offspring, so the odds are that a male will not get to mate well. Females tend to mate regardless, so having a female will tend to carry the genes onward at a higher rate. Thus higher ranking females show a greater tendency to give birth to males while lower ranking females have a greater tendency to give birth to females. This is not a choice, but rather reflects some gradual adaptation that's resulted from the males of top ranking females getting to pass on their genes while the lower ranking females' male offspring did not but their daughters did. However, dominance among the males is not based on nepotism, it's based on strength and power, so a male can ascend if he's able to. And the male offspring of a top ranking female may be entirely unsuccessful. My sense is that there isn't a lot to be gained from this section as it's speculative and, of course, the females aren't really choosing to have a male or a female baby; there's simply some tendency that has enabled the offspring of top ranking male-female combinations to be more likely to produce a male. This notion leads into an upcoming topic, which is intersexual competition.

The bias toward more females during times of ecological duress connects directly to the metabolic demands of males being higher than the metabolic demands of females. The tougher it is on the mother, the greater the odds of the fetus not surviving.

Intersexual competition reflects differing interests in the future reproductive success of the female. In tournament species in which the males migrate, they care little about what happens to the female once they are gone and so aggressive elements are sometimes found within their sperm. These elements help increase the odds of generating a successful pregnancy and set the fetus up to be more metabolically demanding. Females, on the other hand, have evolved ways to neutralize these elements as they are costly and dangerous.

Imprinted genes are genes that have different manifestations depending on which parent they came from. In classic Mendelian genetics, a combination of Aa and AA treats the A's as similar, but with imprinted genes it actually matters whether the A came from the father or mother because the gene will behave differently. Through the process of methylization, the gene's behavior will be altered based on its origin. If you get it from one parent it will be active, if from the other it will be silenced. When you look at imprinted genes that are active if they come from the father, they all tend to be genes that promote fetal growth. If from the mother, they tend to slow down fetal growth. For example, one of the genes codes for insulin like growth factor. Not hard to see how that fits in. The female's version makes for a less responsive receptor for the insulin like growth factor. Another example is choriocarcinoma, which is a cancer of the uterus that can happen if the male's sperm has aggressive growth factors and the female has no counterbalancing genes; this leads to unchecked growth which is bad. Pregnancy hyperglycemia is another example as the fetus is trying to get lots of sugar from mom but mom may have an active gene that checks that (hypoglycemia will occur if she does not). These types of imprinted genes are not typically seen in pair bonding species. Humans are again right in the middle.

Next up is the fun topic of…sperm competition? Yes, research into fruit flies shows that another strategy that's out there is the sperm carrying a toxin that kills off other males' sperm. Sadly for the females, the toxins are also potentially toxic to them. Thus we see females have evolved ways to counteract this.

Exogamy impacts the behavior of animals as well. There is variation in who leaves (females in chimps and gorillas, males in baboon troops) and that influences what happens within the group. For example, chimp groups can be highly aggressive and even genocidal toward other groups ("outsiders" or "them") because the males are all related by kinship ties and thus get along much better than they would if there was male exogamy.

One of the scariest things in the world is when all the males in a given group start getting along really well with each other. Aggression toward the others often follows.

This relates to military techniques that aim to create a sense of kinship among the troops. This makes them a band of brothers that will cooperate with each other, though it can have divisive effects as well, such as was seen in the Vietnam War, because the group may agree to disagree with orders and commands from above, the hierarchical other.

• Founder Effect A bio-geographic (or other) event occurs that separates out a subset from a larger group. This smaller subset soon becomes more inbred than the larger whole, simply as a by-product of being a smaller group. This translates into having a higher degree of relatedness, which introduces the whole business of kin selection. Because these guys are more closely related, they will work together more as a group and will end up outcompeting the original group members when they are reunited.

Another scenario is demonstrated through the example of two chickens, one that's highly aggressive and one that's more laid back. When competing one on one, the more aggressive chicken will lay more eggs, but there's the drawback in which a group of aggressive chickens will harass each other and thus impair their own breeding while the calmer group will lay more eggs because as a group they cause less grief for each other.

Politics comes into play as well, with issues ranging from male domination, sexual aggression, social stratification and more and the question of the extent to which these are a reflection of natural order.

On the other hand, the gradualists were Northeastern Marxists. And the world they want it to be fits smoothly into the notion of dialectical materialism.

Genes as molecules, genes as information, genes as DNA. Here we have proteins emerging for their importance in the structure of cells and cellular activity. Proteins hold the shapes of cells together, they form messengers and hormones, they are the enzymes that do all kinds of important stuff; proteins are the workhorses.

So what codes for proteins? This is where genes come in. Genes specify (code for) proteins. Proteins are built from amino acids, of which there are approximately 20 that commonly occur. Each one has to be coded for with a different DNA sequence, a different DNA sequence of 3 letters (3 nucleotides). He notes that in the process DNA first specifies a code string of RNA which then specifies the protein construction (amino acid string). Thus if you know the DNA then you will know the RNA which in turn gives you a sense of the amino acids which will form the protein and knowing that informs you of the shape of the protein (different amino acids vary in their attraction toward water and these levels influence the ultimate shape) which clues you in on the function of the protein. That is the critical link from the DNA to the function and the notion of a behavior being genetically controlled.

Proteins fit into other molecules like a LOCK and KEY! This is the whole world of hormones and neurotransmitters fitting into their particular receptors.

He notes that prion diseases are an exception to the hydrophobic/hydrophilic structure of proteins.

Enzymes are important because they catalyze reactions. That is they cause reactions to occur which on their own would be unlikely to happen. A simple way of looking at this is to think of it as bringing things together or separating them, as appropriate. Virtually every enzyme is a protein. This affects cellular activity by influencing the opening and closing of ion channels. Ion channels connect directly with the cell's decision to act or not.

Francis Crick is credited with establishing a central dogma of genetics - DNA codes for RNA which codes for proteins. Sapolsky focuses the listener on a subtle element of this dogma, which is that DNA is ultimately in charge, sitting around and deciding what will happen and when, and then releasing the instructions that become the RNA to protein chain. Surprisingly, DNA isn't always in charge. Viruses are mentioned as an example. Viruses are basically snippets of DNA that get into a living organism and hijack its DNA, taking over the plane and directing where it goes, making it function for the virus's desire. In the 1970's viruses made of RNA were discovered. The pathway is facilitated by enzymes which convert the RNA into DNA and start up the whole parasitic process. Accordingly, these are called retroviruses because they are reverting from RNA back to DNA.

Mutations are important because they can alter the orders from DNA. A micromutation occurs when one letter within the DNA sequence is accidentally miscopied. Pairs of triplets (amino acids) are coded for by the DNA. This is a connection of three base pairs. So we can have a change in one of these letters which may impact the ultimate shape and function of the amino acid that is created.

There are three basic types of alterations. First is a point mutation, which consists of one of the letters being changed into a different letter. This may not matter because of the limited number of different amino acid combinations. There are four different letters (nucleotides) and three letters needed, so we get 4x4x4 or 64 different potential combinations, but there are only about 20 amino acid shapes, so there's overlap in that shape 22 GAU may be similar to shape 43 GTU, so the change from A to T may not significantly change the shape (please note that this example is an example for understanding and is not based on a specific shape 22 or 43).

For example: "I cdnuolt blveiee taht I cluod aulaclty uesdnatnrd waht I was rdanieg. The phaonmneal pweor of the hmuan mnid. Aoccdrnig to a rscheearch at Cmabrigde Uinervtisy, it deosn't mttaer in waht oredr the ltteers in a wrod are, the olny iprmoatnt tihng is taht the frist and lsat ltteer be in the rghit pclae. The rset can be a taotl mses and you can sitll raed it wouthit a porbelm. Tihs is bcuseae the huamn mnid deos not raed ervey lteter by istlef, but the wrod as a wlohe. Amzanig, huh ? Yaeh, and I awlyas thought slpeling was ipmorantt ! Tahts so cool !

Changes in the 1st or 3rd nucleotide (letter) may also be of minimal significance as the amino acids have similar shapes so a minor letter change may only result in a minor shape change that produce a minor change in results but does not dramatically change the functioning of the amino acid.

I will now do this. I will mow do this. I will not do this.

However, there can also be a point deletion. This consists of a nucleotide being deleted. In classical genetics a deletion mutation has dramatic effects and is a big deal.

I will nod ot his.

The third type is insertion mutation.

I will now ud othi.

Deletion and insertion mutations tend to have big consequences.

Ok, so there are 64 possible combinations that code for 20 amino acids. Say you look at a mutation and 40 of the combinations have no impact. In this case we have a standard mutation rate with 2/3rds of the changes not impacting the formation of the amino acid and 1/3rd changing it. Contrast this with a scenario in which you examine a mutation and find that 99% of the differences in the base pairs will impact the amino acid's formation. This is an echo of a very strong advantage or adaptation

• there would have been positive selection for this trait. It's not general variation or just hanging

around; it's been picked.

Alternatively if 99% of the mutations have no immediate impact this is a stabilizing gene in which you do not want to mess with its function (it's strongly set against any kind of change, which indicates that change is really bad in this area).

The changes in Foxp2 are positive changes.

Ok, so here's the idea. If 99% of the changes impact the amino acid then we have positive selection. If 99% don't, then we have negative selection. It works this way because the positive elements can build on each other and changes in it can be beneficial while impairments aren't devastating (for example, do any of us write like Marcel Proust? No, but we can still express ourselves poetically). However, when 99% of mutations have no impact, it's a highly stabilized gene. For example, do any of us have no lungs?

Next up is the whole sibling chimpanzee percentage topic. You share 50% of your genes with a sibling, but you share 98% of your genes with chimpanzee. What? This is about the level we look at. For example, chimps and humans have noses, so that's a commonality when compared to a tree, which only has a nose when it's in "The Lord of the Rings" or wandering around Stanford. However, humans can have button noses, aristocratic noses, etc. which is a DNA difference but at a much more specific level.

The carryover to the political element is that if every bit of the advantage or disadvantage that comes from a mutation matters then it follows that every bit of competition (competitive advantage) also matters.

In the 1980's Stephen J. Gould, a paleontologist, and Niles Eldredge, also a paleontologist, came up with a very different model. They challenged the gradualist model, arguing that instead there are long periods of stasis where nothing happens and that the little changes don't matter much. Instead when change happens it's rapid and dramatic. This is known as punctuated equilibrium. Gould was a Marxist, though, so it's worth noting that this model fits in with the dialectic process (thesis - equilibrium; antithesis - mutation; synthesis - new beings). Analyzing the fossil records shows long periods where nothing seems to change and then suddenly there's a big change followed by long periods where nothing's happening. This implies that the vast majority of the small changes aren't that important and that the competition framework is incorrect and serves mostly to create an illusion that nature has a massive hierarchy that's determined by competition when in reality nature permits most varieties to do just fine, thank you. Continuing with the political theme, it's then noted that it's mighty convenient that the competitive model fits in nicely with the environment that its advocates come from and have benefited from.

The first counter is that these are very different disciplines - what counts as rapid for a paleontologist isn't really fast. 100,000 years isn't all that quick (and changes that occur a little bit at a time due to competition over 100,000 years could appear rapid based on the starting point while still being driven by each minor advantage the whole time).

The next counter is that flesh and tissue do not leave a record in the paleontological record. A fossil won't tell you what happened inside the brain (in the sense that minor advantages won't necessarily manifest physically; anyone reading this likely has intellectual advantages over the vast majority of your peers but is unlikely to have a gigantic elephant head that holds a bigger, stronger brain. It's all the same from the outside.) All paleontology can study is forms, morphology.

The third challenge comes from molecular biologists who ask for the actual genes and evolutionary mechanism that would create this pattern.

Sapolsky notes that when the last challenge was brought up in the 1980's the paleontologists didn't have a good, evidence-based rejoinder, but that a lot of the stuff that's happened since then has supported the notion of punctuated equilibrium.

Next he moves onto DNA. When we look at a DNA strand, there are periods that code for genes interspliced with large sections (95% or so is non-coding) that function as an "instruction manual." The genes themselves are not always coded for in just one snippet. Often multiple areas on the DNA will code for parts of the same gene. So you can have a section that codes for the first third of a protein followed by a long stretch that has nothing to do with that protein. This is then followed by a section coding for the next third. And so on. Each of these sections is called an exon. The in-between stuff is called introns. People deduced and then discovered something called splicing enzymes.

The splicing enzymes would come along and snip out the intron section so that the first third of the exon connected to the middle third and the final third to produce a clear read-out.

David Baltimore was the first to introduce the concept that this makes the genes modular and opens the door to massive information within the DNA universe. Because of this flexibility, DNA would then have the potential to abandon the original A-B-C model and create, for example, an A-C combination. This will give you 7 different ways to combine these exons, which means there are 7 different proteins that can result (pacing mutations of course).

This is a massive deviation from the concept that one gene specifies one protein. Different splicing enzymes can thus create very different results. The more they are researched, the more flexibility emerges - different enzymes, splicing at different spots. So we have different items being created by the same basic DNA original set due to different splicing enzymes being activated and activated at different times of life (think Mr. Potato head as DNA and a child as the splicing enzymes - same basic pieces, lots of possibilities).

The instruction booklet part of DNA is all about when and under what circumstances to activate and start and stop creating proteins. (For example, human growth hormone is released throughout life but has peak periods.) For better or worse this means that DNA doesn't "know" what it's doing. Instead it's a read-out that's under the control of lots of other factors. Among these are the regulatory sequences upstream from the gene. These might be called promoter or repressive sequences that promote or repress the expression of DNA snippets downstream. They are like switches. And they are turned on when the right event (internal or external) happens. These events are triggered by transcription factors. These might turn on single genes or whole networks in the DNA. On the flipside, any given gene can have a whole bunch of different promoters that it's waiting to hear from before it does its thing.

So who's in charge? Whoever or whatever controls those transcription factors. Including the environment. Which has something to do with genetic effects (shocker!)

So what qualifies as environment?

It could be something within the cell. For example maybe the cell is getting low on energy. This could release a transcription factor that would result in the cell being activated to take up more energy.

Or it could be something from outside the cell, such as a hormone floating around in the bloodstream. A hormone is a blood borne chemical messenger. Testosterone is used as an example. It would float far and wide and have its effects and those effects would increase significantly when the male hits puberty resulting in changes in lots of areas in the body.

You could have a messenger from the outside environment, such as a scary sight or an olfactory messenger, like a pheromone.

As a consequence of this, Sapolsky notes that the most interesting stuff with DNA now is not the specific nature of the proteins but rather when it does its thing and what elements trigger it.

DNA is covered, stabilized and protected by chromatin. And so there is a whole world of messengers that inform the chromatin of where and when to open up and allow the transcription factors through. Changes can also happen that will permanently impact the chromatin. For example, mothering styles in rats have been shown to permanently change elements in the chromatin in areas relating to anxiety. This leads into the field of epigenetics. Research with monkeys has shown a change in one area impacting 4,000 other areas!

So fertilization is all about genetics while development is all about epigenetics.

So if we have a mutation in one of these splicing enzymes or transcription factors, the kind of changes that would result could well fit into the punctuated equilibrium (not gradual) model of evolution.

DNA as the big boss man is undermined as we learn that 95% of the DNA is simply the instruction manual, that transcription factors have huge roles especially in an if-then manner, that splicing and epigenetic effects impact growth, and on and on. Here he highlights ways in which things are interconnected - environment, genes, etc. In this area we move toward a way of thinking that seems to interest Sapolsky - the whole chaos theory/Heisenberg Uncertainty Principle element of life in which there's a bit of randomness and chance in even the most structured systems. And yet there's also a bit of structure in the seemingly chaotic. This just might be an important theme in evolution…

As promoters change, transcription factors change. Splicing enzymes can change their behavior and create entirely new proteins. Changes in transcription factors can activate entirely different gene sequences. Little changes can have big results, especially when those changes cascade.

Vasopressin and vols (and perhaps humans). One version of the promoter stimulates release of more vasopressin. Correlated with this is an increase in monogamous mating. The more vasopressin, the more likely the vol is to be monogamous. And polygamous vols, when given vasopressin, begin behaving monogamously. There's some evidence that this impacts human behavior too. Sapolsky mentions a study that suggested that the type of vasopressin promoter you have provided some predictive power of the likelihood of you getting divorced down the line. Naturally there are three million confounds here, but it gives one pause in terms of the concept of free will.

Dinorphin (pain receptor) promoters seem to relate to ease of addiction to pain killing drugs in rats. The more promoters that the rat has for dinorphin, the more likely that rat is to exhibit addictive behavior toward pain killing drugs when given the opportunity.

Changing transcription factors changes gene networks. He notes that a disproportionate share of the differences in the genetic code between chimps and humans lie in the genes that code for transcription factors. This leads to the suggestion that the most interesting evolutionary changes are going to be those found in changes in the regulatory structure of the genes, not in changes to the DNA itself.

The more genes you find in a species, the greater the percentage of those genes that code for transcription factors. For example you have 1 gene, A, so there's 1 transcription factor. Have two genes, A and B, and you now have 3 transcription factors - one for A, one for B and one for AB. And so on down the line.

Microevolution is about the proteins; macroevolution is about the networks.

She argued for transposable genes in plants, i.e. genes that are actually moving around on the DNA line, creating new proteins, networks, results. This amazing feature is also seen in the human immune system which adapts itself constantly in order to combat pathogenic invaders (and sometimes, unfortunately, to combat things like the insulin production cells in the Islets of Langerhorn - giving the person Type I diabetes). A plant can't run away from trouble, so it had to evolve another way to handle the world's difficulties. So they have fancy stress response tricks, such as changing genes around to handle new environments and challenges.

This is done by activating transposaze, which is a splicing enzyme that slices out sections of the genes so they can jump around. These types of genes are also seen in animals.

Predictably, and unfortunately, pathogens also get to utilize this trick. Trypanosoma brucei is a nasty protazoan that causes sleeping sickness in humans. It invade the body and in order to evade the host's immune response, uses jumping genes to change its protein coating. So the adaptive immune system stays a step behind it because just as soon as it figures out how to kill the original coating, the trypanosoma has changed its shield. The adaptive immune system takes out pathogens in a sort of lock and key function, but if the pathogen changes the locks faster than the immune system can chisel out the keys, you're in for real trouble.

This phenomenon is known as antigenic variation. In essence the pathogen has numerous shells (for this parasite the estimate is in the thousands) and shuffles through them as it replicates itself. It puts the immune system at a distinct disadvantage. Imagine you're a detective and you can only catch your suspect if he's wearing the exact same outfit he had on when he committed the crime. If he has 1 shirt, 1 pair of pants and one pair of shoes, you'll catch him immediately. If he has 1 shirt, 1 pair of pants and 2 shoes, it's going to take 2 days. If he has 15 shirts, 15 pairs of pants and 5 shoes, you're eating donuts, drinking coffee and peeing in a Mountain Dew bottle for 1,125 days. If the suspect is there to rob 25 liquor stores and 10 banks while you look for outfit #1, he's got a lot of time to get it done.

This happens elsewhere in the body. Neuroprogenitor cells can also jump around - this is neurons moving around, this is the cells in your body that have the most to do with determining who you are being the least constrained by genetic determinism.

So a hormone has the two receptors on it - one on the hormone side to trigger it and other that connects to the promoter. These can be mixed and matched so that a hormone can be triggered and then go out and attach to an entirely new promoter. This is a new if-then clause.

Glucocorticoids are stress hormones that suppress the immune system (there's a lot more to it, but in brief, they suppress it by reducing the inflammatory response). A slight clip and a little shuffling and you can create the new if-then clause if there's progesterone around suppress immunity. What's this about? Pregnancy. This if-then statement prevents the immune system from attacking the fetus.

The downside is that when the immune system recovers, it sometimes overshoots the original mark and ends up getting hyper. In its hyper state it's over-reactive and next thing you know you have an auto-immune disease, which is more common after pregnancy. This can be dangerous and some autoimmune disorders, such as lupus, are severe enough that the affected will be advised to avoid pregnancy.

Next up are copy number variants. This is the world of multiple copies of the same gene. This can allow for experimentation with one back-up copy. At the same time, there can be problems linked to it, such as is seen with schizophrenia. The multiple copies of genes may account for "irreducible complexity," i.e. how can an eye pop up out of nowhere? If the organism has multiple copies of sensory genes and is able to experiment with one without sacrificing the other, it could develop a feature incrementally, slowly growing an eye while using sound and tactile information for guidance until such time as the eye starts working. (This can account for evolution's production of vision while leaving a very big door open in regard to what's out there that we haven't evolved to see. This is the whole world of intuition and spiritual belief. This is the whole world of wackos that claim they can sense things others can't. Or is it?)

For the most part these changes will not be beneficial overall since they have to coordinate with so many different gene networks. Therefore it's generally a stabilizing selection in which you won't see much change. However, when the genes stumble onto something good, you may see a rapid change.

Bottlenecks occur when particular traits enable a subset of the population to survive, regardless of the problems with their other traits. He states cheetahs went through this. Sickle cell anemia is another common example.

In brief, the hominid body is designed to store nutrients. These days our food is loaded with all kinds of everything. So we're seeing a huge increase in average body mass (folks are getting fatter) because the body is storing all the good and bad stuff. The more wasteful your metabolism, the better it is. Get yourself a body that isn't used to a western diet and you are a candidate for type II diabetes as your body grows beyond what it's supposed to. The fat cells get full and start ignoring insulin. Insulin gets angry and calls on the pancreas to make more insulin to help force the fat cells to do their job. The fat cells relent a little but demand ever greater amount of insulin to listen and pretty soon you've got a blood sugar problem and are well on your way to burning out your pancreas.

The Dutch Hunger winter is a great example of this. Due to Nazi shuffling of food, the Dutch experienced a winter of starvation. The women who were carrying babies gave birth to "thrifty" babies whose metabolisms had learned to hold tightly onto whatever nutrients floated by. Thus they are more at risk for all the metabolic problems in adulthood - hypertension, diabetes, excessive weight gain, etc. And so are their offspring since they gestated within a mother's body that was very thrifty and thus shared less nutrients.

Sometimes there are surprising effects from genetic variation, such as the story of the silverfox.

The last fear is that of antibiotic resistance. MRSA, VRE, smallpox, our friend trypanosoma, all with a capacity to evolve faster than our drugs. So there's a continual battle between the cells of our body and the pathogens that want to crash the party.

In brief, this is a field in which scientists look for patterns of shared traits among individuals that have different levels of shared genes and infer relatedness and genetic influence from that. The basic notion being that if you have a behavioral trait that is more common the closer you are genetically, you can infer that the behavior is driven by the person's genes. Because of concerns over the environment's effects, the studies focus on several variants that help control for environmental influence. For example, comparing identical twins to fraternal twins or comparing siblings that are raised in different environments. Unfortunately this approach has flaws. For example, he notes that monozygotic twins and dizygotic twins are not treated the same; the environment is much more similar for monozygotic twins. The environmental differences can start early - if they split within the first five days after conception each will have its own placenta. If they split in the 5-10 day range, there is a shared placenta. This means there will be a difference in the extent to which they share the same bloodstream.

He mentions a Johns Hopkins study that examined differences in math ability between boys and girls. The data set suggested that boys were better than girls at math, with a 13:1 ratio in the upper levels. However, in more equal societies, such as our friendly Scandanavians, the difference is not only diminished, but slightly reversed with girls scoring higher. The lower a society's score when it comes to gender equality, the greater the difference between the sexes on tests of mathematical aptitude.

As he notes the differences in environment for 13 year old boys and girls, it's easy to see that his viewpoint is that this field is, at the very least, difficult to prove scientifically and, more realistically, ludicrous. Simply put, people don't ever share the same environment. There are thousands of different experiences that shape us and influence how we handle situations.

To correct for this, adoption studies are used. Here siblings with similar genes that are raised in different environments are compared. The thinking is relatively straightforward - if these siblings are more like each other than they are like the siblings in their adoptive homes, genes are playing a role.

A big study on schizophrenia based on Danish citizens shows genetic influence in the development of schizophrenia. Using adoption studies and statistical measures, they found a 1% chance of being schizophrenic among the population on the whole, but with no biological basis while being raised in a schizophrenic household the number goes up to 3%. When raised in a household that did not have a schizophrenic parent but in which the biological parent(s) do, the number jumps to 9%. And for the truly bizarre situation in which the kid had a genetic legacy of schizophrenia and managed to get adopted into a household with a schizophrenic adoptive parent, the rate goes all the way to 17%. He notes that this synergistic effect will come up again. Sapolsky also states that this study was the first time a genetic basis was shown for a psychological disorder. As such it's a landmark event because a genetic psychological problem is a medical problem, not just a mere adjustment to society issue.

The new gold standard study model is the identical twins separated at birth model. From this group, the research suggests about 50% heritability of IQ, about 50% heritability of where you are on the introversion-extroversion scale, and about 50% heritability for degree of aggression.

Anxiety levels as an adult can be impacted by the prenatal environment (in rats). The more stressed the mother, the higher the glucocorticoid levels in the bloodstream, resulting in a smaller brain, thinner cortex, more glucocorticoid receptors, fewer benzodiazepine receptors, more of a decline in cognitive ability as you age and a harder time bouncing back from stress - meaning more cumulative exposure to glucocorticoids and therefore more damage. This can be referred to as non-Mendelian inheritance of traits since the thinking is that it's not a genetic thing.

Holland 1944 and the Dutch Hunger Winter. The Nazis divert all the food in Holland to Germany. The Dutch diet thus goes from normal to starvation level. 3rd trimester fetuses develop super thrifty metabolisms due to nutrient deficiency and thus become much more likely (19 fold increase in risk) to develop metabolic diseases such as diabetes, obesity, high blood pressure, etc. because their bodies keep a greater than normal percentage of nutrients - sugar, sodium, fat - all stored. They in turn have offspring who are at a greater risk because the mothers' thrifty metabolisms don't share as freely with their offspring.

Mitochondria, the powerhouse of the cell, have their own DNA and along with other junk in the cell split somewhat randomly during gamete formation. Mitochondria only come from the mother's side.

Indirect genetic traits. Judith Rich Harris and The Nurture Assumption. Here the question is to what extent the environment acts on genetic traits in order to reify them. To wit, where you are on the extroversion/introversion scale is as much a result of how the world interacts with you as it is your genes. Thinking in terms of a good looking baby and an ugly baby - both have extrovert genes but only one of them gets a lot of smiles back in response to extroverted behavior. Other genetic factors will mediate the impact of the gene in question as well the world at large.

Continuing with the example, he points out that height is a heritable trait to a significant extent and that endless studies have shown that taller people are treated better and considered more attractive, "comma, he says bitterly."

Not surprisingly, people who are treated better during the developmental periods end up being more extroverted. Thus with have heritability of a trait that in turn causes you to be treated differently in the world which brings about changes in personality. Again, the genes are having a hard time winning out on their own.

The pecking order - you inherit the color and iridescence of your feathers. Get bad feathers, you get pecked at more often and head to the bottom of the social ladder.

Studies have suggested 70% heritability of political preferences in the US. However, this is actually mediated by personal characteristics, especially comfort with ambiguity. Conservatives tend to not like ambiguity, preferring black and white analyses of situations. He then transitions into the Kohlberg scale of moral development and the notion that there's a theory that tries to link up political preferences with one's stage of moral development. In both examples, conservatives end up looking pretty bad - simplistic worldview and under-developed morals. This is one area where Professor Sapolsky may be presenting a biased view. While your author agrees with him in many ways, the conservative viewpoint has its nuances and there are issues for which adding in ambiguity may be possible but not necessarily smart (crime, for example, which endless studies have shown is significantly impacted by SES and all kinds of developmental elements - yet and still, there's still a crime that's been committed and the why doesn't undo it - is ambiguity correct here? I'm not taking a stance, but am noting that it's an area of ethical debate in which ambiguity isn't necessarily the winner).

Curiously, studies showing heritability of aggression in rats actually have an underlying mediating factor - pain sensitivity. The more aggressive rats are less able to tolerate pain and thus more likely to lash out aggressively when they feel it. Again, the surface behavior is not the one that's being passed along.

Mothering styles of rats impact the robustness of the rat as an adult. Better mothering leads to a healthier rat that's likely to be a good mother when grown. This is accomplished through epigenetic changes in transcription factors.