neuroscience - Which part of the brain needs to be shut down to lose conciousness?

There is no widely-accepted neurological structure that mediates 'consciousness.' Even if some structures have been shown to be necessary for consciousness, they have not been shown to be sufficient. This is true with anesthetic mechanisms as well -- their ability to paralyze and block pain signals is fairly well-understood, but the mechanism of loss-of-consciousness is still unknown.

Still, 'consciousness' has to be there, somewhere between being awake and being dead, states which anesthetics can readily bridge (review):

Nevertheless, at some level of anesthesia between behavioral unresponsiveness and the induction of a flat EEG [indicating the cessation of the brain’s electrical activity, one of the criteria for brain death (22)], consciousness must vanish.

Later in the same review:

The evidence from anesthesia and sleep states (Fig. 2–3) converges to suggest that loss of consciousness is associated with a breakdown of cortical connectivity and thus of integration, or with a collapse of the repertoire of cortical activity patterns and thus of information (Fig. 2). Why should this be the case? A recent theory suggests a principled reason: information and integration may be the very essence of consciousness (52).

This is consistent with my own take. Consciousness itself is the subjective experience of 'brain,' so it can't be lost, just poorly integrated.

digestive system - Why Do Ruminants Require A Multi-Compartment Stomach To Digest Food?

There is more difference than just the parts of plants that are eaten.

Two of their stomachs - rumen and reticulum are not used for digesting food at all. Multiple rounds of chewing and mixing with saliva, wich result in very small particles of undigested food help the bacteria in those stomachs reach, digest and use that cellulose-rich plant material. Cows "eat" the bacteria from their stomachs and the grass is just food for these bacteria. You could say that cows are not herbivores but secondary consumers.

Look at this picture (from Wikipedia article on ruminants, a good place to check all this in more detail but still simpler than most professional books):

See that the ruminants have the same second and third part of their digestive system (though the bacteria use up most of carbohydrates, so some difference in absorbed material), but have an additional part in the front - where the microbes digest and ferment the food, that the ruminant has provived them. The reticulorumen needs to be large in order to provide space for all that plant material and bacteria.

eyes - Perception of artificial light - flickering

It's difficult to give an exact answer without actually observing the light and performing measurements. I have a theory, though.

Your peripheral vision is hyper-sensitive to changes in light - an evolutionary trait that provided quicker reactions to predators sneaking up on you. As such, even the tiniest fluctuations in light can be registered with your peripheral vision; much more so than your primary field of vision. In this case, it may well have been that the light was flickering very subtly, or at a very high frequency, which your primary field of vision could not pick up. When your peripheral vision was in play, it immediately spotted the flicker.

This is reliant on a principle called the flicker fusion threshold, which essentially states that there is a threshold of various light properties (including flicker frequency, colour, intensity, etc.) at which an eye begins to distinguish a steady light from a flickering one. Research has demonstrated that species who have high rod density are good at picking up flickering, whereas species with low rod densities have a much poorer threshold. Cone density doesn't seem to factor in very much, since flickering is primarily a change of intensity rather than hue.

This transfers into the human eye, since we have a high rod density (and low cone density) at the edges of our retinas, i.e. in our peripheral vision. If you had the eyes of another species (as creepy as that would be) with a high rod density, you may well have been able to detect the flicker quite easily with your primary field of vision.

To directly answer your question - yes, I believe this is primarily the "fault" of the eye, rather than the brain. The brain has a role in identifying the flicker at a subconscious level, in terms of fight or flight response, but the eye is responsible for providing the elevated sensitivity at the peripheral.

genetics - How does the modern theory of evolution solve these apparent problems?

OK, I'll have a go although you really shouldn't combine so many questions into one.

1 The mutation protection "paradox"

As already mentioned while many mutations are caught and corrected, not all of them are. You have to consider that a body (the human one, for example) contains several trillion cells, each of which contains 3 billion nucleotides each of which can be mutated. So, if the human body has, say, 50 trillion cells (a relatively conservative estimate), that means that a mutation could occur at any of

                              $3e10^9 * 5e10^{13} = 15e10^{22}$ = 150000000000000000000000

different sites. So even though the cell is pretty good at catching and correcting errors, some are bound to get through from pure statistical chance. In any case, you know that not all errors are corrected, diseases such as cancer are often the direct result of such mutations and errors.

I should also point out that in sexually reproducing species (such as humans) mutations are passed on to offspring only if they occur in one of the cells that become gametes (sperm or eggs) so this does not accurately represent the number of available sites that can give rise to mutations that can directly affect evolution for sexual species. Other species however, do not reproduce sexually. For example, cutting a worm like C. elegans in half will result in two worms so a mutation in any of its cells could be passed on to its offspring.

Anyway, point mutations are not the only way that diversity is generated. Even in the absence of mutations, processes such as chromosomal cross-over during gamete cell division (this is what makes you into a mixture of your Mom and Dad) would still produce differences that selection can act upon.

2 Genetic entropy

This one is a bit harder to answer, largely because it is complete poppycock. I'll try though. Let's see, we do not have "more mutations than our parents", what an absurd idea! The silent assumption here is that there was a "perfect" genome and each mutation is carrying us further from it. Therefore, since my parents were closer to this platonic ideal of the perfect DNA, each mutation that occurs in my cells takes their genomes a further step from that perfection.

This is very simply wrong. There was never a perfect genome, each cell in each individual of each species in the world is constantly undergoing mutations and has always done so. The genome is dynamic, not static and it has never been static, it can't be. DNA is a chemical substance and undergoes chemical reactions (such as mutations) all the time. Like all other chemicals it exists in a thermodynamic equilibrium, but not a static one. The only way that I have "more mutations" than my parents is if you accept as a premise that humanity comes from the perfect genomes of Adam and Eve. Since this is what Mr. Sanford is, presumably, attempting to demonstrate, using it as a premise is, at best, a circular argument.

Unless you assume the existence of a platonic ideal of a genome you cannot say whether I have more or fewer mutations than my parents because how can you compare them? In order to say that I have more mutations than my parents, you would need to quantify the number of mutations that each of us has and that cannot be done. How do you count mutations? You would need a reference genome of the ancestral human and we don't have that.

The rest of the argument is even more nonsensical. Mutations can either be completely neutral and therefore "unselectable" or they can have an effect. By definition, if a mutation has an effect, it can be selected for or against. That's how selection works. So, stating that these tiny mutations (which do exist) cannot be selected for/against and yet are harmful is a direct contradiction. You can only have one or the other. If they are harmful, there will be a selective pressure to change/correct/lose these mutations.

In any case, if these things "are left to build up in all people until the entire human race becomes extinct" all that means is that these things build up in individuals of a species and the species changes. Ummm, well, yes, we have a name for that, it's called evolution.

Just a final point, tRNAs have their own specific genes, a random mutation in an intergenic region will have no effect on them, why should it? This just shows the fundamental ignorance of the author in question.

Oh, and the whole "Junk DNA" is a very complex question. Yes, we now know that a lot of what was termed "Junk DNA" has a function (this was no surprise by the way, "Junk" was never intended to be taken literally). All this means is that mutations in non-coding DNA can also be harmful. OK, fine, then they will be selected against because that is how evolution works.

3 "meta-informaton paradox" (whatever that is)

This idea is often bandied by creationists but is a basic misunderstanding. Mutations are random(ish), evolution is not remotely random. Advantageous mutations that make an individual more likely to reproduce will tend to be selected for and spread across a population while deleterious mutations will tend to be selected against and be removed from the gene pool. This is not a random process at all.

As for the "meta-information", nothing is "independent". The cell is a complex system with extremely complicated interactions and a lot of cross-talk between the different processes. The DNA is not separate from the cell, it is an integral part of it. The Aristotelian idea of reductionist logic where you study complex systems by cutting them into little bits and understanding those bits is all very well as an intellectual tool but that is all it is, a tool. In reality, complex systems should be studied in their entirety, you cannot disassociate DNA from DNA regulation.

4 The pseudo math hypothesis

Let's have a look at these assumptions.

• Assumption 1: "Evolution must occur by a net gain in new information. "
  Of course not. Evolution can create a net loss in complexity (information) just as often (indeed, probably more so) as a net gain. The classic example of this are viruses. They have evolved into lean, mean, minimalist killing machines. They have nothing that is not absolutely essential. Hardly a net gain in information.




• Assumption 2: I don't know where these numbers are coming from, whenever you read a phrase that starts with "scientists have observed", run away. What scientists? How have they observed this? How do they define beneficial? Anyway, let's say these numbers are right (I really really doubt it, but let's say they are for the sake of argument).




• Assumption 3: Huh? Let's just throw some random numbers and see if they stick. There is no magical number of changes that results in speciation. In mutations as in real estate, it's "location, location, location". The question is not how many mutations but where they have occurred and what effect they have had.




• Assumption 4: Wow, this one is just completely wrong. To pick just one problem here, if 10 million species is the upper limit of species living today, and 99% of all species have become extinct, how does it follow that 10 million can also be a good estimate of all the species that have come before? If the 10 million of today are only 1% of all the species that have ever lived (99% are extinct right?) then it follows that the number of species that have existed is around one billion.




• Assumption 5: It is most certainly not true that every beneficial mutation is fixed. Many are, others aren't. Also, bear in mind that the same mutation can be both beneficial and harmful in different contexts. For example, a mutation that makes me more resistant to cold would be very useful during an ice age but less so (and could be harmful) during a period of high temperatures. To take a classic example, there is a known mutation in some humans that makes them susceptible to sickle-cell anaemia. However, the same mutation also protects from malaria. So, is this one harmful or beneficial? That depends on whether you are living somewhere where malaria is prevalent or not.

OK, so now the numbers. These wonderful probabilities all assume that evolution happens through "beneficial" mutations. First of all, that is not the only way that genomes change. I mentioned chromosomal crossing over earlier and you also have things like genetic drift (you also have all sorts of other weird things such as horizontal transfer).

In any case, it does not take X beneficial mutations to make a new species. As I said, there is no magic number and evolution is not restricted to beneficial mutations. Just mutations.

However, the most serious problem in this reasoning is that you are not calculating probabilities, you are calculating frequencies. What the argument you are presenting says is that it will take $10^{150billion}$ events for 10 million species to evolve from a common ancestor. It says absolutely nothing about the probability of such events because you are not taking into account the size of the event pool.

Let me explain, if you toss a coin, you have a 50-50 chance of getting either heads or tails. Therefore, getting 5 heads in a row is not very likely if you throw five times. If, however, you throw a few billion coins a few trillion times, you are very very likely to at some point get 5 heads in a row. In order to calculate the probability of something you need to take into account the number of tests performed.

If we keep the arbitrary numbers you have quoted, we have 10 million species, let's say each of them has a genome of 1 million base pairs and each has just 10 cells whose genome is passed on to their offspring (non-sexually reproducing species are actually the vast majority but most of them are unicellular so let's just take 10 as an average). Let us also assume that the creationists are right, the world is about ten thousand years old and let's say that species live for an average of two years (absolutely wrong of course but let's just pick small numbers). Finally, let's say that each species has only 1 million living individuals (again wildly conservative, just think of the number of ants in the world). This means that we are talking about

10 million species * 10 cells each * 1 million individuals * 1 million bases per cell = 100000000000000000000

If the rate of mutations is a tiny (much much smaller than the real value) 1 mutation every 24 hours, this means that there are $10^{20} * 365$ potential mutations a year. And, therefore, there have been $10^{20} * 3650000 = 365*10^{23}$ opportunities for mutation in the last 10000 years, that's 365 followed by 23 zeroes, that's a hell of a lot of chances. So, yes, if one in a thousand of them were beneficial that still makes it really quite likely that such mutations have occurred and have caused speciation events. This becomes even more likely if we take a realistic estimate of the time elapsed (10000 years is extreme for all but the most bullheaded of creationists).

mycology - How does a fungus protect itself from digestion by other fungi?

In general fungal cell walls are resistant to whatever enzymes or compounds they are excreting to break material down for consumption. Conceptually, it is a little like your stomach lining being resistant to stomach acid. For a more detailed answer you may have to head over to your local university and find a Mycologist.

There is ongoing research on how fungi actually "eat." You can look up fungal endocytosis if you wish to research it more. There may be other mechanisms as Shigeta mentions.

evolution - How exactly are game theoretical evolutionary models described during implementation for computer simulations?

There is no single way to build such a model. They can vary from a simple mathematical statement like Hamilton's rule (rB>C) to the chemical diffusion models used to describe the patterns in animal skin coloring (like zebra stripes, leopard spots and the like).

There are efforts to build molecular models of entire cells like this model of mycobacterium genitalium dividing, which integrates nearly 30 different mathematical models to describe different aspects of the organism. There are efforts to build such a model of an entire brain as well.

Another common sort of model for evolutionary biology is the use of game theory, where different strategies can be posed one against another as in the prisoner's dilemma competition Dawkins describes in the Selfish Gene.

It goes on and on. Basically biological modeling is driven by the sorts of mathematical models that we know. New models will reveal new paradigms of how biology works. They can be highly mathematical, but their relative importance and when they apply and what they mean are more analogy than proof.

For instance in the prisoner's dilemma, the first contests showed that Tit for Tat was the strongest model - generally assisting others, but betraying when there is a history of betrayal. The ideas at the time moved towards general cooperation in populations. More recent replays have shown that if there is a team of entrants that make extraordinary gifts to each other (allow betrayal without retribution), then they can compete against other models quite well.

One can never prove that a selfish model for the prisoner's dilemma will not show up, though biological systems to seem to be highly cooperative. That is a model, not a proof.

neuroscience - What is the difference between different brain regions

The wiring is different as you mentioned. However, perhaps the most important is the brain knows where it's input is coming from. The brain knows where each fibre innervates and thus can compile and present this data to our conscious mind. We show if we stimulate the brain directly, than we feel a sensation in the part of the body that portion of the brain is responsible for. Plasticity means our brain can change what feeds into where, this is most commonly where we learn a motor skill. If we play the piano for example the part of the cortex feeding to this area increases.

Another way is the type of chemical transmitter and receptor. Dopamine is primarily used for things that cause us pleasure for example. However dopamine can affect our movement if it is secreted in from the substantia nigra, as this feeds into the motor cortex. Furthermore, neurotransmitters can be excitatory or inhibitory and this is an analogue rather than binary signal. All of these fine tune, and the position at which they inhibit and the location and the feedback from which they obtain their signal all indicates from where the brain is getting the information or to what it is responding to.

In summary it is wiring, signalling and location. However the components are incredibly similar but it isn't the small differences that have a profound effect.

human genetics - What hair color will result in someone inheriting both blond and ginger genes?

Hair color is not so simple as that. Most traits, especially those as complex as color, are controlled by many alleles at many loci. That's why there are different kinds of brown, blond, and red hair in the population. There is no "hair color gene." A fascinating paper came out a few years ago, identifying dozens of SNPs playing a role in hair and eye color. It's a deep, deep rabbit hole that we have only begun to plunge into.

EDIT: To summarize, it's very complex. This paper performed genome-wide association scans looking at two comparisons each for eyes (Blue and green, blue and brown), hair (red or not, blond or brown), and skin (freckles, sun-sensitivity). The researchers looked in a group of Icelandic and Dutch individuals, which means they only looked at a small portion of human variability (i.e., very few African or Asian genomes, for example). Still, just from those simple comparisons, their scans:

revealed 104 associations that reached genome-wide significance, accounted for by 60 distinct SNPs, of which 32 showed genome-wide association with only one pigmentation trait, 12 with two traits and 16 with three traits.

That is to say, they found 60 DNA bases that explained their data. Roughly half of those only affected one thing (eye, or hair, or skin, but only one), a fifth of those single base changes contributed to two different traits, and a full 25% of those SNPs were related with three traits.

That's still pretty hefty. Basically, they found 60 things that can affect hair, eye, or skin color, and some of those can affect some or all of those at the same time. And they only looked at people from two countries. Here's a figure where they summarize the seven strongest SNPs; you can see how tricky it can be to explain colors.

pathology - Transmission of disease from mother to fetus

Pregnant mothers can indeed pass on various microbes to their fetuses but it is not always directly through the placenta, as the placenta can be protective. Although the blood of the mother and fetus do not mix directly, the two can interact. Maternal proteins can flow across to the fetus, as maternal antibodies are actually the source of a newborn's immune system for a few months, and maternal immune cells have even been found in fetuses, which of course means other cells or viruses can get across.

HIV is a good example for your question, actually. HIV can infect newborns through the placenta, but the majority of infections occur during birth, not in utero. Birth is a pretty bloody process, and the rupturing of the amniotic sac exposes the infant to anything in the mother's blood, which is when most infections occur. For HIV specifically, physicians can all but prevent mother-to-infant transmission by administering anti-HIV drugs just before birth.

Here is a list from the CDC of some STDs which details how infections may be passed on to newborns; most clarify that it mainly happens during the birthing process. That being said, plenty of diseases will cause transplacental infections. Usually they are viruses, as viruses are simply smaller, but there are definitely bacterial and parasitic examples, such as Borrelia duttonii, Trypanosoma cruzi, and Toxoplasma gondii. Here's a list of bacterial ones and here's a list of viral ones.

dna - Difference between viral and human genetic material

I have heard that there is a difference between viral and human genetic material. What is that difference?

If I take my cells and take DNA out of them and insert only a small part of it having a sequence, say, AGTTC, and viral DNA with the same sequence, can my body distinguish between the two? If so, how?

evolution - Why does so much variation exist within species?

I think there are two elements to this answer. To cut to the short answer skip to the bold summary at the bottom...

Firstly, genetic variation exists because of mutation. Genes get mutated every generation, the . Larger populations will have more mutants within them because: more individuals = more nucleotide base pairs (C's G's A's and T's) = more potential sites of mutation. However mutation is not likely to explain the persistence of variation because mutation rates are very low (1 in 100,000 to 1,000,000 gametes have a newly mutated loci at any individual locus) and singleton alleles have only a 50% chance of reproduction (assuming no selection) so are likely to be lost by drift (Falconer & Mackay, Intro to Quantitative Genetics 1996).

You also talk about acne, which is likely to have a large component of environmental variance. Therefore you should remember that not all phenotypic variance is genetic its source and it is highly likely that an individual trait has some degree of environmental variance component. Simplistically:

Phenotypic variance = genotypic variance + environmental variance

So the bigger question is why does variation persist? There are many potential causes of this which continue to be widely debated. Essentially it seems paradoxical because selection should reduce variation as it drives the fixation of all loci to the fittest allele. However, selection is transient, both spatially and temporally, and is not efficient against rare alleles (especially recessive alleles because they are hidden by dominant traits - e.g. disease "carriers"). Another important point is that some mutations will be neutral, therefore remain unaffected by selection.

In the spatial context, this means that selection is not always favouring the same allele in all places a species inhabits. Selection might be different based on the where it is occurring (within a species, traits like fur would be beneficial to populations in cold climates but not to those in warmer climates - here I am assuming that the sole effect of fur is to improve the ability of retaining heat).

Temporally there are also key elements. Principally, over time selection changes. Again sticking with my fur example, climates change. Ice ages come and go bringing with them different selection coefficients for fur growth.

Another variance in selection can be sexually antagonistic selection, where different alleles are favoured in either sex. In this case selection does not deplete variation but instead maintains it. It has recently been shown that sexual antagonism is prevalent throughout the genome.

the divergent reproductive strategies of the sexes could promote the
maintenance of sexually-antagonistic variation (Sharp & Agrawal 2012... yesterday!)

Other hypotheses suggest mechanisms by with selection can maintain variation such as assortative mating.

Long story short, you stated that you expect variation to reduce as a consequence of selection. However genetic variation persists for many reasons, and can even be maintained by selection in several ways. Furthermore, phenotypic variation which is what you actually describe with your acne example (and I with my fur example) can be caused by non-genetic components of variation.

.

Suggested reading:

Cox & Calsbeek 2009, Sexually Antagonistic Selection, Sexual Dimorphism, and the
Resolution of Intralocus Sexual Conflict.

Falconer & Mackay 1996, Introduction to Quantitative Genetics.

Singh & Krimbas 2000, Evolutionary Genetics: from molecules to morphology.

Sharp & Agrawal 2012 (in press, accepted on-line version released yesterday, print may be 2013) Male-biased fitness effects of spontaneous mutations in Drosophila melanogaster, Evolution.

Innocenti & Morrow 2011, The Sexually Antagonistic Genes of Drosophila melanogaster, PLoS Biology.

Arnqvist 2011 Assortative mating by fitness and sexually antagonistic genetic variation, Evolution. (also see his book sexual conflict).

Is there any evidence that a virus can modify human evolution

The simplest example, that I can recall are the flu pandemics. The 1918 pandemic is the first to be described because of its severity, but quite possibly not the first in human history (see for example the Black Death - Yersinia pestis is a bacterium, but in the 15th century in just a few years it covered almost all of Europe, sometimes killing up to 40% of population in a given area).

Influenza pandemics appeared quite regularly during the 20th century, usually every 20 years and killed suspiciously many people compared to yearly influenza strains. Additionally, a person who survived one pandemic, was unaffected or only mildly affected by the next pandemic.

All this suggests, that the pandemics "clear" the population from susceptible individuals, and regularity of pandemics (notice, that 20 years is more or less the time of one human generation!) assures that the new generations also go through this kind of selection. The surviving individuals are more resistant to all strains of influenza then those, who never suffered from a pandemic. Maybe the influenza didn't mutate our DNA, but it could be a major force of natural selection.

And one more note: did you notice the great noise in media every time a new potentially pandemic strain is discovered? Actually, it's not just hyperboly of the danger. Last pandemic was in the '70s, so it's high time for a new one. And, since the last one was almost 40 years ago, the new one (when it happens) will probably be very severe.

Advice on Cell Biology texts by Alberts

I've actually got a copy of Essential Cell Biology on my desk currently, it's one of our core textbooks.

When comparing with the "look inside" feature on Amazon for Molecular Biology of the Cell (remembering I only have access to the first few pages) I would suggest that Essential Cell Biology certainly takes a slower pace, but I wouldn't say that it was less detailed.

It goes into great efforts to explain how we know things experimentally, which I personally find quite helpful. The pictures in Molecular Biology of the Cell look almost identical, however I would say they are more copiously used in essential cell biology. Essential Cell Biology also comes with a DVD including very useful animations of cell processes.

Comparing the glossaries, I would still be inclined to say they are covering very similar levels of material, however Essential Cell Biology is using more 'entry level' language.

The key difference between the two in my opinion is the copious use of images in Essential Cell Biology - it's almost half a picture/diagram book. In your situation (pretty much identical to mine) I'd probably recommend Essential Cell Biology just as a start then move on to Molecular Biology of the Cell as everyone else rates it so highly.

Finally, Essential Cell Biology certainly has some kind of sense of humour:

Geek Spoiler:

The bottom line reads C A G T whilst the top line reads G T C A in semaphore, two complementary strands of DNA bases acted out for your amazement...

genetics - Are there more descriptive ways of naming genes and gene interactions?

I couldn't help but notice just how non-descriptive the gene names that modern genetics is using. Currently I'm reading "The new science of Evo Devo" by Sean B. Carroll and here are some examples of gene names used:

• Fzrb


• Krox 20


• Hoxa2, Hoxb4


• ZPA


• FGF8


• sonic hedgehog

While these names identify genes uniquely, they do very little to express what and where the gene does, or how it is related to other genes (While FGF8 may be related to FGF7, it's relationship to XYZ10 is not obvious).

I get the need to uniquely identify genes , and the book is an example of just how hard it is to presently write about a lot of genes at once. The author creates a picture of what's going on, but the gene names get in the way. Even in cases where a gene has a semi-descriptive name, like "eyeless", the reader has to remember that it's actually the gene responsible for eye formation.

Are there are any efforts underway to systematize or name genes for a given organism in an expressive manner?

As a programmer, I write code for a living, and having descriptive names makes it easier to look at someone else's code, read about code and even discuss it with novices. For example:

• initializeDataModel


• createViewHierarchy


• userDidSelectLayerAtIndex

Modern programming tools make using descriptive names easier, because of autocomplete - typing in the first few letters of a programming structure completes the rest. Even google has a list of autocomplete suggestions.

We are all familiar with the Internet, where biology.stackexchange.com/questionname resolves into a specific page. Stackexchange is the site we are visiting, and Biology is a subset of that site. There are other biology websites, but biology.stackexchange.com uniquely identifies this site. The use of "biology" in the address gives readers a general idea of what the site is about and relates it to other biology sites. Our web browsers resolve the address into a proper string of bytes and get the right page. What if we name genes like like

• com.drosophila.eyeformation


• com.chicken.limb.structure.ZPA


• com.human.development.geometry/XYZ10

,and whatever technology we use would actually resolve that descriptive name into a gene or a series of gene interactions?

Is there any recent evidence for the aquatic ape theory of human evolution?

The Aquatic Ape theory has never gained wide acceptance. This is because it has never had strong evidential support.

The features supposedly supporting the hypothesis only do so under an extremely superficial analysis (e.g. the argument for bipedalism), frequently actually occur in other non-aquatic mammals (e.g. hairlessness in naked mole rats and rhinos, a descended larynx in red deer), show no sign of having arisen at similar times in the human evolutionary record (e.g. encephalisation evolved far later than bipedalism and bipedalism vastly predates hairlessness) and lack fossil evidence of having evolved near aquatic environments.