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Why have humans evolved conciousness?
Why did humans/animals evolve to become self-aware of their own thoughts.  That is, why don't humans act and compute like a machine, or walking zombie.  In my mind, such creatures would still be as smart and equally capable of surviving, the only difference being they don't experience the phenomenon of self-awareness. (To understand my question think: unconsciously sleep walking)

What kind of answer are you looking for? If the answer "It is evolutionary advantageous" or "You might not be able to have one without the other" will not work for you, can you give an idea of what you expect?

"such creatures would still be as smart" - if you aren't conscious can you be aware of others' motivations in the same way? Isn't the ability to develop a theory of mind a big part of "being smart"?

How can you demonstrate that humans are self-aware? How can you demonstrate that computers or worms are not? These are hard philosophical questions not really suited for this site.

@MCM, The answer I personally think is that evolution cannot explain why we have awareness.  I posted the question in-case people who know more about evolution could give an explanation.

@terdon, I can feel my own self-awareness, and I just make the assumption that other humans are self-aware because we look the same, grow up together etc.  But I know I'm self aware, so why I did I evolve to have this self-awareness, which provides me no benefit.

@AlanBoyd, a computer can play chess equally well as a human, and the computer isn't conscious.  I'm sure an unconcious "walking, computing zombie" could navigate his way though motivations of others and appear to be identical to us in everyway.  The only difference is that there would be noone who experiences his subjective point of view.

@Chris - I'm not asking what your opinion is, I'm asking what's an acceptable answer for you. "Why are humans self-aware?" and expecting something other than a variation on "Because it's extremely beneficial evolutionarily speaking" is asking a lot. If you think Natural Selection isn't a satisfactory explanation, you need to explain why.

If I knew of the acceptable answer, I wouldn't be asking the question.  An acceptable answer is one that explains why consciousness helps an organism, or explains why consciousness is essential for intelligence.  Basically an acceptable answer is one that answers the question.

Why do I think natural selection can't explain it?  Because I thought that intelligence doesn't necessarily require self-awareness, and therefore while I see how natural selection would push creatures in the direction of high intelligence, I can't see the survival benefit of being aware of one's thoughts.  Many say that we only become aware of our thoughts after our brain has come up with the thought, so why is such an awareness even necessary, if the subconcious is happy thinking on its own.

The thing is that "feeling" something does not demonstrate it as true. Also, it is virtually impossible to demonstrate that animals are or are not self aware.

Its my self awareness that allows me to be aware of my feelings.  If I had no self-awareness, there would be no "I" who is the subjective observer of my body.  But I am "I", the subjective observer of my body.  The fact I feel the emotions attributed to a specific body, my one, illustrates to me my own consciousness, so my feelings do prove that I am self aware, but to myself only.  I know I am self-aware, but I don't know if you are, or anyone else, and I can't prove that I am to anyone, as noone else can experience my experiences.

-1. Your question and comments are philosophical, not biological, and therefore not appropriate for this site. You seem to believe that evolution can't possibly explain it, and therefore there is really no science to be discussed. Read up on the philosopher David Chalmers, who agrees with you. Then read up on his main rival, Daniel Dennett. Note that when you get into these sorts of questions, your intuition about whether you "know" that you are "self-aware" and how to "prove" it are destined to fail.

np.  I see you are a neuroscientist.  Could you please have a look at this question?  http://biology.stackexchange.com/questions/6794/do-adjacent-axons-in-a-nerve-influence-each-other

Imagine a sleep walker trying to deal with a leopard or learn a new skill and you see the problem right away. A complex brain makes a model of the universe (the world around it) and tries to predict what is going to happen when it does different things, It allows learning by something other than trial and error. As soon as a creature starts including its own possible reactions in its model, it is self aware.

@John I guess then I'm not convinced that self awareness is the same as consciousness.

@Kenshin define conscious and self-aware then, becasue you used both interchangeably in the OP.

@John suppose a robot knows how to catch a ball.  It clearly must be aware of it's own position and the ball's position so it is self aware, but I don't think the robot is conscious, do you?

have you seen the attempts to build a robot that can catch a ball? and no you don't need to model yourself to catch a ball reflexes will do it, but the downside of reflexes is they are not flexible. You should really read up on ethology and animal behavior before you try human behavior, much like learning how a lawn mower engine works before you try and understand a nuclear turbine.

catching a ball does not require consciousness but it is an incredibly complex behavior one that requires some of the most advanced AI we have ever built. http://www.livescience.com/45528-robot-arm-catches-flying-objects.html. By model itself I do not me model your body I mean model your open brain, your own thought process. An example of an advantage is being able to lie and catch lies effectively both require a detailed model of  a brain someone else's or your own through process.

There have been many proposals over the years as to why human consciousness has emerged and how, or even what it is.
Most of us will not be surprised to know that there is no consensus about an answer here.  Its hard to draw a trend from a single example.
Here is a little survey of the one's I've heard.

We are intelligent because we have opposable thumbs and can use tools, which evolved our brains.  This is an old one - maybe as old as Darwin's time.  I think its mostly ignored now because so many animals - including pandas and other non primates have opposable thumbs or use tools or both.  (monkeys and chimps use tools, and recently crows have also been observed to use tools.)
brain size.  We do have a large brain to body size ratio.  There are other animals with similar ratios and they don't have internets.
We are 'self-aware'.  That is to say we recognize ourselves as an individual.  It was proven that other primates can recognize themselves in mirrors (putting a red dot on their forehead. when they see their reflection, they touch their own forehead).  So that's not exclusive either.  its not a bad idea, but so far it doesn't seem to make the
'We ate something' I once read a discussion of how humans might have ingested psychotropic plants or fungi.  As you can see, this was 2010.  Its not the worst idea, but its hard to prove.  Lots of experiments on cats since the '60s have not produced cat's who care to tell us if they are intelligent.  Maybe they are just too smart in the first place.

These theories, from when I was a student are so discounted now, you can't find too much record of anymore since they were pre-internet and also they seem so unlikely now.
More modern theories have locked onto social configurations of human societies which drive intelligent adaptations.  This is stemming from observations that human evolution (the rate at which genetic variants are retained in the gene pool) are accelerating since humans have become social.
These new theories while standing on some amazing evidence are still feeling around in the dark - stuff about how social interactions have created a preference for intelligence-like traits. There is probably something to that - once intelligence gets a toehold it is a clear advantage.  But how did it show up only once and why us? I think that's the hard part that science has, for the moment, given a rest.

Given how we clearly would have no hardship eradicating everything else on earth (though funnily moral objections against doing so), it could be that intelligence/conscience/... is an "absolute advantage" trait similar to, for example, using enzymes rather than ribozymes or DNA in conjunction with RNA - except that we're not yet at the stage where all alternatives are eradicated.

heh - we're so superior we might end up doing the job on ourselves too!  I agree though - nothing seems to be able to stop or trump intelligence...

@Armatus - Are you sure we could easily eradicate everything else (well, all other life) on earth? Viruses might be a tough game, especially those that live in humans. And extremely small things that replicate often and mutate successfully relatively often may adapt pretty quickly to our efforts to eradicate them (not that it would be easy in the first place).

If only the Obama administration had really listened to the Death Star Petition we'd have a running start at it.  Seriously there is an idea that bacteria might have come to earth by hitching a ride on a martian meteorite, so some clearly believe its possible microorgs can survive planetary devastation. (search term: "Panspermia")

A Death Star might be the way to go if we wanted to include ourselves in the noble quest of extermination, but imagine the horror if some tough bacterium would get a foothold on the death star itself! : )
(As for all alternatives that don't include us humans -- it will be tough to get all the bacteria in intestines, mouth, stomach etc out of there)

-1. The substantive part of this answer assumes the common misconception that only humans are intelligent and conscious, and that we somehow know this for a fact.

Why did humans/animals evolve to become self-aware of their own
  thoughts.

Answer is pretty simple. Most mammals are self aware... it is just a matter of degree. It is a lot more advance in humans, but it is there in animals. like pride of Lioness hunting... setting up an ambush together... which means a lion can predict what zebra will do in a situation. And what other lioness will do.
And why have it? The answer is simple... being aware of you own thought, is basically being able to prediction the thoughts of others. And this is pretty useful.
We have the example of lioness pride ambush hunting. It requires a degree of self awareness in order to communicate and in heat of the chase predict what the other members of your pride will do and what will the prey animal will do.
Being alpha (wolf, lion, chimp, elephant, hyena, meerkats) is great. There are many biological benefit (first to eat, drink and have babies). However for a there to be an alpha, there must first be a  group to be alpha over. And when there is a group, there is a beta, and while beta might not be able to beat you individually, beta might team up with delta..to remove you.
So  as you can see, living in groups quickly leads to complications. And if you can understand others, you can use others to benefit yourself. Much selection pressure there for to evolve consciousness.

"being aware of you own thought, is basically being able to prediction the thoughts of others" I don't think these two things are necessarily related. As an extreme counterexample: Many algorithms can predict behaviour (e.g. youtube and amazon suggest videos/items you might be interested in). That doesn't mean they are self-aware. I know I reasoned in the opposite direction as you did (you: self-awareness causes prediction; me: prediction can exist without self-awareness), but I still think yours was not a valid logical conclusion. Or at the very least not an obvious one.

It seems to me like the answer that addresses the core of the question: 1) we need to define what is self-awareness and 2) how humans are different in this respect from other animals.

I don't think you can ever ask or answer for that matter WHY questions in biology. The only answer there is: because it works. Asking why questions implies that there was a reason, and reason cannot exist alone by itself. Reason is held by someone or something. And reason is something that doesn't exist, it is something we created and use for our own purposes and we cannot attribute it to anything else having one. Now, if you asked "how?", that's an answer biology was created for.
There could have been many outcomes to everything in biology but this is the one that appeared and works. This doesn't mean that it is some sort of theoretical or practically optimum, but the law of this universe is survive long enough to improve if needed.
I know that this is an opinion, but it's as close to the answer that you can get. If someone gives an answer to the WHY question, you could never prove it, or you could find evidence for all the possible reasons. And we can't also tap into the reasons of the universe because our intellect and modes of expression are way lower than the universe has.

Asking why doesn't have to imply reason, it can imply a cause.

yes, "why" is different from "what for"

Natural selection doesn't select for the type of consciousness. It selects for brains that work for its purposes. The brain I think is like a Conway's game of life. It theoretically can pull off all kinds of tasks, and that can be explained just by the laws of physics acting on the brain.
The question of how the brain creates consciousness is an entirely different question maybe a philosophical one. I have aspergers. I sometimes do some abstract thinking. I sometimes sort of feeling like I'm conceiving of an object with properties that most intuitive theories prove cannot exist. They would say it's just my brain inventing the sentence "This object has those properties" and they're probably right. However, I sometimes actually have a small bit of feel for thinking in one and would feel like I'm conceiving of a real object which is distinct from its formalization which people would see if they looked at an image of my brain. I think we then decide to define consciousness according to the way the brain is in that kind of way.

Probably density of cortical columns. I tested this on a mouse recently, it was aware I was trying to help it and actually walked calmly into the jar.
Released it but did wonder if it will make an appearance again one day.
Perhaps in this case, neural nets are not complicated enough unless the connectivity threshold is in a critical range. This is apparently why we are one of only three intelligent species on this planet, sharing this with dolphins and African Grey parrots.
Four if you count octopi.
I speculated a while back based on my knowledge that connectivity modulators like psilocin, xenon and other compounds could be used to trace the actual neural connections responsible. This has been linked to Orch-OR and other QC like phenomena, also allowing for strong AI to be developed by synchronizing classical processors with a quantum link using entangled photons.

Welcome to Bio. Thank you for your contribution. However, we appreciate well-sourced answers and by the looks of it they are more a collection of thoughts and opinions, rather than plausible answers. Perhaps even more importantly, you are targeting a how question and the OP is asking why.

Animals are not self aware, sentience is the quality of placing yourself in time and space, and the capability of introspection. We humans know we exist, we know we live in a universe, we ponder what's the meaning of life, where we came from and how we came to exist, where we go after we die, animals don't, they act by instinct and have different levels of intelligence, their behavior is written in their DNA code, but they aren't self-aware, this is the basic trait that separates us from animals.
Concerning how we became self-aware, that will depend on your beliefs (another trait of our advanced intelligence), but those who believe in evolution pretty much agree that we developed sentience because our brains developed much further than that of any other species, our advanced cortex and cognitive system gave us this ability. Different religions also have different accounts to our origin and history, in the proto-Indo-European cosmology for example, we are descendant of aliens, called pleiadians or nordic aliens, they came to earth through a portal in the sun, and brought their seed to our planet and gave origin to us, all our knowledge and manifestation of our humanity, like science, art... come from them.

Animals can be self-aware. There's quite a list of animals that have passed the mirror test.

I down voted this answer because it doesn't answer the question.


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Why do we feel tired if we sleep excessively?
When we eat, finally we feel full. I know which mechanism causes the sensation of being full. But when we sleep excessively we often still want more sleep. Why does this happen? Is there a mechanism underlying this?

Is this a universal phenomenon?

What you think dear Kevin? you didn't experienced?

i doubt there is a good answer to this one.  I recently read an interview with the retiring head of the UCSF sleep center and he said 'to the best of our knowledge, the reason we need to sleep is because we get sleepy.'  Not sure if there is a strong answer to a question like this ;)

No answers, but some speculations: Perhaps "excessive sleep" simply usually happens when people are excessively tired? Or perhaps people who once in a while sleep excessively do it to "make up for lost sleep", but that it is not really possible to make up for lost sleep, and lost sleep in general might lead to lower quality of sleep. Low quality of sleep may make you want to sleep more. In normal cases where you get up early there is perhaps some sense of acuteness or danger that makes you relatively alert (at a cost, perhaps).

People sleep in ~90minute long sleep cycles. Technically, if you decide to "sleep in" by 30-50 minutes, you may start the next sleep cycle and feel worse awakening from that. The logic behind this is that you wake up from deeper sleep. I don't know if there is hard science to back this up though

Studies have proven somewhat the opposite of what you're asking

For example a study from 2004 - "The impact of extended sleep on daytime alertness, vigilance, and mood" found that,

Average daily POMS vigor and fatigue scores also improved during the sleep extension period

And thus concluded

Extended sleep leads to substantial improvements in daytime alertness, reaction time, and mood.

Whilst an older study from '73 -"Performance and Mood Following Variations in the Length and Timing of Sleep" found that,

Neither sleep duration, nor any other sleep parameter consistently correlated with the performance or mood measures.

The study does go on to state however,

Therefore, it seems reasonable to assume that the detrimental effects of acute changes in the length and/or timing of sleep were not directly related to any specific changes in the length or electrophysiological patterns of sleep, but to as yet unknown physiological changes resulting from the disruption of an established circadian rhythm of the sleep and wakefulness.

This perhaps suggests that the question which should be asked should not be why does oversleeping makes us feel tired, but why does the disruption of normal sleeping patterns make us feel tired?

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Does evolution by selection require that individuals consciously change behaviour in an effort to suit their genes?
Imagine an animal that is incapable of digesting a particular kind of food. Now suppose the mutations for digesting that food were to suddenly appear within the population. There still has to be a corresponding change in the animal's behavior, correct?
I mean, I don't go around thinking, "Gee, how could I get the best out of my genes to get ahead of my competition?" There seems to be a need for changing behaviour to get the benefit of the new mutations, which for me allows room for divine providence (e.g. A God) to guide evolution at the level of animal behavior at least.
Am I missing something? Does evolution by selection not require device providence etc?

The fact that there is not, and there cannot be a scientific proof of God makes any (pseudo)scientific argument referring to God a moot point. If you want to explain something using science then you must stay in the framework of the scientific method. Putting God into the equation is a deus ex machina (pun intended) just doesn't work. You can of course explain evolution by means of divine intervention, but you cannot call that science.

@Nico: I am aware of this. I was primarily interested in the philosophical underpinnings of the naturalistic worldview -- i.e. why certain scientists dismiss God from their personal worldview based on the science. (I initially wanted to post this in philosophy but I wanted a good answer to my question from the biology).

OK, sorry I did not understand that was the sense of your question. In that case, may I point you to this excerpt from Carl Sagan's beautiful book "The Demon-Hunted World"?

Going off of your example: I get hypoglycemic if I dont eat well. So if I sat around eating Legos all day I would become ill from lack of nutrients. It would not take long for me to realize I shouldnt be eating Legos. I dont need God to tell me this. The idea of God subconsciously altering someones behavior to "maximize" genes is ridiculous. Why then, does God not prevent two recessive carriers of a disease from mating? What it comes down to is this: Saying "couldnt God do X" is not proof or evidence, so no scientist is going to take it seriously.

I would also like to point out that as a scientist and a devout atheist, it is not science that convinces me that god does not exist but faith. I can no more prove there is no god than you can prove there is one (or more). Scientifically speaking, the absence of a god is the most reasonable hypothesis given observable data, but that does not make it true. That I feel there is no god is an act of faith no different than yours when you feel there is one. Science can only deal with the demonstrable, faith is beyond its purview.

@terdon - we'll try to ignore that the basis of science is the faith that the universe is reasonable and orderly :)

@MattDMo that is not faith, it is an assumption on which our later conclusions are based. Assumptions in logic or science are the equivalents of theorems in math, they are not arguable, they are premises. In any logical edifice, the premises are taken as given and the logic is built on them. You need to accept certain things as premises in order to construct your logic. In a philosophical discussion, I am willing to accept that my perceived reality is likely not real. I cannot accept that premise for a scientific argument or for my day-to-day life though, because that way lies madness.

Why is it that at least 7 people have voted on answers but only I have voted on the question? Whether we agree with their worldview or not, the OP has asked a perfectly valid question in a non-confrontational manner and deserves an upvote. We should not refrain from upvoting valid questions just because we have a philosophical disagreement with the OP.

@terdon - I dont think it was a good question. For starters the title is "Why is there such an argument about evolution" but thats not what he is asking at all. Indeed, what he is asking is clear as mud. He first asks about how / if (?) genes can influence behavior. Not a bad biology question, but then he asks about why scientists ignore this, which is a wrong assumption, and not so much a biology question but a philosophical question about scientists. And he ends by asking if he is confused. Four questions if you count the title, none of them related. Im guessing thats why it got 0 upvotes.

@vonMises I was not suggesting that the question should be upvoted, I was asking people to vote, one way or another. We tend to only vote one answers here and it's a shame. Anyway, the basic question is quite clear, "why do scientists ignore the possibility of a guiding hand in evolution". Yes, it is based on many wrong assumptions but it is clear.

I edited the title as the previous one was really not helpful. Feel free to roll back if you don't like the edit

Understanding Evolution by UC Berkley is a very short and very introductory course on evolutionary biology that you might want to have a look at.

@Remi.b — Although the poster may be a troll, your change of title to something that is neither what he intended or, indeed, a title, is unacceptable. I have changed it again (even though it invalidates the argument of my own answer). I would say a better way of dealing with this is to vote to close it as opinion-based. Arguing on the basis of opinions or belief in the divine is clearly unsuited for a scientific forum of this type. I appreciate people not wanting to be accused of avoiding an argument, but do you argue with Jehovah's witnesses and the like that knock on your door?

The theory of evolution via selection does not require any kind of divine intervention. It proposes that mutations randomly occur within the DNA, this causes changes in the phenotype (e.g. allowing digestion of a common food source), these changes can be good or bad (beneficial or deleterious). As a result, those with "good" mutations achieve more reproductions (the fitness of those mutant allele carriers is higher) and those mutations spread through the population. You can not direct the evolution of your DNA because mutation is random, even if we artificially induce mutations, we can not direct what the mutation does to the phenotype (though we can sometimes induce specific mutations known to have certain phenotypic effects). Selection favours some phenotypes over others but can only work with the mutations it is presented with - it can not direct the evolution of animals with wheels if mutations that allow wheels to form do not occur.
From this sequence you can see the evolution of a phenotype is best explained in a most parsimonious way without the inclusion of divine intervention. It is the principles of Occam's Razor. Calling divine intervention in to this theory would add further, and unwarranted, complication to the model and we would then have to find strong evidence for the existence of a divine being, something which is still yet to happen in the eyes of most evolutionary biologists. Strong evidence has been found which suits the theory without divine intervention (including unnecessary and untestable components to a theory goes against the basic principles of science).
Selection itself, though largely involved in evolution, is not necessary for traits to evolve. The neutral theory proposed by Motoo Kimura and developed in the last few decades suggests that traits can evolve with out selection, via genetic drift. This means traits develop in populations purely due to random sampling of neutral (or near neutral) random alleles. The relative importance of Selectionist vs Neutralist theories remains hotly debated within evolutionary biology.

Explaining your imaginary scenario with a current theory of evolution: A new digestive enzyme
The scene: There is a population of 100 deer. 50 males and 50 females. There is a potential for variance in mating success and that mating success is defined solely by the strength of the male.
Selection affects a trait: Males that digest their food better grow bigger and stronger. Thus selection favours males that get the most out of their food. If the ability to digest is completely genetically determined by a single locus (for simplification lets say it is) and there is only one allelic variant (one version of the gene) in our first generation then mating success will be equal among the males.
A mutant arises: In the next generation a single male carries a mutation in that locus. It is a mutated version of the gene which makes a key digestive enzyme work more efficiently.
Selection acts: This male is 10% larger and stronger than other males, and therefore sires more offspring in the next generation than any other male. These next generation offspring (technically half if it was a single mutation in a diploid organism - the other half have the ancestral haplotype) have the mutant allele. Then those males with the mutant allele also get more of the matings and so on and so on.
The allele is then spreading through the population. It will continue until all members of the population have the same allele (fixation) or will start over if a new allele arises which is even better. That's all evolution is, no divine beings necessary.
What if the allele was neutral? If the gene for a digestive enzyme existed but was not necessary in an organisms diet it would not know it could go out and use that food source. It may not even be able to. For example, a single fruitfly carries a mutation which has no cost and allows it to digest lactose. It is unlikely to be able to utilize that allele, because dairy products are not part of it's diet and not available in the wild. The allele would only drift in the population, eventually being lost (most likely as it starts at low frequency) or becoming fixed in the population. You can see a genetic drift simulation I wrote in R here. You can set f=1 and then play around with population size, number of generations, and replicates to get a feel for this process.
Note it is worth considering the effects of pleiotropy (if an allele has a good effect on one trait but a negative effect on another - including traits in different environments) and linkage (if the good allele is close to some deleterious mutations in the DNA it will struggle to spread until it is separated by recombination).

I think you might improve your answer by telling a bit about what might happen to newly arisen mutation that would be beneficial if the genetic background was different. What is the fate of this mutation allowing to create a new enzyme to digest a food when individuals behave (let's assume the variance in behavior are 100% genetically coded). You might as well give a word about pleiotropy.

The OP was asking what happen if the beneficial effect of the mutation (new enzyme allowing to digest a new food) is hidden because it is genetically coded that deer (to follow your example) don't eat the food it can now digest. In such a case, the mutation (new enzyme) is not beneficial and does not spread (or only by genetic drift).

It doesn't mean that you need a god for evolution to occur, it just mean that a mutation that allow better lactose (milk) digestion has a different effect on the reproductive capabilities of a mammal than of an insect. The effect of a mutation depends on the environment and the genetic background in which this mutation appears.

@Remi.b that's is covered by the neutralist side of things - "..traits develop in populations purely due to random sampling of neutral (or near neutral) random alleles"

I felt that the OP might wanted a explanation of what might happen to the mutation he was talking about. I wanted to be specific to the OP's example where you provided very good general description. +1 good answer mixing basic process of evolution, philosophy of science and Kimura's neutral theory.

@Remi.b I get you now, added in a bit.

@GriffinEvo

if we artificially induce mutations, we can not direct what the mutation does to the phenotype.

I don't think you meant that. Yes we can direct what the mutation does to the phenotype - we routinely do it in organims we can genetically manipulate (bacteria, yeast, mice etc.) and of course only in cases where we understand the
relationship between genotype and phenotype.
Better way of putting it would be that in most cases in natural populations we cannot predict consequences of a given mutation, as there are many factors in nature that can influence the fate of that mutation.

@yotiao by "we routinely do it in organisms we can genetically manipulate" do you mean we can cause a specific mutation to occur?

@GriffinEvo Yes. We can introduce a specific mutation (substitution, insertion or deletion of a single base pair up to large chunks of DNA) into a specific position in the genome. In many cases, we know a good deal how if affects the phenotype. In other cases, we have no idea but this is exactly the reason it's done.

@yotiao but this is using an induced mutation to produce an effect on the phenotype, for which the specific mutation has previously been observed to cause the intended phenotype - it's subtly different to what I said. Without a priori knowledge of how a mutation affects a phenotype, we can not know what effect a mutation will have on the phenotype,  we must first observe it to understand it's effect (though I'm sure predictive models can or will be built that can simulate the effect of specific mutations).

@GriffinEvo Yes, you're right for the majority of mutations (some obvious ones excluding, like stop mutations in housekeeping genes). We must have an idea of a genetic basis of a certain phenotype to be able to speculate about effects of potential mutations underlying the phenotype. But the ability of induction of mutation in a defined genomic position allows us to verify/narrow down these speculations in a really clean and clear experimental way.

AlleleA1 is a great population genetic software that really gives you a good idea how the frequency of alleles is affected by various factors. You don't have to know R to run it, but you need a Mac (a double bonus :-)

@yotiao the point I am making is that it is not possible to know it without any prior knowledge of the mutation's effect - I can't say "I want to start digesting cellulose better so I'll change my 5,694,237th nucleotide from an A to a C" unless I have tested that beforehand or have explicit information telling me such a change will give that result.

@rg255 already did a good job answering the main thrust of your question, I will address this part: "There seems to be a huge amount of room for divine providence to guide evolution at the level of animal behavior, at least. Why then do scientists with a philosophical materialist outlook gloss over this?"
Of course there is "room", there is room in the theory of evolution to posit that small, green, tasty but mean little pixies come and push the new food down the creature's gullets, thus teaching them to use new food sources. There is room to posit that invisible, intelligent lichen from Alpha Centauri are actually using brain waves to guide the evolutionary choices of species in a global scale.
While there is clearly room to posit these theories, there is absolutely no evidence for them. The scientific community is not "glossing over" anything, it is just ignoring various (infinite in fact) theories for which we have absolutely no evidence in favor of those for which we have. This is a classic fallacy that was very nicely put to sleep by Russell's teapot argument:

Many orthodox people speak as though it were the business of sceptics to disprove received dogmas rather than of dogmatists to
  prove them. This is, of course, a mistake. If I were to suggest that
  between the Earth and Mars there is a china teapot revolving about the
  sun in an elliptical orbit, nobody would be able to disprove my
  assertion provided I were careful to add that the teapot is too small
  to be revealed even by our most powerful telescopes. But if I were to
  go on to say that, since my assertion cannot be disproved, it is
  intolerable presumption on the part of human reason to doubt it, I
  should rightly be thought to be talking nonsense. If, however, the
  existence of such a teapot were affirmed in ancient books, taught as
  the sacred truth every Sunday, and instilled into the minds of
  children at school, hesitation to believe in its existence would
  become a mark of eccentricity and entitle the doubter to the
  attentions of the psychiatrist in an enlightened age or of the
  Inquisitor in an earlier time.

If you feel that the world you observe is best explained by assuming the existence of an omniscient god who guides the evolutionary process, then that is your right. However, the fact that you believe this to be true does not make it so any more than my believing it to be false disproves it. We are not glossing anything over when we don't take that belief seriously, no more than when we don't take Russell's teapot seriously. The Christian faith, like many others, is built on the assumption that a god exists, it will never attempt to prove or disprove that assumption because such proof would be sacrilege, the entire edifice is built on faith not evidence. If we do not share that belief, why should we attempt to fit our observations into the ideological scaffold provided by someone else's belief system?
If you feel that one theory explains what you observe better than another, the onus is on you to prove it so. That is in fact the beauty of science, it is what sets it apart from most other areas of human endeavor: we change our minds when presented with compelling evidence to do so. Indeed, the history of science is littered with discarded theories. If you can come up with any decent evidence to support a theory, then that theory will (eventually) be taken seriously. Until you do, asking others to consider it based solely on the fact that you believe it to be true is hubris to say the least.

This is a complicated topic. Basically, we differ on what can be known. Knowledge of God more properly falls into "personal knowledge", like knowledge of a particular person. You're quite right to demand a certain level of "proof"(proof, i.e. 100% certainty, only exists in mathematics), and for that I'd recommend Vishal Mangalwadi's "The Book that Made Your World". But to go from mere propositions about God to a personal understanding takes faith.

@Joebevo exactly, and as such does not fall within the purview of science. That's why nothing is being glossed over, faith is not something that can be approached by the scientific method of observable and repeatable experimentation. Therefore, any theories that base their conclusions on arguments of faith are not relevant to scientific debate. Science only deals with testable, disprovable theories and the existence of a guiding hand in evolution is neither.

But you can of course argue against the existence of god on the basis that in many religions there are beliefs in acts of god(s) or features of god(s) that are in opposition to scientific knowledge (walking on water, wine from water etc.). By asserting a level of probability on things that people say god does you can indirectly assert the likelihood of god existing in the first place. So because nothing god does / what god is is physically possible as far as science can tell, very likely there is no god at all.

@yotiao well, not really, no. If you start with the premise that god(s) exist, by definition they are above and beyond the laws of physics. Therefore, you expect them to be able to do things that are impossible, otherwise they would not be gods. Deities are not expected to conform to the laws of Nature, they wrote them.

Heh, this is way OT so we should not go much longer, but I then ask: what is your argument for the premise (god(s) exist) in the first place?

@yotiao absolutely none, it is not a premise that I hold to be true. However, if you do accept that god(s) exist, then it is to be expected that they don't conform to the laws of physics. If you believe in a creator(s), then you believe that they also created the laws of nature and, therefore, would expect them to be immune to those laws and cannot use these same laws to argue that they don't exist.

@terdon Yes, in this case this is simply out of realm of science.

I think it pertinent to answer the question posed in the original title, although I will make passing reference to the specific argument the poster makes.
“Why is there such an argument about evolution?” This is because evolution is an example of a scientific question which one party approaches from a philosophical standpoint that asserts a particular answer, and so they will never be convinced by scientific arguments that ignore this philosophical position.
Note, that I am not saying that the arguments from those of a particular philosophical standpoint are necessarily wrong, only that its exponents will continue to argue (or try to engage people in argument) when the vast majority of scientists have come to regard the question as settled in favour of the counter-view — indeed when that view underpins their daily work.
There are other historical examples of this. Most well known is the Roman Catholic Church's refusal to accept Galileo’s espousal of the Copernican view of the Solar System — even to look through his telescope to see the evidence. (I think they have thrown in the towel on that one now.) On the political left you have the promotion of Lysenkoism by the Soviets.
I would suggest that philosophical attitudes colour contemporary arguments. I suspect many ‘progressives’ would never accept scientific evidence that indicated one ethnic group were less intelligent than another. And it would be naïve to think the stage at which one regards a life as having been formed is independent of any religious or feminist views one may hold. There now. I’ve lost the friends I made in the previous paragraph.
Finally, your example of an individual acquiring the ability to digest a different food illustrates my point. You are so convinced that you are right that you have never taken the trouble to find out what the arguments for evolution actually are. It is only under circumstances that an acquired trait provides a competitive advantage that it will be selected for. Think multi-drug-resistant bacteria. You’ll find much more sophisticated arguments on the various ‘scientific creationist’ sites on the Internet, but you would be advised to save your breath, because nobody is listening. As I said, la guerre est finie.

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Why doesn't recombination occur in male Drosophila?

"Males do not show meiotic recombination, facilitating genetic studies."

For a while I have known that this phenomenon occurs, this quote comes from the Wikipedia page on Drosophila melanogaster, and I frequently use this feature of Drosophila in constructing hemiclones for my own research in quantitative genetics.
But, until now, I have never asked why doesn't recombination happen? Why would this feature evolve?
Further, why is the absence of recombination sex-limited to males, why do females have recombination?

This is a venerable fact.  Exceptions in D. melanogaster strain Y-007 have been observed and D. ananassae has consistent male cross-overs, but this work dates back to the 1970s.
This Current Biology 2002 paper is not exactly new, but sheds some light on the issue in question.

In male Drosophila melanogaster, meiosis occurs in the absence of recombination or a recognizable synaptonemal complex (SC).

The authors used a GFP-lac fusion to observe a series of sections of the male fly in meiosis with integrated lac - specific binding regions.  They see for the most part that the GFP bound segments of the DNA are not associated in cell division.  That is, homologous chromosomes physically associate during meiosis (via the SC) and in male drosophila, they do not.
It seems from more recent work, that the details of how this work is still being worked out but several gene regions and factors have been identified.  Suspected factors that help conspire to align the various homologous chromosomes are being looked into.  Take a look at the P.I.s biblio for more.
This isn't my main field, but as I understand it, many aspects of meiosis are still being mapped out.
As to the question of how this evolved and why; its definitely strange.
 It looks like there is a gender selected trait where the SC doesn't form in males.  Its easy to imagine a mutation that caused males only to lose recombination - the process is so complex its hard to imagine such a trait not showing up.
Still it's surprising to think that the trait has not only survived but become dominant in Drosophila all over the world.  To be a common traits to so many Drosophila species, it must have happened more than 10 million years ago.  Explanations of the advantages of sexual reproduction often include recombination.  Even the human Y chromosome has a self-recombination mechanism that reduces error in the coding regions.  As such, its hard to believe that this is not a huge disadvantage for the flies.  Still, if if it were such a big deal, you'd imagine Y-007 would have dominated and re-introduced the trait.
The only theory I can think of might be called 'lazy males'; that the males got the females to do one more thing for the offspring and it somehow outcompetes the sperm of the recombining males.  Lots of sperm are non-motile; that's a fact for humans, I have no idea what its like for flies that recombine.  Take a look at the variance in morphology as well - sperm are really crazy ugly sometimes and a good deal of the mating process is to help weed out the defective ones.  Without recombination, might it be that males produce viable sperm at a greater rate, helping them in sperm competition, which I'm sure is the case for fly mating - Drosophila are not monogamous too I'd guess?  Anyway that's not a researched idea, just a guess on my part.

thanks, this is a good answer so far, could you shed any light as to why that might evolve?

thanks for asking this question! the answer is I don't know and it seems like a lot of the speculation behind this would be buried into the fly literature pretty deeply.  I put a guess into the entry.  I'm actually going to write one of the authors and ask them what they think though.  It's the sort of question some of us scratch our heads about while a dozen or so talk about the fine points over coffee every day.

@shigeta The link to the "Current Biology 2002 paper" is broken. Do you remember the reference? Thanks

To the best of my knowledge there is no strong evidence as to the reason why. The most reasonable explanation seems to be that it evolved as a crude mechanism for preventing recombination of the male sex-chromosome.
You might then ask why a mechanism targeted to the sex-chromosome specifically (as in humans) did not evolve to which I'd suggest that evolution frequently continues with "good enough" solutions where the benefits of apparently better solutions are small or don't involve incremental benefits and note that there is some evidence that lower rates of recombination are beneficial in Drosophila (ref]).

This phenomena is known as achiasmy, where recombination is absent in one sex in a species. The Haldane Huxley rule states that in achiasmic species, the sex without recombination will always be the heterogametic sex (XY or ZW). This is basically the only consistent rule relating to recombination. There seem to be exceptions to every other theory and pattern observed.
The Haldane Huxley rule supports the theory that achiasmy evolved to prevent non-homologous recombination between X and Y. However there are species (most mammals) where the X and Y do experience recombination, but recombination is limited to a small part of the chromosomes called the psudo-autosomal region.


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Mitochondrial DNA and recombination
Firstly I could do with a brief description of mitochondrial DNA. How does the structure of DNA in mitochondria compare to animal DNA (for the sake of simplicity let's say human - some animals might have unusual DNA structure) and what living organism is the mitochondrial genome most akin to? (Circular like bacteria maybe?) and are the mitochondria within a single human homogenous?
Secondly, and most importantly to my aim, does the mitochondrial genome recombine in anyway? Is the process of recombination affected by its structure? Are there any patterns/rules in mitochondrial recombination? Is there DNA transfer between mitochondria which could have a similar effect?
I am trying to think about how male deleterious alleles can spread differently in diverged populations given potential recombination to female beneficial (or recombination away from female deleterious mutations).

Mitochondrial DNA is circular, like bacterial DNA, and around 16.6 Kb long. It codes for 37 genes in total but the majority of these are simply the machinery for gene expression (curiously, mitochondria have a slightly different codon->amino acid translation 'table' to nuclear DNA) and so just 13 code for proteins. Single mitochondria usually have multiple copies of the DNA.
Mitochondria are thought to be most closely related to the bacteria Rickettsia, an obligate intracellular parasite that causes typhus. Mitochondria are so degenerate, however, that they've lost nearly all the genes that normal bacteria have.
While there is some small level of heterogeneity in mitochondria in a single person because mitochondria are exclusively transmitted down the female line most people typically only start with a single clonal population of mitochondria. Because of this, there is no other mitochondrial population present that the mitochondrial DNA could undergo recombination with.
Mitochondrial DNA does undergo recombination with nuclear DNA, however, in that genes can be transfered from the mitochondria to the nuclear DNA and because of this the majority of genes necessary for mitochondrial function are now coded not on the mitochondrial DNA but on the nuclear DNA and their protein products transported into the mitochondria after translation.

Thanks @JackAidley - I have a couple of follow up questions now having read your answer, I'll give them some thought and put them to you later.

Addition to Jack Adley's answer:
Evolutionarily, mitochondria are thought to be descended from α-proteobacterium (Rickettsia are also descendants of this bacterium).
There are evidences that nuclear genes have also been imported to organellar minigenome. This can also happen because of recombination. I am not sure about the case of mitochondria, though. Since the current hypothesis is that organeller DNA that got leaked because of organeller damage, got incorporated in the nuclear genome, there not much of a likelihood that active recombination takes place between the two. However inter-mitochondrial recombinations have been reported, which perhaps happen during mitochondrial fusions.

Recombination of mitochondrial DNA does seem to be possible, but it doesn't seem anywhere near as common as nuclear recombination. This is important because mtDNA is subject to much higher mutation rates, and so would be subject to the same kind of degeneration you see in the Y chromosome - i.e. Muller's Ratchet, if it wasn't so small. Nevertheless mtDNA does generate considerably over a multicellular organisms life span and this is one possible mechanism for aging.

Mitochondrial chromosomes do not undergo recombination. They replicate their DNA in an asexual manner, producing identical copies (except for the occasional mutation).  Mitochondria do not exchange or transfer DNA between themselves as they have no mechanism for that.
Very rarely a piece of DNA might get out of a mitochondrion and into another or into the cell's nucleus.  The latter type of transfer is believed have happened multiple times in the more than a billion years eukaryotic cells have existed.  Most of the genes needed for  mitochondrial functioning are located in the nucleus, not in the mitochondria, and many of those genes probably had such a mitochondrial source. Having mitochondrial genes in the nuclear genome is advantageous, exactly because it allows them to undergo recombination and thereby allows improvements to spread through a population of organisms.

Any references to add?


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Primary cilia: what cell types have non-motile cilia that migrate?
My understanding is that there are two broad categories of cilia: motile and non-motile (also called primary.
Examples of the former include sperm flagella and the cilia of epithelial cells that line the airways.
Examples of the latter are mostly single cilia that protrude from the cell and act as an antenna, usually packed with certain receptors (HH pathway, Notch pathway etc.)
In the inner ear, a primary cilium called the kinocilium extends out of the center of the apical side of hair cells and migrates to the lateral side over the course of a few days. This cilium is non-motile, it is simply anchored to a basal body which is pulled to one side of the cell.
Does anyone know of another such example in any other tissue? A single non-motile primary cilium whose basal body migrates along the apical plane of the cell after docking with the cell cortex.
Thanks.

It's hypothesized that planar cell polarity is many cases functionally associated with asymmetry of (primary) cilia (Axelrod (2008)). So, the phenomenon of primary cilium migration could be not that infrequent. One example is the development of ependymal cells in brain ventricules: They are multiciliated and the cilia are motile, but ciliogenesis starts from a single cilium, which is not motile and which migrates from the apex to the rostral end of the cell:

Mirzadeh et al (2010)
Bayly & Axelrod (2011)

Seemingly less clear (for me, at least) cases are non-motile single cilia on the lens fiber cells and may be, embryal node cilia (which are motile in the mature state):

Wallingford (2010)
Sugiyama et al (2010)


text:
Wolf or Coyote?
I took the following pictures in the Yellowstone National Park of a Coyote-like animal. However, when comparing with pictures from the Internet, I see also quite some similarities with a grey wolf. So my question: Is this really a coyote?

Note that these two species have recently formed a hybrid as well: https://en.wikipedia.org/wiki/Coywolf

PBS did a documentary about coywolves: 53 minute video

Related: https://biology.stackexchange.com/questions/93010/did-my-wildlife-camera-take-pictures-of-coyotes

It's a coyote - I think it's too slender for a wolf and has pointed ears...

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text:
How does prolonged exposure to high frequency noise affect hearing?
Is there any research showing how prolonged exposure to background noises, particularly high frequency noises, affect hearing abilities? Does constant high pitched noise cause damage even a low volumes? E.g an alarm sounding, noise of an air plane, or noise from road works and building sites.
If so, what is the effect? and why does it happen?

You're asking about high-pitched noises even at low volumes, but your examples are high in volume, not (necessarily) pitch. Which are you actually interested in?

Rodent protection modules for car engines give off high-pitched but quiet noises :) In any case, I don't think a high-pitched sound has any different effects of prolonged exposure compared to a low-pitched sound.

It turns you into a bat.

The ear uses a series of hairs to parse out sound frequency in the cochlea.  When the cochlear hairs die, we lose some frequency response.
As we get older, even without exposure to loud noises, the higher frequency responses tend to lose their response first.  But loud noises have been linked to hearing loss and high tones are often lost first.
Hot off the presses: there's been some success in regenerating the cells which respond to sound in our ears.
I want to add @Armatus has a good point.  Ultrasonic sounds - above hearing range - seem to not adversely affect hearing at all.  Will humans and animals be harmed by frequencies outside their hearing range?

In regards to your "hot off the press" link... Ear Rogaine? ;-)

Lol - that would be one tricky q-tip!


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One flybase gene number (FBgn), many Affymetrix Id's
I am trying to convert a set of Affymetrix ID's, like this one 143053_at_3745, to Flybase Gene Numbers (FBgn) like this one FBgn0000015. I have downloaded the Flybase file required to do so (as described here) but I have noticed that most of the FBgn's have more than one associated Affy id.
My question is, how do I know which to assign to my data? From the list of affy-ids that I have, how do I label each one with the appropriate FBgn? I am using data from the Ayroles et al 2009 (DGRP) which has a column of AffyID which look similar to the ones in the Flybase file but shorter (1638273_at). Perhaps I don't grasp why there would be more than one.
Some have one affy id which is repeated across 15 columns in the file, whereas some seem to have several affy id's associated with them.
Some questions this problem raises:
Why does a singular FBgn identifier have more than one associated affy identifier?
Why do some datasets, such as the dataset I have, have shorter versions of the affy identifier?
Where can I find an up to date and appropriate list matching these Affy id's the FBgn identifiers correctly?

perhaps @shigeta knows this...

Is it possible that there are multiple probes for the same gene? You've said that most of the FBgns have multiple Affy IDs associated with them, but you haven't said the converse.

I suspect that is the case, but I am not familiar with the technicalities of affymetrix chip design, and was confused as to why there would be some with the same - though further examination shows that the latter part (after the final underscore) changes within that subset.

I can answer this - I may not have time to dig though the file you are pointing to... but here's some explanation - lmk if you need more.
The shorter names (123456_at) are the original names for the probe sets that Affymetrix gave.  The file you area asking about has been extended for FlyBase's purpose and I'm only dimly aware of its existence. It looks like Flybase has tried to rename the probe set to a minimal gene list and create less ambiguous mappings.  I'm not familiar with it.  If I have time Ill try to look at it and put something here, but I'm fairly slammed this week.
In general you should know, there is a many to many relationship between probe sets from arrays and genes.
There are a few reasons for this.  The most common reasons:
More than one probe set per gene
1) More than one start sequence per gene. The IVT arrays such as you are looking at read only the 3' end of the gene.  If there are  more than one such terminii, you will have more than one probe set.
2) Duplicate genes.  If the 3' end of the gene has been duplicated recently, then a probe set may read more than one gene and not be able to distinguish them, so it will have both gene references in its annotation files.
3) Duplicate probe sets. For older arrays, this did happen where the probes in two probe sets will be mostly or entirely the same.
4) formerly separate genes are now joined into a single gene.  This is similar to (1) above, but with the added reason that two neighboring transcripts seen separately at the time of the array design are currently known to be part of the same transcript.  This is something we often don't think about, but the array may have been designed before your current gene of interest had a full length sequence.
In several cases the transcription behavior of the two probe sets will be quite different and you can decide which one to take based on how it behaves experimentally.  for example one of the probe sets may never respond while another one may register large changes with biological sample conditions.  Sorry I can't be of more help here. There are too many possible scenarios to consider to write about cogently.
More than one gene per probe set
1) a single stretch of DNA, even on the same strand, may simply be associated with more than one gene and the probe set will read both of them.
2) Even if they are not exactly the same, some genes resemble each other in nucleotide sequence that is impossible to choose probes which do not read both of them.
Since they have similar read length to a probe set, all this is also true to some extent for short read NGS sequencers in RNASeq data.
As you can hopefully see, ambiguity is something you have to expect to some extent when deciding to work with a biological system.  In many cases (~ 80%) you will have a single gene read per probe set, but with those odds you'll be looking at the genome browser for a half dozen of your favorite experimental results.

glad it sufficed - there's always more... lol

seemingly so...


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What makes drosophila eyes red? and is it stable?
I have Drosophila melanogaster which I am doing an eye pigmentation assay on in the future. To do this I will dissolve the heads, 10 of them removed from frozen whole flies, in acidified ethanol for at least 48 hours (in the dark at 25 degrees) and then measure the colour of the liquid using a nanodrop. Specifically, this measures how well the liquid reflects red light, quantifying how much red pigment is in there.
I would like to know what causes the red colour in the eye and if leaving it dissolving for extended periods of time will (or is likely to) result in changes of what I measure? (ie is the material causing the redness in the eye susceptible to deterioration, which would change the colour of the liquid it is dissolving in over time)
Have any methods type papers tested this by comparing those dissolved for longer periods to those over shorter periods?

Just on a detail - a red pigment doesn't absorb red light, it absorbs light at "all other" wavelengths.

There's been a fair amount of work on this subject but a lot of it is old - see for example this 1945 paper and this 1948 paper.  That latter one in particular goes into some good stuff: color in the wildtype is due to red and brown pigments, which the authors separated by using acidic ethanol (after grinding up the flies).  Here's a 1961 paper from JSTOR that goes into a bit more detail on some of the red pigments (drosopterin, and isodrosopterin, and neodrosopterin) and looks like a good reference for some other, more basic work on Dmel eye pigmentation.  More to the point, here's a 2013 minireview on the chemical synthesis of drosopterins, which is useful mainly for referencing a lot of other work, in particular this overly detailed chapter from 1970.  That last one has tons of info about some of these pigment-causing proteins in insects.
The only particular reference to stability I could find was from that chapter, on page 144:

The simple pterines (group 2) are chemically stable under normal physiological conditions, while the substituted (groups I and 3) and conjugated pterines are unstable. Light catalysed oxydation of the polyhydroxy side chain at C-6 is a normal phenomenon. The hydrogenated pterines are extremely unstable, especially at pH 7. Tetrahydrobiopterin, for instance, is oxidized within seconds in the light, but more slowly in the dark. [sic]

Thanks @amory - I spoke to my supervisor and we'll do a mini test of it, looks like it could be something we need to consider if it is likely to be unstable. I'll post the result in a few months!

@GriffinEvo Good luck!

you never know, it may lead to the first ever Biology SE publication!


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Can Omega 3 Fatty Acids prevent chest pain in periodic Atrial Fibrillation?
It is debated if omega-3 polyunsaturated fatty acids (N3PUFa) may be effective in preventing AF (atrial fibrillation), meta-analysis here.
However, much less has been considered this: Do N3-PUFAs prevent acute symptoms of periodic Atrial fibrillation?
The meta-analysis concentrate only in the long-term effects of prevention.
My proposal focuses on the short-term i.e. the fact that the user can recognise AF first and then uses N3-PUFAs.
Please, assume that there is a validation method by which the user can easily detect that he has AF - he does this if he suspect it, i.e. feels special discomfort and special wave-like-pain the chest.
He takes each time in this case 20 ml of Müller omega-3 oil which has also vitamin D.
The effect of recovering is immediate in prophylaxis.
Assume the user has less than < 20 ng/ml vitamin D in blood each case, most of the time, 9 ng/ml so avitaminosis.
My conjecture is that N3-PUFAs can prevent the acute symptoms of periodic AF.
How can N3-PUFAs prevent the acute symptoms of periodic AF?
What is the role of vitamin D here?

Does it matter what the cause is of said atrial fibrillation? IHSS, CHF, valvular disease, DM, HTN, MI, other?

@anongoodnurse Thank you for your good comment! It does not matter what is the cause. I will specify this when I understand what could be most practical to study and detect.

Omega 3 Fatty Acids cannot prevent the the acute symptoms of periodic A Fib, nor is there a role for vitamin D in the treatment of acute symptoms of periodic AF.
Atrial Fibrillation with the symptom of chest pain is very worrisome and requires urgent or emergent treatment. The most common treatments are heart rate control via IV antiarrhythmics, or cardioversion, either electrical or chemical, usually done in the emergency room.
There has never been a study wherein AFib accompanied by symptoms of chest pain was treated by Omega 3 Polyunsaturated Fatty Acids and there never will be, because N3PUFA does not cardiovert arrhythmias nor does it effect heart rate in AFib.
No medical body of any kind would support such a study.
Finally, there is no convincing evidence that N3PUFAs decrease the incidence of AFib, and this has been studied often, because eating 4-5 servings of fish per week has been shown to have a beneficial effect on A Fib. That gives reason to hope that N3PUFA supplements might be similarly beneficial. However:

The role of omega-3 polyunsaturated fatty acids in the setting of AF is controversial. Although some studies demonstrate a lower incidence of AF recurrence with omega-3 polyunsaturated fatty acids use, others have shown an increased risk. Further studies are needed to assess the role of N3-PUFAs in the prevention of AF.[1]

If N3PUFAs have not been proven to help AFib long term, there is no hope whatsoever that studies will be undertaken to shown their effect in the acute treatment of symptomatic AFib, which is the scenario you have described.
Atrial Fibrillation becomes symptomatic when the arrhythmia results in decreased perfusion of various organs. If there is decreased perfusion to the heart, the presenting symptoms may be of ischemia (usually chest pain or pressure) or shortness of breath due to decreased cardiac output and decreased oxygenation in the lungs. If it is severe enough, fainting may occur from decreased blood pressure, and decreased perfusion of the brain. If it is not severe, it may result in a sensation of flip-flopping in the chest, or palpitations (irregular, thumping, or pounding heartbeats). There are other symptoms of A Fib but since you mentioned chest pain, I won't elaborate.
[1] Atrial Fibrillation in the 21st Century: A Current Understanding of Risk Factors and Primary Prevention Strategies

Actually, I read somewhere that high doses in the case when the patient feels flip or flop in the chest can actually worsen atrial fibrillation. So the admission of this in high amount should be avoided in such cases. No positive effect shown. The elevation of the sleeping position is the way to go until the patient feels go unless no other approach made for the particular patient.


text:
To understand side-effects for nebivolol's beta1 selective pathway in PubChem?
Assume you have a drug nebivolol.
When nebivolol is used as beta1 selective drug, beta2 is mostly for side effects, but this is not clear from PubChem.
I do not know any cases where nebivolol is used as beta1 and beta2 selective in the treatment.
Its first two pathways of interaction from PubChem.
Assume this pathway to be selective for some indication

and this nonselective (where side-effects stems mostly with large doses)

There no such differences in this section.
No explanations when side-effects come in each case of treatment plan (dose).
How can you understand side-effects of this adrenoblocker from selective beta1 pathway in PubChem?
Like in which cases beta2 selection becomes possible when beta1 is selective.
When beta2 is nonselective when beta1 is kept selective?
In other words, how can you read pharmacodynamics of this adrenoblocker in PubChem?
I.e. what the drug does to the body at any given dose.
I think there is little pieces of informations about it.
Implicitly, the side-effect can be read from Mechanism of Action:

where it refers at high doses to bronchospasm.
However, I would refer explicit discussion about side-effects and what we are trying to find and what are suspected as side-effects.

I don't understand the question. If you're talking about clinical effects, the distinction between "effects" and "side effects" depends on patient characteristics and the goal of therapy, so it would not be possible to differentiate these in a chemical database. If you're talking about something intrinsic to the molecule....I don't understand the question.

@Susan Thank you for your comment! Nebivolol is beta1 selective. Beta2 is only for side effects, but this is not clear from PubChem.

Again, if you're talking about clinical effects, I beg to differ that any particular effect or receptor activity can be labeled exclusively an effect or a side effect. For instance, the beta2 antagonism is likely responsible for the efficacy of these drugs to treat essential tremor, so  your statement beta2 is only for side effects doesn't seem correct.

The information that you have shown as a snapshot of pubchem is insufficient to comment about side effects.

How can you differentiate between effects and side-effects of this adrenoblocker in PubChem?

I think PubChem will list all sites (receptors) at which a drug reacts, rather than the preferred sites, which I think is appropriate.
The pharmacological properties are listed in Section 8: Pharmacology and Biochemistry:

Pharmacology
  Bisoprolol is a competitive, cardioselective β1-adrenergic antagonist. Activation of β1-receptors (located mainly in the heart) by epinephrine increases heart rate and the blood pressure causing the heart to consume more oxygen. β1-adrenergic blocking agents such as bisopolol lower the heart rate and blood pressure and may be used to reduce workload on the heart and hence oxygen demands. They are routinely prescribed in patients with ischemic heart disease. In addition, β1-selective blockers prevent the release of renin, a hormone produced by the kidneys causes constriction of blood vessels. Bisoprolol is lipophilic and exhibits no intrinsic sympathomimetic activity (ISA) or membrane-stabilizing activity...

From this, one cal tell that if there is activity at a beta-2 receptor, it is not the major intended site.
PubChem is a valuable resource, but it's not a one-stop-shopping site. That's the reason there are extensive references given for sites of interaction. It's a great starting place for investigation of a drug.

Thank you for your excellent answer with details! I completely agree with you that you need to consider the pathways of interaction parallel with Pharmacological properties to understand the selectiveness. It would be great if the selective pathways would be pinpointed explicitly, and those nonselective/selective corresponding to side-effects (often only with large doses) separately. My teacher says that use SmPCs to understand better PubChem. Do you know any source which collects SmPCs in one place?

@Masi - I'm afraid I don't know what SmPCs are. :(

SmPCs are Summaries of Product Characteristics found in most packages of drugs. Here is European guideline for them http://ec.europa.eu/health/files/eudralex/vol-2/c/smpc_guideline_rev2_en.pdf

US is enough, since I need to follow AAMI standards in my work that means US is the best choice. Thank you for the comment!  Is this the resource which you use http://www.pdr.net/ ?

@Masi - Yes, that's the one. Try to get your hands on a hard copy before subscribing, to make sure it will suit your needs.


text:
Why do we get runny noses in the cold?
The most annoying thing for me about being cold is a runny nose. Is there an advantage to having a runny nose when cold? What does having a runny nose achieve?

possible duplicate of What causes a 'stuffy' or 'runny' nose when you have a cold?

I added a duplicate badge to this question because I think the other question is better formulated. We do not get runny nose in the cold. We get runny noses when we have a cold. That is a big difference. I see this question as a very simplified question in Physiology which aims to explain difficult concept in Pathophysiology by concepts in Physiology.

I'd have to disagree with that. I get a runny nose when it's cold, even if I don't have a cold.

@jarlemag Yes, I agree that some people do get easily runny nose in the cold. Badly formulated sentence from me. My point is that the cause is not the cold weather. It is a secondary thing for the runny nose. Some people however do not get runny nose in the cold. The cold weather is not the cause itself - only a mechanism or a condition that triggers the runny nose.

Well, the important thing is that we both agree that someone can get a runny nose, when they are in a cold environment. I don't see a need to argue about the semantics of "triggering condition" vs. "cause". :-) Anyway, I vote to keep open as not a duplicate.

There are two reasons for this:

Nasal mucus helps warm inhaled air before it reaches the lungs. In cold weather, the mucus tends to dry out, so the membranes increase their production.
At the same time, exhaled air is warmer than the surrounding air, so it contains more moisture than the outside air can hold. This moisture condenses around the tip of the nose.

Explanation found here.
So there's no particular advantage to getting a runny nose; it's just a normal reaction occurring in extreme conditions.

Just to add, cold air has a lower capacity to solve water. Hence why cold air tends to be drier than warm air.

I do not agree with this answer. These are mechanisms, not the cause. I added a duplicate badge to this question because I think the other question is better formulated.

Rhinorrhea, or runny nose is a response used by our nasal membrane to get rid of foreign particles including pollen dust and infection. As such we get runny noses when we have a cold, allergy or are exposed to high densities of air-born particles. Cold air may irritate our nasal membranes, both because of temperature differences relative to our body and due to the lower amounts of moisture cold air holds. Cold air thus also results in a runny nose.

It would be great if you added some references to support your response!

There are definite advantages to getting a runny nose in cold weather. Rhinoviruses prefer cold weather and deploying large amounts of mucus is a good way to trap them (instead of letting them get in to infect the nose). Additionally, severe dry nose can cause nosebleeds and the mucus helps prevent this from happening.


text:
Decreasing the alcohol proof and faster in hangover, why?
My russian friend says that the USSR agents used/use the trick that they offered the victim first vodka and then last wine.
I have noted that this puts you faster to hangover: decreasing the alcohol proof.
Some people lose their motor function immediately and some their memory only.
Why does a decrease in the alcohol proof cause you a) faster intoxication and b) faster hangover?
Probably the change in the concentration of alcohol inside cells of brain tissue affects some parts of your brain like the cerebellum. I would like to have an explanation in Biochemistry.
Is there any truth in my friend's argument?

Are we speaking of faster hangover or faster intoxication? In the second case the answer is trivial I would say... in the former I wouldn't see the utility for a secret agent to do that

@nico I am interested in the both cases. I do not know why decreasing the alcohol proof causes faster intoxication. Can you please explain.

well, it's not the decrease, but the fact that if you start with vodka rather than wine you'll get intoxicated faster, as there is more alcohol in it.

@nico I am not sure whether your point is the case here. Like taking "shot, wine, shot, beer, shot" will get you faster down than "beer, wine, shot, shot, shot". I do not know why, but the changing alcohol proof seems to affect some structures in the brain or tissues that affect your motor functions or memory. So in the first, there are two decreases, while in the latter zero.

This has more to do with the person's tolerance to alcohol than the trick itself. People will be affected by different amount of alcohol differently. From personal experience in college, I have seen many people take several shots of vodka and still carry on a conversation. In the same night, I have seen others take a glass of wine and be out for the night.

Without supporting references only an expert in this area could evaluate your answer. Consequently, answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). ——— You may also wish to take the [tour] and then consult the help pages on the standards for additional advice on [Answer] effectively. Thanks!


text:
What is the maximum amount of different bacteria in the drinking water in Europe?
I am looking for a statistical amounts which are allowed.
Some students say it is 0 for all bacteria, which I think is false.
I found this USA source.
I found there

Total Coliforms (including fecal coliform and E. Coli) mg/l. No more than 5.0% samples total coliform-positive (TC-positive) in a month.
Giardia lamblia: 99.9% removal/inactivation.

What is the right place to look for such information?

According to a text I'll reference later, humans face larger risk with microbial contaminants that chemical ones. This is the reason why most water quality standards and guidelines (including who) recommend (or allow) 0 counts per 100 ml for bacterial indicators.

No, your colleages are right: There should be no coliforms in drinking water in Europe following the Council Directive 80/777/EEC.
This PDF from the Northern Ireland Environment Agency (which follows the directice mentioned above) shows this a bit nicer.
It makes sense, since coliforms are a sign of mixing sewage and fresh water. Nothing you want to have happening.
This is the relevant table from the linked PDF:


text:
How does activation of adenylcyclase lead to increased cAMP and diarrhea?
I am trying find explanation for these mechanisms

Tox plasmid -> exotoxin (enterotoxin) -> activation of adenylcyclase
  -> \up cAMP enterocytes -> release of H2O, electrolytes in gut lumen -> diarrhea.

Tox plasmid is a toxin generated by the genus enterobacteriaceae.
I read this as that exotoxin Tox activates adenilciclase enzyme (protein) which increases the amount of cyclic AMP in the enterocytes, and releases water and electrocytes into gut lumen consequently resulting in diarrhea.
How does the activation of adenylcyclase lead to increased cAMP heparis and diarrhea?

The crypt cells of the gut can actively secrete electrolytes (ions) via special channel which finally leads to water secretion. This is usually tightly controlled, since uncontrolled loss of water is obviously not good for the cells.
Have a look at this schematic figure, (from this webpage):

Sodium, Potassium and Chloride ions are co-transported into the cell,
sodium and potassium are transported back out via other channels.
If the adenyl cyclase is activated (for example by bacterial toxins,
cholera does this), then cAMP is made.
cAMP aktivates Protein Kinase A (PKA) which in turn phosphorylates the the Cystic fibrosis transmembrane conductance regulator
(CFTR)(this channel is also important for cystic fibrosis) which leads
to the secretion of chloride ions from the cell. This builds up a
negative potential across the membrane (positively charged ions are
missing).
This leads to the secretion of sodium ions through the tight
junctions, resulting in the netto secretion of NaCl.
The secretion of salt builds up and osmotic gradient across the
membrane, which leads to water secretion and can also lead to hyponatraemia.

To overcome this problems, the so called "oral rehydration therapy" is used. The solution contains of an isotonic solution of sodium chloride and glucose. This is taken up by the sodium-glucose symporter (a special class of transporter, that transports two molecules in the same direction) and builds up a gradient which is directed in the opposite direction of the diarrhoea, helping to fight dehydration.

What is netto secretion of NaCl?

I think the water goes inside cells wit the transport of Cl- ions. Then, NaCl accumulates in the cells. The gradient across the membrane may increase if the water does not follow enough Cl-. This then leads to the water secretion into the cells. Right? Since there is too much water in the intracellular space, more water stays in the extracellular space which then is released as diarrhea stools. Right?

No: Cl- ions are secreted through the CFTR channel. Then sodium is "secreted" through the tight junctions to neutralize the negative charge, which is building up on the outsite. The results in the net secretion of NaCl (which is of course still ionic and not there as a salt.

@DeNovo Thanks for the correction, I have edited the answer. BTW: In such cases it is perfectly ok (and also in line with the stackexchange philosophy) if you edit an answer (or question) to correct mistakes.


text:
Normal position of Electrical axis only in the III lead?
I found this sentence in my notes which is not exact enough:

Electrical axes

Excitatory processes have definite direction and magnitude and could therefore be represented as vectors. At any moment there are two
  points in the heart with the biggest potential difference, which is
  called electrical axis, characterized by the angel α.
Under normal conditions -> 30°< angel α < 90°
Electrical axis gives information about the position of the heart, where the normal position ([arrow to south-east]) represents the
  biggest amplitude in the III lead

What is the exact electrical axis and of what they are talking about?

@kmm This is not anymore discussion-type answer. I specified the question. Please, see also my answer to my question which clarifies something.

If your answer to the question clarifies it, then why not just edit the question?

The other question I have: Why do you permanently post questions and their answer within minutes? This is kind of absurd.

@Chris Because I like the Q&A style, and try to first improve the notes so well as I can and ask your opinion because I cannot be sure that I am right in my thoughts.

Ah, ok. Most of this is not my field of experience, though.

Let's consider the definition of the electrical axis.
The text does not specify which type of electrical axis and of what.
For instance, Guyton discusses Mean Electrical Axis of the Ventricular QRS only.
However, Guyton says that the mean electrical axis of the normal ventricle is 59 degrees.
In many pathological conditions of the heart, this direction changes markedly, sometimes even to opposite poles of the heart.
So the original author must have considered the Mean Electrical Axis of Ventricular QRS.
I would change the paragraph to

Mean Electrical axes of the Ventricular QRS

Excitatory processes have definite direction and magnitude and could
  therefore be represented as vectors. At any moment there are two
  points in the heart with the biggest potential difference, which is
  called electrical axis, characterized by the angel α.
Under normal
  conditions -> 30°< angel α < 90°
The Mean Electrical axis of normal ventricles is 59 degrees, which gives information
  about the position of the heart, and it represents the biggest amplitude in the lead III.


text:
How to deduce if RNA virus infection or DNA virus infection
Is there any general rule to say this must be RNA virus infection and the other one DNA virus infection?
Example of a case: 5 children develop a bright red rash on the face and turns violet after a few days and then disappears. Then maculopapular rash appears on the trunk, buttocks and extremities. It soon fades from the trunk but persists on the thights and forearms. Two children have also had a slight fever and a sore throat, but all were not terribly sick. What is the genetic material of the most likely causative agent?
Right answer is: Single-stranded DNA, since most probably causative agent is erythema infectiosum caused by parvovirus B19.
I do not want to remember all microbes by heart.
How can you deduce that this must be a DNA infection and probably single-stranded?

Regarding 1st q) I will wait in hopes that I'm wrong, but I think the answer is you can't. There is still a lot of work being done just show bacterial vs viral using host markers, let alone breaking down viral.  There would also be little clinical significance to knowing, other than epi.  I think this is why the red book is now in App form: you ID the pathogen, and then you can know more specifics about it. 2nd question is a totally different question that I would be happy to answer separately (unless someone who can answer 1 in the affirmative can tie them).

Just as an example of where you can't.  Let's say you have a PT with an URI. Most likely cause is viral. Could easily be RSV (-ssRNA), Adeno (dsDNA), HRV(+ssRNA), or any number of others (these were listed for types).  Just on the numbers your best guess is HRV, but that could easily be wrong.

@AtlLED The second question moved here: http://biology.stackexchange.com/questions/9934/how-can-a-respiratory-infection-lead-to-a-skin-infection You are welcome to answer. I want to know.

@AtlLED You're right, there's no way to tell. It's a false dichotomy based on the wording of this exam question.  This exam is actually asking us to consider a chain of three questions: What is the disease described; What causes this disease; and How does this causative agent store genetic information.  The instructor in this case assumes that if one can answer correctly the last question in this chain then one understands the first two as well.  In short, this more a matter of pedagogy than pediatrics.

@Gossar Off idle curiosity, what is the class you two are taking?  Seems like ID, but it's an interesting approach given the questions.

@AtlLED I'll have to let Masi answer that question; I'm not in a class with him.
Perhaps I should have phrased that previous comment differently.  The us there was an editorial we.

@AtlLED Microbiology course, 2nd year, in Medicine.

If you mean simply by looking at symptoms, then there is no way, especially if in the context of a medical visit.  You're better off learning the usual suspects and figuring out the patients risk and likelihood for a given infection.  A good example is Hepatitis.  Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) have similar (enough) outward symptoms, but the former is a DNA virus and the latter an RNA virus.  In fact, looking at enWikipedia's list of acute causes, it's all over the place!
If you can actually assay for it in the lab, then of course.  Although...


text:
Regional circulation and Cardiac output?
I am reading my study materials and think what is the systemic POV here

Regional circulation Blood flow within the tissue/organs based on the functional demands of the tissue.
      E.g. The blood flow to the brain should remain relatively constant from a systemic POV (13% of CO at rest).

What is the POV here?
Extension to the question and explanation.
The last part is just 13% of maximal cardiac output.

I'd guess venous P[O_2], maybe. Who gives abbreviations without a key? Although the suggestion of "point of view" make sense in context.

Use the homework tag?

Given the answer this is more of an English Language question than Biology so I'll close it.

This question appears to be off-topic because it is about an abbreviation commonly used outside of the field of biology.

It might be as simple as 'point of view'.

Thank you very much! I really sometimes get confused by the abbreviations used in my study materials.


text:
Which processes are during the latent period of ventricular contraction?
The latent period is the time between the start of depolarisation and the start of contraction.
I know that the contraction of ventricles starts after sufficient influx of Ca2+ and threshold potential is met.
The influx of Ca2+ is at start of Phase 2, so Phase 0 and 1 are included in the latent period.
Comparing to electrocardiogram is not simple, since there is always at least some time lag between the event and the recording.
I think there not much sense to compare cellular model events to ECG recordings here.
Which cellular processes does the latent period include?

During the latent period of ventricular contraction, excitation-contraction coupling takes place.
There may be other processes, but I think most are these from Wikipedia:

An action potential is initiated by pacemaker cells in the Sinoatrial node or Atrioventricular node and conducted to all cells in the heart via gap junctions.
The action potential travels along the surface membrane into T-tubules (the latter are not seen in all cardiac cell types) and the depolarisation causes Ca2+
to enter the cell via L-type calcium channels (also known as Dihydropyridine receptors) and possibly sodium-calcium exchanger during the early part of the plateau phase. This Ca2+
influx causes a small local increase in intracellular Ca2+
.
The increase in Ca2+
is detected by ryanodine receptors in the membrane of the sarcoplasmic reticulum which releases Ca2+
in a positive feedback physiological response. This positive feedback is known as calcium-induced calcium release and gives rise to Calcium sparks.
The spatial and temporal summation of ~30,000 Ca2+
sparks gives a cell-wide increase in cytoplasmic calcium concentration.
Contractile mechanism similar as in skeletal muscle about cytoplasmic calcium binding to troponin C and so on.

Note that to fully answer this question you should include figures about mechanisms of excitation-contraction coupling, cardiac action potential -figure and permeabilities of different ions.

The phases from the stimulus to the force contain latent period, contraction phase and relaxation phase. This applies to all muscles, not just muscles associated with ventricular contraction.
So the Latent period, about 5-7ms, contains the following:

skeletal muscle prepares for contraction

phase between stimulus and beginning of contraction (response)

the muscle doesn’t change length or tension

influx of Ca2+

inhibitory proteins of contraction:

binding to Troponin and removing Tropomyosin
Troponin: T binds with tropomyosin, I binds with actin, inhibits ATPase, C has high affinity to calcium ions.

ATPase activity increases

where some parts such as biomechanics is mostly ignored.


text:
Antihistamine's effect on insulin secretion and tiredness?
Antihistamines are known to cause tiredness.
The essential hormones of the body are insulin (glucose), parathyroid hormone (calcium) and aldosterone (Na-K ATPase, sodium).
I am thinking how this tiredness symptom can come.
There are so many different antihistamines so I am confused about the mechanism how they cause tiredness.

Histamine acts on parietal cells of stomach via H2 receptors to stimulate hydrogen ion secretion - cephalic phase.
Excess of antihistamines can lead to decreased acidity of stomach so change in conversion of pepsinogen into pepsin.
So less pepsin breaking down peptides and proteins.
Body has to do something else to break those components - and this consumes much energy and makes you tired.
Small mucus food mass stays in the intestines.
Delayed absorption.
Nutrients needed so liver has to work and make essential things - amino acids and something else.
Some waste management also may happen - because of tiredness.

Changes in blood sugar level.
Delayed most probably after food intake.
Very fast and fast insulin secretion mechanism starting during wrong times - all of the sudden.
So less insulin secretion cumulatively:

very fast mechanism - change of permeability of membranes (Na-K ATPase and sodium channels) reacting during times when not suitable - long after food intake
fast mechanism (phosphorylation of different things) happening more, since sympaticus apparently is not so inhibiting here
slow and very slow mechanisms however preferable (increased permeability of amino acids and mitoses)

So I think the tiredness of antihistamines is because of the increased amount of active fast mechanisms of insulin secretion, while less very fast mechanisms.
To carry the raw food mass in the intestines also require much energy.
What is the physiological mechanism behind the tiredness of excess antihistamines?

What class of antihistamines are you referring to? (Those used to treat allergic responses act against the H1 receptor, not the H2 receptor.)

Both, since I do not understand how the tiredness can come only through the receptor H1.

Thanks to studies on animal behavior and on histamine dection in the Central Nervous System, researchers found out the "histaminergic system".
It's thought that histamine-containing neurons regulate sleep-wake cyrcle, immunity, memory, body temperature, drinking, feeding rhythms. By the way, knockout rats who lack of histamine system don't show big defects in any function.
H1-Receptors for Histamine are distributed in the CNS and in the rest of the body. H1-antagonists (such as Promethazine, Chlorcyclizine, Loratadine...) have different effects on CNS, depending on dose. At conventional doses central depression appears and patients are sedated. They can even experience an antihistamine "hangover" in the morning, even if they take these drugs at bedtime. By the way, antihistamine overdose typically shows with convulsions.
The "non-sedating" H1-antagonists, or "second generation" have a lot less effects on CNS. They have polar chemical structure: they can not cross the blood-brain barrier.
By the way, a lot of typical and atypical anti-psychotic drugs have H1-antagonism effects on the brain (with H2 and H4 antagonism): their main goal is sedation to stop the patient from hurting himself (or others) during manic episodes.
So I think the last two sentences explain that sedation is almost a totally CNS-mediated side effect of antihistamine drugs.
H1-antagonists don't suppress gastic secretion, do not inhibit salivary, lacrimal or other exocrine secretions. Older H1-antagonists have an anti-colinergic effect on muscarinic receptors: they may reduce ACh-mediated secretions, typically in mouth and in the respiratory tree.
H2-antagonists are used to treat acid-peptic desease (as PPIs, proton pump inhibitors). CNS-related side effects are not commons, and include: confusion, delirium, hallucinations, slurred speech and headaches. These effects are mostly related with IV infusion of the H2-antagonist.
I just made a very small research on PubMed. I found this:
http://www.ncbi.nlm.nih.gov/pubmed/3529778
as you can see it is a study (on only 9 patients, in 1986), about insuline-glucose-Cpeptide and ranitidine (H2-antagonist) relations. Their conclusion is "Ranitidine significantly increased the area under concentration/time curves for glucose and insulin but not that of C-peptide. Our data indicate that ranitidine does not affect pancreatic insulin release nor peripheral glucose utilization and are consistent with the hypothesis that ranitidine influences the hepatic clearance of glucose and insulin both of which undergo high first-pass liver extraction."
I think that tiredness is a typical CNS-mediated side effects of H1-antagonists (anti-allergic) but is not a side effect of H2-antagonists (anti-acid). Maybe H2-antagonists affects insulin action via hepatic effects.
*I'm italian (sorry for any english mistake) and I am a last-year medicine college student.
I wrote trying to summarize some chapters (8, 32 and 45) of:
- "Goodman & Gilman's The Pharmacological Basis of Therapeutics" - L. Brunton, B. Chabner, B. Knollman - 12th edition; McGrawth Hill 2011

This is wrong statement: [second generation] antihistamines cannot cross the blood-brain barrier. They can! Particularly, they can in the old and special medication (Montelukast).