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Re: Tears

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  • Alain
    Hi, Greg, It seems to me that continual loss of amino acids in fresh or salt water represents a significant waste of resources. However, as all the
    Message 1 of 60 , Jan 22, 2013
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      Hi, Greg,

      It seems to me that continual loss of amino acids in fresh or salt water represents a significant waste of resources. However, as all the physiological effects activated in response to hormonal stimulation will continue for some time after being triggered, it may not be necessary to produce limbic tears continuously, but only periodically. By producing them at the most appropriate time we can limit losses and maximize the desired effects. The best time seem to me to be when the diver surfaces to catch his breath.

      As Cecil said: "... I spend a lot of time in (sea) with my eyes open, and it does not sting when immersed only when I resurface."

      Maybe it is the stinging sensation that happens when the diver surfaces, who is responsible of triggering the secretion of tears under limbic control. From this view point, during the dive, only basal tears are shed (they are cheaper). But the hormonal effects of limbic tears will persist until the diver's next breathing.

      Greg thank you for sharing your great work!



      --- In AAT@yahoogroups.com, "gcgiltmead" wrote:
      >
      > Here is the long, more detailed, explanation of how Limbic Tears protect the cornea from hypoxia, and thus are an adaptation to swimming and diving. Although all of the details of this are in the literature, I don't believe anyone put it together to reach this conclusion till I did last month. If they did they have not successfully gotten the word out.
      >
      > This is not in a publishable format. I can provide references but have not organized that yet. It's that new.
      >
      > The group consists of people from a wide variety of backgrounds and the ultimate goal is to explain this to the general public so I've attempted to write this so that people with limited scientific background can understand it.
      >
      > :)
      >
      >
      > Elaine Morgan correctly identified weeping as a characteristic of humans that is rather unique, and thus a candidate to be a trait stamped by our ancestors semi-aquatic phase. However, she mistakenly likened our production of copious tears to certain aquatic birds that excrete excess salt in their tears. She has since acknowledged that error but I continued to suspect that she was right, though for the wrong reason. More is known about tears now than twenty years ago which made my investigation of the matter easier.
      >
      > A possibility to consider regarding vision when swimming is refraction of light.  There is an elementary school experiment any sighted person can do where you stick a pencil in a glass of water, with at least a third of the pencil sticking out.  Looking down from above the pencil appears to be bent, but when you pull it out it is still straight.  Put it back in and it looks bent.  Slide your finger down the side of the pencil and you can feel it is straight.  This illusion is caused by refraction of the light as it passes from air to water.  Refraction occurs to some extent whenever light passes from one density to another, such as from a layer of corn syrup into a layer of water.  It also occurs when light passes from water to our tear layers.  This refraction is different than air to the tear layer so vision would be expected to be adversely impacted by going into water (fresh or salt).  Placing another layer of liquid between the tear film and surrounding water would generate two interfaces, both slightly different than that seen without this extra tear layer.  This could be a benefit of tears shed when swimming, but the idea has flaws.  Most obvious, the extra tear layer would have an inconsistent thickness making it unreliable.  I don't know enough physics to do the math on the refraction created by these various interfaces, but I frankly doubt there is enough benefit (if any) from this to produce the dramatic evolutionary changes that "psychic tears" are. The answer must lie elsewhere.
      >  
      > When ophthalmologists (eye doctors) refer to tears they start with the three layers of fluid that cling to the outside of the eye, specifically to the cornea.  The first concept that must be understood here is hydrogen bonding and hydrophilic versus hydrophobic chemicals.  Water molecules are polar molecules, meaning that the electrons spend most of their time around the oxygen nucleus rather than circling the hydrogen nucleus.  This causes the oxygen end of the molecule to have a relatively (but incomplete) negative charge and the hydrogen ends of the molecule a relative positive charge.  When exposed to other polar molecules their positive and negative ends attract each other, but since their is flux in the charges due to the cycling electrons the attraction is somewhat fluid.  When a polar molecule encounters a non-polar molecule (such as a fatty acid tail, composed of carbon and hydrogen atoms that share electrons fairly equally) there is no attraction and the molecules slide apart with the polar molecules drawn away if they find a polar atom to interact with.  Likewise, the non-polar molecules tend to clump together.  The polar molecules are called hydrophilic (water loving) and the non-polar molecules are called hydrophobic (water fearing) or lipophilic (fat loving).  One of the special properties of free fatty acids is that they have a polar end with a long lipophilic tail.  If these molecules are aligned properly they can form a neat layer with one side of the layer the polar heads and the other side the lipophilic tails so that they can stick to both lipophilic and hydrophilic molecules.  This is a basic molecular characteristic of living systems and the fundamental building block of cell walls.
      >  
      > The cornea itself is very hydrophobic/lipophilic so water or saline will not adhere to it.  Nature's solution is the Mucin Layer that coats the lipophilic cornea and provides a hydrophilic outside coating that allows water or saline to adhere.  The watery layer next to the Mucin Layer is called the Aqueous or Lacrimal Layer (I prefer Aqueous as Lacrimal can lead to confusion) and is key to not only moistening the cornea but also contains antibodies and other substances that are essential to the health of the eye.  The cornea is avascular (free of blood vessels) so the Aqueous Layer also plays a key role in bringing oxygen and nutrients to the cornea and carrying off waste products.  The Lacrimal Layer is covered by a Lipid Layer which appears to function as a seal of sorts, slowing evaporation of the Aqueous Layer and maintaining the thin film of tears over the cornea.
      >
      > Another function of the tear layer in addition to moisturizing, nourishing and protecting the cornea and outer layer of the eye is to create a smooth optical surface on the front of the microscopically irregular corneal surface.  Since the primary purpose of the eye is vision it is hardly surprising that tears actually participate in capturing a more accurate image.
      >
      > These three layers have three separate functions and each is secreted by a different gland: the mucin layer primarily from the conjunctival goblet cells, the lacrimal layer by the lacrimal gland and the lipid layer principally from the meibomian glands in the lids as well as some secretion from the glands of Zeis.
      >  
      > Aqueous tear production is also three separate processes: basal, reflex and "psychic" tearing.  Basal tears are those tears produced somewhat continuously to maintain the moisture, nutrition and health of the eye.  Reflex and "psychic tears" are released in larger volumes than basal tears so are not confined to the space between the two lipid layers but spill across the eye, and often down the cheek.  Reflex tears are produced in response to an irritant such as an irritating chemical or wind.  "Psychic tears" are tears we produce in response to emotions.  It is "psychic tears" that are of greatest interest here as they are rare or absent in most of the animal kingdom but a prominent feature of modern humans.  Although both reflex and psychic tears are produced by the lacrimal gland, reflex tears are produced in response to autonomic stimulation via the ophthalmic nerve (and inhibited by sympathetic nerves) while psychic tears are produced in response to stimulation from parasympathetic nerves which are believed to originate in the limbic system.  The limbic system is a somewhat nebulous complex of structures in the mid-brain that is involved in emotions, smell and memory.
      >  
      > Basal and reflex tears are believed to have a similar composition of water, mucin, lipids, lysozyme, lactoferrin, lipocalin, lacritin, immunoglobulins, glucose, urea, sodium, and potassium.  They differ in volume, reflex tears having much greater volume than basal when excreted ("psychic tears" being even more voluminous) and in what stimulates their production.  "Psychic tears" are different in composition containing about twenty five per cent more protein, especially the protein-based hormones prolactin, adrenocorticotropic hormone (ACTH), and leucine enkephalin. 
      >  
      > The issue of "psychic tears" in other animals is rather controversial and poorly studied.  A variety of animals including gorillas, seals and crocodiles have been photographed with a tear on the face.  I am not aware of any instance in which such a tear has been captured and analyzed to see if the composition is more consistent with reflex or emotional tears.  Having a tear is not the same as crying, but it does raise a valid question.
      >  
      > So those are the facts we start with.  The questions that need addressing are why do we cry, is there any other purpose for "psychic tears" other than expressing emotional stress and does this have anything to do with the AAT?
      >  
      > The popular explanation for why we cry is that it provides social benefits.  It is much easier to imagine humans developing a social response to crying than developing crying to generate a social response in others.  For a species to evolve a system that includes a separate nervous innervation and connection to the brain and an altered secretory function of the lacrimal gland to not only produce vastly greater quantities of tears but tears with a markedly different chemical composition in order to elicit an emotional reaction in others is really a rather preposterous idea.  Evolution occurs one step at a time. There is no imaginable advantage to selectively excreting prolactin, adrenocorticotropic hormone, and leucine enkephalin in response to emotional stress. This point is further emphasized by the claim by some that there is no function for these three peptides being in "psychic tears" and that modern science has here to fore not found ant reasonable explanation for their presence.
      >
      > Could it be that these "psychic tears" evolved for a different purpose and later evolved into the emotional tears we regard them as today?  After all, fish evolved fins to swim, not so that primates could grasp tree limbs a few hundred million years later. Consider the origin of the innervation involved in producing these tears; the stimulus originates in the limbic system.  The limbic system, also known as the Paleomammalian brain, is a fairly primitive part of the brain that is engaged in several functions.  It plays a key role in the formation of new memories.  It is intimately involved in olfaction (smell).  It is closely associated with the superior calliculus, which is a primitive optic cortex (as opposed to the optic lobes of the cerebrum).  The superior calliculus is engaged in detecting movement sensed by the eyes and directing the animals attention to the movement.  The limbic system is believed to be the center of emotional behavior.  Could it be that a system for flooding the eyes with tears of a different composition than reflex tears evolved which was controlled by the limbic system and was later hijacked by the behavioral aspects of the limbic system to generate emotional tears?  Such an origin could explain the different chemical composition of "psychic tears" and the need for such a large volume of tears when excreted.  It would not only require a minor adjustment to become hijacked during emotional outbursts but this could occur incidentally (picture intense emotions causing somewhat disorganized limbic stimulation, somewhat akin to a mini seizure, or perhaps a cross connection within the limbic system developed).  The later evolution of a sympathetic response, wether biological or learned, to the emotional tearing would be a single step rather than supposing six or more steps at once (an evolutional mathematic impossibility).
      >
      > Since "psychic tears" must have evolved from a non-psychic purpose I will use the more objective term "Limbic Tears" instead of "psychic tears" from here on.
      >
      > Is there any way to imagine a beneficial function for tears with the unique composition of Limbic tears cascading down the cheeks?  Absolutely not!  The purpose of tears relates to the eyes, not washing the face.  Yet within the context of a purely terrestrial evolution of the hominid line tears primarily run down the face, and their effect on vision is to make it blurry!  It is not possible for a complex system to evolve that has a clearly deleterious effect and no benefit!  Yet according to the terrestrial theories that is what we are left with.
      >  
      > What about the AAT?  An ape or hominid on land that shed psychic tears would normally be holding its head/face upright causing the tears to run down the face instead of across the eyes.  In fact, the lacrimal gland is situated on the inferior margin of the eye so the bulk of the tears don't even wash across the eyes before being shed or running down the lacrimal duct into the nose.  The only tears going over the cornea are ones backing up due to the volume produced.  A totally dysfunctional system.  If that same creature is swimming and sheds Limbic tears, the face would likely be facing down and the tears would have a slight tendency to pool up across the eyes.  Is there anything about tears that could make them useful to shed while under water?
      >  
      > While keeping the eyes, and especially the cornea, moist is essential, there is a fine line to how moist it must be.  Too much or too little water distorts the cornea and interferes with vision.  Fresh water is obviously hypotonic compared to human plasma.  Sea water is actually hypertonic compared to plasma.  Some believe that the intracellular salt concentration is the same as it was in sea water hundreds of millions of years ago when life began and that today ocean salinity is higher due to further accumulation over the eons. When swimming in fresh water, water will seep into the cornea causing it to swell, and making the eye more myopic.  When swimming in sea water, water will seep out of the cornea and it will shrink, causing the eye to become more hyperopic.  Within the context of the AAT it is hypothesized that our ancestors in a sea side environment survived by diving repeatedly to gather seaweeds and mollusks.  After a few hours of diving it would be expected that water would seep out of the cornea causing hyperopia, or farsightedness.  The real significance of this is the inability to see clearly up close.  When diving to gather food from the sea floor this would raise the risk of grabbing a sea urchin, scorpion fish or other hazard.  Such incidents would not be just inconveniences.  A scorpion fish sting can kill and a sea urchin spine can cause a serious infection.  Even if not fatal, not being able to gather food for a few days would endanger both the injured individual and any dependents. 
      >  
      > If a system evolved to secrete tears in response to diving, these tears would tend to form a layer over the eye which would decrease water loss from the cornea.  Since a system had already evolved for producing reflex tears in response to chemical stimuli, the stimulus for this more copious secretion would more likely come from the brain itself.  Diving does cause a degree of angst even among modern humans so the limbic system would likely have excitation with each dive.  It is a small step to have that limbic excitation result in autonomic stimulation that in turn becomes associated with excretion of a stream of tears by the lacrimal gland.  (The word stream is used in a relative sense compared to basal tears and not meant to be an actual stream any greater than normally associated with "psychic tears".)  A stream of tears is essential here as they would quickly dissolve into the vast expanse of surrounding water.  One detail to keep in mind here is that it is not required to keep vision normal, just good enough.  This is a classic case of "I don't have to be faster than the tiger, just faster than you". If individuals with this trait have a higher survival than those without it, it will become predominant.
      >
      > So what about the composition of Limbic tears?  The main difference from other tears is the presence of three peptides: leucine enkephalin, prolactin and ACTH.
      >  
      > Leucine enkephalin is an Endorphin, or naturally occurring opioid. It's value seems somewhat obvious as it has an anesthetic effect which could be valuable to reduce stinging when opening the eyes under water, but it is much more complicated than that.  Leucine enkephalin binds to delta opioid receptors.  While delta opioid receptors function like other opioid receptors in diminishing the perception of pain they have another effect that is more important here.  Delta opioid receptor stimulation mimics "ischemic preconditioning".  Ischemia refers to a lack of oxygen. Ischemic preconditioning is a phenomenon by which when a tissue is subjected to repeated brief episodes of ischemia (less than five minutes) that tissue develops resistance to more profound ischemia (meaning that the cells of the tissue are less prone to die under the stated conditions).  It has been studied primarily in relation to the heart but is by no means limited to cardiac tissue.  It is likely that this function of Leucine Enkephalin is related to stopping or delaying apoptosis which would otherwise occur in the aftermath of hypoxia. Apoptosis, which is initiated by Mitochondria, functions to remove damaged but still living cells as a first step in the regenerative process. When the cell dies during this process a variety of chemicals result in an inflammatory response. While this can be crucial to healing, it is often more damaging than the original injury. The bottom line is that exposure of tissue to Leucine enkephalin makes the tissue somewhat tolerant to ischemia or hypoxia via stimulation of delta opioid receptors.
      >  
      > Prolactin was discovered and is usually thought of as a hormone that stimulates milk production but it has a history among vertebrates far older than mammals and is know to have over 300 hormone like effects on various cells.  A prominent effect is to stimulate lymphocytes through cytokene receptors, but it is difficult to relate this to its presence in tears.  Prolactin also inhibits angiogenesis in the cornea.  Angiogenesis, or the growth of new blood vessels, within the cornea directly interferes with vision.  The most common cause of angiogenesis in modern humans is corneal hypoxia related to contact lenses.  It is not the contacts that cause the angiogenesis, but the hypoxia.
      >  
      > ACTH is usually thought of as the hormone that regulates the Adrenal Cortex.  It was first discovered in relation to Addison's Disease and Cushing's Syndrome and has been employed to stimulate release of steroids from the Adrenals for a variety of conditions.  However, ACTH receptors are not confined to the Adrenal Cortex but found throughout the body and especially throughout the brain.  Embriologically, the eye develops from the same neuro-ectoderm that gives rise to the central nervous system and thus is more closely related to neurons than other cell lines in some ways.  The adrenal cortex is derived from medullary tissue but during its early development neuro-ectodermal cells from the pre-adrenal medulla migrate into the pre-adrenal cortex and may account for the prominence of ACTH receptors in the adrenal cortex.  What role ACTH plays within the brain has not been well studied, but it does stimulate dopamine production and it is possible that it functions as a neuro-transmitter.  It is also likely that the function is somehow related to it's function in stimulating the adrenal cortex.  The hormones released by the adrenal cortex have several effects but prominent among them are their anti-inflammatory properties and elevation of glucose levels.
      >
      > Biochemically, ACTH triggers several processes when it attaches to ACTH receptors of various tissues. The immediate effect is to increase cAMP which activates Protein Kinase A. Protein Kinase A has several effects, prominent among them being to increase Glucose levels and increase Glycolysis. ACTH also stimulates Mitochondria to increase production of proteins used in oxidative phosphorylation. This does not directly increase ATP production but prepares the mitochondria to do so.
      >
      > These actions of ACTH combine to allow cells to increase anaerobic metabolism while preparing to increase aerobic metabolism, an ideal combination for dealing with transient hypoxia.
      >
      > Looking at it like a detective what we have is profuse tear production that protects the cornea from osmotic injury (wether in fresh or salt water) and three peptides that work together to make the cells of the cornea more tolerant to hypoxia, increase anaerobic metabolism in the cornea while preparing it for faster recovery from hypoxia and prevent neovascularization in response to hypoxia. All of this information is well established and readily available but no one has put it together simply because no one has considered the possibility that Limbic tears function to protect the cornea from hypoxia while swimming and diving.
      >
      > The cornea is a very thin avascular structure. It obtains oxygen by direct diffusion from the atmosphere.  The eyelids are thin and highly vascular so unlikely to cause corneal hypoxia even when closed for hours at a time. There is clearly much less oxygen in water than air which must lead to corneal hypoxia with diving and swimming. I know of no other common occurrence of pre-modern humans that would lead to corneal hypoxia.
      >
      > A final piece of evidence that Limbic tears protect the cornea from hypoxia is that contact lens wearers are more likely to suffer hypoxic corneal injury such as neovascularization if they have decreased tear production.
      >  
      > Do we shed tears under water?  Did our ancestors shed tears underwater more than we do now?  Do aquatic mammals shed tears under water?  Do other vertebrates? Do fish cry?  Why do people rub their eyes when they emerge from water? Is it to stimulate tear production or perhaps to remove excess tears? How can we test such questions?  Given time some clever person may figure out how to investigate those questions but for now it remains appears that our ancient ancestors did evolve a reflex to shed tears when under water to protect the cornea from osmotic injury and hypoxia.
      >  
      > The scenario proposed here is that when hominids or pre hominids began obtaining their food from the sea two of the hazards they encountered were distortion of the cornea from water molecules leaching out into the saltier sea and hypoxic injury of the cornea when diving repeatedly.  Most likely, they first gathered seaweeds and mollusks that were in close to shore and in shallow water.  Some of these might even have been gathered without dunking their heads under water.  Over the ages they would have had to venture further and dive deeper to obtain their food.  Two factors would have driven this process.  While the increasing scarcity of "low hanging fruit" would have required venturing out further and deeper, the evolutionary process would have simultaneously been equipping them with better adaptations to do so in a variety of ways.  Thus the stress on the eye from diving would have gradually become more intense over tens of thousands of years rather than all being encountered at once.
      >  
      > Producing copious tears of the same composition as reflex tears to combat the drying effect of sea water would likely have been the first adaptation.  This step would have had to be first as the three peptides needed a way to be carried to the lens before those adaptations could occur.  All that was needed to begin producing these tears was stimulation of the lacrimal gland to pump out greater quantities of what it was already making.  Parasympathetic innervation was undoubtedly already present so the pathway existed from the limbic system to stimulate the lacrimal gland.  Wether the first stimulus was related to fright or not is pure speculation but the creature who experienced it had a competitive advantage due to better preservation of near vision after repeated dives.
      >  
      > Once copious tears were being produced in response to the stimulus of diving the stage was set for these tears to carry other substances that would aid eye health.  As diving became not just more frequent but longer corneal hypoxic damage would have become more of a problem, with hypoxic induced neovascularization one of the most severe consequences.  Over time those individuals with higher levels of prolactin, ACTH and leucine enkaphalin would have experienced less corneal damage and thus better survival rates.  Eventually natural selection would have assured that the tears produced by limbic stimulation would be high in these critical substances.
      >  
      > There is no way to determine when this system was adapted to crying, but that change would also only require one change within the limbic system to occur once the rest of the mechanism had evolved to protect the cornea.
      >  
      > This scenario is a gradual step by step alteration of existing systems for readily apparent reasons by natural selection with at least six different traits evolving (including emotional tears or crying).  There is no imaginable reason for a purely terrestrial animal to have evolved to have prolactin, ACTH & leucine enkaphalin as prominent components of tears.  It is also unimaginable for five different genes (three of which are irrelevant to the process) to have evolved in this way to elicit an emotional response in others.  When seen this way, the nature of Limbic tears is powerful evidence in favor of the AAT!
      >
    • cecil tamang
      regarding amniotic fluid: http://www.ncbi.nlm.nih.gov/pubmed/7450565  http://www.ncbi.nlm.nih.gov/pubmed/2952913 this one is counter intuitive- lower levels
      Message 60 of 60 , Jan 28, 2013
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        regarding amniotic fluid:
        http://www.ncbi.nlm.nih.gov/pubmed/7450565%c2%a0

        http://www.ncbi.nlm.nih.gov/pubmed/2952913 this one is counter intuitive- lower levels of amniotic fluid endorphin in labour than before labour

        http://www.ncbi.nlm.nih.gov/pubmed/6318561 includes ACTH concentrations in amniotic fluid


        And no worries Greg regarding info on narcan- only curious.
        --cecil

         
        After ruminating on this a while, I am very impressed with the Prolactin role here. This may be an evolutionary step on the way to Prolactin being in Limbic Tears. I am always trying to look at new ideas with an attitude of "What might prove this wrong?" Each time such an investigation fails to disprove it and especially each time the challenge provides more evidence the hypothesis gets stronger.

        It's been >20 years since I stopped doing newborn care. I will need to see if Narcan is still used that way today, but I've seen it work. I am going to be very busy with other stuff the next 10 days, but if I don't get back to you (Cecil) privately in a couple weeks please remind me. You make a good point regarding endorphin levels, but do we know what the levels are in amniotic fluid? There's more to this and I will keep working on it as time permits. Too much speculation right now, but making progress.

        It's so helpful to collaborate. This concept raises lots of questions and the ones brought up by the group have helped!

        Greg

        --- In AAT@yahoogroups.com, cecil tamang wrote:
        >
        > Thanks for this Greg, very interesting.
        > Prolactin in certainly present in amniotic fluid http://www.ncbi.nlm.nih.gov/pubmed/1280539, but endorphins in newborns I would assume come directly from placental circulation rather than diffusing into amniotic fluid, and besides we would expect highest levels around birth which would still leave the last 15 weeks of gestation unprotected by that mechanism. 
        > I have never heard of Narcan being used unless opiates have been administered in labour- it is certainly not common practice here (NZ)  do you know if this has been studied? please feel free to answer by personal email if you wish, as this is pretty tangential to AAH c_tamang@...
        > Thanks again for your thorough answer!
        > Yours, Cecil
        >
        >
        > ________________________________
        > From: gcgiltmead
        > To: AAT@yahoogroups.com
        > Sent: Saturday, January 26, 2013 9:55 PM
        > Subject: [AAT] Re: Tears
        >
        >
        >  
        > Fascinating question Cecil, and one I hadn't given any thought to. I think it is very relevant.
        >
        > The lens is not on the surface of the eye until near the end of the first trimester. By then the hyaloid vessel, a branch of the ophthalmic artery, has developed. It runs straight through what will become the vitreous and supplies the lens and nearby tissue. This vessel breaks down around 25 weeks gestation and is pretty much gone by birth. Those last 15 weeks of gestation are the focus of this question. By then the lens is present and avascular, and the (human) eyelids can open.
        >
        > The adult lens has over 5,000,000 cells. At the start of the third trimester the lens has less than 1,400,000 cells and the number does not increase much by birth. Most of the growth and development of the lens occurs prior to the hyaloids vessel breaking down.
        >
        > I have not found a reference that directly addresses what happens during those last 15 weeks, but I agree that the lens probably is relatively hypoxic. My guess is that a combination of a low metabolic rate within the lens (it is not growing then) and its small size, which makes it easier for O2 to diffuse through it, allow it to tolerate the hypoxic state of being bathed by amniotic fluid. However, hypoxia is a poisonous state that leads to the accumulation of substances that can trigger an inflammatory response and apoptosis. Fetuses are undergoing vascularization all over so I also expect that there would be a high propensity to develop neovascularization of the lens in the third trimester. Mediators are needed to block these adverse consequences of hypoxia.
        >
        > Maternal Prolactin levels are high in late pregnancy, and it crosses the placenta so should be present in amniotic fluid. I expect the placenta plays a role in producing other mediators that protect the lens. Leucine Enkaphalin could be present. It is an endogenous endorphin. Near term fetuses have significant levels of endogenous endorphins. I have personally resuscitated
        > a number of newborns and Narcan, an opioid blocker, is often effective in stimulating respirations even in newborns whose mothers have received no opiates. The theory behind its use is that the fetus has high endogenous endorphins physiologically, to help tolerate the birth process. I don't see the functions of ACTH being as useful with chronic hypoxia. There remains the possibility of other mediators.
        >
        > Once again, this can be tested. It would not be complicated to test amniotic fluid for these two substances. It would also be interesting to know what the glucose level is in amniotic fluid. The cell's alternative to aerobic generation of ATP is glycolysis.
        >
        > The very fact that the lens seems to suspend growth and development in late pregnancy is unexpected evidence. This is admittedly a somewhat circular argument as it must suspend growth and development after losing its blood supply when the hyaloid vessel breaks down. That raises the question, what happens in fish and amphibians?
        >
        > --- In AAT@yahoogroups.com, cecil tamang wrote:
        > >
        > > Hi Greg,
        > > More out of interest than anything else, is hypoxia of the cornea an issue in utero? You suggest that the highly vascular nature of the eyelid is enough to maintain oxygenation when eyes are closed. But except in species whose eyes are sealed at birth, according to your logic the foetal cornea would be exposed to potential hypoxia whenever the eyes are open in amniotic fluid. If it is a problem, it is obviously dealt with by some other mechanism besides tears (maybe something in amniotic fluid?), given the delay in production of tears in human newborns- (4 weeks for 'limbic' tears to reach adult levels, but usually much longer than that for noticable tear flow. Also delayed tear production with prematurity). and the presumed total lack of such tears in most other mammals.
        > > partial answer to my question of the other day if you are interested: http://www.ncbi.nlm.nih.gov/pubmed/12036663
        > >
        > > http://www.ncbi.nlm.nih.gov/pubmed/16354631
        > >    Curious if you have any thoughts, though as I said probably has no bearing on you ideas. Anyway newborn visual acuity is not particularly necessary, as our basic newborn ability to crawl to the breast and self-latch appear to be guided by smell.
        > >
        > > Another thing:
        > > in the discussion of leucine enkephalin as potentially reducing stinging of the eyes in water, just throwing in my observations: I spend a fair amount of time in (sea) water with my eyes open, and it doesn't sting when submerged, only when I resurface. This can sometimes be a very potent motivator to keep swimming underwater!
        > > .
        > > Ok thanks, Cecil
        > >
        > >
        > >
        > > [Non-text portions of this message have been removed]
        > >
        >
        >
        >
        >
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