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Tears

 

AAT Group discussion and theories from January 2013

Though I've been interested in the AAT for >10 years and was referred to this group 5 yrs ago I finally got motivated to join after researching psychic" tears.

This subject got Elaine Morgan a lot of criticism, but when I read her view of it I kept saying her conclusion is wrong (about tears being used to excrete salt) but there's something there. Being a physician with a background in biochemistry I approached the question from a different angle.

When I began researching it I thought maybe tears played a role in light refraction but I stepped back & just studied the (Ophthalmology) literature before reaching conclusions. What I found stunned me!

Both "psychic" and reflex tears are produced by the lacrimal gland, but reflex tears are made in response to noxious stimuli and produced in response to autonomic stimulation via the ophthalmic nerve while "psychic" tears are produced in response to stimulation from the brain's limbic system via parasympathetic nerves.

Seeking objectivity regarding what "psychic" tears really evolved for I prefer to call them Limbic Tears.

The most significant difference between reflex tears and limbic tears is the presence of significant amounts of three peptides in limbic tears: Prolactin, ACTH and Leucine Enkaphalin. According to the Ophthalmology literature, these three peptides have no function in tears and their presence there is a mystery. Saying natural systems do something for no reason always strikes me as arrogant and ignorant so that caught my attention.

It turns out that each of these three peptides works in a different way to protect the Cornea & Lens of the eye from hypoxic injury.

A key factor here is that the Cornea & Lens of the eye are avascular and depend on Basal Tears to deliver oxygen and nutrients. The oxygen is transferred from the atmosphere, not blood.

Today, hypoxic damage to the cornea is usually caused by contact lenses. More than 100 years ago the most likely circumstance to subject the cornea to hypoxia was swimming and diving. Infact, I can think of no other situation in which the cornea and lens would be subject to hypoxia while the rest of the body is spared!

Being new to the group, I don't know if this is old hat or news to you so I will await comment before saying more...

Greg

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@ Marc: Yes. there are 3 types of tears: Basal. Reflex & Limbic. Details 1/19. As to the reports of "weeping" in Gorillas, Elephants, Seals & Crocodiles, I believe these are observations of tears. No one has ever analyzed them to see which type they are. It is a huge question; but it is testable!

@ Cecil: Reflex and Limbic Tears have different chemical compositions and are produced via different nervous stimulation. They are completely separate even though both come from the Lacrimal gland, kind of like an auto factory making cars and trucks. As to when each function is mature, I doubt anyone has looked. As to "Do we shed tears under water"; that is the 64 million dollar question, and a hard one to test. More to come. The question regarding other species is also a big key. Do fish have tears? I think they must but again I don't think anyone has ever asked before, at least not anyone but philosophers and comedians.

I did stretch the point regarding the Lens as it is not proven that the Lens gets O2 from osmosis through the Cornea but that is a more direct route than through the vitreous and the SpO2 in air is much higher than in blood. There is no question regarding O2 delivery to the cornea.

I believe that this issue provides tremendous support for the AAT and is therefore very important. It is also important because it is testable (though I do not have the resources to do that). It also has significant potential spinoff value; which could attract dollars for research. As an Emergency Physician I am intrigued by the thought that an infusion of Prolactin, ACTH and Leucine Enkaphalin might prevent cell death in the hypoxic penumbra around the infarcted area in a stroke. Preserving that tissue is the target of a tremendous amount of research today and the methods we are using are of limited value and very dangerous. I can imagine Big Pharma pumping millions into research on this, and answering some of our questions in the process.

Because Reflex Tears and Limbic Tears have different compositions it is possible to collect a small sample and test it to see which type is being shed. I think this could be done with just a capillary tube, less than a ml. That means we can actually find out if a non-human shedding a tear is shedding reflex or limbic tears. That's a tremendous opportunity for a grad student! The species most likely to be useful for this seem to be seals and crocodiles.

I am also wondering why people rub their eyes when we come out of the water. It seems to be reflex behavior. Does the rubbing stimulate Limbic Tears? And how much tear fluid is needed to provide protection from hypoxia?

What about fish and amphibians? They do have a mucus film over their eyes. Has anyone explored its composition? How do fish get enough O2 to their corneas?

Lots of far reaching questions remain, but unlike many other AAT issues most of these can actually be tested in a lab.

Then there is the question of what does this mean to the AAT? A wading animal or one that swims a little has no great need for this trait. This is the trait of a diving animal, such as one that gathers shell fish and sea weeds from the sea bed.

Lots to ponder and I am very interested in others thoughts/info. I will post a detailed explanation of the tears issue this weekend.

Greg

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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.

Alain

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Excellent point and I agree 100%!

Most people rub their eyes when we surface or emerge from water (or even a shower). I hadn't given that any thought till after posting, but some comments here brought it to light. I tried to pay attention to exactly how we rub our eyes when I was swimming 2 days ago. Rather unscientific but it seems like I was rubbing across the upper 1/2 of the eyelids, where the lacrimal gland is located. Maybe that stimulates limbic tears. This can be tested so if we generate enough interest we will get an answer.

Greg

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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!

GCGiltmead

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Some comments:

"... the lacrimal gland is situated on the inferior margin of the eye ..."
Is this so, Greg? I thought on the upper margin? What about this in other tetrapods?

"... Some believe that the intra-cellular 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."

You mean the inter-cellular Na+concentration?
IIRC the theory of sea-water having been 4 x or so less concentrated 500 MA or so has been abandoned, it's now generally thought that fishes-tetrapods at some time had fresh or brackish water ancestors.

______

Excellent thinking, Greg, but producing a large amount of tears would mean a loss of energy.Perhaps there evolved (cf outside the water) a double system underwater:
- basal underwater secretion, protecting against continuous osmotic, refractory, hypoxic etc problems in sea &/or fresh water,
- "real" tears against/after certain dangers underwater (eg, you mention sea-urchins & scorpion-fish) containing enkephalins, ACTH etc. (explaining the emotional component & the connection to crying).

Sea-urchin > copious tears + Leu-enkephalin, ACTH etc. + crying aloud.
Tears post-aquatically became a sign of distress, calling for mother or father.

Thanks a lot, Greg!

--marc

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Thanks for the feedback Marc. Yes those two points are in error.

The Lacrimal Gland IS on the upper margin of the eye, which does make it more efficient. Just have to strike most of that paragraph. It was a nebulous and insignificant claim anyway. I guess that's the price of rushing something out when sleep deprived.

Yes, extra-cellular fluid. Reflex tears have a composition similar to serum, not to intracellular fluid.

I'll consider the London Conference but I live in the US and the cost of attending is significant. What about sending a poster?

Greg

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Marc Verhaegen wrote:

What are the dangers for the eyes themselves when diving? any ideas? --marc

_________

Off hand I see 3 types of dangers:

1) Chemical; depending on wether one is in fresh water salt water, water molecules move into or out of the lens which distorts its shape as discussed. In modern times we do see chemical contaminants (mostly petro-chemicals) cause problems occasionally but this was not an issue even a couple hundred years ago.

2) Biological: Organisms in the water can infect the eye tissue. All 3 types of tears contain antibodies (mostly IgA) to reduce this risk. As a physician I can say that eye infections are not normally associated with swimming, even in nasty polluted water.

3) Hypoxia, as the avascular lens depends on direct diffusion of oxygen from the atmosphere.

Greg

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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

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Sorry for the delay, I am just back from a 2 week road trip & had not been on the site for a while.

I have been researching this question for the last 3 years and hope to submit my findings in an article titled "The Meaning of Tears" for publication next week. That process may take a while and in the meantime I need to be careful what I say so as to not violate any publication requirements. One of the biggest barriers to getting the paper accepted may be that my conclusions are completely novel, you will not see them anywhere else, and that requires a long paper to document it all. I was inspired to do this by Elaine Morgan, who got it wrong but I couldn't get out of my mind her suggestion that emotional tears originally evolved for a non-emotional purpose and where later hijacked. I am convinced of that now! As Marc said it is very complicated (and very different than what I originally expected). I will simplify things and leave a lot out, then comment on stuff not in my article.

A key to understanding tears is that the cornea of land animals is completely avascular. It gets its nutrients and eliminates waste via tears and gets its oxygen directly from the atmosphere.

To start, there are 3 types of tears. Basal tears are produced at a constant rate by a couple different tear glands and provide lubrication and nutrition to the cornea. What has been called "reflex tears" are produced by the lacrimal gland in response to sympathetic stimulation and are chemically the same as basal tears. They simply flush the eye in response to various irritants. There are numerous receptors on the cornea that trigger sympathetic tears including one that responds to fresh water and one that responds to salt water. The sympathetic tears shed when water gets on the cornea maintain the osmotic state of the cornea so it is less prone to swelling or shrinking, which distorts vision. The third kind of tears are traditionally called "emotional tears" and are made by the lacrimal gland in response to parasympathetic stimulation. Parasympathetic tears contain a large amount of 3 proteins that are scarce in other tears. The literature
states they have no function. The literature also states that all mammals shed parasympathetic tears yet claims they are shed in response to stimulation from the limbic system of the brain in response to emotions. Largely true in humans, this is wacko for most species. It is these Parasympathetic tears that we are interested in. That is where I began sorting out the info, some of which we discussed here a couple years ago. Input from this group and at the London conference were vital to figuring some of this out.

The paper is over 6,000 words but the conclusion is that the lacrimal gland produces tears in response to parasympathetic stimulation as a previously unrecognized component of the Diving Response and that these tears protect the cornea from hypoxic injury when under water. The 3 proteins are the key to preventing apoptosis of cells in the cornea from temporary hypoxia.

The article goes into great detail on the neuroanatomy of this. The brainstem nucleus that initiates parasympathetic lacrimal stimulation is the Lacrimal Nucleus. It may be activated both by stimulation of the same receptors that initiate the diving response and by a neural tract from the thalamus which has been believed to be the way limbic stimulation triggers it. However, this tract originates from a nucleus within the thalamus which is intimately involved in a variety of aspects of the diving response.

This whole thing has repeatedly reminded me of the struggle to get people over their prejudices in seeing the merits of the AAT as similar prejudices are why there is significant misunderstanding of the tear mechanism!

The rest of this is not in the article and needs lots of research as it is mostly speculation, but it pertains more directly to the Elephant tears question.

I believe this mechanism for protecting the cornea from hypoxia evolved at about the time that vertebrates emerged from the sea. Vision is much more effective in air than in water so was very useful but major changes were needed in the tear film to avoid drying and to adapt to the different optics of vision in air, including the water/air interface at the cornea which is a minimal issue under water. At the same time these amniotes went back into the water frequently. The adaptation to getting O2 from the atmosphere allows a higher metabolic rate in the cornea so is a good trait, but that makes the cornea vulnerable to hypoxic injury when under water. Thus this complex adaptation should have evolved by the time amphibians emerged.

Mammals are mostly land animals and the aquatic and semi-aquatic mammals evolved from ancestors that were land animals. Millions of years of selection occurred before some of us (mammals) returned to the water, though this happened several times.

Now some real speculation. When a species returns to the water part time it will benefit from increased flow of parasympathetic tears, both in volume and frequency. This requires a change in gene expression (epigenetics) not the genes themselves (and there are a bunch involved here). One important factor is that neural pathway from the thalamus. It is well established that various aspects of the diving response are modulated by input from the thalamus. Some of these aspects can even be voluntarily controlled by higher centers in the brain (breath holding for example). As such higher control of a trait evolves it requires more connections with higher brain centers. No surprise that new functions develop (consider something as far off as breath holding when bearing down to move one's bowels, this likely has a degree of connection with the diving response, which may explain why the pulse drops with voiding). This type of mutation probably happened
to bring about our human triat of weeping.

So back toward the elephant. A single tear on the face has been documented in many mammalian species but is meaningless as it could easily be a sympathetic tear. Frequent shedding of tears that overflow the eyes is well known in several species such as seals, hippos and elephants. To my knowledge ALL of these species are either semi-aquatic or have a semi-aquatic ancestor in their fairly recent evolution (elephant).

So why did this tortured elephant cry? He is not the first documented case, though maybe the best documented. Intense emotion causes rather diffuse stimulation of the mid brain (which includes the limbic system and the thalamus). People and other animals are known to sweat, urinate and deficate in response to happiness, fear and pain. My belief is that this poor animal had diffuse and marked mid brain stimulation and that since elephants have a well developed parasympathetic tearing system as a result of their evolutionary background, prominent tearing resulted. The same event in a camel would not be expected to cause prominent tearing as it does not have such a robust parasympathetic tear system.

I think that is also the answer to why humans weep, and is another brick in the wall of evidence for the AAT.

Greg

< Re: Other past semiaquatics - a crying elephant?
Wed Jul 9, 2014 4:22 pm (PDT) . Posted by:
"Marc Verhaegen" aquape
Greg Jones (who posts here regularly) knows everything about protective (in
or outside salt or fresh water), emotional etc.tears. It's quite complicated
stuff. --marc



Elaine Morgan touched on other mammal species being "over looked" past
semiaquatics, as she argued humans were. I have seen biological families
like elephants, rhinos, tapirs, suids and shrews being mentioned in the
debate as potential past or present semiaquatics. Elephants seems to be the
best supported by fossil evidence, e.g. back to the hippo-like Moeritherium
37 mya.

Another thing Elaine touched on was human emotional tears being an aquatic
"marker", originally citing e.g. sea birds exuding wast ammounts of salt
water from their eyes. Personally, I remember a documentary of a large sea
turtle having laid eggs on the beach, being studied by biologists while held
captive for a short while, and then from the stress of the situation exuded
a form of thready slime from its eyes. If human tears are somehow an aquatic
remnant, other possible past semiaquatics would cry also as an aquatic
marker.

http://www.news.com.au/world/indian-elephant-raju-cries-after-50-years-in-captivity-during- rescue-by- wildlife- sos/story- fndir2ev- 1226983355252


This news story reminded me of this. A male Indian elephant was rescued by
Indian activists from quite brutal human captors, who had kept it chained
for years in a quite inhuman (hm!) fashion. The third picture listed in the
article shows the male just as it's leg chains (having invert spikes!) is to
be removed, and shows tears rolling down from its eyes.
Quote: "'The team were astounded to see tears roll down his face during the
rescue,' Pooja Binepal, of Wildlife SOS-UK, told the Daily Mirror."
(And in the last picture, we see another potential aquatic marker in
elephants, which we also share with them: Their bathing behavior.)

Are there any further studies into emotional tears in elephants or other
past semiaquatics? Or can such "stress tears" occur generally in any
species?

 

Thanks a lot, Greg, splendid.
I summarise a bit:

The cornea of land animals is completely avascular:
- nutrients & waste via tears (role of circulation),
- O2 directly from the atmosphere.

There (in all mammals? --mv) are 3 types of tears.
- Basal tears are produced at a constant rate by a couple different tear
glands, to lubricate & feed the cornea.
- (Ortho)sympathic (OS) or "reflex" tears flush the eye in response to
irritants, produced by the lacrimal gland (OS), chemically the same as
basal tears, triggered by numerous receptors on the cornea (incl.one
responds to fresh water, one to salt water). OS tears shed when water gets
on the cornea to maintain the osmotic state of the cornea (to prevent
swelling or shrinking, which distorts vision).
- Parasympathic (PS) or "emotional" tears are made by the lacrimal gland
in response to PS stimulation. PS tears contain a large amount of 3
proteins that are scarce in other tears. The literature states they have
no function, and that all mammals shed PS tears, yet claims they are shed
in response to stimulation from the limbic system in response to emotions.
Largely true in humans, this is wacko for most spp. It is these PS tears
that we are interested in. That is where I began sorting out the info,
some of which we discussed here a couple years ago. Input from this group
& at the London conference were vital to figuring some of this out.

The paper is over 6000 words.
The conclusion:
- the lacrimal gland produces tears in response to PS stimulation as a
previously unrecognized component of the Diving Response,
- PS tears protect the cornea from hypoxic injury when under water.
The 3 proteins are the key to preventing apoptosis of cells in the cornea
from temporary hypoxia.

The article goes into great detail on the neuro-anatomy of this.
The brainstem nucleus that initiates PS lacrimal stimulation is the
Lacrimal Nucleus.
It may be activated both by
- stimulation of the same receptors that initiate the diving response,
- a neural tract from the thalamus which has been believed to be the way
limbic stimulation triggers it.
However, this tract originates from a nucleus within the thalamus, which
is intimately involved in a variety of aspects of the diving response.
This whole thing has repeatedly reminded me of the struggle to get people
over their prejudices in seeing the merits of the AAT:
similar prejudices are why there is significant misunderstanding of the
tear mechanism!

The rest of this is not in the article and needs lots of research as it is
mostly speculation, but it pertains more directly to the Elephant tears
question.

I believe this mechanism for protecting the cornea from hypoxia evolved at
about the time that vertebrates emerged from the sea.
Vision is much more effective in air than in water, so was very useful,
but major changes were needed in the tear film to avoid drying & to adapt
to the different optics of vision in air, including the water/air
interface at the cornea (which is a minimal issue under water).

These amniotes went back into the water frequently.
The adaptation to getting O2 from the atmosphere allows a higher metabolic
rate in the cornea, so is a good trait, but that makes the cornea
vulnerable to hypoxic injury when under water.
Thus this complex adaptation should have evolved by the time amphibians
emerged.

Mammals are mostly land animals, and the aquatic & semi-aquatic mammals
evolved from ancestors that were land animals.
Millions of years of selection occurred before some of us (mammals)
returned to the water, though this happened several times.

Now some real speculation.
When a species returns to the water part time, it will benefit from
increased flow of PS tears, both in volume & frequency.
This requires a change in gene expression (epigenetics), not the genes
themselves (and there are a bunch involved here).
One important factor is that neural pathway from the thalamus.
It is well established that various aspects of the diving response are
modulated by input from the thalamus.
Some of these aspects can even be voluntarily controlled by higher centers
in the brain, eg, breath holding.
As such higher control of a trait evolves, it requires more connections
with higher brain centers.
No surprise that new functions develop (consider something as far off as
breath-holding when bearing down to move one's bowels, this likely has a
degree of connection with the diving response, which may explain why the
pulse drops with voiding).
This type of mutation probably happened to bring about human weeping.

So back toward the elephant.
A single tear on the face has been documented in many mammalian spp, but
it could easily be an OS tear.
Frequent shedding of tears that overflow the eyes is well-known in several
spp, eg, seals, hippos, elephants.
AFAIK all of these spp are either semi-aquatic, or have a semi-aquatic
ancestor in their fairly recent evolution (elephant).
So why did this tortured elephant cry?
He is not the first documented case, though maybe the best documented.
Intense emotion causes rather diffuse stimulation of the mid-brain: limbic
system, thalamus etc.
People & other animals are known to sweat, urinate & defecate in response
to happiness, fear & pain.
IMO this poor animal had diffuse & marked mid-brain stimulation:
since elephants have a well-developed PS tearing system as a result of
their evolutionary background, prominent tearing resulted.
The same event in a camel would not be expected to cause prominent
tearing, as it does not have such a robust PS tear system.
I think that is also the answer to why humans weep, and is another brick
in the wall of evidence for the AAT.
Greg

:-) Thanks a lot, Greg.

Tears can have different functions (not only cornea-protecting), eg,
shedding of waste products after a stress period, eg, corticoids?
= why we weep after stress??

Could there be 4 types of human tears IYO: basal & protecting, in & out
the water?

--marc



 
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