Extinct Species

                 I listened to a podcast the other day about the pros and cons of zoos.  As with just about everything nowadays, it’s a controversial topic.  Unfortunately, it’s hard to land in a place of knowing exactly what you’re talking about when you’re basing your opinions on feelings.  I feel like that on just about every controversial topic known to man.  So, I'm not going to put up opinions.  Instead, I’m going to offer you some of my experiences with zoos, some pros and cons, and talk about one success story that just warms my heart.

                The last time I visited a zoo was about two years ago.  I live ~ 3 miles from the Philadelphia Zoo.  With its giant Zoo Balloon floating over the river as a serious advertisement, I was drawn to go for the third time.  The zoo had recently opened their new Big Cat Falls exhibit (sponsored by some company – it changes and I’m not about to perpetuate the advertisement here).  Lions are my absolute favorite so I was pretty psyched.  

This new enclosure is supposed to mimic their natural habitat as best as possible.  The male lion, Merlin, and his three female companions, in addition to the jaguars, leopards, pumas and tigers, can frolic among large rocks, waterfalls, and fallen trees.  The lions are also miked in some way so that we can hear them roar (or grumble, as the case may be).  It was an impressive and overall happy experience.

Following the lions, we saw the lone polar bear.  This is where my heart broke.  It was 90 degrees and hovering at 90% humidity.  That bear looked sad, confused, and mostly especially, hot.  All the animals, which came from everywhere on the globe, were subjected to the climes of Philadelphia – meaning summer highs of 95 degrees F and winter lows of 20 degrees F.  The polar bear had to deal with the Philadelphia summer just as much as the African lions have to deal with the winter cold.  The zoo’s website claims the big cats are fine with it, but they do heat some of the rocks so they have a warm place to hang out during the cold days. 

Are zoos bad for animals?  In the case of elephants, zoos were ultimately deemed to be bad.  Elephants are quite social and like to walk long distances each day.  The small pens were not conducive to them and a movement was started several years ago to close all elephant exhibits.  I was able to see the Philadelphia elephants before they were re-homed in 2007.  Figure 41.1 is a picture of Petal, Callie (African elephants) and Dulary (Asian elephant) in their old pen.  Beautiful animals.  They are now in Tennessee and Baltimore and (according to reports) are happier.  Elephants are hardly the only animals to suffer in zoos, unfortunately.  Some develop weird, repetitive behavior that is only seen in captive animals.  So far, only elephants have received the push to be removed, however.

On the flip side, zoos do allow us to see animals we may not have an opportunity to view otherwise.  In this way, zoos offer an educational experience.  They also are highly involved in conservation projects around the world and have played a key role in re-introducting extinct species back in the wild.  Case in point: Père David’s Deer.

Have you heard of these animals?  I had not until yesterday.  You can see a picture of them in Figure 41.2.  Aren’t they amazing?

Elaphurus davidianus (Père David’s Deer) was originally found in East Asia, but was extinct in the wild before the close of the 19^th century.  Interestingly, from 1890 to 1900, the 11th Duke of Bedford collected the remaining deer from Berlin, Paris, and Antwerp and created his own herd at Woburn Abbey in England.  By 1945, this collection had grown from 18 deer to 250.  

These deer were then transferred to other reserves and zoos throughout the world with eventual reintroduction to the wild.  Beginning in 1985, three separate herds of deer were introduced into China at Beijing Père David’s Deer Park, Dafeng Père David’s Deer Nature Reserve, and Shishou (Tianezhou) Père David’s Deer Nature Reserve.  As of 2005, over 1500 deer are now living in these parks and maintaining their own populations.  Genetic diversity among the deer is still low, but scientists are working to develop ways to increase it among the current populations and any future reintroductions.

Accordingly to Soulé et al and Frankham et al, thousands of terrestrial vertebrates may require captive breeding programs with subsequent reintroduction in the next 200 years to stave off extinction.  

One of the issues I always consider when looking at animals in zoos is whether they accurately represent the animal in all ways.  Sure, we can look at a gorilla.  We can appreciate its size and its features, but does it actually act like a gorilla when in captivity?  Are we really looking at a fully functional gorilla or a nice replica of what the animal merely looks like?  How much of their natural disposition is removed and/or bred out by living in zoos?

Père David’s Deer were actually studied to this effect.  In a paper published by Li et al in August 2011, the deer were subjected to various pictures and sounds of common animals and natural predators.  The scientists wanted to know if, after years of captivity, the deer could still respond to their natural predators with fear and caution.  

Interestingly, they do.  Tiger roars especially led to strong reactions among the deer.  The last sentence of their abstract reads, “Our study implies that Père David’s deer still retain the memories of the acoustic and visual cues of their ancestral predators in spite of the long term isolation from their natural habitat.”  It seems that, at least for these deer, captivity didn’t completely dampen their senses to predators. 

 

This is an interesting function of zoos that I hadn’t considered before.  It seems that with most controversial topics, we get a healthy serving of good and bad points.  Obviously, we are all left to make our own opinions about zoos and I won’t offer my own (somewhat misinformed and emotional) opinion to cloud this topic until I have time to fully research it.  I merely wanted to convey the success story of Père David’s Deer.

Along the same lines, did you know that we have seed banks?  Started by the botanist Nikolai Vavilov in Russia, seeds have been collected from all over the Earth and stored with the idea to avoid extinction of plants.  Such dedication the men had who looked over the seed banks that one died instead of eating the edible seeds during a long famine.  Very interesting concept that deserves some study! 

REFERENCES

http://philadelphia.about.com/od/philadelphiazoo/a/zoo_elephants.htm

Zeng, Jiang and Li. “Genetic variability in relocated Père David’s deer (Elaphurus davidianus) populations – Implications to reintroduction program.” (2007) Conservation Genetics. 8 pgs 1051 – 1059.

Soule et al. “The millennium ark: How long a voyage, how many staterooms, how many passengers?” (1986) Zoo Biol. 5, pgs 101 – 113

Frankham, R. “Stress and adaptation in conservation genetics.” (2005) J. Evolution Biol. 18, pgs 750 – 755.

http://www.philadelphiazoo.org/

Li et al. “Do Pere David’s Deer Lose Memories of Their Ancestral Predators?” PLoS One. (2011) 6(8) pgs 1 – 6.

Figure 41.1 Images: http://www.virginmedia.com/digital/features/endangered.php?ssid=6 and http://www.independent.co.uk/environment/nature/a-quarter-of-the-worlds-mammals-risk-extinction-952989.html?action=Gallery&ino=2  

Batman Likes Equilibrium

               It’s getting on towards Halloween.  Lots of grim reapers, skeletons and one tied up Barbie doll line my trek from the train station to work.  The Barbie doll creeps me out actually – her hands are tied behind her back with duct tape.  That ain’t right.

                Keeping that spirit of death alive, I’m going use this post to explain the following phrase:

A cell at equilibrium is dead.

                What does that mean?  Why is it dead?  Did the Devil come and steal its life?

                In order to understand it, we’ll need to learn a few things.  I’ll try to make it painless.

Thing #1: Batman likes chemistry.

                I’m sure you’ve seen chemical reactions written out as in Figure 40.1.  I’m not going to use real chemicals.  We’re going to keep it simple with A and B.  A and B are related to each other in that they can turn into each other: think of A as Bruce Wayne and B as Batman.  

Pretend we have 100 Bruce Waynes in a room.  All those Bruce Waynes look around and decide there’s way too many of them so some become Batman.  For simplicity’s sake, let’s say 25 Bruce Waynes become Batman.  Now we have 75 Bruce Waynes and 25 Batmans in one room.

25 Batmans / 75 Bruce Waynes = 1 Batman / 3 Bruce Waynes.

            Everyone in the room is happy with this mix of Bruce Waynes and Batmans. 

Let me take a minute and describe this moment when everyone is happy with the ratio.  It is called equilibrium!   The room likes being 75% Bruce Wayne.  However, this does not mean that individuals in the room stop changing back and forth between Bruce Wayne and Batman.  If one guy really wants to become Batman – he’s welcome to! - as long as one Batman then agrees to become Bruce Wayne.  Equilibrium is about the overall numbers.  Individuals within the room are still changing back and forth, but the total number of Bruces Waynes and Batmans are no longer changing.

Oops. We wasted too much talking about equilibrium and now 20 Batmans have left the room. 

           Our room now has 75 Bruce Waynes and only 5 Batmans.  

We established above that the room likes 1 Batman for every 3 Bruce Waynes.  In this new situation, we don’t have enough Batmans.  How do we get more?  

Some more of the Bruce Waynes need to change.

            And so, 15 Bruce Waynes become Batman.

20 Batmans / 60 Bruce Waynes = 1 Batman / 3 Bruce Waynes.

We’re back at equilibrium!

I’m sure you can see that there are many ways we can adjust the above situation. 

Examples:

What if 20 Bruce Waynes left the room? (You’d need more Bruce Waynes!)
What if 200 Bruce Waynes entered the room? (You’d need more Batmans!)

What if you made the room bigger? (They don’t care about the room size, they care about how many Batmans and Bruce Waynes there are.  Duh.)

Whatever you do the room, the overall numbers of Bruce Waynes and Batmans must adjust themselves to fulfill the ratio.

Thing #2: Chemistry likes the Bruce Wayne and Batman Scenario.

                Chemical reactions work like the above example.  To bring it back a little to the real world, consider again the equation in Figure 40.1.

                A will turn into B (and B can turn into A!).  If you put a bunch of A in a test tube, it will start turning into B until enough of B builds up that A says “okay, we’re done.”  The reaction is now at equilibrium.  Remember, individual molecules of A and B will still flip back and forth, but the overall numbers of A and B will no longer change.  

What governs how much B needs to be made before the reaction says enough?  A lot of things.  Suffice it to say that each chemical reaction has its own equilibrium point.  

A reaction is always trying to get to its equilibrium point.  Science, our cells, and life exploit that one fundamental fact mercilessly.

Thing #3: Equilibrium is not for live cells.

                Let’s go back to our test tube example with A turning into B.  Instead of allowing B to build up so the reaction reaches equilibrium, we’re going to continually remove B from the test tube.  Each time A turns into B, we’re going to take out the B.  

                A chemical reaction is always trying to reach equilibrium.  If we keep removing B, A is going to keep turning into B.  It’s going to keep trying to get to equilibrium, but we are foiling its plans.  We are ensuring that A keeps turning into B.

                Why is that useful?  In the Diabetes mellitus post, I told you that glucose is a precious energy source for the body.  The way that energy is extracted is to break down the molecule through a series of steps.  The first step turns glucose into glucose-6-phosphate.  Glucose-6-phosphate is then quickly turned into something else.  

Think of glucose as A and glucose-6-phosphate as B.  B is continually being removed from the reaction because it goes on to be something else.  This means that A will keep turning into B.  A is trying so hard to reach equilibrium with B but it can’t because B keep disappearing.   As long as glucose keeps turning into glucose-6-phosphate and glucose-6-phosphate keeps turning into C, glucose keeps getting broken down and our cells keep getting energy.   

   

What if glucose reaches equilibrium with glucose-6-phosphate?  Overall numbers of glucose becoming glucose-6-phosphate won’t change, which means that glucose is not being broken down efficiently anymore and that our cells are no longer getting energy.  

This pulling of reactions towards B is used in every chemical reaction within our bodies and keeps the reactions happening that keep us alive.

A cell at equilibrium is dead.

REFERENCES

 

Zumdahl, Steven S. “Chemical Principles, 4^th Edition” (2002) Houghton Mifflin Company, Boston, MA.

Alberts et al. “Molecular Biology of the Cell, 4^th Edition.”  Garland Science, New York, New York. (2002).

Me, myself, and I 

               

               

Further into Nardoo (cont'd Australian Expedition)

                My last post Beriberiand a Rough Australian Trip discussed the Wills-Burke expedition and the death of three out of four key participants due to a thiamine deficiency.  Near the end of that post, I explained that the men were eating foods rich in thiaminase I, which was breaking down any thiamine in their bodies.  Lack of the essential vitamin thiamine led to neurological disorders and was eventually fatal to all except John King.  One place that gave the men too much thiaminase I was fresh water mussels.  The other was nardoo, which is commonly prepared by the Aborigines without incident but was cooked incorrectly by the European explorers.

                I wanted to do a brief follow up to explain the differences in their preparations and why thiaminase I was still active in the European dish but was inactive in the Aborigine version.

                Nardoo is prepared from the plants of the genus Marsilea.  It is a fern but resembles a four-leaf clover (Figure 38.2).  The fronds, which are ground up to create a type of flour, are rich with thiaminase I.

               

                  Let’s take a step back and look more closely at the protein thiaminase I.

               

                  Figure 39.1 shows you a picture of the protein.  It is an enzyme, meaning that the protein helps a chemical reaction occur (Fun with Radioactivity post).  The particular reaction it catalyzes is shown in Figure 39.2.

                  In short, thiamine and another organic molecule (several molecules fit the bill here so the specifics aren’t important) bind to thiaminase I.  The enzyme then breaks thiamine into two pieces.  A broken thiamine is then unable to do its job in the body and leads to large problems, as demonstrated by Wills, Burke, King and Gray.

                 What are ways to ensure that this enzyme can’t do its job?

One: Destroy it.  I’ve told you previously that protein structure is essential for function (Cancerous Mutational Problems post).  If it doesn’t have the correct structure then it can’t do its job.  There are several ways to destroy protein's structure, but the simplest and most familiar one is heat.    Heat that protein up (ie. cook it)!  Heat is ruining that carefully folded protein and turning into a blob of amino acids with no function.

Think about when you cook an egg.  When it is first cracked, the whites are clear with a slightly yellow tinge.  As it cooks, the whites become opaque and stark in color.  Why?  You’re destroying all the protein inside the whites.  They are falling apart and forming a big clump of unfolded proteins.  It is safe to eat an egg after it has been cooked because any proteins in there are now dead and won’t function inside your body.  It’s also helpful to your digestive system, which further breaks down the proteins into their individual amino acids, transports them to cells, and your cells then use those amino acids to make new proteins that they need (Central Dogma post).  The circle of life.

Two: Take away its substrates.  Thiaminase I requires two things to function: thiamine and another organic molecule.  Clearly, minimizing thiamine is not an option, but it is possible to keep the other organic molecules to a minimum.  

Look at the cars outside.  They require two things to get them to move: gas and keys.  You can dip that entire car in gas but if there are no keys, you car isn’t going anywhere (unless you can hotwire a car, I suppose).  Same idea with thiaminase I.

                Our explorers went the route of #1 because that is how Europeans prepared grains: grinding and cooking.  Unfortunately, let’s quickly consider the Australian bush.  It’s HOT.   The proteins in the plant are going to be used to the hot temperatures so to destroy them, they must be cooked even hotter to mess up their proteins.  According to an article by Earl and McCleary in the journal Nature, these ferns can be boiled for 15 minutes and still have functional proteins.  That’s a hearty plant.

                The Aborigines choose route #2.  The plant is mixed with water and ground into a paste.  They are very careful to keep it away from anything else that might contain organic compounds and this minimizes how many organic molecules are present (how many keys are around to start the car).  Further diluting the paste with water ensures that if any organic molecules are present then they will be few and far between (spreading keys among 1,000 people as opposed to ten people).

                To be clear, no one knew exactly what the problem was with preparing nardoo.  It’s not like they held the plant up and said “Oh yes, there is thiaminase I here!  We will need to plan accordingly.”  It was obviously much more trial and error with preparation over time.  Whatever worked (and didn’t kill anyone) was kept around.  I would imagine it’s similar to discovering wild mushrooms or even rhubarb (the flesh of rhubarb is okay but the leaves are quite poisonous.  Crazy!).

Link to Protein Folding post, referenced in Figure 39.1.

REFERENCES

Earl and McClearly. “Mystery of the poisoned expedition.” Nature (1994) 368(6473) pgs 683 – 684.

Campobasso et al. “Crystal Structure of Thiaminase I- from Bacillus thiaminolyticus at 2.0 A Resolution.” 

Biochemistry (1998) 37, pgs 15981 – 15989. 

Protein images were created in PyMOL with PDB code 3THI

Beriberi and a Rough Australian Trip

         My other blog, Dr. Amedeo, is currently sporting a blurb about Aboriginal Australian ancestry (Ancient Humans post).  I thought an excellent parallel this week would be for this blog, Amedeo, to discuss the lost Australian expedition of 1860-1861 and how it relates to a problem called beriberi.

                Let’s meet the stars of the show.

                Robert O’Hara Burke

Born in Ireland, member of Australian army, police inspector

                William John Wills

Born in England, studied in Melbourne with interest in astronomy, meteorology and chemistry

                John King

                                Born in Ireland, military experience in India, camels

            

                Charles Gray

                                British sailor

                So what did these guys do?  In 1860, an expedition set out whose purpose was “for transversing the unknown interior of the Australian continent.”  While the coasts of Australia had been settled, the vast interior of the continent remained both unexplored and widely unknown.  The hopes for the expedition were to study the plants and animals of Australia as well as collect meteorological, geographical and astronomical data.  The leader would be one Robert O’Hara Burke and he chose William John Wills as his deputy.  They amply supplied themselves with both useful and illogical items.  Interestingly, the party became convinced that camels were essential to the journey since both deserts and the Australian bush were extremely hot (but had very little else in common).  

                No one had crossed Australia from the south to the north before so an added bonus of their trip would be the notoriety of being first to do so.  Unfortunately, competition for the title came in the form of John McDouall Stuart.  Burke became increasingly concerned that Stuart would beat his expedition (which was large and moved quite slowly), so he split the party by leaving groups behind in different places.  Eventually, the whittled entourage became Burke, Wills, Gray and King.  These four men took rations and successfully reached the north shore of Australia before Stuart.  

                This is where things start to go downhill for our explorers.  Monsoon season was upon them so traveling home was slow and rations were being depleted.  Their (arguably) biggest mistake was turning to the land, which they knew little about, to supplement their food supply.  Upon seeing signs of Aborigines eating mussels from a fresh water creek, our explorers procured some and ate.  They also began making nardoo, which is commonly made from a local fern by Aboriginal tribes.

                Not long after, Charles Gray died.  He had suffered on the journey home: he was unable to walk and spoke incoherently.  One night, he was found eating directly from their extremely depleted flour rations.  He had claimed he craved it and couldn’t help himself.  The others did not understand how he could steal from them, especially since the others were also finding their health to be failing.  Their legs felt paralyzed, they felt inexplicable exhaustion, pain and listlessness.

                Their exploration originally was large and those left behind knew Burke, Wills, Gray and King would need supplies on their return, so rations had been stored in known places.  These stores helped the men’s health greatly and their odd symptoms began to recede.  

                However, the men still wanted to supplement their supplies with food from the land so they went to back making nardoo. Burke and Wills would pound and clean the plant while King was out trying to collect more.  Hypothermia began to plague them in addition to fatigue, weakness, low pulse rates, and their bodies began to waste away.  Wills and Burke died.

                Miraculously, King was discovered by local Aborigines who nursed him back to health on a diet of nardoo, fish and local animals.  He was eventually rescued and returned to Melbourne, but his health was permanently damaged.

                What in the world was wrong with these men?

                They suffered from beriberi, which is a deficiency of thiamine (also called vitamin B₁, Figure 38.1).   This little molecule is essential to many cellular functions and must be obtained through our diet.  One of the first signs a body is lacking thiamine is neurological defects, such as confusion and irritability.  This eventually progresses to serious problems with the peripheral nervous system and cardiovascular problems followed by death.

                Unknowingly, the men were ingesting large amounts of thiaminase I, a protein whose job is to break down thiamine.  The mussels they ate were Velesunio ambiguus, which contain thiaminase I.  From the journals left behind, it is unclear whether the men cooked the mussels or ate them raw.  Proper cooking would have destroyed the protein and saved their health.  

   This is about to become a common theme.

                When nardoo is prepared by the Aborigines, ferns are ground into a thin paste, kept separate from other food, and diluted with water.  The expedition men ground their plants then boiled it in water.  The fern is full of thiaminase I (Figure 38.2).   The Aboriginal preparation ensured that thiaminase I was inactive.  The explorers way did not.  The men continued to eat the protein, which continued to break down any thiamine they were able to eat and their health plummeted.  Obviously when they recovered rations left behind, their health improved, but only went downhill again when they returned to nardoo.

                The most interesting part of all this was Gray’s eating of the flour.  Flour is full of thiamine.  Gray’s body clearly knew what it needed and forced him to crave the one food it knew had it.

                I had never heard of this story before listening to a podcast from “Stuff You Missed in History Class” from the website www.howstuffworks.com.  You can find it on iTunes by searching the podcast name and hunting through their archives of shows.  I highly recommend these podcasts if you have time in the car and get sick of music! 

Nardoo – a food prepared from the fern Marsilea Drummondii

Beriberi – a disease caused by a body’s deficiency in the vitamin thiamine

Vitamin – any organic molecule that is required by the body but the body cannot make itself (so it must be found in the diet)

Thiaminase I – a protein that breaks down thiamine

REFERENCES

http://adb.anu.edu.au/biography/burke-robert-ohara-3116

Earl and McClearly. “Mystery of the poisoned expedition.” Nature (1994) 368(6473) pgs 683 – 684.

Diabetes mellitus

Let’s start with some basics.

Hormone: A chemical or protein released by a cell in one part of an organism that travels and binds to cells in another part of the organism.   This chemical is transferring information.  It is acting like a letter sent through the mail.  Upon receiving the letter, you have new information and can act accordingly.  Hormones are one way that cells “talk” to each other and convey information.

Insulin: a hormone that is released to control the amount of glucose in your blood.  The food we eat is full of nutrients that our body needs.  So, after we eat a meal, our body breaks down the food into small pieces that it can use to rebuild things.  

Glucose: A sugar that is really important to biological processes.  Following a meal, your food is broken down into a lot of glucose molecules which are eventually absorbed into the blood stream.  

          

                Okay… we got a lot pieces.  Let’s fit it all together.  After eating a meal and your body gets a lot of glucose from it.  All the glucose is put in your blood stream so it can be delivered to the cells around the body that need some fuel.  As I told you in the CentralDogma post, cells have the protective plasma membrane around them to keep things out.  How does the glucose get in?  Insulin.  Your body recognizes that the glucose level in your blood is high (also called your blood sugar level) so insulin is released to the blood stream.  Insulin then travels around, binds to your cells and basically says “There’s a lot of glucose out here – let it in!”  Glucose then goes inside your cells to be further broken down to energy and carbon dioxide (CO₂, which we breathe out).

                Whew.   

                So what is diabetes mellitus?  The loss of or resistance to insulin.

                I worked in a diabetes laboratory as a research technician for two years and became familiar with several different versions of the disease.  I’ll try to briefly describe them here.

Type 1 Diabetes (aka Juvenile Diabetes): Insulin is produced by the beta cells in the pancreas.  In Type 1 diabetic patients, these beta cells are lost.  No beta cells = no insulin in the body.  Children typically presented with the disease, which is how it got the name of Juvenile Diabetes, however it is possible to develop it as an adult so it is commonly referred to as Type 1 now.

Type 2 Diabetes: Insulin is still made in the body (at either the same or lower levels) but the body no longer responds to it.

Gestational Diabetes: During pregnancy, the body either inadequately makes insulin or stops responding to it.  This is somewhat similar to Type 2 Diabetes.  A very low percentage of pregnancies are affected.  

MODY (Maturity-onset Diabetes of the Young): A genetic mutation limits the amount of insulin that can be made by the body.  Symptoms, which are often mild, manifest in adolescence or early adulthood.

                Please be aware that these are not the only kinds of diabetes.  Other rarer kinds or more specified problems of diabetes further breaks down the names of the disease.  These are the kinds I was most familiar with but I don’t pretend to be an expert.  Feel free to research the topic!

                Common signs of diabetes are increased thirst, hunger and urination.  One way test for diabetes is to determine if glucose is present in the urine.  When insulin can’t do its job, then the glucose remains in the blood stream and is eventually excreted.  Since glucose is a precious energy source for the body, excretion should never happen.  If the body has no current use for the glucose, it will store it as fat instead of eliminating it.  Just like if your wallet has extra $20 bills (because that always happens), you wouldn’t drop the excess on the street!  Instead, you’d put it in the bank.  Several other blood tests and whatnot also exist to more accurately determine what is going on.

                Literally, this topic can now go a hundred different ways.  I could discuss how doctors have tried pancreatic beta cell transplants to cure patients or how Type 2 diabetes is most common in industrialized countries.  An interesting topic may also be current research on gestational diabetes since many of my readers are of my own age.  Clearly, this may have to turn into a series.

                However, with my last little bit here, I’d like to step away from the research and discuss the history of this disease.  Before injectable insulin became available to Type 1 diabetics in 1921, diabetes was a devastating problem.  People suffered and starved due to their inability to uptake glucose from the blood.  As a technician, I remember seeing a presentation which embedded a movie of diabetic children.  They were gaunt with hallow faces and serious eyes.  They looked traumatized and desperate.  Left untreated as they had to be, they died while suffering from blindness, starvation, and kidney problems.  It was a haunting presentation.

                As early as 1552 BC, the Egyptians recognized frequent urination as a symptom for a weird disease they named emaciation.  In Ancient Greece, the disease gained the title “diabetes” from the Greek word meaning siphon.  Doctors felt the disease was siphoning or melting off the patient’s very limbs.  By 1675 AD, doctors noted that urine of diabetics tasted sweet so they added the word “mellitus” meaning honey.  (For real, they employed people to taste urine and determine its sweetness.  Who wants that job?)  Finally, after several studies surrounding the pancreas and diabetes, Frederick Banting and his collegues successfully treated a diabetic patient with insulin.  They were awarded the Nobel Prize in Medicine in 1923.

                I do not know any diabetics personally, but I had a class immediately following lunch during my freshman year of college.  A senior in that class would walk in, take out a large kit, test his blood sugar, measure out insulin and inject himself before the professor arrived.  I watched him every day and he was so nonchalant about it.  Sadly, I have no further personal stories about diabetes.  If anyone would like to share some, please feel free!

REFERENCES

Alberts et al. “Molecular Biology of the Cell, 4^th Edition.”  Garland Science, New York, New York. (2002).

History of Diabetes: http://www.everydayhealth.com/diabetes/understanding/diabetes-mellitus-through-time.aspx

 

Me, myself and I