Snacking Sensations

Squirrels know where it's at, as usual, and apparently nuts are a very good snack, especially if you want to lower your cholesterol levels! This is because they have a relatively high levels of Mono-unsaturated fats and Poly-unsaturated fats. Recent research has shown that while Trans-fats still greatly increase heart disease risk, and Poly and Mono-unsaturated fats still decrease heart disease risk, Saturated fat is actually a fairly neutral substance compared to carbohydrates. So while nuts tend to have some Saturated fat, the Mono and Poly-unsaturated fats make them a beneficial food. Especially good for you is Poly-unsaturated fats.

Substituting 2% of your daily calories (that's only like 25 calories people) from Trans fat to Poly-unsaturated fat reduces your risk of coronary heart disease by more than HALF.

Don't eat Trans fat! Don't do it!

A scary problem with avoiding Trans fat is that a food with up to a half a gram of trans fat per serving is allowed to be labeled as containing zero grams trans fat, or as trans fat free. Since the recommended daily limit of trans fat is only 2 grams, you can get over this limit pretty easily by eating only "trans fat free" foods. Also remember that this is per serving; a serving of Oreos is 2 cookies, and I know you haven't ever had just two Oreos.

Trans fat is not found in nature, so only processed foods will contain them. Food manufacturers started using them because they turn liquid fats, which are more perishable and messy, into handy solid fats (think margarine). Things to avoid:

Stick Margarine, and any tub Margarine that doesn't say it is trans-fat free

Donuts

Fast Food

That fake cream stuff in twinkies and the like

(Have you ever heard of the cardiologist's diet? If it tastes good, spit it out.)

All right, back to the nuts. The BEST nuts:

1. Hazelnuts (these are like superfood)

2. Walnuts (has the most poly-unsaturated)

3. Pecans

4. Almonds

The not-so-great nuts (sorry dad):

1. Brazil Nuts

2. Cashews

3. Peanuts

So eat your walnuts and hazelnuts! (Trader Joe's, and probably other stores, make delicious spicy or caramelized walnut/pecan snacks which make an excellent substitute for mixed nuts. You should all try.)

When Your Body has Poor Financial Judgement

McArdle's Syndrome

McArdle's Syndrome is a glycogen storage disease (Type V, for those counting), so it's a problem with our savings account. These patients are allergic to exercise which makes this the dream disease of nerds everywhere (McArdle even sounds like a good nerd name, doesn't it?). People with McArdle's syndrome are lacking the muscle form of glycogen phosphorylase, so they are unable to convert stored glycogen (savings) back into glucose (checking) to use in glycolysis (ATM). So when they begin exercising, their muscles use up the available glucose, and then are left with no fuel source, which understandably causes some problems (in this case muscle cramps). Luckily for the lives of those with McArdle's, the liver version of phosphorylase is still active, so these patients can still convert glycogen stored in the liver to glucose, and get the necessary energy to all cells, but in strenuous exercise the liver just can't keep up with the muscle.

Those who can't convert the liver glycogen into free glucose get the much worse.....

von Gierke's Disease

Patients with von Gierke's are missing glucose 6-phosphatase, which is a key enzyme in turning liver based glycogen into free glucose. So these patients can accumulate money in their savings account, but never take it back out again- trust fund! Kinda. This is a major problem, because once the free glucose from meal has been used up, the patient's body has no energy source to turn to. This can cause severe hypoglycemia (low blood sugar) with even short lengths of fasting, such as the time between normal meals. Patients present in infancy with massive enlargement of the liver (because of glycogen buildup), hypoglycemia, acidosis (low blood pH) and growth failure. The disease is relatively easy to control in adults by frequent ingestion of corn starch which is slowly digested to provide a continuous source of glucose. However infants usually require a 24-7 nasogastric feeding tube until they are old enough to be persuaded to eat cornstarch all day.

But of course glycogen metabolism isn't the only process that can have problems....

Beriberi

I love tropical diseases. They have such fantastic names, which means they are about the only diseases I remember over long periods of time. Beriberi is a severe thiamine (vitamin B1) deficiency. It is a tropical disease because thiamine isn't that rare of a vitamin, so severe deficiency usually only occurs in populations that rely entirely on polished rice for food. Thiamine deficiency in the developed world occurs in alcoholics who are mostly relying on alcohol for their caloric intake. It is given the much more dull name of Wernicke-Korsakoff syndrome, or as I like to call it, AlkyBeriberi.

Thiamine is necessary for the TCA cycle, which we haven't talked about yet. The TCA cycle is like glycolysis, in that it produces ATP (cash). It actually takes glycolysis byproducts, and further extracts ATP from them, but requires other inputs as well, such as oxygen. The TCA cycle, though, is much more efficient than glycolysis, and actually provides the majority of our ATP.

So people with Beriberi have a severe lack of energy supply in their cells, which means that their bodies' systems begin to gradually shut down. The nervous system is the first affected because the brain is much more dependent on glycolysis and the TCA cycle for energy. Other tissues are also capable of using fats and proteins through other pathways. So patients exhibit mental confusion, unsteady gait/lack of motor control, vomiting, and coma. Those with Wernicke-Korsakoff also sometimes exhibit a strange type of congestive heart failure that is characterized by high cardiac output.

Also interestingly, Arsenic and Mercury poisoning disables the same enzyme that is disabled in Beriberi, leading to similar mental/neurological problems. This is the origin of the phrase "Mad as a Hatter", because hat makers used mercury nitrate in their hat making processes, frequently succumbing to mercury poisoning.

Glucose, my Cruel Mistress.

Or, what happens when there is too much biochemistry.

So, we eat. We eat to give our body energy. You would think that something this straightforward would be simple, but no. It's not, in a big way. And, it's only like 10 freaking percent of the material on the next biochem quiz, but I'm not bitter. And it gives me a lovely ridiculous analogy!

Specifically, we eat carbohydrates, which are turned into glucose in our stomachs, and then absorbed into our blood and carried everywhere, because our cells transform glucose into ATP, which is the cell's unit of energy, via glycolysis.

ENTER THE ANALOGY (stay with me here)

So glucose = my mother's electronic transfer of money into my checking account. It's great, because I now have more money, but I can't actually spend it at the local farm. Because the farm doesn't take checks or credit cards, and neither do your cells. You have to turn your electronic money into cash (or ATP) because this is what the farmer (your cells) uses to pay the rent. You do this via an ATM machine, or glycolysis.

So whenever your cells need a little spending money/energy (ATP), they go to the ATM (use glycolysis) to get some from the checking account (glucose). But cells are just like me- I get one big transfer each month, the cells get a pile of glucose each meal. You don't want all that extra glucose/money just floating around- a thief (the kidney) might steal your debit card, and spend (pee) all your money (glucose). And then you would be broke (dead) for the rest of the month (forever).

So along comes insulin! Insulin is released when there is lots of glucose in the blood. It causes the uptake of glucose into the liver and muscle via glycogen synthesis, where it is stored in a more stable form, glycogen. In our fancy analogy, the money in the checking account (glucose) is transferred (by glycogen synthase) to the savings account (glycogen in liver and muscle) in response to insulin (your good sense).

So now your body is trucking along after its meal, and it uses up all its free glucose. Aka, it's the middle of the month, and I've eaten out one too many times. Now I need to buy groceries from the farmer, and your cells still want to keep living, like the pesky things they are. But just like in my real life, you can't withdraw cash from your savings account. (Electronic transfers only. ING Orange. Over 1% interest. Check it out people.) You have to first transfer it to your checking account.

So- You need more ATP (money), and for that you need Glucose (money in your checking account) but you've used it all up. Glucagon signals a need for more glucose, so you go to your liver and muscle for glycogen (savings account). You convert your glycogen into glucose via gluconeogenesis (electronic transfer from savings to checkings), and then convert the glucose to ATP via glycolysis (get money from checking via ATM).

YAY!

Of course it is too late for me to get to the interesting disease parts, but that will come tomorrow.

The Twisted Ways My Brain Works

Here is the TCA cycle (important in cellular respiration aka life)

Citrate -> Isocitrate -> alpha Ketoglutarate -> Succinyl coA -> Succinate -> Fumarate -> Malate -> Oxaloacetate

Here is my "mnemonic"

Lemon -> Kind of Lemon -> tricky one -> Even though your friends suck on cigarettes, you shouldn't suck on cigarettes, because if you smoke, it is bad for you, and the have to give you oxygen.

I wonder at my brain sometimes.

Words of Wisdom

"There is no doubt that the first appearance of the mammal, with his unexplained need to push his testicles out of their proper home into the air, made a mess of the three-layered abdominal wall that had done the reptiles well for 200 million years."

-Sir William Heneage Ogilvie

A-licious

One of the liver's many functions is to store Vitamin A. There have been reports of Vitamin A intoxication after eating various livers, especially polar bear livers. When the time comes in your life that you are eating a polar bear, avoid the liver.

Scared....muscleless?

And now back, after a brief encounter with what was hopefully H1N1 (so I don't have to deal with it later) and the subsequent biochem quiz!

I present to you this fantastically funny video (don't worry, the goats aren't hurting):

http://www.youtube.com/watch?v=RGz97dxGHV8&feature=related

Myotonia is a disease that is thought to be caused by a defective ion channel in muscle. The chloride channel is responsible for allowing muscles to relax after they have been stimulated to contract. In people and animals, a defective chloride channel in skeletal muscles leads to a short delay (about 5-7 seconds, if you watch the video carefully) before the muscles can relax. This is normally only triggered when there is extreme muscle stimulation, so people learn to cope with this disease by moving slowly. Fortunately for our amusement, goats have not figured out this little trick.

Collapsed Lung- House vs. Real Life

If you have been introduced to the formulaic awesomeness that is the weird-shit solving of House MD then you have probably seen a representation of a collapsed lung, because it's basically their second favorite thing to do (right after anal bleeding). Here is a rough summary of House's version of a collapsed lung:

Patient has weird symptoms. Patient suddenly starts gasping and choking and maybe flailing. Incredibly hot doctor put a stethoscope on the chest and shouts "his lung's collapsed". Second incredibly hot doctor runs over and pokes a thin metal tube through patient's chest. One hissing sound later, and the patient is perfectly fine again and no one mentions how he's now got a metal tube through his chest.

REAL collapsed lung is much more boring. It also has a much more complicated name, pneumothorax (pneumo=air, thorax=chest). To understand pneumothorax, you have to understand how we breathe.

Our lungs are sitting in our chest cavity, which is created by our ribcage on the top and sides, and our diaphragm on the bottom. And maybe some muscles in there too, if you're not a skeleton. But just the diaphragm on the bottom. In the active portion of breathing, inhalation (inspiration), we contract muscles that pull the diaphragm downward which enlarges the chest cavity. However, there is no way for air to get into the chest cavity (important-remember this later) so this creates a negative pressure. This negative pressure basically pulls the lung tissue outward, transferring the negative pressure to the inside of the lungs. This negative pressure in the lungs causes air to rush in, just like a vacuum.

Exhaling (expiration) is the easy part- all muscles relax, the diaphragm rises to its natural position and air is pushed out.

The simplest scenario to create a collapsed lung is if there is an injury to the chest cavity (say, like, someone poked a thin metal tube through your chest. Huh.) Now what happens? The diaphragm moves downward, and the chest cavity expands, creating a negative pressure in the chest cavity. NOW however, there is a way for air to get into the cavity. So instead air rushes in to fill the chest cavity. Your lung does not get pulled open, so no air enters them, so you don't get oxygen. You breathe out and the air gets pushed back out, but when you try to breathe in the air again just fills the chest cavity and not the lungs.

The fortunate catch is that your chest cavity is actually divided, one for each lung, so lung collapses occur individually. You can still breathe with your other lung. So a collapsed lung is not in fact a medical emergency- people can go quite some time with a pneumothorax, and most small pneumothoraxes actually just fix themselves.

So does House lie?!

Only a little. What House is showing is actually a tension pneumothorax. Same deal as before, but instead of an open hole, you have a little flap that can bend into your chest but not out. When you try to breathe in, air fills your left chest cavity (because your injury is on your left cause I said so). But when you try to breathe out, the pressure holds the flap closed and no air escapes. Breathe in- a little more air in the cavity. Try to breathe out- air doesn't leave. Basically, you are blowing up your left chest cavity like a balloon. Unfortunately, there are other things in your chest, like your heart, good lung, esophagus, trachea, and other mildly important things that don't appreciate being squished. As they start being compressed, the tension pneumothorax becomes an immediate medical emergency. And this is when the thin metal tube comes in.

Basically, what House (and real doctors) are doing here is turning a tension pneumothorax into a plain old boring pneumothorax. Sure, one lung is still collapsed, but at least your heart and other lung are functioning, and breathing and beating are useful for living. The actual collapsed lung will take several days to weeks to fully re-inflate, and will probably require some suction of air out of the chest cavity.

It is good to note that normal pneumothorax should be treated as well, because it does place some strain on the heart, and this can be damaging over time.

Whoa.

Bone Sawing + Open Chest Cavity + Stethoscope= Doctor.

Boniva

Those who watch an excessive amount of Lifetime or Food Network (which I would never ever do) probably have seen a commercial for Boniva. Boniva is an osteoporosis treatment whose claim to fame is that you only have to take it once a month, instead of once a week like all those other osteoporosis pills.

Now if you're anything like me, you're sitting there wondering who on earth is so lazy that it makes that much a difference to take a pill once a week or once a month. But it turns out that bisphosphonates like Boniva (which inhibit the resorption of bone by cells called osteoclasts, your bone's natural recyclers) also are very hard to absorb through the stomach. This means you have to take them on an empty stomach, which causes severe upset stomach, gastric reflux, and erosion of the esophagus. So APPARENTLY I should judge less, and all Boniva users are happy to only go through this once a month.

Prions: birth without life.

Days 2,3 of Med School.

So most people have heard of Mad Cow disease.  Caused a meat panic, made England kill a whole bunch of cows, and revealed some creepy practices about feeding cows other cows.  But what many people don't know is the really cool scientific discoveries that came from Mad Cow, and its less glamorous sheep cousin, Scrapie.

When Mad Cow and Scrapie started popping up big time, people were scrambling to identify the causative agent, since it was obviously transmittable from one animal to another.  But they found that beyond even identifying it, they couldn't even kill it.  Anti-bacterials, anti-biotics, anti-virals, extreme heat, everything that would kill any living organism or virus, wouldn't kill whatever was causing Mad Cow.

Eventually, they found that what did stop Mad Cow from spreading was protein denaturing chemicals.  This meant that the Mad Cow infectious agent wasn't a virus, wasn't a bacteria or a microscopic organism, but just a protein.  And not just a protein- a protein that is in everyone's body already.

So here's what happens.  The Prion protein is the protein involved in Mad Cow.  It is a normal protein that is produced in everyone, and is now thought to have some sort of a neuroprotective function.  But it's not a perfectly stable protein.  It can twist, and change its shape a bit.  After it changes its shape, it may bump into another perfectly normal Prion protein.  When it does, it causes that normal Prion to change shape as well.  And so on, in a cascading fashion until there are thousand of millions of misshapen Prions.  When a misshapen Prion from one animal is introduced into another animal, it acts as a seed, initiating this cascade of protein shape changes that causes Mad Cow disease.

It is unclear whether the misshapen Prions are actually poisonous in some way, or if the shape change simply inactivates the good Prions, which may cause a problem if normal Prions are very important in the body.  However, in an interesting twist, very recent research indicates that normal Prions may suppress Beta-secretase, whose action is key in creating the plaques that occur in Alzeheimer's disease.  The plot thickens.

WTF is Histology anyways?

Day 1 of Med School (for reals).

Histology is the study of microscopic anatomy.  Basically you look at cells under a microscope.  Why do you need to do this?  Imagine:  You are at the doctor's and have a lump.  Somewhere.  And the doctor, fearing this lump may be cancer, takes a biopsy.  So now the doctor has a chunk of your lump.  You go home, and tomorrow the doc tells you if you have cancer.  How does he know this?  Not magic.

The object of the game is to look at the lump (also known as tissue) under a microscope and see if it looks normal.  However, this is complicated.  Because microscopes basically have to shine light through something in order to work.  So the tissue has to be cut in thin strips (about 60 micrometers).  To do this, the tissue is first dehydrated in alcohol, and then has wax poured over it.  This wax gives stability so that the tissue can be cut into such thin layers without making it into something resembling cream of wheat.  Then, the layers are dunked into stains, which stick to certain cellular structures and make them show up in colors, because unstained lump basically looks like lots of vaguely pink mush.  Then, and only then can you look at stuff that looks like this:

http://path.upmc.edu/cases/case263/images/figure03.jpg

Which will apparently one day tell me lots of things about your lump.

But that's the boring stuff.  The cool stuff is when you use Scanning Electron Microscopy.  Instead of those big bulky lightwaves, you use itty bitty electrons.  And instead of all that slicing and staining, you just dunk the thing in heavy metals, and that gives you a sweet 3-D image of really really tiny things:

(blood cells)

http://upload.wikimedia.org/wikipedia/commons/8/82/SEM_blood_cells.jpg

(gills of a mudskipper)

http://www.vcbio.science.ru.nl/images/TechniqueFig3B_Zoom.jpg

(ant)

http://upload.wikimedia.org/wikipedia/commons/c/ca/Ant_SEM.jpg

Seriously the prettiest thing science has come up with for a while.  But aside from making pretty pictures, Scanning Electron Microscopy (SEM) is the only way to visually identify viruses.  SARS?  

http://www.sciencedaily.com/images/2009/03/090313150254-large.jpg

ID'ed by SEM.  Useful.

Busy lives make it hard to post.

Med School Day 3,4,5 (Kinda)

Last Day of Orientation, White Coat Ceremony, Saturday

• White Coats are cool
• Swipe cards are even cooler
• Check out Ovid because it's so much better than Pubmed
• Parents make life busy
• Always have balance in your life, so go to the zoo often

Some things never change.

Med School Day 2 (kinda)

Second Day of Orientation

Today, mixed in with the usual orientation bureaucracy and being informed that we have 8 (count 'em, 8) different passwords, we had our first real class.  Med students today don't take the real hippocratic oath, because it's 2500 years old and that may mean it's a bit outdated.  Instead, most schools use some revised version encompassing the main ideas of the oath, and here we get to write our own each year!  Really, this just means that each class looks at last year's oath and changes a couple words to make themselves feel warm and fuzzy inside, but anyways.

So, the school sent home a bunch of example oaths and ethics papers, so everyone could read them over the summer to develop their own ideas of what a Physician's oath might entail.  Then today we met in small groups to discuss.

And there we are, 10 of the "best medical students in the country", as we have been told all week, sitting with one of the school's foremost experts in Medical Ethics.  And...the silence descends.  It really is comforting to know that for all the overachievers and geniuses that are supposed to be in this class, it still takes pulling teeth to get anyone to speak up in class.

Eventually, we came to the conclusion that no one really cared if our oath was different than last year's oath, so we looked at the real hippocratic oath.  Some of the pledges ancient Greek Physicians made are definitely no longer held true:

I will provide medical education free of charge.

I will financially support my teacher in times of need.

Some are still the foundation of today's oaths:

I will only seek to benefit my patients, and not do harm.

I will speak of nothing that I learn inside a household, whether learned during treatment or not.

I will not have sex with my patients.

And the most interesting are the "no" statements.  Today's oaths largely do not have any negative statements.  They say what the physician will try to do, but do not say what the physician will refuse to do.  Probably because they were trying to avoid the controversy of:

I will not give a deadly medicine to anyone, even if I am asked.  Apparently scholars are unsure if this means no euthanasia or assisted suicide, as it is often interpreted, or is more directed at not supplying assassins.  Since we are told that there was plenty of euthanasia in Ancient Greece, either a bunch of Physicians weren't good at following instructions, or it really meant the latter.

I will not give a woman a harmful pessary.  A pessary, in my understanding, is when a sharp metal instrument is poked into the uterus to initiate an abortion.  Many people interpret this as no abortions.  However, the pessary METHOD of abortion had a ridiculously high death rate, because you just poked sharp metal things into soft tissue.  So, since again there were plenty of abortions performed in Ancient Greece, many scholars believe that this was outlawing only this method of abortion, not abortions in general.

And now you know.

My monthly payments are going to be WHAT now? And other things you did not want to learn.

Med School Day 1 (kinda)

First Day of Orientation

56% percent of America's graduating physicians in 2008 had debt greater than $150,000.  We are told this to emphasize that we are not alone.  Over half of your class is probably scared shitless as well.  Of course, my school is very proud to announce that their average student indebtedness is 20 grand lower than the nation's average.  But considering 20% of the class is MSTP (aka no debt), and this is the largest percentage in the US, the fact that they're only 20 grand lower doesn't comfort me.  But anyways, we're going to try not to think of this, and pray that the financial aid team didn't screw up and think that sister is still in school, cause otherwise bye bye all aid.

OTHERWISE... we learned:

We have a cool library (duh).

We have an IT department (duh).

We have a class picture (duh).

We have to pay tuition (damn).

We have individual study carrels (cool).

Its impossible to get any work done in said carrels (oh well).

The second years say if you study outside of exam week in first year you're working too much (...yay?).

We have a school tab at the bar tonight (SWEET).