Ubergeek Theatre

This is for Susan over at The Rickety Contrivances of Doing Good, who was tagged by N=1, and was kind enough to expand the invite. I’ve seriously addressed Highly Pathogenic Avian Influenza (HPAI) H5N1 in a previous post, so I won’t go through the nitty-gritty again, but here’s a few helpful tips to keep you prepared for a possible pandemic (my tongue is firmly in my cheek):

1) Don’t be a doctor. Or a nurse or any sort of medical assistant or tech. They will be the first to get sick and the last to admit that they’re actually ill.

2) Avoid all small children. Never forget that they are plague bunnies of the apocalypse.

3) Just say no to all possible disease-carrying animals, including (but not limited to), all birds, pigs, housecats, Siberian tigers, ferrets, quaker parrots, and laboratory mice. Be especially careful of the tigers - they’re sneaky.

4) Install a UV sterilizing light in your mailbox, over your front door, and have a portable one handy so that you can irradiate all potential houseguests/invaders. Skin cancer can’t possibly be as important as avoiding bird flu, and I’m sure the mailman will agree with you.

5) Wear gloves and a face mask everywhere. I realize that this is incredibly unfashionable, but the good news is that the Japanese have created fashion surgical masks to help you look good while avoiding all the bad.

6) Shop till you drop! The worst outcome of even a small pandemic is the total collapse of global economy. Do your part to keep the planet going by at least buying a few things on the internet (like the aforementioned surgical masks, or maybe some lovely tea from southeast asia, where the most human bird flu cases have been - those poor people will really need economic help if the pandemic strikes).

7) While being a good citizen consumer, try to also keep to yourself. You want to emulate survivalists and by remaining in hidden and silent contemplation of your life and its safety level in order to avoid contamination. I might suggest reading Leviticus 13 repeatedly to help keep your resolve strong in the face of necessary isolation in your duct-tape sealed room.

8) For God’s sake, wash your hands! Again! Do those look clean to you? Again! Have you bleached the house yet? Well, what’s stopping you?!?!?

9) Stay fit. Not only will this help your immune system remain healthy, but it will make you more attractive to the other few remaining survivors. When you emerge in the post-pandemic sunshine, you will have top pick of potential mates and can happily do your part to save the world, or at least mankind, from certain extinction. Make sure you do some yoga to stay flexible in anticipation of this.

10) When all else fails, Don’t Inhale. It will all be over soon.

((okay, Susan, I did my best. I hope this qualifies for bonus points ;) … ))

in lieu of anythign to say, I was tagged by my brother over at Music on Your Pizza at some point before finals, so I’m getting around to it now. I’m not going to tag anyone else (especially as any of you who read this have probably already gotten this one), but I’ll answer:

Meme premise: I am to list ten (somewhat) interesting and (relatively) unknown facts about me/opinions of mine/habits/etc. I am also to tag ten other people, but as I said, I’m not going to. Given that I’m not particularly forthcoming on this blog, this may be a big first, but so it goes….

1) I don’t actually like doing research, though I’ve worked in multiple labs over the years in different bioogical fields. Now that I’m in medical school, I’m very happy that I won’t have to do basic research ever again. Obviously, however, I like talking about it.

2) At one point, I did, in fact, have an investment license (and I was a public notary). Amusing.

3) I’ve always suspected that my father’s side of the family plays up their Scottish heritage more than is strictly true, but I’ve never cared enough to truly dispute it. I find it more entertaining to carry on the possible vast exaggeration than to be the whistleblower.

4) A nun once hit me on the head with a bible for falling asleep during a prayer service. I think it’s an even funnier event considering that I’m not Catholic, and never have been, but happened to go to a Catholic high school.

5) I have serious issues with programming a VCR. For no good reason, really.

6) I often appear younger than my younger brother, so when we’re out together, I invariably get carded, while he does not. When he’s not around, I appear about as old as I am, but there’s something about his presence.

7) I’m convinced that if I work hard enough, I can grow almonds in Wisconsin.

8) I secretly love shoes, and if I ever have the money, I intend to have lots of them. I feel rather guilty about this, but it seems a harmless secret passion. The only real problem is that I tend to leave all my shoes by the door, having taken them off when arriving home.

9) I didn’t really have an interest in dolls as a child - I had My Little Ponies instead. Dolls seemed boring.

10) If I weren’t in medicine, I’d sort of love to be a bohemian artist. Of course, I realize it’s not all my mental image thinks it is, but I still sort of like it. For a little while.

As I said, no tags, but I didn’t want to be totally remiss in my “having-been-tagged” obligation.

And then I will be done with finals. I have promised myself to do a better job of updating here, especially as I will have a relatively relaxing summer (some research, some patients, some gardening).

To the woman named Eileen who commented and apparently has lovely hair. I seem to have misplaced your comment, and I’m terribly sorry. All I saw before it disappeared was that you have never gone gray, to which I say, nice genes!

Now for the throwing open of the topics. If any of you are still reading this, and would like me to address something in a future post (a.k.a. in the next three months), drop me a comment, and I’ll do my darndest not to lose it.

Last Thursday, in the wee hours, a friend of mine had a kidney transplant (after a long wait). Her old kidneys definitely had to be removed, and, as you can see in this image, this is why:

The ruler underneath is six inches long. Each kidney is about the size of a football and weighs 10 lbs. (and yes, I have her permission to post this image here)

This is something I wrote for the Lost Writers ‘zine, that I’m posting here because I thought it was decent. It’s not technically a “science article,” but it is “science-related.”

Behind the Veil

During the first week of medical school, I and a hundred other recently-arrived students crossed a strange line, perhaps one of the single biggest demarcating lines of the field of medicine. Like the thousands of physicians before me and after me, and unlike almost every other human on earth, I began the process of systematically taking another person’s body apart. Admittedly, I’d dissected pieces of people before, and I’d observed anatomical dissections. But I’d never dealt one-on-one with an entire corpse. If any of you, on a lark, decided to do what I and my compatriots engaged in, you would be arrested. It seems strange that the auspices of Medicine and the cold tile walls of an anatomy lab mean the difference between crime and education.

The night before that first day, I thought about that first cut, from the hollow of the throat, down the sternum, around the bellybutton, then down to the beginning of the pubic hair. I was prepared to be that first person to cut into another’s body. As it turns out, the idea of the “first cut,” is largely antiquated. Upon arriving at the lab, there were four scalpels, one for each of us. And while one person did make that longitudinal cut, the other three of us were not a passive audience. Instead, we were busy making cuts that bisected his line, creating flaps of flesh to be pulled away minutes later. There was no tense moment of held breath, no wooziness or moment of philosophical horror. We simply all began cutting. This may sound more uncaring, but I think it was our first lesson in the true meaning of “necessary detachment.” On a cadaver, we could all have afforded to be hesitant and stuttering, but that sort of behavior would never be acceptable for a living patient, and we all instantly accepted the idea that practicing now would make it easier later.

Let me disabuse you of some common misconceptions. For one, the anatomy lab is not in a damp, dimly lit basement. It’s on the first floor, has many windows, and is brightly but not garishly lit. The bodies are encased in free-standing stainless steel tanks, completely submerged in an ethanol-based embalming fluid. Granted, not every medical school runs things quite like this, but there are never piles of uncovered cadavers lying about slowly atrophying, as is portrayed in many stereotypes. We do not name our cadavers - they all had names (and no, we don’t know them, and never will), and to re-name them would be to deny their lives before we met them. We do not play bongo-drums with their skulls or make their jaws talk, or dangle their kidneys like yo-yos. Each body is kept by itself, including a separate bin for each body to hold the pieces of skin and fat we must remove. At the end of the semester, each body and all its pieces is cremated, and the cremains returned to the family if they so desire. The smell is nasty but not overwhelming. However, the urban legend that dissection makes you hungry is absolutely true - the ethanol embalming solution seems to be a potent appetite stimulant.

That said, it would be easy to see the necessary actions of anatomy as somehow being cruel and unusual. The typical first lab involves removal of the skin from the chest and the back. Until you’ve tried skinning a human for yourself (and I don’t really recommend it), you have no idea how hard it is, nor how violent you will become within a half hour’s time.

During the initial cuts, everyone is tentative, trying not to cut too deep and usually failing to make it all the way through the skin on the first go round. Even on the skinniest of bodies, the chest skin is at least a quarter of an inch thick, and on large cadavers, it can be an inch or more. It’s fairly easy to develop the confidence to cut with the right amount of depth and certainty with a few minutes’ practice, but the subsequent removal of the skin is much more trying.

The textbook offers hints to the difficulty of the task, stating: “To facilitate the removal of the skin flap, make a stab wound in the flap large enough for one or two fingers. Insert a finger into the hole and PULL very hard on the flap.” The textbook isn’t wrong, except in that it significantly understates what you need to do. If you merely stab a hole in the skin, stick your finger in it and pull, almost nothing happens. Rather, you have to wriggle your finger into the larger cut you’ve made, and start working it vigorously back and forth under the skin, tearing through little strands of tissue and feeling small globs of fat slip away, until you’ve created a loose edge, much like the loose edge of a label on a wine bottle. At this point, you can either be brave or be slow. Slow means using your scalpel and, lifting the loose edge of skin, carefully cutting away the fascia - the connective tissue between the skin and muscle - and pulling the skin away as you go. Brave means inserting your finger into the smaller stab wound and pulling, HARD, working another finger underneath the loosening skin as you go.

This is the real moment of philosophical crisis. Up until this point, you’ve been fairly respectful, merely violating the flesh with the blade of a knife. Now you are literally ripping the skin off of someone’s body, and the sound emanating from that flesh as you go is akin to a room full of school nurses yanking the band-aids off a room full of children’s knees at the exact same moment. At some point early on in the process, you are gut-wrenchingly aware of committing an act from which you can never return. Five minutes later, you are in a state of frustrated detachment, cursing the body for being so stubborn, tearing the skin away viciously, in an attempt to just get the job done. You’re not just wriggling your finger viciously, you’re engaging in some sort of primeval Neanderthal flesh-tearing rite of passage. The people with thin bodies quickly become the alpha anatomists, grinning smugly as the groups with large cadavers struggle to remove thick slabs of skin and fat.

Having succeeded on the chest, the body needs to be turned and the back skin removed. This is when you learn that the skin of the chest is peanuts compared the back. Never let anyone tell you that their skin is getting loose with age. Trust me, even the loosest, most ancient skin is clinging tightly to the underlying tissue, especially on the back. The skin there is easily twice as thick as the chest skin, and it’s not even the thickest skin on the body. In anatomical terms, both are considered “thin skin.” You want thick skin? Go for the palms. I don’t even want to think about trying to get that stuff off without a scalpel.

Having engaged in almost bestial blunt dissection, each student then retreats into a clinical shell, carefully analyzing the cutaneous and lateral nerves, looking for the thrombocolumnar aponeurosis and other structures of muscle and tendon. We show them to our lab mates, analyze other bodies, and retreat back into mild intellectual status. The grisly and potentially criminal nature of our afternoon is safely caged within the rules and logic of scientific endeavor.

It is later that you reflect on the act of dissection. After the sun has set and your homework has been done, you may find yourself pondering the body that has been freely offered to you. Do you remember it as specimen or man? Do you remember the raw muscles or the external pubic hair? Does it feel like you’ve invaded someone’s ultimate privacy? Clearly, this man (or woman) gave permission for this to happen to him after his death, a decision that requires both humility and bravery. He offered strangers the chance to marvel at his personal blend of perfection and flaws. Will he be more human to you because of this purposeful choice, one that none of us can honor without temporarily dehumanizing him?

In six months, the student comes to know more about this stranger’s flesh than they have ever known about their closest loves, more about his body than his family can even guess. They will share an intimacy unknown in the rest of society, by the cadaver’s choice, forced on the student by the necessities of education. The students will be using his muscles to further understanding, at no benefit to him, requiring no awareness on his part, with his permission but still using him solely for their own ends. Perhaps that is the true crime in this act - the ultimate experience of intimacy without love, coupled to an act that is so inherently cruel amongst the living that we can barely accept it for the dead. If we all dissected cadavers would that make us more compassionate or more monstrous? Medicine may be, in the end, the secret home of gods and monsters. Is this why we all seem to have a love-hate relationship with physicians? Is the social fascination with doctors because of that anatomical line that separates us from them - that doctors have the ability to enact animalistic violence in the name of science and life-giving, which the rest of us rely on completely? Perhaps, it is not just the act but its finality that give us pause. In the path to becoming a physician, it is this moment of anatomical dissection, much like the first patient consult, the first patient death, and the first infant delivery that are points of no return. In the rest of the world, there are few careers as cluttered with choices after which there can be no real turning back. Perhaps the real line medical students cross in that first week is not from sternum to pubis, but the starting line of one of the most life-altering racetracks in life, each choice further alienating us from other individuals while tying us more inexorably to humanity and our need to serve it.

It’s New Year’s, and the hair is down, the shoes off, the party really hopping. Some of the shoes may even be sopping champagne onto the carpet, but most people prefer to keep their shoes sober, thank you very much. We, on the other hand, may find ourselves well beyond the point of finding our shoes, let alone ascertaining their sobriety. In the morning, we will welcome in the new year with a raging headache, parched throat, and general malaise. In honor of this apparently entertaining repast, today’s UberGeek Theatre focuses on the timely topic of Alcohol and its metabolism, effects, and the best way to deal with hangovers (because, really, isn’t that the only thing you want to know?).

For the most part, we all understand what it means to be pleasantly drunk. The world is warmer, the lighting better, you know you’re good-looking, brilliant, and fascinating, and everything is a hazy sort of loose. Some of us probably know what it means to be unpleasantly drunk - when the timing of drunkenness has fallen apart and we are disoriented, nauseous, lethargic, and can’t quite put together the fact that we’re really not together, epitomized by a sad attempt to point to one’s nose that ends up almost taking out the left eye. That’s what it may feel like to our minds, but what does it feel like to our bodies?

Anthropomorphically, I can only imagine the liver facing a night of heavy drinking the way a levy engineer in the Netherlands faces a sudden flood - frantically and constantly until it passes out in exhaustion (well after you have already passed out yourself). Alcohol is highly toxic, and as the main job of the liver is to deal with toxins, it works unpaid overtime every time you have one for the road.

The general process looks something like this: Mr. T. Collins slides down your throat, and - magician that he is - walks through the wall of your intestine into your bloodstream. Your blood gives him a waterpark ride to the liver, where he’s taken hostage by a savage tribe of proteins, who proceed to break him into pieces and eat him. He’s converted from alcohol to acetaldehyde and then eventually to acetic acid and then water and carbon dioxide. His ashes are exhaled to the world through the lungs and washed out to the septic system via the urine, as are the remains of all intruders successfully captured by the body.

While this might make a great adventure movie, it’s not something your body enjoys reliving on a regular basis. In the process of detoxifying your blood, the side effects are particularly nasty. Ethanol, aka alcohol, is first converted to acetaldehyde, which is for starters, a potent carcinogen, binding to your cell proteins and DNA and causing all sorts of genetic mutations, cell death, and general havoc. After that, your body eventually converts the acetaldehyde to acetic acid and so on (However, about 40% of people of Asian descent lack the enzyme for this step, thus showing the linguistic lie of the stereotype that “Asians can’t hold their liquor.” They can and do hold onto it, in fact, for a far longer period of time than non-Asians. Sadly, this is the real problem.)

If you drink enough, acetaldehyde escapes from your liver into your blood and travels to the brain, where it inhibits the function of neurotransmitters like serotonin and enhances the function of neurotransmitters like GABA. In the case of serotonin, the acetaldehyde actually binds to it, turning it from a neurotransmitter into something that looks very much like morphine. Some people might suggest that this lends alcohol some of its addictive quality. In terms of GABA, alcohol’s enhancement of it means that your brain starts shutting down (GABA is a giant “off” signal). Interestingly enough, this happens to a greater extent in men than women, however women are more likely to report feeling drunk. The gender difference thus suggests that alcohol makes men stupid and makes women feel stupid, which could lead to some very awkward social circumstances. On top of that, acetaldehyde interferes with vitamin absorption and directly destroys folate which is needed to make DNA. So not only are you drunk, you’re drunk and malnourished.

The nutritional problems of excess alcohol intake are greater than a mere folate deficiency however. Alcohol is calorie-rich, at 7 calories per gram (an average U.S. beer has 12 grams of alcohol, and you could easily work your way through a daily calorie intake on just a few stiff martinis), and completely nutrient-deficient (the few vitamins that may exist in beer are usually destroyed by the co-habitating alcohol). Moreover, alcohol is not metabolized directly to energy, the way most foods are. Instead, a small amount of its energy is immediately metabolized to fat through a process called, uncreatively, lipogenesis. A large portion of its energy is directed into the “electron transport chain” via a molecule called NADH. The electron transport chain is literally a water-bucket brigade of electrons that generates energy for your body. Usually, this process is fueled through sugar and fat metabolism, but when alcohol is in the picture, it tends to crowd those guys out, so you end up not metabolizing the fats you normally would, and they hang out in your bloodstream, creating potential heart problems and generally being a nuisance. By drinking often and copiously, therefore, you tend to develop the traditional “beer gut” consisting of newly generated fat and abandoned un-digested fats, collectively schlumped around your midsection dreaming of the good old days.

Lest you think this is the worst of things, let me continue to the “unpleasantly drunk” part of things. The NADH molecule is fairly pervasive in biological processes - it’s a good gopher for energy. When alcohol is broken down into acetaldehyde, it produces NADH, which can proceed as I mentioned above, or it has one other option: it can mess with your sugar. You may have always thought that alcohol was a great way to “get some sugar,” but let me disabuse you of that notion. NADH actually stops your body from making glucose, aka sugar, forcing it to produce lactic acid instead (think of the smell of buttermilk, and you’ll be onto the whole idea of lactic acid). Lactic acid is responsible for post-exercise muscle cramps, which becomes a part of your hangover the next morning. Moreover, the lack of blood sugar makes you tired, sleepy, and ravenously hungry - alcohol-induced binge eating is another good source of the infamous “beer gut.”

What about the rest of the hangover, you ask? Well, all this work on the part of your liver takes a lot of oxygen, which starves your brain. Moreover, your brain is being randomly turned “off” by alcohol-induced GABA signaling. The morning after, therefore, your brain is left in the same place as you are: confused, starving, grouchy, and just trying to figure out where it left its clothes. In the same way that you might cause great pain to your coworkers that morning, your brain will cause great pain to you. The dehydration (and thus dry, icky throat) is simply because alcohol makes you throw everything up, makes you pee, and again, all these processes to detoxify you use more water than they create. When the cops put you in the holding cell to “dry you out,” there’s more truth to it than they know.

Over time, chronic drinking leads not first to liver cirrhosis (though it’s certainly one graphic side effect), but first to muscle degradation, heart problems, cancer, and the side effects of malnutrition: anemia, hair loss, tremors, poor posture, nerve damage, blindness, general grouchiness and so on. In part because this is a second metabolic system kicks in when you drink a lot - the Cytochrome P450 pathway. This pathway detoxifies your system, but creates dangerous free radicals, which, when drunk, your body doesn’t have the energy to fight. Couple this with an overabundance of fatty acids in your blood, and you’ve got a recipe for all sorts of tissue damage, as there’s nothing a free radical likes more than a big piece of fat to chew (and, if you think about it, that seems to hold true on a larger scale as well). Of course, that’s only in chronic alcohol consumption cases, and evidence supports the idea that moderate drinking is really quite good for you, as long as you make sure that your idea of moderate and your doctor’s idea of moderate are the same thing.

At this point in my little alcohol diatribe, some of you are probably saying, “well, this is all pretty bad, especially that hangover bit, so it’s a good thing I�ve started drinking those energy drink cocktails to counteract these problems.” This is the point where I laugh at you, because you’ve been snookered by a great advertizing campaign (kindly overlook my irrational preference for bottled “mountain spring water” over the tap).

I’ll say it once (and then ramble on about it): caffeine does not counteract alcohol. In fact, it may make the whole mess worse.

At face value, it seems sensible: caffeine is an “upper,” alcohol a “downer,” so you should be left in the middle after drinking both. The problem is that they don’t work in even remotely similar fashions. Once ingested, caffeine can act directly on your cells, binding surface receptors called “adenosine receptors.” As you might have guessed from the name, adenosine receptors normally bind adenosine, which is a calming little molecule - it makes you sleepy and slow. It’s your body’s feedback response to unnecessary “fight or flight” stimulation by epinephrine and norepinephrine. Caffeine prevents adenosine from slowing you down, and so the effect is to maintain a primal responsive state of increased heart rate, blood pressure, and blood flow to the skin. You’re flushed, hyper, and ready for action. Simultaneously, this also decreases the blood flow to your internal organs and causes your liver to release sugar from its stores into your blood. “Aha!” You say, “so it will prevent alcohol-induced hypoglycemia!” Possibly, but look at it this way: suddenly, your heart’s racing, which uses much more energy, your skin is flushed, losing heat - aka energy - to the outside world, and your liver isn’t getting enough blood, losing the energy it needs to detoxify your blood alcohol.

Add to this scenario a few other effects of caffeine. Caffeine is broken down into three compounds: paraxanthane, theobromine, and theophylline. Paraxanthane might seem initially reassuring, as it promotes the break-down fat molecules (even in the beer gut). However, this adds to the concentration of fatty acids in your blood, and so raises your risk of heart damage, especially with the increased heart rate and blood pressure. Your risk of alcohol-induced heart attacks goes way up, therefore, if there’s caffeine in the mix. Theobromine causes your blood vessels to widen, your bladder to fill, and sends oxygen to your brain. This could be a good thing, except that again, you get less oxygen to your liver. So your brain may be more awake, but it’ll be drunk that much longer. And the combined diuretic effect of alcohol and theobromine is the fastest way to cause self-inflicted raisin-hood known to man. Kindly, theophylline causes your lung passages to open, so at the least you’ll be breathing easily while you’re shriveled up and unconscious in the bathroom.

Now that I’ve cut off your last hope of saving yourself from horrid regrets New Year’s Day, I feel I need to give you a small consolation: there is, in fact, something you can do to minimize a hangover besides the obvious method of not drinking. You have probably seen all these pieces of advice before, but now they should make sense.

Things that don’t work: “hair of the dog” cures - you’re really just putting off the inevitable, so you should really just suck it up and get through it now. Weird concoctions of raw eggs, juice, etc - not such a good idea given the nausea thing and the difficulty our bodies have in digesting complex foods (then again, if you can get it down, you’re probably not all that sick). Sticking your head in icy water - you’ll be awake, sure, but all the water will still be on the outside of your poor little desert of a brain.

Things that help:

1) Drink lots of water while you�re drinking, and after you’ve stopped drinking. This will keep you nice and hydrated.

2) Take a vitamin - alcohol causes vitamin deficiencies, which can actually make you feel crappy long before you show signs of deficiency.

3) Eat while you drink - this won’t actually prevent you from getting drunk or getting a hangover, but it does slow your alcohol absorption down, so it gives your liver a better chance to deal. Remember, no matter how much you drink, your liver can only completely get rid of about 7-10 grams an hour, or somewhere between a half and almost a whole beer. Eating moderately will also help prevent you from binge-eating later (which is far more likely to lead to an intimate relationship with the toilet) and keep your electrolyte levels up so you don’t feel as bad the next morning.

4) Stick to clear liquors, avoiding wines and beers - this is an extreme prevention step in some people’s opinions, but there are many people in the world who are sensitive to the other compounds in wine and beer - sulfites and dead yeasts, etc - which can compound the hangover response with an allergy response.

5) The morning after, eat very simple foods, like toast and honey. Drink more water. Put off having any caffeine as long as possible in order to minimize further dehydration.

These, sadly, won’t be an instant cure, but they do help quite a bit.

I should, perhaps, point out that I do not intend to remain completely sober on New Year’s, nor am I opposed to drinking. So while I may have given you good reasons not to drink excessively, keep in mind that the key word is “excessively,” and a key co-conspirator is “chronically.” One of the best ways that I’ve discovered to avoid becoming an excessive and chronic drinker is to become a consummate food and alcohol snob. Not only will your tastes become expensive, you won’t want to muddy the experience with something so plebeian as overwhelming intoxication. With that in mind, Happy New Year’s, and I hope your brain forgives you in the morning.

Sources:

Wikipedia
Virtual Chembook, Elmhurst College, 2003
The Medical Council of Alcohol (UK) Student Handbook
www.wellesley.edu/chemistry/chem101/caffeine/caffeine.html
Poschl, G. et al. Alcohol & Alcoholism 39(3):155-165, 2004.
Wang, GJ et al. Alcoholism: Clin. & Exp. Res 27(6):909-17, 2003.
McDonough, KH. Toxicology 189(1-2):89-97, 2003.
Adachi, J. et al. Journal of Nutritional Biochem. 14(11):616-625, 2003.
Cunningham, CC et al. Alcohol Res. & Health 27(4):291-99, 2003.

Back in September, I was asked to work on several topics. I haven’t forgotten, so I am now starting to work my way down the list.

If you’re like me, you’ve got a little gray going on. If you’re like most people, that makes you, unlike me, over the age of 35. Among Caucasians, the statistics show that 50% of us are 50% gray by age 50. I’m one of the people who will be close to 100% gray by that age, and so will help balance the people who dye their hair and lie to the statistician. Maybe you’ve done what I’ve done, and begun naming your gray hairs after the people you think stressed you to the point of grayness. I have one I half-jokingly call “Joe.” You know who you are. Perhaps you’d like a better word for your condition. I suggest you use the technical term: poliosis, which comes from the Greek “polios” aka “gray.” People at dinner parties might think you mean Polio, and either avoid you or offer you extra pity. Cough a few times; see how fast you can clear the room.

So why do we turn gray? There are several approaches to this question. Some anthropologists might tell you it’s a status symbol - it shows you are a mature member of “the pack” and are therefore in a senior status position. Some cynical anthropologists might then point out that gray hair lets the young know you’re available as a baby-sitter.

Aside from the potential cultural benefits (apparently feeling old isn’t enough of a cultural cost to prevent grayness), what, scientifically, is going on?

The human hair is an individual trying to act independently within a larger set of sweeping controls. You might say that each of our hairs is representative of a general human condition. While philosophically deep, this is not such a big deal scientifically - it’s pretty much status quo.

Each hair has two main parts: a shaft and a root. The shaft is the part we see, and consists of a long tube of dead cells. Pigments trapped within these cells give hairs their color. The root is the part of the hair under the skin, and is surrounded by a tube of tissue called a follicle. The follicle is the control center of each hair. Each hair is independent of every other hair (unlike animal hair, which works in a coordinated fashion), so each follicle is its own little command-control center. The follicle controls the “growth” cycle of each hair, which is broken into three parts: anagen (growth), catagen (a brief period of regression, sort of like adolescence), and telogen (a rest period, which some people erroneously suspect retirement is). Growth, Regress, Rest, Repeat.

Hair pigment is created by the same molecules that color our skin: melanins. Eumelanin lives in brown and black hair, while pheomelanin causes blond or red hair. Cells called (not a creative moment in science nomenclature) “melanocytes” produce these pigments, and then transfer them to hair “keratinocytes.” In turn, the pigment-containing keratinocytes obligingly commit suicide and are pushed out of the skin by your follicle to form the hair shaft.

Simply speaking, hair graying happens when your melanocytes stop producing melanin. They don’t necessarily die, although they can. In a larger general sense, I’m sad to say, no one really knows why. “Genetics” is the catchall answer, but there’s no “graying gene” that anyone’s found so far. There are some interesting correlations: B12 deficiency, low bone density, thyroid problems, anemia, and smoking are all correlated with premature graying.

And no, so far, there’s nothing you can do to prevent it.

Historically, there are many anecdotes about “overnight graying,” caused by stressful situations. This has been dubbed “telogen effluvium,” but the evidence for its actual occurrence is spotty. Henry IV supposedly went gray overnight after escaping the St. Bartholomew’s Day Massacre in 1572, and Marie Antoinette supposedly went gray overnight before her execution (but with that wig, how would you know? Moreover, if her hair only had one day to grow before her head was chopped off, how do you know she went gray right then?). Evidence is pretty much non-existent on the stress-related sudden graying. There is a rare condition called “diffuse alopecia areata” (use that in a sentence, see where it gets you), which causes large quantities of pigmented hair to suddenly fall out. If you’ve got gray hair hiding on your head that doesn’t fall out, you might look like you’ve suddenly gone gray, when you’ve really suddenly gone bald.

There’s no link between grayness and hair loss, by the way. Look at all the old people with gray hair in odd places (ears, etc), and you’ll see this is definitely true.

Scientists, not content with mere correlations, have looked into the specific mechanisms of graying, though mainly in mice, so it’s hard to say how applicable these findings are to human hair (then again, we’re remarkably similar to mice in most ways). The most recent evidence, reviewed by researchers from the University of Iceland and the National Cancer Institute in Maryland, point towards something called “stem cell maintenance.” Other research, from the Free Radical Research Group in Paris (which sounds amazingly like a group of protest-studying sociologists, but apparently is not), points towards - you guessed it - free radical damage to cell machinery. Little radical scalp insurgents are making you gray, but in this case, there’s no real way to win the war on “hair-or.” Ahem. Sorry. Moving on……

On the free radical side of things, scientists argue that superoxide molecules (they’re not that super, really, it’s a misnomer. They’re really just oxygen molecules with extra energy, and therefore extra capability for harm) cause mutations in cell machinery that either breaks the pigment production line, or kills the cell. This would clearly cause graying, but it doesn’t appear to be the end-all be-all. Your cells, especially melanocytes, are amazingly capable of dealing with superoxide molecules without conking out. Scientists on the stem cell side of things say that there’s a break-down in the molecules that regulate the growth cycle and the ability of melanocyte stem cells to replace melanocytes that die. All cells have finite lives, and your hair follicles keep a stash of melanocyte stem cells in a region called “the bulge” (where cells apparently battle to be the next pigment monopoly in each hair society). When melanocytes die, these stem cells receive a chemical kiss, awaken from a dormant Snow White sort of state, and migrate from the bulge to the pigment-production area and gear up to color your hair. Anything that prevents the awakening and migration of these stem cells would also result in graying.

Here’s what’s funny. The two arguments, from my perspective, don’t look so opposite. Some oxidative damage surely causes stem cells to stay asleep forever (killing Prince Charming to prevent the magic kiss is not as impossible in the real world as it is in the movies, apparently). This may just be an example of “drama in science,” which seems to lurk in the oddest corners (Stem cells versus Free radicals! This Sunday on Discovery!).

In the end, however, the cause of hair grayness probably does come back to that modern-age-old answer: “It’s in your genes.” Somewhere in your DNA are the messages that control how well your cells produce pigment, respond to free radicals, and regulate cell cycles. Perhaps some day science will show that the fastest-cycling hairs gray earlier than the slow-cycling hairs. Maybe they’ll show that people who worry too much tend to go gray because they’re more susceptible to free radicals, or that stressful events cause more damage to your melanocytes than to the rest of you. Perhaps all this new evidence will be covered up by the powerful hair dye industry and you’ll never know the answer. Until then, while you may blame your parents, remember that your early graying is probably karmic justice for all the gray hairs you may have “given” them when you were a child.

Sources:

www.thestraightdope.com
Scientific American
Popular Science
Eirikur Steingrimsson, Neal Copeland, and Nancy Jenkins; “Melanocyte Stem Cell Maintenance and Hair Graying,” Cell 2005 Apr 8;121(1):9-12.
Article by the Free Radical Research Group, University of Paris: Photochemistry & Photobiology 2004 Nov-Dec;80(3): 579-82.
Experimental Gerontology 2001 Mar;36(3): 591-2.
Journal of Clinical Endocrinology and Metabolism 1997 Nov;82(11): 3580-3.

A few days ago, a friend kindly broke my long writer’s block (so many subjects, so little time), with a question about vaccines. She had heard a radio ad for a study in which a new AIDS vaccine candidate would be tested. The ad stated that the vaccine was perfectly safe. Is that possible, she inquired? While I can’t speak to that particular vaccine in question, I thought I’d provide a dose of UberGeek Theatre on the kinds of vaccines and how they might (or might not) be safe, effective, useful, and so on.

Most of us have a working definition of vaccine: that shot they give you so you don’t get sick. This is a good generalization for the everyday person. Of course, vaccines can be given orally (polio), nasally (mostly experimental), by gene gun (also experimental), as well as via injection. And there’s different types of injection from the “stab-and-jab” of the subcutaneous (aka: anywhere under the skin) injection, to the more carefully poked intravenous (aka: into the blood) injection. Beyond that, vaccines are indeed supposed to prevent illness, in essence, by giving you a little bit of what could ail you in an attempt to get your body on the permanent alert.

Without going into pages and pages of detail (and trust me, there’s books and books of detail, and even larger books of what we don’t know), let me explain how your body goes on permanent alert at the sight of a vaccine.

Your immune system has scads of different components that I’m just not going to touch on here. The important parts for this discussion are the big two, your T-cells and your B-cells (and why are they called thusly: A different essay for a different time). These cells are coated in claw-like proteins that respond very specifically to different proteins that enter your blood. Each T-cell/B-cell has its own set of specific claws and thus responds to a different protein. How does this happen? Well, through the miracle of genetic recombination, which is a nice way of saying “useful slip-ups,” your body never produces the same set of “claws” twice, no matter how many times it runs through the same T or B-cell assembly line. Your body compensates for this by having a very rigorous T and B-cell selection process (think Marine Corp boot camp, only more deadly) so that you don’t produce cells that think your own proteins are suspect (this does, however, occasionally happen anyway, causing all sorts of terrible autoimmune disorders). So a system of studied inefficiency leads to a very elegant and wide panel of possible immune cells.

Why is this important? Because viruses, bacteria, and parasites, the Big Three in the germ world, contain more individual differences than you or I or even Stephen Hawking for all his universal wisdom can imagine safely without our heads exploding. So your body has to be equipped to recognize tens of thousands of proteins without ever having seen them before. And that’s what’s so amazing about the immune system - somewhere in your body is a T-cell or a B-cell that can bond and respond to a protein that you’ve never encountered, that perhaps has not yet been created. No kidding.

But one cell in a body of trillions is not a particularly good guard against, say, an invasion of measles. If measles invades, your guardian cell has to find it, bind to it, send out alert signals, cause your immune system to swing into action, and try and save you. As history proves, disease is often faster than your immune system. This is where vaccines come in.

Not only does your immune system have an incredibly complex recognition system, it also has a memory system. If you get measles as a kid, chances are you’ll never get measles ever again - your immune system makes sure of it.

T-cells are killers. When a T-cell finds its target, it proliferates, creating an army of T-cells to fight off the invader using a complex series of deadly weapons, especially poisons. Like a Cold War spy stereotype, your immune system is very good at poisoning its enemies. Once you recover, some of those T-cells are given desk jobs for valor in battle, and become T-memory cells, keeping a watchful eye on the borders of your body in case the invader ever returns. When a B-cell finds its target, it not only proliferates, it turns into a little war machine and begins pumping out antibodies. Antibodies are like little disembodied claws with flags on their wrists. They float around, bind to invading germs and act like signal beacons for other immune cells who come and kill the virus (either through the T-cell poison method or by simply ingestion. We’re also very good at eating our enemies). These antibodies don’t disappear when you recover. Instead, they float around like a satellite monitoring system (think of Reagan’s “Star Wars” plans), ready to act in case of another attack.

Vaccines, then, are intended to be a safe induction of that memory response. Your given an injection of a harmless form (or something very similar - more on this later) of the germ in question, you mount a successful immune response to it, and then your body remembers the enemy, so that if it invades, you kill it before it has the chance to make you sick. Memory not being perfect, you sometimes have to get a booster shot a few years after the initial vaccine, and sometimes you have to get a series of shots (hepatitis, for example), in order to build up the level of memory you need to protect you from particularly nasty diseases. Antibodies are of chief importance here, as they are the floating alert system that can save you - you want to create as many antibodies as you can to ensure permanent immunity.

Vaccination isn’t a modern, post-industrial invention. In fact, 11th century physicians in China and India were known for injecting the pus from smallpox lesions into their patients. The hope was to cause a mild form of the disease and grant permanent immunity thereafter (Smallpox being a “once in a lifetime” virus). This process, now called variolation, is not the most efficient, nor, as you might imagine, the safest way to immunize a populace - despite the best efforts of these doctors, smallpox persisted on a wide scale until the last century.

Edward Jenner is the name commonly associated with vaccines, although if you had asked people in the 1780s who he was, the educated would point to him as a great birdwatcher, and author of a seminal paper on Cuckoo behavior (the same people would later accuse him of perhaps emulating his beloved birds). In 1796, in a completely unethical experiment, Jenner injected a young boy with pus from a woman’s cowpox wound, (cowpox is a benign bovine relative of smallpox and was often caught by milkmaids), and then two weeks later deliberately infected the boy with smallpox (that would be the unethical part). Fortunately, the boy survived, and Jenner’s name went down in history (although it was another man, William Woodville, who conducted the first large-scale study to prove Jenner’s one-time experiment).

The way science works is not always fast or forward. Often, scientists are no more progressive in their labs than they are in their lives, and reflect the culture around them. This is probably why it took another 100 years before vaccines were given a second chance, when Louis Pasteur invented his rabies vaccine (and coined the word “vaccination”). Other vaccines, however, were a long time coming.
Why did it take humanity so long to embrace what has become a modern mainstay of public health policy? The single biggest reason is probably a lack of technology. “Germs,” as we know them remained a somewhat murky theory until the early 1900s, first with Koch’s postulates involving disease elements (which established how to prove something actually caused disease), and second, with the development of microscopy. Bacteria-observing microscopes had been around throughout the 1800s, but microscopes that could observe viruses (which make teensy-weensy seem large) weren’t developed until the 1930s. Prior to this, the cause of any given disease was mysterious - for example the term “malaria” comes from the Italian words for bad air (mal aria), because the Romans believed swamp gas caused what we now know is a parasitic illness. We couldn’t see what killed us, so we tried to explain it the best we could - bile imbalances, bad air, evil spirits, etc…

Now that you have some history, I’ll skip ahead to the point in time that is the present. We know what ails us most of the time, we can sometimes look at it, and if we’re even luckier, we can make a vaccine to prevent people from getting it. To that end, there are currently four types of vaccines, though only three are in widespread commercial use. Some of these are safer than others, which gets back to the original question.

The first kind is the “Live Attenuated” Vaccine. This type is probably the most common of the vaccines you’ve had, as it includes measles, mumps, rubella, and chicken pox vaccines in America. Military recruits sometimes also get the live attenuated vaccine for adenovirus and yellow fever, and some of us and/or people from other countries may have gotten the live attenuated polio vaccine as children. So what is it? A live attenuated vaccine is at heart the same virus that can make you sick. It has, however, been effectively brainwashed into submission. This is usually done by growing the virus in the cells of another animal until it no longer thinks of itself as a “human virus.” This could, for example entail injecting it into a rabbit, removing it from the rabbit, injecting it into another rabbit, and so on and so forth for several generations. Usually, the progression is a little more complex. For example, the measles vaccine currently in use was isolated from humans in 1954. It was then grown in human kidney cells (in a dish), human amnion cells (the fluid that surrounds babies in the womb), sheep kidney cells, and chicken embryo cells. After this, the “brainwashed” virus doesn’t make us sick anymore, but it’s also not quite as good at inducing memory as the original virus, so it takes a few shots to create a protective level of antibodies (for measles you usually get two shots, one as a baby then another between the ages of 6 and 12). Live attenuated vaccines are generally very effective and very safe, and some, like the polio or adenovirus vaccine, can be given orally as opposed to injected. So what’s the problem? Well, occasionally, the virus will revert to its original nasty self. You’ve already mounted an immune response, so you’re safe, but unvaccinated or immune-compromised people around you may not be. So you may not get sick, but you can make others sick (which does wonders for your social calendar). This tendency to revert is one of the biggest obstacles to making effective live attenuated vaccines for most viruses.

There is an off-shoot of the live attenuated vaccine that has returned to use in the past four years - the viral vector vaccine. This sounds big, but what it really means is “using a harmless virus that looks a lot like the bad virus to induce immunity.” You know it as the smallpox vaccine. The vaccinia virus, aka cowpox, is still used to provide immunity to smallpox. However, as I’m also sure you know, side effects do occur, and occasionally, the harmless vaccine can, in fact, cause disease. Experiments are currently underway to take even more harmless viruses and give them some of the genes of the harmful viruses, again providing immunity without disease. At least one ebola vaccine trial in animals has so far been very successful with this model, and some experimental HIV vaccines have shown promise using this method.

The second kind of vaccine is the Inactivated or “Killed” virus vaccine, and includes the vaccines for influenza (the yearly flu shot), hepatitis A (only given to travelers), Japanese encephalitis, some polio vaccines, and rabies. This vaccine is exactly what it sounds like: virus that has been “killed” (disregarding the debate over whether viruses are actually “alive” in the first place). Dead virus can’t make you sick, but you still mount an immune response to it. Often, viruses are inactivated with harsh chemicals like formalin or something called beta-propriolactone (not on the quiz). On the surface, these vaccines sound ideal. The big problem is this: viruses are super-duper-small, so what if you don’t kill every single one? What if another virus sneaks into the batch? In 1950, a batch of polio vaccine wasn’t “quite dead yet,” and led to over a hundred children getting polio from their vaccinations. Last year’s flu shot was in jeopardy because of contaminated culture materials. The third problem is that some viruses, like influenza, change so frequently that last year’s vaccine is no longer effective. This is why you have to get a new flu shot every year - you’re facing a new and very different flu every winter. Last but not least, while our bodies do respond to killed viruses, they don’t mount quite as large an immune response as to live viruses, especially if you’re an adult. So the flu shot is not 100% effective in the elderly population, who sadly, is in the greatest need of protection.

The third type of vaccine is the Subunit vaccine, which in humans is currently a family of one: the Hepatitis B vaccine (that series of three shots, each one more painful than the last). Experimentally, many subunit vaccines are in the works, but only the HepB series has been commercially and medically successful so far. The theory is straightforward: take the virus apart, purify out the bits that your body can respond to, leave behind parts that make the virus complete (and therefore dangerous) and use the reactive subunits for a vaccine. Viruses are often little bits of genetic material inside a series of coats. So if you take just the jacket and inject it into the patient, you should theoretically get a great immune response with no chance of disease. Hepatitis B outer proteins are grown in yeast cells (yeast, our usually harmless beer-making friend! How we love yeast), then purified and injected into your arm. This works well for hepatitis, but so far nothing else. Why? Well, first you have to know which bits of the virus will cause a good immune response. Then you have to find a way to produce/extract/purify just those bits. Then you have to test them, and oddly enough, even if you’ve got the first two things down pat, you often don’t get a very good immune response. We don’t really know why, but subunit vaccines are just not as effective as whole virus vaccines. So while in theory these vaccines are perfect, in practice, they are mostly confined to lab experiments. The HepB series, however, works very well, so don’t worry about that one.

The last type of vaccine is purely experimental still. The DNA vaccine is a variation of the subunit vaccine, and basically consists of a piece of viral genetic information injected directly into your cells. The gene or genes would be produced in your cells, and the viral proteins displayed on the outside of your cells like giant red flags to your immune system. Your body would then produce a fairly good immune response. As farfetched as the idea of injecting DNA straight into your cells to cause immunity sounds, lab results in animals have been very successful. At least one lab is working on a DNA vaccine for tuberculosis (a bacteria, but the idea is the same) and producing decent results in mice. There’s too much we don’t know about this approach to make it useful in humans yet, but it looks promising.

To get back to the original question: are vaccines safe? The answer is yes. Perfectly safe? Well, that depends on the type of vaccine. At the moment, the only “perfectly safe” vaccine is the subunit vaccine (with the caveat as long as your not allergic to what its grown in, like yeast or eggs - the vaccine itself, however, is perfectly safe). The new viral vector vaccines (not smallpox), that offshoot of live attenuated vaccines are incredibly safe, and live attenuated and killed virus vaccines are almost completely safe. There have been accusations that the thimerosal, a preservative in some vaccines is linked to autism, but the evidence is shaky still (and is, again, another essay for another time), and due to public pressure, thimerosal was eliminated from U.S. vaccines in 1999. Is the particular experimental AIDS vaccine that my friend heard advertised on the radio safe? It’s probably mostly safe, but not perfectly so. I doubt very much that there’s any chance it could give you HIV, but there might be a chance of many side effects. Any vaccine, especially for such a deadly disease, that’s made it to human trials must be a very safe vaccine indeed, but in some ways, perfect safety is still a trade-off for immune response, so it may be perfectly safe, but not perfectly effective. The perfectly safe, perfectly effective, perfectly priced vaccine is still the Holy Grail of vaccine technology, and the great quest of many budding graduate students.

Sources Cited:

Flint, et al. Principles of Virology, 2nd ed. ASM Press, 2004.
Kuby, et al. Immunology, 5th ed.W.H, Freeman and Co., 2003.
Desowitz, Robert. The Malaria Capers, Norton, 1991.
Immunization Safety Review Committee. Immunization Safety Review: Measles-Mumps-Rubella Vaccine and Autism, National Academy Press.
Henderson, D.A. �Smallpox: clinical and epidemiological features� Emerg. Inf. Dis. 5:537-539, 1999.
Jones, SM et al. �Live attenuated recombinant vaccine protects nonhuman primates against Ebola and Marburg viruses.� Nature Medicine 11(7):786-90, Jul 2005.
Unpublished data: Talaat Lab, UW-Madison.

And I am working on a few ideas, just as soon as I get all the appropriate educational paperwork out for the season.

Until that point, it has occurred to me that I should present a disclaimer for the general public.

The author of UberGeek Theatre (being me) would like to acknowledge that I am not an expert. I do my best to find scientifically sound, peer-reviewed, legitimate resources upon which I base my columns. I have not cited them thus far, but I am tempted to start, as it is important to give you the opportunity to evaluate my sources for yourself (so far, I have only used three web sources, everything else has been from peer reviewed journal sources and/or collegiate textbooks). I cannot prescribe medications, diagnose diseases, or claim “ultimate knowledge” of anything. I can and do take the factual information I know and discover and attempt to present it in a readable fashion, and I try as much as possible to be apolitical, or least non-partisan. I always welcome factual debate and challenge to my points as long as all debate is respectful (less of me than of other readers, really, but you get the idea).

What prompted this, you might ask? Well, here are two links, one to a post on pseudo-scientists and science quality on the net, specifically pharmaceutical advice. These got me thinking that I did not want anyone misled or misinformed, and therefore I should make a proper disclosure so that anyone stumbling across the site would know exactly where I am coming from in these entries.

Disclaimer stated, more columns will be forthcoming in a few days.

After a long hiatus, call it a mental health recovery period, perhaps, UberGeek Theatre is proud to announce its return to scientific rambles with a step outside our (royal “our”) usual forays: physics.

“Physics? Gah, no, really, physics?” you might ask… and rightly so. After all, it’s not really my area, barring a few lower-level collegiate experiments with springs. But a recent article in Discover caught my eye, and hopefully I won’t blunder too greatly (those of you out there with the mad physics skills - I’m relying on your feedback) in today’s topic, titled:

What Holds You Down: Why You Can’t Be Everywhere for Everyone.

In an effort to be totally clear, I’m going to start with a few definitions.

Hypothesis: a question, usually one that is tested scientifically after it is posed.

Interpretation: a potential answer that cannot be scientifically verified, but makes darn good sense (and is well-argued).

Theory: a successfully answered hypothesis that withstands rigorous testing by multiple persons over long periods of time, under different experimental conditions whenever possible. In physics, theories cannot always be tested physically, but must withstand rigorous mathematical and logical testing if physical tests are not possible. There are very few actual Theories in the scientific world because of this, so the term “theory” is vastly different than “theoretically speaking,” “music theory,” or “I have a theory as to who killed your brother.”

Law: In physics, this is something that has progressed beyond Theory status, and is something so amazingly provable that it is considered generally unnecessary to prove it further. The Law of Gravity falls into this category.

Gravity: Well, now, that’s a very good question. It is, in one way, an attractive force that exists between two objects of mass, proportional to their relative masses and various other mathematical multipliers. If you throw something into the air, the force between it and the Earth eventually slows the object and forces its return to a state of attachment to the ground. What goes up comes down, etc. The moon’s orbit is partially a product of gravity; the Earth’s orbit around the Sun is gravity as well, and so on and so forth. But gravity is strange - it is the only major “fundamental force” that cannot be explained in terms of quantum mechanics. Which leads us to:

Quantum Mechanics: According to Merriam-Webster, this is “a theory of matter that is based on the concept of the possession of wave properties by elementary particles, that affords a mathematical interpretation of the structure and interactions of matter on the basis of these properties, and that incorporates within it quantum theory and the uncertainty principle — called also wave mechanics.” In my terms? The counting, mathematical evaluating, and measuring of the little fiddly bits that make up the Universe. And I would like to insert here that I absolutely hate it when a definition includes one of the words being defined (as in “quantum”).

Okay, I’m done with definitions. As if the mystery of gravity isn’t enough, there’s an on-going problem of particles and jealousy. Yes, jealousy. I would suspect that many physicists are green with envy (heck, I’m green with envy) over the fact that atomic and subatomic particles can exist in two places at the same time. Just think of all the things I could get done! All the postcards I could send myself from obscure foreign locales! How many more UberGeek books I could read! All the trash I wouldn’t have to haul to the dumpster! And so on! But for as of yet unknown reasons, not only can I personally not exist in multiple places at once, nothing larger than a photon (a wavelike particle of energy, it’s not really that important for this paragraph, just really, really small) can.

So how did they, the marvelous Physics Lords, figure this out? How many of you took and remember physics? I thought as much. Me too. But maybe you can dredge the old “light-bulb” experiment up from the depths of your subconscious for a moment for the sake of discussion.

Light, if you recall, moves in waves. It also moves in particles, so let’s say light moves in wavelike particles called photons (aha! We meet again!). However, for most of us, the light we deal with is in massive quantities of photons, so we just think of light as a wave, beam, tunnel-definer, whatever. So, you have a screen (no this isn’t a launch into my vacation slides - another time, perhaps), and in front of that, you have another screen, this one with two slits in it, an arbitrary foot apart. In front of that, you have a light-bulb. If you turn the bulb on, lots of light will hit the screen with the slits, and only a tiny amount of light will go through the slit. You may notice that light radiates outward from its source, much like ripples radiate outward from a witch or a duck dropped into a pond. Like the light-bulb, the slit acts as a single source, and so light radiates outward from it in the same rippling fashion. Some of the light from Slit A hits the light from Slit B. If the light from Slit A is in the crest part of its wave (”up”) and the light from Slit B is in the trough part of its wave (”down”) you get a complete cancellation of signal, a.k.a. Dark. If the lights are in the same part of their respective waves, you get a magnification of that part, a.k.a. “Extra-Light.” On the screen you’ve placed behind all this, the resulting image is alternating bands of light and dark. And if you’re considered safe with a box cutter and a light-bulb, you can indeed try this one at home.

But what if you had the capability to pass a single photon through either slit? Instead of massive photons that can then radiate outward from both slits, you would be sending a single particle of light through either Slit A or Slit B. Conceivably, you could observe where it lands on the screen and perhaps learn something about photons.

The problem was that when this experiment was actually performed with individual photons in 1909, the same “light-dark-light-dark” pattern emerged. Weird, very weird. As only one photon was going through at a time, the only explanation for its cancellation, according to the Physics Lords, was that the photon was meeting itself on the other side of the slit and canceling itself out. This is to say, the same photon was going through Slit A and Slit B at the same time, and hitting itself on the other side. Just think about that the next time you want a Doppelganger - apparently you might not be so pleasant to yourself on the sidewalk.

So photons can exist in two places at once. Researchers have run all sorts of experiments and established that only tiny things like photons, atoms, electrons, etc, can do this. Thumbtacks, however, cannot, and you should always make sure the grad student isn’t standing behind the screen if you attempt to double-check this fact. It’s all fun and physics….

To curb their disappointment that they’d never be able to send themselves to the store and the Hawking lecture at the same time, physicists began hypothesizing as to what might cause their “location” handicap. Some sort of cosmic “obesity?” Were they, perhaps, just too dense? How could they ever get out of trash removal and other boring household chores? When dealing with particles that you cannot even hope to observe in their natural habitat (what do quarks do for fun? How do gluons attract mates? Do physicists get out much?), there are a lot of “What in the hell is going on?” questions floating about.

The prevailing explanation is the Copenhagen Interpretation, formulated by Werner Heisenberg (Mr. Uncertainty himself), and Niels Bohr (who was actually quite interesting). They postulated that we do not see the effect of multi-location in daily events because the minute we actually observe an object, we see one particular version of the object anchored in our given reality. So, if you’re outside, the contents of your room are jiggling about in multiple places, but when you look in the window, they all suddenly snap into their given places in your given time. Is it just me, or does that sound really silly when it’s worded without scientific terms? As Einstein said, “I like to think that the moon is there even if I am not looking at it.” Amazingly, most physicists seem to think the Copenhagen Interpretation is the right answer, and go about their quantal studies as if all was well in the Universe, whichever one they’re looking at.

The second interpretation is one that shows up periodically in science fiction. The Many Worlds Interpretation is by far the more fun of the two ideas, and can generate the best novels. In 1957, Hugh Everett III postulated that objects do indeed exist in multiple places at the same time, they just do so in different universes. So in one universe, you are reading UberGeek Theatre, in another you are writing it, and in another, you’ve eschewed humanity altogether, grown gills and returned to the oceans. You can see a) why this makes for good works of fiction/episodes of Star Trek and b) why this is the runner-up as far as explanations go. The potential number of universes is infinite and eventually seems to degrade into Monty Python levels of silliness. Which, I suppose, doesn’t make it invalid, just silly.

So either our eyes determine the world, or we are trapped in one particular universe (perhaps longing for another). Really, I was a bit disappointed in modern physics when I found this out. Surely, there’s something more, well, reasonable than either of these interpretations, I thought. Surely, there’s more to life, location and quantum liberty than this.

In fact (and you saw this coming), there may just be a new, somewhat more reasonable interpretation. An interpretation, no less, that might be testable, and therefore has the potential to become (drum-roll please) a Theory, given enough time, money, and grad students eager to slog long hours dealing with the super-microscopic and hopefully inanimate world.

Roger Penrose (”Sir” to you or I), is a bit of a Physics Maverick, a Cowboy among the Quanta, you might say. He’s created designs for M.C. Escher, championed a controversial link between consciousness and quantum processes in the brain, and staunchly refuses to buy into the Copenhagen or the Many Worlds Interpretation, belonging to a group of “steady-state” idealists, who believe the Universe is eternal. (He also rustles quanta with a lasso rather than a string theory. Okay, that was a bad joke. Really bad. Oy.)

Penrose holds that the field of quantum mechanics has too long overlooked the one force it cannot seem to explain: gravity. For most atomic and subatomic particles, the force exerted by gravity is so weak that physicists often leave it out of their equations entirely. Rather than ignoring it, or assuming that someday we’ll be able to explain it in terms of quantum mechanics, Penrose suggests we start looking at its real impact on objects of all sizes, particularly those like photons and specks of dust, which live at the shadowy edges that divide visible from invisible. His idea, potentially called “The Gravitational Interpretation,” is that all objects exist in multiple places until they interact with gravity. Gravity exerts a different amount of force on the object depending on its location. Since the Universe is inherently lazy (that’s my excuse, anyway), and it takes more energy to maintain two locations and thus two gravitational forces at the same time, the object eventually settles on the path of least resistance - one place, one gravitational force.

Of course, this idea has its detractors. One physicist has pointed out that just because Penrose doesn’t like the way the Universe is, that isn’t justification to call an accepted interpretation wrong. In my view, this is a tad reactionary (a bit like saying “the Earth is flat, just deal!”). After all, Penrose thinks he can test his idea. For the sake of space, I won’t go into the details of the experiment - it involves a photon, a beam splitter, and a few very small mirrors. Without more long-winded details (this is getting uber-long enough), if the photon doesn’t cancel itself out, Penrose has some serious evidence for his hypothesis. It’s not proof, but neither is it just a well-reasoned argument. Whoever figures the experimental design out (and doesn’t just cheat and look it up), gets a cookie, maybe several cookies (if you eat them with your eyes shut).

So, sadly, it turns out that the main problem with humans in terms of location is that we are larger than a speck of dust, or unable to see into multiple universes. And as we haven’t overcome gravity; the odds of getting away with the excuse of “I did take out the trash! Just not in this Universe!” are slim to none; and the trash itself fails to go away just because we’re not looking at it; I’m afraid we are all stuck with our chores and obligations until a better interpretation comes along.