The Chasm and the Collision: Chapter 7 is now available


My apologies to those who were expecting CatC chapter 7 to be available in the middle of the month.  That was the plan, of course, but I have been in transition back to Florida, into a new dwelling (that sounds more impressive than “little house”, doesn’t it?), and restarting my “day job,” after a bit of a hiatus, so things have been a bit erratic.  It is, in any case, available here, now.  The schedule should self-correct now, and I plan to release Mark Red:  Chapter 14 at the end of November as planned…which will only be a few days from now.

I think this chapter of CatC is a particularly good one.  Our heroes are caught up in what seems to be a peaceful discussion with the people who abducted them from near their school, and they learn about a monstrous danger that threatens…well, everything.  They also learn that something they have done, quite unwittingly, seems to have made that danger far greater.

Then, of course, they are faced with an immediate and surprising threat to their own lives, and that’s rarely a good thing.  To survive, Alex is forced to do something truly horrible that he doesn’t understand.

If you want to find out more…well, you know what to do.

On an unrelated note, I’ve decided to expand the publication of Paradox City, and instead of one novella, it’s going to contain three stories of mine.  The title of the compilation will now be “Welcome to Paradox City,” unless some clearly better title comes along, and the cover will be suitably adjusted.  It should come out sometime in the next month or so, I suspect.

In the meantime, Son of Man is in the process of being edited, which of course will take some time, given the fact that it is a full-length novel.  We’re also not ready with a cover yet, but there’s still time for that, so don’t panic…

I’m also going to be making an announcement soon about a change in the process of my non-publishing/writing-related content in the future, so keep your ears pricked and your eyes open (but please, don’t keep your eyes pricked…that can lead to expensive visits to the ophthalmologist).

Lest anyone worry about what’s happened to my writing during my transition, I can at least reassure you:  I have continued to write at least 5 to 6 days a week, never less than 1400 words a day, and usually more.  So, much that is new will continue to be forthcoming.

Well, that’s everything for the moment.  I hope you all had a wonderful Thanksgiving and a reasonably sane Black Friday.


“I Am” (Soy) Isoflavones, and I (probably) Decrease the Risk of Prostate Cancer

I recently had a friend ask me whether eating and drinking soy products can increase the risk of prostate cancer; he had heard that it can, and that all men should avoid soy “like the plague.”

This question really surprised me, because most of the medical information I have encountered has tended to point in the opposite direction…and for reasons that made good, sound biological sense.  However, I know that good, sound, biological sense doesn’t always pan out.  This is why we have to do actual experiments.  After all the Universe is complex, and the human body is arguably the most complex thing we know of in it.  Often an expected biological effect of some dietary or medical intervention, that seems inescapable on its face, can turn out to be utterly undetectable or at least thoroughly confounded by other consequences.  So, bearing this in mind, I did a little reading, and I learned about at least one source of data that might have been behind what my friend had heard.

First, though, to get back to the believed protective effects of soy:  Soy products contain chemicals called flavones and isoflavones, which are part of a group of biological chemicals called phytoestrogens.  Now, “phyto-” is just a word root that means “plant,” and estrogens are, well…estrogens.  I think most people in America are at least passingly familiar with estrogens, especially given the current controversy over the required coverage of birth control pills.  So phytoestrogens are just estrogens from plants.  In human females (we often refer to them scientifically as “women”), estrogens are among the hormones that control fertility and related processes, and they are quite abundant.  However, in the male body–including that little devil, the prostate–estrogens tend to counter the natural effects of testosterone.

Testosterone is also, I suspect, a hormone of which most Americans are aware.  It is the substance, to paraphrase Dave Barry, that makes men take league softball seriously.  Its actions produce such male secondary sex characteristics as increased muscle mass, facial hair, deeper voices and bar fights.  It is also the hormone responsible for the fact that almost every man who lives long enough–if he isn’t testosterone deficient–will develop prostate enlargement (so-called “benign” prostatic hyperplasia, or BPH), with its lovely constellation of maddening symptoms.  The presence of testosterone can also stimulate the growth of many kinds of prostate cancer, and in fact some treatments for testosterone-sensitive tumors include drugs that directly block testosterone, such as bicalutamide (the name isn’t really that important).

It is thought that the effects of phytoestrogens in soy products are responsible for the protective effects that they may have against prostate cancer.  These effects are not tremendous, nor are they absolutely demonstrated, but they are probably real and the science is sound.  So whence comes the idea of soy actually increasing the risk of prostate cancer?

Well, I found out about a study in Japan that covered a number of different dietary sources of soy and its isoflavones on the risks of development of several subgroups of prostate cancer, including localized and advanced cases.  This was a good country in which to study those effects, because the traditional Japanese diet includes a number of soy staples, including tofu, miso and natto (a kind of fermented soybean concoction).Not too surprisingly, this study actually generally supported the idea that soy intake in foods (not necessarily supplements) reduces the risk of prostate cancer overall…but there was ONE little peculiar exception.

The study found that increasing intake of miso soup may be associated with a small increased occurrence of advanced prostate cancer in men 60 years of age and older.  Now this reallyis peculiar, because it seems very specific to miso soup, which raises the question of whether there’s something ELSE in miso soup that’s causing this measured increase.  Also, such studies are always inexact because there are so many potential variables that could be influencing the outcomes by other means.  In addition, the number of cases of advanced prostate cancer in this study, compared to the size of the study, was VERY small, which means the statistical connection is quite a bit less robust than it might be.

Nevertheless, I can at least tell my friend this:  Unless he’s eating a LOT of miso soup (and is over 60), he probably doesn’t need to curtail, let alone avoid, soy products.  In fact, he can probably indulge in all the soy milk, tofu and natto he wants, and if anything, it may decrease his risk of prostate cancer a little bit.  It’s even possible (though not clearly demonstrated) that it might reduce his future problems with prostate enlargement.  Of course, the trade-off is that he may find himself caring a little bit less about who wins a particular sporting event.  Still, having treated a good number of men suffering from prostate problems of various kinds, I can assure you, that would be an extremely small price to pay.

Diabetes For Beginners – Part 2

Welcome to Part 2 of my “freshman lecture” on Diabetes.

Now we get to Type 2 Diabetes Mellitus. Interestingly enough, although this is “Type 2”, it is in fact by far the Number 1 form of Diabetes numerically, with 90 to 95% of Diabetics falling into Type 2…and that number is likely, if anything, to become larger.

Individuals with Type 2 Diabetes do produce insulin, despite what you might think. In fact, oddly enough, many of them produce way MORE insulin than is good for their bodies. So what’s the problem, how can they be Diabetic? Well, the problem in Type 2 Diabetes involves insulin resistance by the cells of the body…especially the fat cells.

This insulin resistance usually starts off as just a sort of predisposition, where some people’s cells respond to insulin a bit more sluggishly than others. At first this doesn’t produce any obvious clinical results, because the pancreas responds to that sluggishness by just putting out more insulin when the glucose doesn’t get taken up fast enough. Unfortunately, this only works for a little while. That’s because the insulin resistance tends to increase as the cells respond to the higher amounts of insulin. In a way, they get used to it, rather like someone losing their hearing when being surrounded by loud noise all the time. Eventually, despite the fact that the islet cells are putting out way more insulin than they would in a healthy state, the body just stops responding well to it at all, and the blood sugar goes above normal levels. This is the clinical onset of Diabetes Type 2, but I think you can see that the real disease starts a long time before this happens.

Type 2 Diabetes is only very rarely associated with the horror of ketoacidosis, but that doesn’t mean it doesn’t have horrors all its own, and though they are subtle, they affect far, FAR more lives than any aspect of Type 1 Diabetes. Long before the blood glucose starts to goes up, individuals heading toward Type 2 Diabetes have chronically elevated blood insulin levels, and this has effects on more than just the blood sugar. It leads to elevation of serum triglycerides, for one thing, and as you may know, this is one of the “bad” forms of lipids (often collectively referred to as “cholesterol” though that’s not strictly accurate). The triglycerides in particular—and elevated insulin itself—increase the risk of coronary artery disease and other vascular diseases, and it’s probable that the chronically high insulin contributes to an increased risk of hypertension (also known as high blood pressure). The heart, the kidneys, the blood vessels, the eyes…eventually all the systems of the body are damaged by these processes.

Once the blood sugar is elevated, the overall effects of Type 1 and Type 2 Diabetes overlap a great deal, except as discussed above. Unfortunately, having extra blood sugar, as you might guess, doesn’t give a person extra energy. Quite the contrary, it usually leads to low energy, partly through dehydration as the sugar spilled in the urine takes water away with it, and partly from a simple inability of the body to use the glucose appropriately. People with untreated Diabetes tend to lose weight, but it’s not a good kind of weight loss. They lose lean body mass for one thing, and lean body mass is the tissue that responds best to insulin and helps lower the blood sugar and improve the overall health.

People with Diabetes also, unfortunately, develop a lot of complications from having just too much sugar throughout their system. You see, sugar is not a completely benign substance. Your mother probably made this clear to you long ago, but you may not realize just why it’s so. Glucose is a very chemically active substance, which is why it’s useful as a source of energy. But when it’s around in large quantities for a long period of time, it tends to react chemically with things with which we don’t really want it to react. For one thing, it binds very nicely—without any help—to various kinds of proteins, and then doesn’t tend to unbind itself. This can actually be useful in measuring how the long-term blood sugar has been, and is the subject of a test called the hemoglobin A1C, which measures how much of a certain type of glucose-bound-hemoglobin there is in the blood, giving a good estimate of how the blood sugar has been over about the last 4 months (Why four months? Red blood cells live about four months in the body, and they are where all the hemoglobin is).

Still, glucose binds to lots of other proteins in much less useful ways than this, and over time this binding tends to create dysfunction in the proteins, and in the structures of which they are part. Such binding happens in the proteins that make up small blood vessels—such as those that feed nerve endings, for instance—narrowing those vessels down until the nerve endings or any other tissues the vessels supply start to die. This (plus a bit of contribution from thickening of the vessel walls due to elevated insulin in the Type 2 Diabetes patient) is the cause of “Diabetic Neuropathy,” a numbness that develops, usually starting in the extremities and working its way up. Though the inability to feel pain might sound nice at first, it leads people to be unaware when they have, for instance, developed blisters and cuts on their feet. Cuts and blisters that are unknown tend to be untreated and thus prone to infection. To top that off, the elevated blood glucose itself makes a person with Diabetes an especial treat for many kinds of bacteria, and it interferes directly with the function of the immune system. This combination of factors leads many uncontrolled Diabetics to face the frightening prospect of infections that cannot be adequately treated and that lead to amputations.

Elevated blood sugar also affects the eyes in a number of ways: The effects of elevated insulin and sugar narrow the arteries in the retina (the sensing surface on the back of the eye) and lead to various consequent visual problems. In addition, the sugar causes fogging of the lens of the eye as it binds with proteins there, producing cataracts.

The kidneys, dealing with the high load of fluid and with the glucose that gums up its complex structure by binding to the proteins—complicated by the often-coexisting problem of high blood pressure—tend to deteriorate under the influence of Diabetes, and many Diabetics progress to kidney failure, requiring dialysis to stay alive.

There are, of course, many treatments available for the complications of Diabetes, though none are quite perfect. There are also treatments for Diabetes itself. Type 2 Diabetics can receive extra insulin to help overcome their insulin resistance, but this extra insulin can cause problems of its own and tends to lead to weight gain…and that gain is often in the fatty tissues, which leads to increased insulin resistance, and so the spiral continues.

There are medications—called sulfonylureas, not that the name is that important here—which stimulate the pancreas to release more insulin in response to blood glucose. But as with giving extra insulin from outside, this tends over time to increase resistance and can thus only go so far.

There are a number of other medications that can help with Type 2 Diabetes. Some suppress the liver’s uncontrolled creation of new blood sugar when it’s not responding to normal suppression by insulin. Some try to increase the body’s cells’ sensitivity to insulin. These medications all have their place and they all work to one degree or another. Yet none of them work as well as avoiding Diabetes in the first place, when possible.

Yes, in many people Diabetes can be avoided and/or largely corrected by some simple changes in lifestyle—well, they’re simple in concept, though carrying them out requires willpower and determination. The main interventions are: diet and exercise. Simply put, keep the intake of simple carbohydrates (that’s sugars and white starches, basically) to a minimal amount, and do regular exercise, especially aerobic exercise (exercise where you keep moving without break, such as walking, swimming, running, biking and so on) three or more times a week for a good half hour or more at a time. Of course, if you have underlying health problems, you need to check with your doctor before starting an exercise routine, and you certainly shouldn’t try to achieve Olympic level results right from the start. But the problems of Diabetes in individuals who are predisposed CAN often be minimized and even sometimes reversed by appropriate lifestyle choices, for as long as those choices are continued. It’s not literally a cure, but it can sometimes be the next best thing.

Well, this has been a very quick rundown of Diabetes, aimed at those who don’t know much more than the term itself and that it’s related to high blood sugar (and is NOT a good thing). I hope it’s answered some questions and…just maybe…stimulated some new questions in the reader. If you have any such questions, please, by all means, leave a comment with your question, whether it’s about something you’d like to know more about or just about something I wasn’t clear enough on in my explanation. I’d be delighted to respond.

Trying to help more people understand more about medicine and science is, after all, the whole reason I’m doing this.

What Are Black Holes?

[Another reprinted article]

A very old friend of mine—that is, one I’ve known a long time, he’s no older than I am, and I hope I don’t yet count as “very” old—suggested that I write an article about what exactly black holes are. So, I thought about it, for all of about two seconds, and realized that black holes would be a great topic for a general science article.

So, what are black holes? Well, in their most common form, black holes are the final remnants left behind after the deaths of the most massive stars. You see, during their ordinary, active lifetimes, stars are at a constant balance point between the force of gravity that tends to make them contact, and the force created by nuclear fusion and its consequent heat, that makes them tend to expand. This balance is maintained for a very long time…though interestingly, the length of time is inversely proportional to the size of the star. That is to say, the bigger the star is, the shorter its lifespan.

Sooner or later, though, every star will run out of its nuclear fuel and won’t be able to provide enough internal heat to keep from collapsing further. There’s usually a sort of contraction and expansion phase as stars get near this stage, and it’s during these times that especially the bigger stars start fusing heavier and heavier elements…but that’s really an issue for another article entirely. In any case, when a star runs out of usable fuel and gravity is no longer opposed by fusion, the star collapses. In some stars this collapse is so powerful and releases so much energy that a “supernova” occurs, a HUGE stellar explosion, where a lot of the star’s matter gets shot back out into interstellar space. This is how every element we know of other than hydrogen, helium and lithium came to be.

Now, depending on how big the star is to start with, when it collapses it will have one of only a few possible fates. Since gravity is dependent on the mass of the star, smaller stars will have less of a contracting force, and they—as our sun is expected to do—become white dwarfs. Gravity shrinks them down until their individual atoms are only separated by the quantum mechanical forces between the electrons (not the electrical repulsion, but the simple resistance electrons have on a quantum level to being too close together). This is about as densely packed as atoms can get and still be atoms. Our sun will probably shrink until it’s about the volume of one of its rocky inner planets like the Earth…although the Earth will almost certainly have been incinerated by the sun before that ever happens. Still, you get the idea.

A star that’s maybe two times the mass of the sun will have enough gravity that the electron forces won’t hold it up. Only the nuclear forces will be strong enough to resist this much gravity. These stars are among the ones that become supernovas, in part because of the tremendous energy released in this collapse that overcomes electron repulsion. The gravity of these stars is so huge that it squeezes the former atoms all in on themselves, sort of mashing the protons and electrons together and creating a huge ball of neutrons…a neutron star. This is about as dense as matter can get in a form that we can recognize as being made up of any kind of individual particles. What you’re left with after this collapse amounts to a single gigantic atomic nucleus…though without any protons and an unthinkably large atomic mass. It’s so heavy and the gravity is so huge that any human—or indeed any other unfortunate entity of normal atomic constituents—would be squashed immeasurably flat on its surface.

It would at least be a pretty fast death though.

Now we come to stars that start out at about three times the mass of our sun or more. When these star collapse, there’s nothing even nuclear forces can do to resist the gravity, and in fact, no known force can resist the collapse. These stars become black holes.

There’s a bit of trouble in describing what really goes on inside a black hole. According to general relativity, the mass of the star becomes compressed to an infinitesimally small and infinitely dense point called a singularity. Now, scientists are pretty sure this isn’t exactly accurate, since infinities are usually not literally achievable within the universe as we know it. Also, a truly infinitesimally small concentration of matter would violate the Uncertainty Principle, which is a law of nature that seems every bit as immutable as gravity. So here in the heart of a black hole we arrive at the notorious point of conflict between general relativity and quantum mechanics. I’m not going to try to explain how that conflict is to be resolved, because so far no one knows.

One reason why it will be hard to resolve this conundrum is because black holes are, well…black. The reason they are called black holes is because when gravity is that strong, even light can’t escape it. Yes, gravity effects light, though for anything short of a black hole that effect tends to be unnoticeably tiny. Yet the principle of why a black hole is black is fairly simple. It has to do with escape velocity.

Escape velocity is a measure of how fast something has to be going when leaving the surface of a body such as a planet or a star or a galaxy in order for it to fly completely away from the body and not remain at least in orbit (or come crashing back down on the head of the people below). From the surface of the Earth, you’d have to throw something upward with a speed of about 7 miles a second (ignoring air resistance) to keep it from coming back down or getting stuck in orbit. That’s pretty fast, but it’s TINY compared to the speed of light (about 186,000 miles per second).

Then again, the Earth is also really tiny, on the scale of stars. A very large star that has collapsed completely can have a gravitational pull so powerful that its escape velocity is greater than the speed of light. Well, so far as we know, light is still the fastest stuff in the Universe (rumors about neutrinos notwithstanding), so if light can’t escape from that gravitational field, then NOTHING can. That’s why black holes are black.

The blackness of black holes doesn’t just stick around right at that tiny point called the singularity. The gravity is strong enough that any light—and thus anything else as well—that gets closer than a certain distance to the singularity will never be able to escape. That distance from the center of the black hole defines a sphere of inescapability called the Event Horizon, or just the Horizon. This is a good name, because the horizon on the surface of the Earth is the point you can’t see past because of the curvature of the Earth, and the Horizon of a black hole is the point no one and nothing can see past because of the curvature of space-time (in other words, gravity). The size of the Horizon of a black hole is based simply on its mass. As more matter falls into a black hole, the horizon grows…though what exactly happens to the singularity in the center is unknown, and may remain so forever, since even in principle there’s no known way to get information from inside an event horizon.

Though they are all very similar in character, black holes come in a lot of different sizes (by which I mean their masses and the areas of their event horizon are different). There are “ordinary” black holes that are the remnants of large stars. There are also “super-massive” black holes, believed to be at the center of most galaxies—including ours—and which have the mass of millions or even billions of suns.

Theoretically, there may also be very small black holes with the masses of mountains, which might have been formed during the early Universe by the enormous pressures associated with the big bang. These black holes wouldn’t so much have collapsed as have been squeezed inward, and they wouldn’t have to have a very huge amount of matter. Yes, you can make a black hole that way. Well, YOU can’t, and I can’t but it’s theoretically possible, though not demonstrated. Still, some relatively small black holes could still exist out in the Universe, remnants of the tremendous forces unleashed when the Universe began.

There even could be submicroscopic black holes created by VERY energetic collisions of fast-moving particles, as in very large accelerators or in cosmic ray collisions. These would be black holes whose Horizons are on the size-order of subatomic particles. These are nothing to worry about, by the way, because—and this is something many people don’t know—black holes don’t last forever. They have a limited lifespan due to a quantum mechanical phenomenon called Hawking radiation (yes, it’s named for THAT Hawking). This describes the fact that all black holes are actually radiating particles and photons from just outside their Event Horizon. I’m not going to go into how that works right now (it’s not all that difficult to understand, but it would take quite a bit of explaining), but it means that the mass of a black hole does go down over time and eventually it will disappear, like water boiling out of a pot. What’s more, the smaller the black hole is, the faster it evaporates. Any black holes made accidentally—or deliberately—in particle accelerators would be so small that they’d evaporate before we could even directly tell they were there. Such black holes may pop into existence in the upper atmosphere every day…many times a day…when highly energetic cosmic rays hit the earth. So don’t freak out about CERN making a black hole that would swallow up human civilization. If that was going to happen, it would be happening several times every day at least, in the sky above our heads.

Well, I hope this article answers at least some questions about what black holes are, as well as giving some related and interesting information. I’ve left out a lot, but I know I’ve also covered things at a bit of a breakneck pace. If there’s anything that’s unclear or confusing, please let me know. I’m happy to receive constructive criticism on this most destructive of topics.

And to my very old…well, to my “long-time” friend who suggested this article: I hope you found it helpful.

Diabetes For Beginners – Part 1

Diabetes is an illness of which I suspect almost all adults in America are aware. I also suspect that most people know that it has something to do with high blood sugar and that having high blood sugar is a bad thing. Still, I imagine there are a fair few people out there who haven’t really got a lot more understanding of it than that—including some people who have the disease—because they haven’t really had it explained to them in terms they can follow. After all, doctors—of which I am one—don’t often take the time necessary to make sure that their patients fully understand the ins and outs of a disease process. Partly this is because, when one understands something on a very complex level, it seems like it’s going to take serious effort to explain it to someone who doesn’t have the same educational background. However, I think this is a failure of imagination and a bit of mental laziness on our part as doctors. The Nobel-Prize-winning physicist Richard Feynman used to prepare “freshman lectures” about physics subjects when laypeople asked him about topics they didn’t understand. If he found that he couldn’t prepare one, he recognized that failure as an indication that the subject wasn’t well-enough understood!

I just love that philosophy and attitude. So, since Diabetes in general is pretty well understood, I’m going to try to give a “freshman lecture” here on Diabetes.

First off, “Diabetes” is actually only part of the name of the disease we’re going to be discussing. The full name of the disorder is “Diabetes Mellitus” and this diagnosis is then subdivided into Type 1 and Type 2. The term “Mellitus” serves to differentiate the common disease known as Diabetes from the far-more-obscure disorder “Diabetes Insipidus,” which I will not really be discussing here.

You see, the word “Diabetes” is a Late Greek word meaning “excessive discharge of urine.” That’s originally all the word referred to, since that is the most noteworthy presenting problem in both kinds of Diabetes. The meaning of the second words in the disease names is going to gross a few people out, and that’s completely understandable. You see, “Mellitus” means (more or less) sweet-tasting, whereas Insipidus—and this will be obvious when you think about it—means “tasteless”.

Sweet? Tasteless? What is sweet or tasteless?

The answer is: That excessive discharge of urine. Yes, in the old days, one way they used to diagnose things was to taste the urine, and the urine in Diabetes Mellitus tasted sweet. Why? It tasted sweet because it was just full of glucose.

Well, urine is not SUPPOSED to be full of glucose! Nature has designed our bodies to want to hold on to glucose, either so we can use it directly as fuel or convert it into one or another storage form that we can use for energy later. Nature doesn’t deal very kindly with creatures that waste precious energy…when survival is at stake that’s a really bad strategy. So the kidneys ordinarily filter the glucose out of urine before it’s passed to the bladder for elimination. Only when the glucose is quite a bit above normal range is the kidney’s ability to do this overwhelmed, and sugar (glucose) starts to spill into the urine and be wasted.

So, how does the blood sugar get so high? Well, ordinarily, the level of sugar in the blood is pretty tightly controlled, mostly by the actions of two major hormones: glucagon and insulin. Most people who have heard of Diabetes have probably heard of insulin. Insulin is a type of hormone called a peptide, which means it’s a small, clipped version of a protein. It’s produced in the pancreas by a group of specialized cells called beta islet cells in an area called the Islets of Langerhans. The name isn’t really that important, except that things have to be given names so we know what we’re talking about when we’re talking to each other. The cells in the pancreas that make insulin were first described by a scientist named Paul Langerhans, so they got named after him. That’s how it works with a lot of obscure medical terms.

Insulin is secreted (released, in other words) by the islet cells in response to the sensed level of glucose in the blood. The more glucose there is, generally, the more insulin is released. Why is this necessary? Because the cells of the body only take up glucose when they’re stimulated to do so by the action of the hormone insulin. Insulin is, quite literally, the signal that tells cells to activate the machinery they use to take glucose in, after which they can digest it for energy to run their metabolism, or they can store it for burning later. So, when we eat and our digestive systems bring glucose into our blood, the glucose level rises, the islet cells release more insulin and the cells take up more glucose. It’s a good system, and usually it works brilliantly.

Incidentally, glucagon, which I mentioned before, is in a way the opposite of insulin. It is released in response to lower blood sugar, and stimulates the release of glucose from storage or the creation of new glucose by the liver. These two hormones—insulin and glucagon—in a healthy person, work beautifully in counterpoint, and maintain the blood sugar between roughly 60 and 100 milligrams per deciliter at all times. It’s a lot like the cruise control on a car, which applies a little more or less power as needed to keep the speed where you set it. A healthy body has a very tight and responsive glucose cruise control.

Diabetes happens when the insulin system breaks down. There are two main ways that this happens, and there are, therefore two main kinds of Diabetes…very cleverly called Type 1 Diabetes and Type 2 Diabetes.

In Type 1 Diabetes, there is a failure of the beta cells in the Islets of Langerhans…usually caused by some kind of inflammation destroying those cells. When this happens, there is no longer any production of insulin to speak of, and without insulin, the cells of the body don’t take up blood sugar. Without blood sugar, many of the cells of the body cannot get new energy, except by very specialized and limited means that have their own downside to the body when they operate without restraint. A person with Type 1 Diabetes absolutely requires the administration of insulin from an external source. This is usually done by injection into the subcutaneous tissue by a fine needle, generally a number of times a day. Without this treatment, a person with Type 1 Diabetes will not be able to get glucose into their cells. They will lose oodles of glucose in their urine, they will rapidly lose weight and dehydrate (because all that spilled glucose in the urine carries a LOT of water with it), and ultimately they will go into a catastrophic state called “Diabetic ketoacidosis.” I won’t get into the specifics of this right now, but it DOES involve the blood becoming quite a bit too acidic, among other things. None of the effects involved are good for the function of a human body, and unless treated quickly and given replacement insulin, a person in Diabetic ketoacidosis will die.

Wow, that’s pretty scary, isn’t it? Fortunately, nowadays we have a number of different forms of readily available and inexpensive injectable insulin for Type 1 diabetics to use…and there are scientists working all the time on better ways of treating this disorder, including working on developing insulin that can be given without injection and transplantable replacement islet cells. Stem cell research may be able to deliver that last modality in readily workable form, without the worry about tissue rejection, so we should all do everything we can to support such research.

Well, this has already gotten pretty long, so that’s going to be it for the first half of the article. I’m going to continue this discussion, of course, in Part 2 which will, appropriately, start with the subject of Type 2 Diabetes Mellitus.

So What Is All This GeV Stuff, Anyway?

[This is a reprint of an article I wrote for my hubpage…but I want to focus here on my own page, now, so hopefully no one will be too upset by the re-use.]

Recent news about events at the Large Hadron Collider in Switzerland has brought particle physics more into the mainstream, as scientists have discussed hints that they’re getting closer to finding and defining the Higgs particle…the messenger particle of the Higgs field.

I’m not going to try to rehash the meaning and nature of the Higgs field here. Most of the articles I’ve looked at do at least a decent job with that subject. If you want an even better treatment–as well as a fantastic summary of the state of modern physics that is thorough but extremely understandable–I recommend getting a copy of “The Fabric of the Cosmos” by Brian Greene. He does a better job of explaining difficult subjects in easy-to-understand terms (that nevertheless don’t dumb down the material) than just about anyone else I’ve ever read.

No, what I’m going to talk about is a term that’s thrown around an awful lot in articles about particles: The GeV (and more generally, the eV). The term eV is shorthand for “electron volt,” and “GeV” is the notation for “giga-electron volt”…a billion electron volts, in other words (MeV, mega-electron volt would be a million electron volts).

But wait…the articles about the Higgs (and other writings about atom smashers) refer to measures such as 125GeV as being a measure of a particle’s mass! What does that have to do with volts!? Don’t volts have something to do with electricity? Isn’t household current measured in volts? Does that mean that it takes a Billion times as much voltage as in household current to find a Higgs particle?

Well…not exactly. In physics, the electron-volt is actually a measure of energy, not the voltage in a circuit. Specifically, it’s the amount of kinetic energy (the energy of motion) a free electron would accumulate after being accelerated through a potential difference of one volt. You see, voltage is to electrical fields a lot like what pressure is to water. Voltage differences push things that respond to electric fields…and electrons are one of the most well-known of things that respond to electrical fields, and have been since at least Benjamin Franklin’s time. In other words, falling through a “pressure” difference of one volt will accelerate an electron until it has a kinetic energy that is defined as one electron-volt.

So what the heck does the kinetic energy of an electron have to do with the mass of a Higgs particle? Well, as you probably know, energy can change its form, but it doesn’t disappear, and if need be can always be measured in the same units. At every day energy levels, physicists are more likely to use joules as a measure of energy…a joule is the amount of energy put out by something that has one watt of power in one second. So a one hundred watt bulb puts out 100 joules of energy every second.

Now, when you’re dealing with smaller scale things–like electrons and protons and Higgs particles (Oh my!)–it’s better to use a smaller unit of measure. The eV is a VERY small amount of energy, and can be excellent currency when describing what goes on in interactions between subatomic particles. Just as you wouldn’t use a brick of gold to try to buy a gumball out of the grocery store gum machine, but would instead use your pocket change, you don’t usually use joules in particle physics. You COULD, of course…but you’d be using REALLY small fractions of joules and it’s just easier to use the particle physics version of pocket-change, the electron-volt.

But still, what does this have to do with the mass of a particle? I’ve been talking about energy here!

Well, now we come to probably the most famous equation in all of physics, at least as far as the general public is concerned: E=mc2 (the two here means “squared”, or a number multiplied by itself). This equation explains that matter and energy are interchangeable. Matter and energy are just two forms of the same thing. So you can describe how much Stuff something is made of by describing it in ordinary terms of Mass (such as grams and kilograms), or, if you’re feeling like it and if it’s useful, you can describe it in terms of energy. Now, the “c” in that famous equation is the speed of light, which is mighty fast: about 300,000 kilometers a second (about 186,000 miles per second). It’s already a big number, but when you multiply it by itself, it’s MUCH BIGGER. So even a little mass converts into an awful lot of energy. That’s why nuclear reactions are so powerful: they convert a fraction of a percent of the matter involved in the reaction into energy, and you get all the glory of our sun and all the horror of nuclear weapons.

So finally we arrive at the reason for using eV’s and MeV’s and GeV’s in particle physics. It turns out that, like joules, working with ordinary mass units like grams gets very cumbersome when talking about really tiny things like subatomic particles. You have to use extremely small numbers with a lot of zeroes after the decimal point. If you’d rather not deal with all those zeroes, well, since matter and energy are interchangeable, you can instead describe very small masses in terms of a pretty fair number of a similarly small unit of energy. An electron-volt is just such a useful small unit.

In other words, when they say that the Higgs particle doesn’t look like it can be more than 125 GeV in mass, they mean that, if you took its mass and turned it into free energy, the amount of energy you’d get would not be more than 125 billion electron volts. That may sound like a lot, and on the scale of subatomic particles, it IS. However, it really is a very small amount of energy, and thus an exquisitely small amount of matter.

Of course, the Higgs fields is thought to permeate literally the ENTIRE universe, and the Higgs fields effects are all carried out by Higgs particles, so the mass equivalent of the field would add up to a pretty big amount in total. In fact, ALL the ordinary things with which we are familiar are made up of particles whose masses can be described in terms of electron volts, and most of those “weigh” a lot less than the Higgs appears to. So big things are made up of small things, just lots and lots of them. Like, lots and lots of electron volts of energy can equal the mass of one small but very important particle.