A Tenuous "Alli"ance

It appears that GlaxoSmithKline has recieved approval to market Alli overseas to our European cousins.

This means the product will now be proposed for final approval by the European Commission and marketing authorisation could be granted in the coming months. On licence grant, orlistat 60 mg would be the first licensed weight loss aid available without prescription throughout Europe.

You hear that? An FDA-approved weight-loss supplement! It's a miracle!

Alli was actually released to US markets last summer as one of the more unusual Rx-to-OTC product conversions that we've seen recently. Popular once prescription-only Zyrtec I expected, but Alli was really out of left field. I actually meant to blog about Alli when it was released, but somehow it got away from me. Now I can do so to commemorate its release across the pond.

What is Alli? Alli contains the same active ingredient as a prescription drug that was developed by the Swiss company Roche Pharmaceuticals--the generic name for it is orlistat. It is the first over-the-counter drug approved as a weight loss aid by the FDA, mostly because there's good clinical data that it's actually effective when used properly.

OTC "diet pills" generally contain high doses of stimulants/caffeine, claim to suppress appetite, or somehow purport to "melt fat" or "block calories." Some stimulant weight-loss supplements contain as much caffeine per capsule as three cups of coffee and have "serving sizes" of two or three caps at a time! Clever wording is usually employed to conceal the simplistic nature of these products--Zantrex-3 refers to its caffeine content as "a proprietary xanthine-based stimulant." Caffeine is part of a chemical family called methylxanthines. Other times numerous herbal ingredients or Latin names for botanicals obscure the true content of the supplements except to the most attentive consumers.

Alli, true to its claims, is different. How does it work?

First, a bit of basic biochemistry. There are three major "macronutrients" required for human nutrition--carbohydrates (sugars), lipids (fats), and proteins. All of these are absorbed through the intestine whenever you eat. Macronutrients are then delivered to the liver or various cells of the body that can use them. Carbohydrates are easy; the body breaks them down into smaller units and uses them to produce ATP, a small molecule that is the primary source of energy for the body at the cellular level.

Proteins and fats cannot be used directly by most cells. Instead, the liver processes them into more readily useful forms. Some proteins can be converted into glucose, the most basic (and preferred) form of fuel for body systems, especially neurons. Fat metabolism is more complicated and involves many steps that ultimately culminate in the release of free fatty acids; these are also usable as fuel by many body systems.

If you eat too much of anything, be it proteins, carbohydrates, or fats, the body is remarkably efficient at storing the excess energy produced. The most energy-dense form of stored energy is fat; fats produce the most energy (in calories) per gram. This fat winds up getting stored throughout the body as a reserve for times when food sources are scarce. Each pound of fat on your body represents a total stored reserve of 3,500 calories. Yum!

I've heard it mistakenly stated that you "can't get fat" eating a high-protein diet because "carbs make you fat" or, more obviously, "fat makes you fat," but this is completely false. Your body can (and will) make fat out of anything the liver can get its...um...lobes on.

What does this have to do with Alli?

Alli is not actually absorbed into the bloodstream. Instead, it floats around in the intestines and binds to fat molecules, preventing those from being absorbed. If your body doesn't absorb the fat molecules, it can't process them--in a sense, it's like you never ate them in the first place. Alli binds an average of 25% of consumed dietary fats, potentially reducing caloric intake from a fatty meal significantly.

Problem: Alli is not magic. It cannot break the laws of physics and destroy matter (and I suspect converting fats to energy in your intestine would have odd effects, were it possible). If you don't absorb the fats, they still have to go somewhere. Since they're already 3/4 of the way through your digestive tract, and getting the whole system to flow in reverse is both very unpleasant and very difficult, I'll let you think about it on your own for a second.

A funny aside: The makers of Alli recommend that you not wear light-colored pants while taking it.

I personally like to think of Alli as "negative reinforcement." Operant conditioning is basic psychology. Continuously eat fatty meals on Alli and you're going to suffer chronically oily stools. You're either going to learn to control your dietary fat intake or you're going to throw away your Alli.

This isn't to say that Alli is bad. As part of a comprehensive diet and exercise plan, it will help you lose more weight, even if it's only a few extra pounds. But the reason Alli can get FDA approval, aside from the fact that it's been subjected to more rigorous clinical trials, is that Alli doesn't claim to be magic. "Eat all you want and still lose weight!" "Melt fat away while you sleep!" Due to loose regulations, dietary supplement manufacturers make these kinds of claims all the time. But the makers of Alli had to be realistic about the potential benefits of their drug to get it approved. This isn't a bad thing. It's what we should expect from all drug and supplement manufacturers--indeed, it's what should be legally required.

Anyway. Now Europeans can experience the thrill of Alli without a doctor's prescription!

...just remember to wear dark pants.

Thank You, Orac, or: A Little Knowledge

This is what happens when people who know absolutely nothing about how to do science get their hands on a little bit of scientific data. An excerpt from Orac's post:

According to Mrs. Janak, less than one milligram of histidine is going to cause nausea, vomiting, and irritable bowel syndrome. Mrs. Janak needs to learn some units before she embarrasses herself by posting such burning stupid to the web. But she's just getting warmed up. She fixates on an observation that histidine is involved in the regulation of of trace minerals and concludes that getting all that histidine (remember, 0.78 mg worth, to be precise!) must somehow mess up the body's metabolism of heavy metals and cause heavy metal poisoning.

Orac, know that if I could, I would have your children. You've probably already found someone else to do that by now, assuming you want them, and I lack the essential plumbing, but the offer stands in some sort of metaphysical context.

Repetition =/= Truth

Apparently Tim Pawlenty, governor of Minnesota, was recently questioned about his position on teaching creationism/intelligent design--mostly because it's something that's come up with VP Sarah Palin, who favors "teaching the controversy."

GOV. PAWLENTY: I saw her comments on it yesterday, and I thought they were appropriate, which is, you know, let's -- if there are competing theories, and they are credible, her view of it was, according to the comments in the newspaper, allow them all to be presented or allow them both to be presented so students could be exposed to both or more and have a chance to be exposed to the various theories and make up their own minds.

Emphasis mine.

That's it. Full-stop. If they are credible. They aren't.

Evolution is a scientific theory. So is natural selection. They are supported by data, research, and observation. They don't just explain something, they invite further questions. How do things evolve? What pressures favor which adaptations? What conditions affect the visible "rate" of evolution? Thousands of issues are being explored by biologists using what we know about evolution as a starting point because it's been thoroughly demonstrated that it happens.

Creationism doesn't invite any serious questions that can actually be answered ("so, who is this designer, anyway?"). It doesn't present any hypothesis other than "stuff was designed," and that hypothesis isn't scientifically valid because it isn't testable. It is not a competing theory because it is not science.

It's disgusting that people are offended that their children are learning science in science classes because science apparently offends their theological sensibilities. And the politicians that are using this talking point--"it's a local issue"--are doing the smart thing, politically, and dodging the issue altogether. They're not saying they don't have an opinion. They're saying that they won't voice their opinion because they're afraid of alienating some portion of their constituency. No political candidate who wants to keep his career is going to stand up in front of America's 75% Christian population and tell them that their faith and beliefs are irrelevant when it comes to determining what is and isn't verifiably true.

Even if local school boards don't want their kids exposed to scary ideas like evolution, it's a waste of taxpayer dollars to teach them bullshit instead just so that they can be sheltered from theologically unpalatable truths.

All Antibiotics Are Equal

...but some are more equal than others. Or so patients seem to think.

Here's the bottom line. If you take nothing else away from this post: Antibiotics are not "strong" or "weak." They are targeted.

Patients ask me some questions about antibiotics that sound truly strange if you know anything at all about microbiology and antimicrobial agents. Granted, most patients don't have that background, and it would be unfair for me to expect them to know the difference between Gram-negative and Gram-positive bacteria or to know anything about activity spectra. Probably the most common question, in some form or another, is "is this a good one?"

The answer is not as simple as yes or no. Are the antibiotics on the market effective for treating bacterial infections? Yes. Will this antibiotic be effective against your bacterial infection? I don't know. And, chances are, neither does your doctor, at least, not for certain. Are the risks of taking this antibiotic going to outweigh the benefits? Probably, unless you're taking telithromycin for acute bacterial sinusitis (which is not an acceptable use of the drug).

That bit about telithromycin was a bit of pharmacy dark humor. If you didn't get the joke, forget I mentioned it and move on with your life.

The only way to know if a given antibiotic will be effective in treating a particular infection is to culture the microorganism causing the disease. This means taking a sample from the patient, growing the sample on a petri dish, and then trying to grow the sample in the presence of various antibiotics that are released by little discs inserted into the growth medium. The bacterial growth results are then compared to a table for each antibiotic to determine whether or not the antibiotic sufficiently inhibited bacterial proliferation to say that the antibiotic will be effective against an infection in a living person.

This process takes anywhere from three days to a week to get right. Most patients are not willing to wait that long, and the lab tests are both costly and time-intensive. Most doctor's offices are not equipped to do a lot of lab testing. As a result, most doctor's visits where patients complain of what sounds like an infection result in the patient being sent out the door with a prescription for some antibiotic that the doctor thinks will be appropriate.

You can't blame physicians for not taking the time to culture everything, though I imagine most infectious disease specialists would bite your head off for suggesting that it's acceptable to start throwing around prescriptions without doing a culture. My microbiology professor would have a heart attack if I showed him the script I transcribed from a phone conversation on Saturday; Tamiflu and an antibiotic. Tamiflu kills influenza A viruses, but not bacteria. Antibiotics kill bacteria, but not viruses. You could argue that the physician is just covering his bases and trying to help the patient.

You could also argue that this is a little bit like using a blunderbuss to kill a mosquito.

The point of culturing bacteria is that antibiotics are not like a set of progressively bigger guns. They're specific tools in a toolbox. Using the wrong antibiotic is like using a hammer instead of a screwdriver. The problem is not that the tool isn't "strong" enough, it's that it isn't specific enough. Even healthcare professionals throw around terminology that makes it sound like some antibiotics are explicitly more "powerful" than others, but what they're really talking about is antibiotics that are used as last resorts. There are certain antibiotics that are used after everything else has failed--not because they're better and the others are "weaker," but because bacteria are less likely to resist them.

Which brings me to my second point. Bacterial resistance.

Bacterial resistance is a matter of evolution, i.e., natural selection. Suppose that 99% of all bacteria exposed to genericillin die. The 1% of the population that survives does so because it has randomly developed a means to protect itself from genericillin; perhaps it breaks down genericillin by secreting enzymes before the drug can affect the bacteria. That 1% of the population goes about its life and continues to reproduce, so that 1% of the old population is now billions of bacteria. The population rebuilds itself rapidly (due to lack of competition for resources), so we expose the bacteria to genericillin again. But this time, it doesn't work, because these bacteria are immune to genericillin. They were never susceptible to genericillin. What we have done is selectively bred the organisms most fit to survive in a genericillin-laden environment and killed off all of their competition, permitting their population to explode.

You do not become "immune" to an antibiotic because antibiotics don't do anything to "you" (at least, not ideally). This is probably the biggest misunderstanding of antibiotic resistance that I encounter--patients who think that they have become "immune" to genericillin because they took too much of it.

This is a little like expecting to be immune to bullets because you've shot too many people.

Unfortunately, the situation is much worse than that. You aren't the only one who has to deal with the consequences of resistant bacteria. We all do. And we have no one to blame but ourselves. Every unnecessary antibiotic prescription, every antibiotic that someone stops taking halfway through their therapy or that they "save for later," every "borrowed" medication--all of these contribute to resistant bacteria. The resistant bacteria already exist, for the most part, results of genetic mutations. But we're selectively breeding them by killing off their competition. Curing syphilis today requires eight times the dose that was required in 1960.

I've said it before, and I'll say it again. I would rather see physicians overprescribe narcotics than antibiotics. Drug addiction and substance abuse are bad, from a public health perspective, but breeding "superbugs" is a great deal worse. Addicts are, as a rule, only hurting themselves; overuse of antibiotics hurts everyone.

Diabetes Discussed: Part 3

Thus PalMD and I continue our cross-blogging endeavor to explain what researchers have figured out about diabetes in light of recent proclamations from the mouthpiece of science that type II diabetics may not benefit from dropping blood glucose levels to their minimum levels as much as previously thought.

Treatment of diabetes is multifaceted. As Pal pointed out, insulin is the mainstay of therapy, especially for type I diabetes. In type I, insulin is the only reasonable therapy; right now, nothing else works. They don't make insulin. They need insulin. Simple enough.

Insulin was the first protein drug product developed and widely used--it was originally derived from pigs or cows. Nowadays, we get our insulin from E. coli that have been genetically "reprogrammed" to produce human insulin through bioengineering. And we also have a huge variety of insulin products that are essentially just modifications made to the basic insulin design. Some insulins act more rapidly (like Humalog or Novolog) whereas others are intended to last up to 24 hours to provide an insulin "baseline" (like Lantus or Levemir). Insulin dosing may initially be based on weight, but after that, dosages are recalculated based on trial and error. It is difficult to predict precisely what quantity of insulin will produce the desired result, and there are several different rules and protocols for optimizing insulin dose. In short, insulin doses must be individualized to the patient, requiring a lot of careful monitoring by both the health care provider and the patient (with a home blood glucose monitor).

Treatment of type II diabetes is way, way more complicated.

Because type II diabetics can create insulin, but their cells are less responsive to its effects, the initial treatment of choice is usually metformin. Metformin is amazing. It's the only drug in its pharmaceutical "family" on the market, and nearly every type II diabetic is on it. It works by increasing the sensitivity of cells to insulin and by decreasing the amount of glucose the liver makes--it's that gluconeogenesis process again--which results in an overall decrease in blood sugar. It even causes some patients to lose weight, which is excellent; losing weight generally decreases the severity of type II diabetes.

Pal covered metformin and the other "oral hypoglycemics" already--sulfonylureas, like glipizide, force the pancreas to spit out more insulin. And thiazolidinediones (TZDs for short; that word is quite a mouthful) have multiple body effects, including increasing insulin sensitivity, but by a different mechanism than metformin--which means that they can be combined, and sometimes this produces better results.

I would like to stress at this point that if you or a loved one have diabetes, while this series may be thought-provoking and raise interesting questions, that you should discuss the matter with your primary care physician when it comes to individual treatment recommendations--not here. I'm not a licensed medical practitioner*, just a student of pharmacy with a flair for words and a desire to share his knowledge with the world. And even if I were licensed, reading some article written by an anonymous blogger is not an appropriate substitute for face-to-face medical advice.

With that out of the way. What does recent research tell us? Past research tells us that blood glucose is important. But new research says other things might be just as important--maybe more.

Heart disease is a number one killer of patients with type II diabetes. Kidney failure is more common in type I. They're both considered to be manifestations of the same disease. But they're clearly different in several ways. Pal mentioned ketoacidosis--that's common in type I, but incredibly rare in type II. What explains these differences?

If I wanted to indulge my inner conspiracy theorist I'd blame the drugs used to treat type II diabetes, which is kind of like the absurd claims made by tinfoil-hatwearing HIV denialists that AZT causes AIDS.

Much more likely is the difference in co-morbidities ("other diseases/conditions the same patient has") for both type I and type II patients. Type II patients are typically obese, or at least overweight. The Framingham heart study has demonstrated that being overweight (as defined by medical science, not People magazine) is a risk factor for cardiovascular disease. So is having wonky cholesterol levels--and those are pretty common for type II diabetics, too.

This study is kind of interesting. Essentially, cholesterol deposited on beta-cells--the part of the pancreas that secretes insulin--can induce beta-cell failure. Cholesterol essentially "clogs the pipes." Even more interesting is the fact that this whole problem may be tied to a gene that codes for a protein called ABCA1. ABCA1 is essentially the "conductor" responsible for regulating lipid transport in and out of beta-cells. People whose genes incorrectly code for the ABCA1 transmembrane protein may be more susceptible to lipid-based damage to the pancreas. It is entirely possible that controlling lipids is at least as important as controlling blood sugar in type II diabetes, which means that dietary modifications, exercise, and cholesterol-lowering drug therapy may all play an even greater role in achieving good treatment outcomes than previously thought. This is exciting research!

That study's too neat to just be a throwaway link. I might come back to it later.

I think the point of recent research basically demonstrates that we can't just treat blood sugar. It doesn't mean we're completely mean about how we're treating diabetes. It just gives us a new direction to focus our research. Diabetes may be conceptualized as a problem with glucose metabolism, but that isn't the end of the story. Physicians, pharmacists, and patients have to work together to design treatment regimens that address cholesterol and sugar, among other factors.

*Well, I have a pharmacy intern's license. Which permits me to practice pharmacy, compound medications, and counsel patients under the guidance of a licensed pharmacist. But it's essentially a learner's permit. And you shouldn't be using the internet as your sole source of health advice anyway. It's not a good resource. In pharmacy, we call using a drug by itself that shouldn't be used alone "inappropriate monotherapy." Getting all your medical information online is the same. Go talk to your doctor!

Diabetes Explained: Part 1

The medical world is abuzz regarding the recent revelation that driving blood sugar to its lowest theoretical level may not be the optimal treatment regimen. PalMD of WhiteCoat Underground has already addressed the issue in a short post, noting wisely that this whole issue just raises more questions about the nature of diabetes and how it should be treated.

But what is diabetes, anyway? There are a lot of misconceptions, perhaps the most popular being that diabetes is a disease you contract as a result of eating too much sugar. My own mother was convinced that a diet proportionally high in carbohydrates was likely to cause diabetes until I made an attempt to explain otherwise. It also gets likened to a sort of food intolerance--the idea that diabetics can't eat sugar because it will cause acute damage. Naturally, the truth is far more complicated; patients with diabetes won't keel over and die in minutes if they eat cake.

Diabetes is often conceptualized as a problem with glucose metabolism. When you or I eat, the body breaks down complex carbohydrates into simple glucose units. Certain amino acids, the building blocks of proteins, are converted into glucose by complex pathways in the liver (the big, scientific word for this is "gluconeogenesis"). Glucose then circulates through the blood and is delivered to various sites; it is the preferred fuel for every cell type in the body, especially neurons. Something like 80% of the glucose in your body is utilized by the brain and nerve tissue.

The issue is that glucose is unable to enter cells unless the drawbridge is down, because glucose molecules are too big to freely pass through cell membranes. In order for glucose to enter cells, special pores on the cell surface need to open. And the trigger that opens those pores is insulin. Without insulin, most of the body's cells have no way to utilize glucose--and therefore, they are unable to fuel themselves efficiently.

It isn't that sugar is somehow toxic to patients with diabetes--the problem is more like having a blocked fuel line in your car. No matter how much gas you put in, your car can't get the gas because of the obstruction. And if you keep filling the tank anyway, you're going to cause it to overflow and spill gas onto the street, harming the environment with damaging emissions.

There are two types of diabetes. Type I diabetics are unable to make insulin; this could be because of a genetic defect, damage to the pancreas by infection or trauma, etc. The net effect is that no matter how much the type I diabetic eats, he is essentially starving, because his body's cells have no way to use glucose. Instead, they rely on far less efficient fuel sources like ketone bodies, which is sort of like putting the lighter fluid-soaked charcoal remnants from last night's bonfire into your car's gas tank and expecting it to operate well. The typical untreated type I diabetic is thin and malnourished. There is tons of glucose floating around in the bloodstream and none of it is accessible, so it gets excreted in the urine.

Type II diabetics make insulin--in fact, they frequently make tons of insulin, especially in the early stages of the disease. The problem is that their cells are less responsive to the effect of insulin, so they use glucose very inefficiently. If type I diabetes is an obstructed fuel line, type II diabetes is a leaky gas tank. Type II diabetics are commonly overweight--having large amounts of fat cells decreases the body's response to insulin. Fat doesn't just sit there; it secretes hormones that regulate glucose usage and appetite, among other things. The bizarre thing is that from a metabolic standpoint, your type II diabetic, despite being overweight, is functionally starving.

If I were stranded on a desert island with nothing to eat, my body's metabolic machinery would switch gears in less than 24 hours. We're starving, it would say, and the pancreas would release a hormone called glucagon to remedy the situation. Glucagon would tell my body to break down my fat stores (the few that I have), cannibalize muscle tissue, and instruct the liver to release its glucose hoard to feed the brain. Eventually, the stores would run out and my brain, cut off from its supply of necessary glucose, would shut down, taking the rest of the body with it. My heart, ever a trooper, would keep on truckin' until the autonomic nervous system crashed, because it is perfectly happy to feed on metabolic scraps.

An untreated diabetic's body is doing this all the time, and the only reason it doesn't kill them is that the brain, kidneys, and nerves don't need insulin to take in glucose. They're the exception to the rule, and if they weren't, diabetes would be fatal a lot more quickly than it actually is.

The reason sugar is harmful to diabetics has less to do with the essential properties of sugar itself and more to do with the effects of wildly fluctuating glucose levels on those three tissues. When glucose levels are high, glucose rushes into the big three--the nerves, the nephrons (the functional units of the kidney), and the retina of the eye. When blood glucose finds its way back down, frequently by being excreted in the urine, there is a huge disparity between the amount of glucose in the nerves and in the blood.

Those of you who remember basic chemistry will recall that such concentration differences are considered unfavorable in accordance with physical law. If we put a tablespoon of sugar in a glass of water, the sugar molecules would slowly spread out throughout the glass (though more slowly than we might like, which is why most people opt to stir the glass). Given enough time, the concentration of the sugar will be uniform throughout the water, and we will have a solution.

But what if we put a barrier in the glass dividing it in half from top to bottom, and the barrier permitted the passage of water, but not sugar? If we put sugar in one partition, the sugar-water on that side will be much more concentrated. Physics doesn't especially like this scenario; equal concentrations on both sides would be preferable. Sugar can't move through the barrier, but water can. As a result, water is going to pass through the no-sugar side to the sugar side in an attempt to equalize the concentrations.

This is the precise scenario that takes place in the human body. Once sugar concentrations in the bloodstream go down, the sugar concentration inside cells (retina, nephron, and neuron) is higher than the sugar concentration outside the cells. Since the sugar can't come out, water goes in. But the cells are limited in size by the boundaries of their membranes. When enough water rushes into the cells, they burst and are destroyed like overfilled water balloons.

So the big problem with sugar and diabetes has less to do with sugar itself being harmful and more to do with osmotic pressure, the situation described above with the barrier that will permit water to cross but not glucose. This is why diabetics with poorly-controlled blood sugar--blood glucose that fluctuates from low to high with great frequency--are more likely to suffer nerve damage, blindness, or kidney failure.

The recent study suggests that type II diabetics (NOT type I diabetics) were just as likely to die from their condition if they maintained low blood glucose levels than if they didn't (this isn't the whole story, so nobody panic). This is a surprise mostly because prior research has fairly conclusively confirmed that controlling blood sugar reduces the risk of those three problems I mentioned earlier in addition to reducing the likelihood of heart attacks, strokes, and other cardiovascular complications.

Why might this be? To understand this issue, we'll need to look at the way diabetes is treated, which will make absolutely no sense without an understanding of what diabetes is. Next post, we'll explore the issue of treatments for diabetes, how they work, and what this new research might mean.

The REAL Cutting Edge of Medicine

Has anyone else ever noticed the fact that proponents of alternative/integrative medicine, most notably the NCCAM, are always talking about altmed like it's the "cutting edge" of medicine? As though CAM "research" and the use of "holistic" therapies are what separate the wheat from the chaff in today's medical world? After all, they're the ones that are really curing diseases. "Allopathy" can only subdue symptoms with toxic drugs, enslaving patients with chronic illnesses to big pharma for life. (Somehow buying supplements for the rest of your life is different.)

I'm going to abandon professionalism and make a rude gesture at those talking heads for a moment, because they (obviously) haven't the faintest idea what they're talking about. You want to see the cutting edge of medicine?

This is some amazing stuff. According to JAMA and several other sources, Swiss researchers are working on a promising new vaccine that may be a more effective way to control high blood pressure. The vaccine works by stimulating the body to create antibodies against a human protein called angiotensin II.

When the kidneys are recieving insufficient blood, the kidneys secrete a substance called renin. Renin, in turn, stimulates the formation of angiotensin, which is then transformed by angiotensin-converting enzyme (usually called ACE) into angiotensin II. Angiotensin II has a powerful effect on blood vessels, promoting constriction and increasing pressure. This system is a major means of controlling fluid volume in the human body. In fact, you may have heard of ACE before. ACE inhibitors, such as lisinopril, are commonly used to lower blood pressure; these drugs work by blocking the formation of angiotensin II. Other drugs for hypertension, such as angiotensin-receptor blockers (ARBs) and the new direct renin inhibitor Tekturna all work to accomplish the same goal--reducing the effect of angiotensin II.

The new vaccine works by stimulating the human immune system to produce antibodies to attack and break down angiotensin II. This is an absolutely incredible use of biochemistry--modifying the immune system to eliminate a protein that the body is making in excess. Because the effects of the vaccine are long-lasting, patients shouldn't need to take daily medications to decrease their blood pressure. In fact, it may be necessary for patients to have medication on hand to raise their blood pressure in the event of an emergency, much like diabetics who carry glucose tablets to rapidly raise their blood sugar in case of an insulin overdose. Further time and testing will tell, but early trials are very promising--4 and 12-month follow-ups suggest that the vaccines are well-tolerated.

And this same theory is being applied elsewhere in medicine as well. Cancer vaccines are in development that can be used to treat various cancers by reprogramming the body to attack cancer cells without harming healthy cells. Even Alzheimer's disease might be treatable with a vaccine that degrades the "plaques" that form on neurons and are understood to be a major cause of the disease.

What kills me is that this is the sort of thing that altmed is always claiming to do--modification of the body's immune system to produce a long-term cure for a disease that isn't caused by an infectious agent. Forget about balancing vibrations or whatever. This is real high-tech medicine. If human beings are going to someday conquer all forms of illness, the work will be done by biochemists, not reiki masters.

Paleovirology

A discussion thread on one of my favorite blogs included this fascinating link to a story that is just incredible. The article is a little lengthy, but not too bad, and it's definitely worth the read, especially if you have any interest in biology or science. Thanks to Sid Schwab for providing the link.

Essentially, when geneticists mapped out the human genome, they discovered that while only 2% of it was entirely necessary for life, as much as 8% consisted of "junk" DNA believed to have been incorporated due to infections from retroviruses. Retroviruses, for the uninitiated, are viruses capable of permanently altering the DNA of organisms they infect, occasionally causing the changes that they make to the human genetic code to be passed on to offspring. The most notorious retrovirus, of course, is HIV, the virus responsible for causing AIDS. A few innovative geneticists studied these fragments and managed to sequence the genetic code of one of the retroviruses that might've insinuated itself into the genome of more complex organisms tens or hundreds of thousands of years ago.

Using biotechnological methods for creating recombinant DNA, these scientists effectively resurrected an extinct virus. And their creation was capable of infecting mammalian cells.

According to the article, there's evidence that the incorporation of retroviral DNA into our genome influenced our evolution. The formation of the placenta, for example, may have been a result of retroviral infiltration. And retroviral incorporation may explain why monkeys are carriers for HIV but are unaffected by it; there's a huge chunk of retroviral DNA that they have that we don't. So sequencing and experimenting with "extinct" retroviruses gives us more concrete evidence for evolutionary pathways and may have medical applications.

Read the article. It's totally worth it.

Interesting to think that there are "fossils" of extinct organisms in your DNA, no?