There really isn’t much to debate.

The US healthcare system, in its present state, is a failure. It fails those with and without coverage. We spend more, care for fewer and are sicker than the citizens of any other industrialized nation.

We’ve studied it. Americans of all socioeconomic strata are less healthy on every measured basis than their UK counterparts–before or after adjusting for the less healthy lifestyles of Americans. Putting it even more bluntly, the richest Americans, lavished with the finest private health insurance our nation can muster, in the epicenter of global medical and biological research, have more diabetes and higher blood pressure than the poorest of English citizens. Even within our country, Americans within the Veterans Affairs system, a little socialized corner of our healthcare system, are similarly healthier than their privately insured doppelgangers.

As far as the uninsured in this country, an unprecedented phenomenon in the industrial world, allow the independent Institute of Medicine to state the case:

Lack of health insurance causes roughly 18,000 unnecessary deaths every year in the United States. Although America leads the world in spending on health care, it is the only wealthy, industrialized nation that does not ensure that all citizens have coverage.

The case for socialized medicine in this country has been made, and it has won. Back in June of this year, an overwhelming supermajority of Americans were in favor of a public health plan option. After the long summer–filled with hideous farces of Town Hall meetings, Teabaggers and endless anti-reform propaganda–support remained at supermajority levels. The Senate vote on the package seems to be a fait accompli.

The core of the opposition is an all out appeal to selfishness. Think of the taxes you’ll pay. Seniors, think of what you’ll be forced to share with those younger than you. You might have to wait in line for care if anyone can get it. The hideous core throbbing at the center of all this summer’s hysterics is the toddlerization of Americans as selfish and self-centered consumers–relentlessly stripped of any sort of adult notions of empathy, responsibility for others, investment in the future or delayed gratification. The whole movement has been lead by paid-for shills for the moneyed interests endangered by healthcare reform.

The mob of mooks compelled by these appeals to selfishness–capable only of braying about ‘socialism’ and ‘the constitution’ with no sense of what either really represents–are the rhetorical equivalent of suicide bombers. This summer’s protests reminded me of nothing less than Kermit Roosevelt‘s handiwork, undoing Mosaddeq’s attempt to nationalize the Iranian oil industry. The intent was to drive terror into the hearts of the elected representatives Democratic supermajority–to generate the illusion of mass discontent. The absurdity of the arguments posed at the Town Halls–Death Panels! Marxism! Obama is Hitler for trying to provide Americans with healthcare!–was the entire point. The feeling of being strapped to a bomb generated by having these cretinous and credulous fools
as countrymen is best diffused by ignoring it as bad theater.

It’s worth considering why American doctors are so expensive, where the costs of drugs and medical devices arise. Healthcare reform is, astonishingly enough after nearly a century of struggle, about to happen. These are the points we should be debating and struggling with as the end details are being written.

Layers of cost build up as we dive deeper and deeper into the life of a medical drug or device. At the shallowest depths are the most obvious additions to costs, the vast sums of money spent on marketing to consumers and doctors alike. Next down are the costly FDA trials, phase I, II and III that must be completed before a medical device or drug comes to market; it’s these studies that also ensure safety and efficacy. At the beating heart of all of this, typically, is in an idea from a publicly funded academic research lab.

The basic biological research done in the United States is the envy of the world. From the investments of the National Institutes of Health (NIH) an the National Science Foundation (NSF) and even more esoteric government sources (the Department of Energy largely bankrolled the Human Genome Project), legions of academic labs have been pumping out the foundation of the medical revolutions of the past few decades. The massive, freely accessible and well-curated libraries of genes, genomes, proteins and even entire metabolic pathways were built through US government funding. Simply put, it would not be possible to do modern biological or medical research at any level without these tools. It’s from these laboratories that we know how, say, cholesterol is absorbed, made processed, eliminated and even turned pathologic in the human body. This knowledge is how drug companies figure out how to test new drugs, measure their effects and safety.

It’s at this level, in academic labs, where the epiphanies behind new devices and meds occur. The discovery of a new pathway, the teasing apart of a bit of physiology, or simply a new understanding why some are protected from disease when others are not all lead to ideas of new drugs and devices. If it’s a really good idea, if the potential seems ripe, it becomes the core of a startup company.

The idea is teased out. If it really looks good in animals, the phase I human trials start at about this point. (Phase I trials are small scale, and focused on establishing safety and reasonable doses or ways of application.) Money is raised (the first big cut of cash taken by the parasitic financial industry). Most often, the goal is to make the idea look good enough for one of the supersized biotech companies (essentially a pile of money and lawyers blended into the equivalent of the Borg cube) to buy up the whole company, idea and all. (The next major step where the financial industry takes a cut.) Somewhere about this point, Phase II human trials begin (small scale, but now focused on both safety and efficacy.)

The last step before a drug or device can be sold is a phase III human trial, large scale and required to statistically demonstrate in a randomized and controlled trial efficacy and safety of the new idea. A typical phase III trial costs ring up at about a billion dollars. Only the Borg-cube level of biotech can really take them on. For a genuinely new idea–an entirely new kind of drug or device–this is the riskiest step. All sorts of unexpected things happen–sometimes for the better, sometimes for the worst. (Both Minoxidil and Viagra started as entirely new blood pressure pills; they worked terribly at controlling blood pressure, but excellently at helping old men feel better about themselves.) The payoff is an exclusive, time-limited, patent. For a new drug or device that genuinely solves a large and unaddressed problem, this adds up to tens of billions of dollars over the ensuing years of legalized monopoly.

The patents for drugs work as the founders intended; they’re just long enough to make the investment worth it, but not so long as to prevent real competition forming while the drugs are still useful. Generic drugs are those that have gone through this whole process, and been on the market long enough for their patent to expire. These copycats mimic the molecular structure of a drug already proven through the phase I, II and III human trials by someone else. Without the R&D costs (or marketing costs), they become instantly cheaper than their parents.

Most drugs on the market today, including new drugs, are actually based on old ideas. Prozac was followed by a dozen or so drugs that work in the same way. (Viagria was followed by Cialis and Levitra.) It’s here where consumers get soaked. As soon as a lucrative drug is about to go off patent, the parent biotech company will typically come out with a new, improved (in some minor way) version. The repeated phase III trial tends to be much cheaper, and with a near certain outcome. The new drug is then relentlessly marketed, driving as many customers as possible away from the imminent generic competition. For the big biotech companies (heavy on money and lawyers, light on genuine risk taking science), developing new ideas isn’t a strength. Instead, they devote vast sums of money into promoting these derivatives, certain that the government funded labs will keep churning out new ideas worth picking off in the future.

In a somewhat ugly way, the whole process works surprisingly well. At this point, most of the drugs most of us will need to take (statins like simbastatin to reduce cholesterol, ACE receptor antagonists and HCZ for blood pressure, SSRIs for depression) are available in generic form. They work well, are cheap and safe. Find a doctor who still reads, and doesn’t have to learn about new drugs from a rep paid to tout the newest (but not necessarily meaningfully better) and more expensive drug, and you can game it all fairly well. That’s to say, the problem of expensive drugs and devices is as much one of this system as that of the poor continuing medical education of many physicians.

The average family medicine doctor in the United States pulls down about $200,000 a year. The average internist or pediatrician earns about $175,000 a year. A general surgeon earns about $290,000 a year.

In comparison, a primary care physician (comparable to an internist, family doc or pediatrician) in the UK, under the NHS, earns between £53,249 to £80,354, about $90,000 to $130,000 at current currency rates.

The salaries of American doctors are huge, terrifying, for anyone trying to bring down health care costs in the United States. Why are American doctors so damn expensive? Medical school is a big part of the answer.

Per the American Association of Medical Colleges (AAMC), the median cost per year (tuition, fees and health insurace) to attend a private medical school in 2008 was a whopping $42,622. Public medical schools were only slightly cheaper, $41,429 for out-of-state and $22,984 for residents.

Add in at least $15,000 a year in living expenses, and the cost of a four-year bachelor’s degree and a newly minted medical student in the United States is easily hauling around three-quarters of a million dollars of debt by time they saunter out with an MD degree. The obligate first job of any medical school graduate is residency, typically a brutal three to five years of work, paying about $40,000 a year.

Running right down the median costs, paying off that $800,000 or so in debt (financed at about 5% a year) over the next thirty years of work eats up about $4300 a month; paying it off in ten years would cost nearly $8500 a month. A pediatrician or internist can expect to make about $14500 a month before tax; paying off this debt over thirty years will cost them about a third of their gross income. About half of that money will go to the financial services industry, in the form of interest.

If you want physician’s salaries to come down in the United States, without a true reduction in physician compensation, the natural choice would be to aggressively subsidize medical education and ensure young doctors come out of school carrying much less debt. A small amount of public investment up front will reduce a massive and ongoing source of inefficiency in the American medical system.

Ah, turfed. Allow me to introduce you to one of the cherished terms of medical care in the United States. You turf difficult, or undesirable, patients to someone else. The insurance industry has succeeded, more than anything else, at transmitting this hatred and fear of sick people down to the lowliest depths of the health care system–from the mightiest administrator to the lowliest medical student.

People with easily treated maladies–high blood pressure, high cholesterol, high blood sugar and so on–go untreated (despite the huge potential long-term benefits from cheap therapy) because the entire health care system hates the ill with a deep and embittered passion.

Let’s think for a moment what the product of health insurance entails. For a fee, a company will pay your medical costs for a fixed period of time. These contracts are never lifetime–often they are annual. The multitude of insurance companies offering these contracts operate in a genuine market. Being efficient–successful–in such a market means figuring out any way to avoid providing healthcare costs, avoiding providing care. If you know you’ll only be writing a short-term contract, caring about long-term cost savings is a totally losing move.

The market has worked well: Insurance companies (for profit or non-profit) have proliferated a multitude of caps, fees, co-pays, deductibles and ‘preferred provider’ lists all oriented on reducing short term costs, regardless of consequence. The very concept of a “pre-existing condition” was generated to prevent sick people from becoming customers, and whole mechanisms have developed to kick people out of their contracts if they become ill. The better the market for health insurance works, the more these mechanisms become inevitable.

A big part of the proposed reforms floating around congress are attempts to subvert these market forces without fundamentally changing the nature of the market. Laws preventing exclusion based on pre-existing conditions or dropping people from plans due to illness seem like obvious ways to improve the situation. But the dynamic will remain, and the clever people at insurance companies will come up with new ways to turf those who need care that tip-toe right up to the new lines being drawn.

The great turf in the sky, right now, is Medicare. All of us, when we hit that magical age, become eligible. A public option, as proposed and under fire as a part of this reform, would probably end up serving a similar role: a government-chartered floor beneath which no American could fall. Stuck with these patients for the rest of their lives, suddenly the dynamic would change. Any clever administrator of a public option health plan would be tremendously motivated to provide preventative care; success of such a plan would be contingent on reducing long-term, not short-term, costs.

A model for such a plan already exists–the Veterans Affairs system. Patients in that socialized American health care system are demonstrably and objectively healthier than their privately insured compatriots in every measurable way.

Barring requiring private insurers to cover people for the rest of their lifetimes, there is no other way to achieve a similar focus on long-term health and cost-reduction than a public plan.

My transcript:

What we’ve really spent our money on, in this system, is trying to figure out to not cover people who have paid for their premiums.

There was a hearing last week, with no network covered, including mine (CNN). And they had witnesses, people who had paid their health insurance premium for months or years and then committed the sin of getting sick. And then insurance companies kicked them off.

And then they had insurance company executives and they were asked, under oath, ‘Will you stop doing this? Will you stop kicking people off unless they’ve committed fraud?’ Ok. Short of fraud, will you cover the people who pay their premiums?

And they all, under oath, said ‘no.’

That’s why we need a public plan. Because they’ll keep kicking you off.

As a pathogen, influenza is the cat’s pajamas; influenza puts the ortho in orthomyxovirus, the segments in its RNA genome and the misery in sneeze droplets everywhere.

Let’s unpack H1N1 and H5N1. The ‘N’ in both stands for neuraminidase, a fancy way for saying “snot eating enzyme.” The virus needs to get to the juicy cells at the back of the throat. Our bodies pour out copious amounts of snot in defense, forming a sticky wall of doom for all manner of pathogens. Stuck on the outside of every flu virus is a sea of this neuraminidase enzyme. The enzyme gobbles up the snot, allowing the virus to reach the cells lining our throat. In comes the ‘H’ or hemagglutinin protein, also located on the outside of the virus. Hemagglutinin binds the salicylate receptors located on the outside of almost all cells (salicylate is a special way of saying aspirin), dragging the virus into the cells. Once inside, you’re infected. Huzzah for our little virus. Go team!

Influenza has been around for a while–co-evolving with many other species beyond man. As a result, different versions of the H and N enzymes have split off over time. The numbers after H and N in a flu virus name indicate the rough genetic heritage of a given flu’s enzymes. H1 and H5 are like Montagues and Capulets–alike in kind if not kin. A given H (or N) is accomplishing the same task, but in slightly different ways.

In comes the home team. If the B-cells in our immune system can make antibodies against the neuraminidase and hemagglutinin, blocking their function, we can stop the virus. Making antibodies takes time. While we’re waiting, CD8 T-cells (cytotoxic T-cells) come in and kill any of our own cells that are infected with virus, a sort of controlled Kamikaze mission in defense of the Home Islands. (Dead cells can’t make more copies of the virus; once you’re infected, brother cell, it’s too late to save you.) With each kill, the CD8 cells release a little bit of activating cytokine and become a bit more bold. This self-death is a large part of the misery of the flu. You are sore because your body is literally killing itself in battle. It takes a week or two for the B-cells to start pumping out antibodies to a new(-ish) virus, at which point the CD8 cells are told to lay off, and take a break.

What we have here is the co-evolution of a host and parasite. My favorite! This sort of host-pathogen interaction is an evolutionary saddle-point, with two possible resolutions:
1. All out battle to the death! Host and pathogen strike fast and hard, in an all-out effort against the other. This is true misery for both, with the eventual true end to this situation the extinction of the pathogen, or host and pathogen together.

2. A detente. The pathogen tries to go out its business in the least offensive way possible, with the host ignoring the pathogen (due to the lack of mayhem perhaps making the pathogen invisible to the host). The eventual end of this evolutionary path is the pathogen becoming commensal, completely harmless. Tons of viruses end up this way, including Kaposi Sarcoma virus. Eventually, a once-pathogen can actually become symbiotic, helping its host out in life, and benefiting as a result. Consider this the environmentalist bug gameplan.

Which path a host and pathogen take is dependent upon a bit of other environmental factors, and also pure random chance. A typical year’s influenza tends towards plan #2, thanks to antigenic drift. Even within a given family of the viral enzymes, thanks to mutation, the surface proteins of the virus are constantly drifting. For example, the 2007-2008 and 2006-2007 flu seaons both had H1N1 influenzas in circulation. In a year’s time, the viral proteins had mutated enough to ensure that people infected with the 2006-7 version of H1N1 could be reinfected with the 2007-8 version. The antibodies we developed in the 2006-7 were good enough to slow down the 2007-08 virus, but not stop it entirely. The CD8 cells still needed to be activated, but not as much as they would for a totally new virus. This is the start of a detente, with the full-scale war held back by the similarity between the 2006-7 virus to the 2007-8 H1N1 virus allowing the older antibodies to work a little and hold the infection in check. So long as a given influenza virus has been around humans for a while, it’ll trend to a detente-style interaction with the human host, holding back the carnage.

What makes this new swine H1N1 virus so concerning is that it’s never been seen by humans before. As a result, none of our existing memory B-cells have an antibody that even wings these H1N1 proteins. We cannot hold back the initial infection at all. The initial defense against the virus is completely reliant upon those destructive CD8 T-cells. This can select for viruses employing strategy #1 (all-out battle) this Spring, Summer and Fall until the next flu season starts; this H1N1 might have a detente with swine, but has no such arrangement with the human immune system.

If the CD8 cells get excited enough by the unusually aggressive virus (a cytokine storm), the lungs of the young and healthy get trashed during these early stages of meeting. People in their twenties and thirties will die in numbers not seen during the more typical detente-style human-flu interaction.

We honestly have no clue how this virus will re-emerge in the Fall. It could be just like a regular-old flu, or it could be a monster that has undergone extensive selection for virulence. The furious-paced efforts to develop and manufacture a vaccine are our safety net.

It’s a pretty clever idea. Nobody has been able to make it work. Tumor cells seem to know the trick, and have potent means of telling the immune cells “back off, guys. We’re cool.”

Dendreon, focusing on prostate cancer (very common in older men), figured it out. In this most recent trial, they demonstrated efficacy of this new treatment to the satisfaction of the FDA. Since this therapeutic method is so new, the trial and standards were more stringent than for a more typical chemotherapy drug.

Not only is this really good news for prostate cancer patients, it’s also good news for the local economy. The intellectual property generated by the company should be applicable to other forms of cancer. Prepare for billions of dollars to start flowing into the state, as we are now the global leaders in a new way of tackling cancer.

Let’s look at the bios of the CEO and scientific leadership team:
Dr. Mitchell Gold: President and CEO.
“Dr. Gold is a former urologist at the University of Washington and currently serves on the boards of the University of Washington/Fred Hutchinson Cancer Research Center Prostate Cancer Institute and the Washington Biotechnology and Biomedical Association.”

Dr. Urdal: Chief Scientific Officer.
“Dr. Urdal received a B.S. and an M.S. in public health and a Ph.D. in biochemical oncology from the University of Washington.”

Huh. UW. You know, the highly productive public research University that brings in a billion dollars a year (or so) of out-of-state funding and is the largest employer in the city of Seattle. Also, the same University facing a 25-35% budget cut from the State and is planning to lay off 1000 people in a couple weeks, while jacking up tuition and cutting student rolls. After these cuts, Washington State will be 42nd out of 50 in State funding for higher education.

Who needs higher education? Taxes are baaad for the economy. The Republican superminority in State government tells us so. We already have a raging state economy. Raging! Sure, Boeing needed billions of dollars of state-funded life support during the boom years, has a commercial aviation division that can’t build aircraft and is facing cuts in orders to its most profitable aircraft, and a military division still reeling from the unexpected collapse of the Soviet Union twenty years ago. It’s not like China is going to figure out how to build aircraft! Never! And Microsoft’s monopoly is firmly entrenched, with no serious competitors on the horizon. Businesses are snapping up Vista and cannot wait for Windows 7. XP is long forgotten. Nobody wants that stuff. Nor is piracy of Microsoft products a serious problem, certainly not in the future markets of Brazil, Russia, India or China.

And our high tech economy has no need for well-trained employees. None at all. Sure, public universities are incredibly efficient at generating superbly trained and prepared staff for companies. But, why would Boing, Microsoft or other tech companies want to hire Washingtonians? If UW is gutted, all it’ll take is more H1B visas. With all the tax dollars we’ve saved, we can make our kids happy in the burger-flipping and car washing jobs that are the future.

Yes, our governor and democratic supermajority in the state legislature are faced with an impossible set of circumstances: a gaping budget hole caused by ill-advised earlier tax cuts and subsidies for failing industries, one of the world’s largest collections of idle wealth residing in the state, and an antiquated and ultra-regressive sales tax based revenue structure. What possible solution could be crafted from this raw material? Mysterious clues have been found in a yet-indecipherable code: aiseray axestay onay ichray. To help them in their quest of balancing the books, the governor has crafted a website where you can cut funding, and pick exactly which seed corn we should feast on now.

Should be a smashing success. Thanks, UW spinoff Dendreon, for showing us what we won’t miss at all.

In the past few months, I bet you’ve seen at least one ad like these. When I first saw these ads, I was impressed.

Most direct-to-consumer drug advertising is loathsome, filled with moronic non sequiturs–what does kayaking have to do with a nucleoside analog used to treat herpes–or simply build up anxiety about a problem, offering no explanation as to how the drug helps.

These ads, for a combination pill meant to treat high cholesterol, are actually quite clever in explaining how the drug should work–a combination of blocking cholesterol production by your liver (a gift of your parent’s genes) and blocking the absorption of cholesterol you eat.

Memorable, clear, informative; too bad the drug doesn’t work.

The results of our study showed that the addition of ezetimibe to the highest recommended dose of simvastatin did not reduce the intima–media thickness of the carotid-artery wall in this cohort of patients with familial hypercholesterolemia, despite significant incremental reductions in levels of both LDL cholesterol and C-reactive protein. The primary outcome, the change in the mean intima–media thickness, did not differ significantly between the two study groups, nor did the secondary outcome measures.

In plain English, this combo pill didn’t stop the arteries from getting clogged with cholesterol any better than the older drug alone. In fact, the older statin drugs–available as much cheaper generics now–do a better job on what you, as a patient, would care about.

The vast majority of people exposed to these ads probably don’t know this, and will never know that the drugs didn’t work, that you’re better off with a vastly cheaper drug, that the company that makes Vytorin sat on the negative results in this study while racking up billions of dollars in sales. My suspicion is that many people will continue to ‘ask your doctor about Vytorin,’ as the ad suggests. And this is why even exemplary direct-to-consumer drug advertising is so damn irritating.

A few things to note:

1. Day-to-day variation in my weight is somewhat typical. The churn is probably from water. Hence, the seven day moving average as a more accurate measure.

2. Each pound of fat contains 3500 (kilo) calories. Therefore, the half pound gain over the week represents about 250 extra calories a day. (Hey, it was the holidays.)

So, how many calories did I average on a given day? About 2126. Subtract the 250 or so extra a day, and we’ll say that 1875 calories a day would be about right for me to just maintain weight. To lose a pound-a-week, I need to eat no more than about 1400 calories a day. A half-pound-a-week? 1625 calories a day.

1875 calories a day is an interesting number. Per the USDA charts, a typical person of my height, age, gender, activity level and weight would need 2858 just to maintain weight. I do it with a third fewer calories. Here is some empiric evidence that I’m an energy sparing person–with the combination of genes, epigenetics and microflora that is more efficient than most at extracting and saving energy from food.

If I ate as many calories as a typical person like me ate, their weight would stay the same; I’d gain about a hundred pounds a year, two pounds a week.

I’ve known this qualitatively for a while, coming from a family of big people and always being prone to gaining weight. Still, seeing the numbers is pretty startling. If I wish to lose weight, I have to eat less, much less, than the average person.

Now I know the number to target. I’m starting at a goal of a half-pound a week, or about 1625 calories.

On my slight five-foot-ten frame, that represents about a fifth more of me since 2001. How did that happen? Very slowly, and with both fat and muscle gains contributing.

Arriving at 135 pounds to Seattle, I was close to being underweight, my BMI above 18.5. Now at 165, I’m not officially overweight, my BMI is still below 25.

BMI isn’t the greatest measure of health. According to the Met Life tables, my ideal body weight is about 155 pounds. Putting aside the numbers for a moment, it’s where I’ve gained fat that matters more from a health perspective. Belly fat, like many men gain as they exit their twenties, is the most worrisome, with negative effects upon blood sugar, lipid profiles and general health.

At some point in the near future, I’m sure to find myself telling a patient to lose weight–ten, twenty, thirty, fifty pounds. How hard is it? By many of the measures I’d use with patients, I could stand to lose ten. Using the best available scientific data, can I do it?

Well, let’s try.

The first step: for the next week, each day I’ll carefully record what I eat and my weight. The goal is to stay about as close as possible to a “typical” week of eating for me, in an attempt to figure out my particular equilibrium between the calories I consume and use in a given day.