Introduction

I am a regular reader of Dr. Rob. And a big fan. Very cool site for both patients and medical professionals. He has a clear focus on advocacy and education (both us and patients). Recently he posted an entry about vaccines which I felt to compelled to comment on. I was going to reply to his but it got out of control long way too fast. So a post I will make.

Dr. Rob was talking about the rise in cases of Haemophilus influenzae type B infection. It can cause inflammation of a flap of tissue in the throat called the epiglottis–which normally serves the function of covering up your airway when you swallow, so you don’t choke. Bad things can happen when you have epiglottitis. Like the flap swelling up so large the child cannot breathe. In fact, when examining a child with epiglottitis we are told to have an anesthesiologist on hand ready to intubate, and if possible, defer the examination to a specialist in pediatric ear, nose, and throat disease. Nasty nasty stuff.

Where he lost me was invoking argument by anecdote and the use of the picture of an admittedly cute 7 month old.

I have a tragic tale to tell regarding vaccines myself. I’m not nearly as cute as the kid in Dr. Rob’s post though. After my second hepatitis B shot, a little more than eleven years ago, I developed a painful atrophic condition called Neuralgic Amyotrophy. And so a young swimmer’s career ended, a young musician found it a struggle to hold the bow of his violin, and his right arm withered away. I have worked hard to gain functionality, spending anywhere from 8-15 hours a week in the gym, rehabbing and gaining strength. I have developed an absurd pain tolerance. And have just barely failed to make an athletic comeback on 4 separate occasions (currently on my fifth, in an attempt to become a strongman and powerlifter). Even though I can shoulder press a barbell weighing as much as I do, I still struggle to shave, hold a phone, or write. And it was worse before I got this strong. Despite my passion for fast cars, I’m stuck driving an automatic, because my stupid hand can’t manage a stick shift. But the ravages of nerve damage and muscle imbalances have continued to take their toll. Today I suffer from cervical and thoracic radiculopathy, facet syndrome, and rib dysfunction syndrome. Next week, I’m being evaluated for wrist surgery due to the atrophy of connective tissue in the affected arm.  But to me the best way to sum it up is, at the age of 25 years old, I’ve actually forgotten what it’s like not to hurt.

That said, I am not in the anti-vaccination camp. I doubt that the mercury in vaccines causes autism. And I think that vaccines play a very crucial role in public and personal health. I am however, a trained scientist, and was taught to value epistemology, background knowledge, and study design in research. If I ever get around to blogging regularly again, you will see that those are core values of mine in the appraisal and pursuit of science and medicine. There are glaring issues and gaping holes in the evaluation of vaccines for safety, in post-marketing surveillance, and in attempts at exoneration of vaccines from charges leveled at them.

Dr. Rob stated: ‘As sad as your experience is, it was not due to negligence or ignorance.’ This is where I beg to differ. Negligence and ignorance (willful or otherwise) in vaccine safety studies is rampant. Even worse, people continue to trumpet vaccine as ’safe’ when they don’t have any reliable data from which to draw said conclusion.

Potential Vaccine Side Effects

There are known risks to vaccines, and there are theoretical risks to vaccines. A lot of people faint when they get vaccines. Others develop pain at the injection site. Neither are all that surprising, and, assuming a person is watched for 15-20 minutes after their vaccination, no harm is likely to come from fainting. However, there are two categories of side effects that can be debilitating and/or fatal. One type is the anaphylactic/allergic response, which can manifest as anything from excessive bruising and redness at the injection site to a rash to, in a full-blown anaphylactic response, swelling of tissues leading to respiratory compromise and in the worst cases, death.

The other class of worrisome reactions are autoimmune reactions. Autoimmune diseases are nasty situations in which your body’s own defenses turn against you. Both infections and vaccines can precipitate an autoimmune reaction. Reiter’s Syndrome is a famous (among medical students) example in which a gonorrheal infection leads to arthritis and eye irritation. Peripheral nerve damage is another relatively common complication of viral infection. Up to 50% of those who suffer from my condition developed it after an infection. Even relatively benign infections like uncomplicated upper respiratory infections can lead to these devastating sequelae. In some cases this is due to the fact that certain properties of these viruses are shared by properties of certain populations of our own cells. Antibodies that attacked one could thus potentially attack the other. This is believed to be behind the high rate of neurological symptoms in people with Hepatitis B infections.

Case reports have also consistently implicated vaccines in the precipitation and exacerbation of autoimmune phenomena, from lupus, to rheumatoid arthritis, to kidney disease, to multiple sclerosis. Anywhere from 15-25% of the sufferers of neuralgic amyotrophy are believed to have developed it due to vaccination.  Given that we think these kinds of things are caused by an immune reaction, it makes sense that if an immune reaction to a virus can cause autoimmune problems, than an immune reaction to a vaccine for that virus could as well.

The Problems with Vaccine Safety Studies

There are two components to assessing the safety of vaccines. The first is pre-marketing safety trials, and the second is post-marketing surveillance. Both are found sorely wanting. I am most familiar with these processes with respect to Gardasil and the Hepatitis B vaccination, so my examples will mainly come from there. My discussion will center around autoimmune and neurologic phenomena, which I and many health professionals believe are the most concerning potential side effects (whether in fact present or not).

As indicated earlier, I believe that proper study design involves the judicious application of background knowledge. A full immune response can take anywhere from 3-6 weeks to mount. It would make sense then, that we monitor for at least that long in order to detect any possible autoimmune side effects. Arguably it would be better to monitor patients for at least 6 months. The immune effects of vaccines can last anywhere from 1 year to a lifetime, so arguably side effects could manifest anywhere within this time period. Furthermore, it may take significant time for autoimmune damage to mount to clinically detectable levels. In the case of the Hepatitis B Vaccine, adverse events were monitored for 5(!) days. At 5 days, I pessimistically think that I would have been reported as a ‘minor’ localized ‘pain at the injection site’ despite the fact that my entire arm tingled and throbbed and I wasn’t able to swim, play tennis, or the violin. At one month, it would have been a different story. Likewise, the Gardasil safety trial monitored adverse events for only two weeks. Better, but still not very good.

A second problem comes in the choice of ‘placebo’. Now, the definition of a placebo is an inert substance with no innate biological activity. 4 of the 5 Gardasil safety trials used a compound called Amorphous Aluminum Hydroxyphosphate Sulfate or AAHS as the ‘placebo’. First problem, this compound is used in both the HPV and HBV vaccines (and many others) as an ‘adjuvant’. An adjuvant is a compound used to amplify the immune response to an antigen. Aluminum compounds do this in two ways: First, by making the antigen more available to be recognized by the immune system. Second, by increasing the activity of our immune system in a more general sense. Although Merck did not provide separate data for AAHS versus saline solution among side effects that potentially signaled the development of autoimmune phenomena (Table 5, page 7), they did do so for local reactions in Table 2 and Table 3 on pages 4-5. It is plain to see that the rates of infection are similar in the Gardasil and AAHS groups, and significantly lower in the saline group. In the real world, you either get a vaccination or you don’t. Your pediatrician doesn’t say ‘well since you’ve turned down Gardasil, I’m going to have to go ahead and inject you with this aluminum salt’. Since adverse effects are measured in terms of how much more often they occur in relation to placebo, it is plainly evident that such trials obscure the real incidence of adverse effects. They also obscure the role that the aluminum adjuvant may have in causing the side effects.

Aluminum salts have been implicated in a number of side effects and even vaccine-related syndromes such as gulf war syndrome, Macrophagic Myofascitis, seizures, joint aches, muscle pains, and a host of other ailments that also top the list of the most common and serious adverse events associated with many vaccines. Aluminum buildup has also been implicated in alzheimer’s disease, autism, infantile seizures, demyelination, and motor neuron death. And we know that vaccinating with aluminum leads to transient increases in brain levels (perhaps what is behind the scary increase in seizures in those who receive aluminum versus saline placebos). But I want to avoid belaboring the point. The take home message is that aluminum compounds found in vaccines can increase the intensity of the immune system and potentially precipitate autoimmune and neurologic phenomena in and of themselves. A starting list of citations can be found here which deals with everything from the effects of aluminum adjuvants to the reduced ability of infants to clear aluminum from their system. Another good overview can be found here. I should note before moving on that I don’t necessarily agree with everything the author has wrote but many of his concerns are valid and largely unaddressed.

So from pre-marketing safety trials, we learn that neither are people monitored long enough to determine the rate of serious side effects, nor are we given a true placebo rate with which to determine how much more likely one is to suffer from a potential side effect if given the vaccine (which is composed of two potentially harmful substances; the antigen, and the adjuvant).

Moving on to post-marketing surveillance. It is perhaps here that willful ignorance is most obvious. Post-marketing surveillance is achieved through something called the Vaccine Adverse Events Reporting System. This is a voluntary reporting system in which doctors must put forth extra effort to phone or submit online a report of an adverse event. Estimates of how often adverse events are actually reported range from 1%-10%, by the FDA and CDC’s own admission. Part of this is because VAERS is passive, rather than active. Another, more insidious reason is that some doctors will actively refuse to report an adverse event to VAERS because they don’t believe it was caused by the vaccine. VAERS works (if something with a 1-10% rate of reporting can be said to work at all) by comparing the rate of events in the vaccinated population to the rate of background events. This means, whether or not it was caused by the vaccine, it should be reported. I know for a fact that I am nowhere to be found in the VAERS database, despite seeing three different doctors and a physical therapist within a few months of the incident.

Yet, despite this known, severe, and asymmetric reporting, VAERS figures are frequently, if not always, used uncorrected. That means that if the reported VAERS rate and the background rate of a given adverse event are even similar, it is likely that the rate of adverse events for vaccinated individuals is actually significantly higher than background. This study is an enlightening read, in which VAERS-captured rates were identical to background. While real-world rates of intussusception following rotavirus vaccination were between 5 and 10 times higher than that in individuals who weren’t vaccinated. (Note: This is the old rotavirus vaccine and not the currently used vaccine). This must give pause, given that the VAERS rates for symptoms potentially heralding the onset of autoimmune disease, neurologic phenomena, and morbidity and mortality for many vaccines are at least at background rate or worse. More worrisome is that despite the well-known phenomenon of under-reporting of adverse events to VAERS, the uncorrected figures are frequently used without any discussion of the problems associated with them. Clearly, if post-marketing surveillance is going to be of any benefit, reporting rates need to be closer to 100% than 0%.

Although not necessarily a part of safety monitoring, there exists a third category of study that can be helpful in determining the relationship between vaccines and adverse events. And that’s the retrospective case-control study. In recent years, we have used such studies to examine the link between various vaccines and autism, multiple-sclerosis, seizures, lupus, rheumatoid arthritis, and others. I’m not linking to any studies because quite frankly everything is contradictory. Some find associations, some don’t. But even here, these studies don’t truly help out in developing a picture of the overall safety of a given vaccine. The biggest problem is that they are far too specific in the illnesses they look at. For example, lupus–one of the more common and devastating autoimmune disease–can manifest as a rash, as psychiatric problems, obstetric problems, arthritis, a propensity to develop dangerous blood clots, or kidney disease. Similarly, the Hepatitis B Vaccine–like the infection itself–has been implicated in any number of neurologic derangements from peripheral demyelination and axonopathy to multiple sclerosis-like disease (emphasis on ‘like’). The latter disease and a possible link to HBV has been the subject of several of these case-control series, with some finding associations and others not. But if you look at the actual case reports that prompted this discussion, you find that although in some ways the pathologies appeared similar to MS, in other ways they didn’t. By taking only a subset of the greater issue (neurologic sequelae) and then using perhaps too restrictive criteria for the definition of illness, they in effect do nothing to resolve the larger question.

Conclusion

In his original post, Dr. Rob said:

But there are some who would suggest that I am deluded. I am brainwashed by the vaccine manufacturers, drug reps, or narrow-minded training. Yes, I can be trusted to rescue their child from the brink of death, but can I be counted on when I recommend vaccines?

I don’t happen to think anything of the sort about Dr. Rob. I do however feel that the knee-jerk reaction to counter the anti-vaccine posturing with hysterics of our own is both counter-productive and disingeuous. We really have very little idea about just how safe or unsafe vaccines are. And anti-vaccination groups are more than cognizant of this fact. Much of what I’ve written about here is likewise trumpeted by many anti-vaccination groups. These criticisms are valid and ultimately our failure to answer them will only cause vaccine skepticism to increase. Yes, vaccines are no doubt effective in reducing the incidence of infectious disease. But do they outweigh the potential negatives? I don’t know, and you don’t. None of us do. And as long as this remains true, the case against vaccination can always be made.

Initial safety trials do not monitor adverse events long enough to reveal the incidence of the most debilitating adverse events. Many fail to use proper placebos. Post-marketing surveillance is subject to under-reporting such that actual rates may be an order of magnitude or more higher. And most retrospective case-control studies do little to advance our knowledge of the broader issues of vaccine safety.

To me, these are glaring problems. But how many in our profession look at the uncorrected VAERS data, or the pathetic nature of initial safety trials and take them as gospel? How many even think about the methodologic problems associated with our methods of assessing vaccine safety? The height of our ignorance in this matter far outweighs the depth of our knowledge. So when we find ourselves troubled by the number of parents refusing vaccinations for their children, when we see un-vaccinated children becoming sick, being hospitalized, and dying from vaccine-preventable illness, it is imperative that we correct this error. It is not enough to argue from authority: ‘I am a doctor and I say this is good.’ We have been doing this, and it hasn’t been working. There is no doubt that irrational fears play a part in the rise of anti-vaccination sentiments. But we should not dismiss rational concerns about vaccine safety. We must be able to argue from a convincing position of knowledge, something not currently possible. Furthermore as physicians we (well, not me personally until June when I graduate) owe it to our patients, our profession, and ourselves to know the truth about vaccines.

Perhaps there really is nothing to the assertion that certain vaccines can cause or exacerbate autoimmune phenomena. Perhaps aluminum adjuvants really do pose little to no risk of neurologic sequelae. Then again, perhaps the risks are real and large enough to make us sit up and take notice. Perhaps the side effect profile is poor enough that the risk of vaccination isn’t outweighed by the risk of infection. And if this is true, if the vaccination skeptics turn out to be right in some respects, shouldn’t we as physicians know that too?

I welcome dialog with doctors and other health professionals on this issue. And I hope that we as a profession learn to open-mindedly tackle the as-yet unresolved issue of vaccine safety.

Americans spend more on healthcare than any other industrialized nation. With the election looming closer, it’s almost impossible to pay attention to current events without hearing it every single minute of every single day. Unfortunately, we never hear the two corollaries. 1) The quality of our medical interventions and management is superior in every single way. 2) The United States leads the world in living as unhealthily as possible. If our outcomes are worse, look to the latter. If our costs are higher, look to both.

Every day I hear pundit after talking head waxing poetic about what we can do to avert the healthcare crisis. Doctors get paid too much (really, how about you suspend your life, goals, and dreams until you’re AT LEAST 28 before you start doing what you’ve wanted to do all your life, with mountains of debt, paperwork, regulation, and other little nuisances looming over your head?). HMOs make too much money (true, in no small part to government regulation). Drug companies are after profits (well, yeah. That’s what corporations do. Physicians can accept some blame here for flawed studies, ever more pervasive medication guidelines, and NBT-ism*).

What I never hear from any of the people who supposedly have the answer to this, is the importance of the American public taking their health into their own hands. The simple truth is that the vast majority of the day-to-day costs of healthcare are rooted in our own lifestyles. Diabetes, heart disease, depression, anxiety, low back pain, arthritis, all of these things are if not 100% preventable, at least largely within our control. What we cannot prevent, we can alleviate and manage by living our lives as best as we can.

The philosophical model of the individual under which the majority of the public seems to operate under is that of a powerless pawn in the grip of fate. Diseases, conditions, and injuries happen to people. They aren’t expected, they aren’t incurred, and god forbid anyone even imply that how you live had anything to do with your current predicament.

It’s not surprising that this is what they want in healthcare coverage. Pay a yearly fee, go to the doctor, get tests, get medications, get interventions, without any further expenditure of time, effort, or money. They want as little an active role as possible in their own health care. This is not insurance folks, this is health maintenance.

What the public seems to want is for doctors, pharmaceutical companies, and the healthcare industry to manage every aspect of their health. And they seem shocked when as their health deteriorates and their demands grow greater, that costs grow.

I came to medical school with a different model in mind, a model that’s only been reinforced as my third year draws to a close. Something not so far off from what Edison voiced when he said that “The doctor of the future will give no medicine, but will interest her or his patients in the care of the human frame, in a proper diet, and in the cause and prevention of disease.” As a 10 year sufferer of Reflex Sympathetic Dystrophy and as someone who spends no small amount of time counseling informally, there is no value I hold higher than the Agency of the individual.

Whether the ailment be physical or psychological, the most important thing to me is to promote the individual’s sense of free will, their belief that they can effect a change in their own destiny by their own hand. In my one year on the wards, I’ve seen heart disease in 30 year olds with no family history, 70 year olds as thin as a rail telling me that their children have diabetes but they have no health problems themselves, and I’ve seen more sedentary, obese, low muscle-mass people with disability for low back pain than I can count. And I’m not even going to mention the rate of COPD in the great state of Oklahoma. This is not the picture of a world in which bad things occasionally happen to people. This is what it looks like when individuals fail to take the maintenance of their own health as seriously as they do Oprah and SportsCenter. This is the failure of the individual to recognize and accept responsibility for their own agency.

The nature of healthcare has changed dramatically in the past few decades, from one in which visits to the doctor were infrequent, pillboxes were tiny one-chambered affairs, and people with chronic conditions were few and overwhelmingly elderly, to one in which our doctors are on speed dial, personal organizers have sections for medication lists, and healthcare utilization has become a part of our everyday lives.

The only way out of this mess as I see it is to stop being Enablers. As the American public eats, sits, and poisons itself into oblivion, instead of allowing them to continue to ask “who’s going to clean up this mess?”, we need to ask them who made the mess in the first place. We need to follow Edison’s advice and return the patient to their position of power. We must act as advisers and educators first, stepping in to manage illness, trauma, and chronic conditions only as they lack the capacity and power to. But patient agency goes far beyond just taking an active role in one’s own health, but also in the decision-making process of paying for medical care. From what level of coverage to who they choose to carry it out. Anything else would be to only further the deteriorating healthcare situation.

One of my philosophical influences, Garret Hardin, wrote about The Tragedy of the Commons. In such a scenario, some see the benefits, while everyone pays the costs. In such a scenario, we are ill-motivated to curtail the costs we incur as we never feel them directly. Such is the situation of our current healthcare structure. Even though we continue to bemoan the increase in out of pocket expenses, premiums, and denial of coverage, the direct costs of our own personal health situations are still very much spread out, and even when not, can be heavily concealed from us.

Premiums have risen dramatically, as my meager pocketbook can attest to, and while much of this is due to graft and greed on the part of HMOs, a good deal of this is due to the fact that the average person and thus the average health insurance enrollee incurs greater costs. Frequent PCP visits for minor ailments, antidepressants, anti-reflux medication, BP medication, diabetes medication, pain intervention, specialist visits. All of these things have seen dramatically increased utilization over the years. More people utilizing more healthcare, of course insurance will go up. And yet nary a mention of this I’ve seen on the news our out of the mouths of politicians.

In such a situation, it would behoove the individual to have the ability to choose their level of coverage and who their provider would be. Two of the greatest disservices that have been done to health care consumers was the coupling of employment to health insurance, and the comprehensive health insurances mandates currently inundating the country. Your employer doesn’t ‘pay for’ your health insurance. You do. ‘Employer contribution’ for social security, unemployment, and healthcare are actually part of your pay, you just never take it home. But when you relinquish a part of your income to your employer for HMO purchasing, you run into an ugly little problem: Your employer may be legally bound to use your money to buy ‘comprehensive’ health insurance by law, but that only means they will try to find the cheapest coverage that satisfies legal requirements regardless of how well it actually takes care of you. This is pretty well evidenced by the fact that although I’m a medical student spending all day in the finest academic hospital in my state, we are offered the most pathetic health insurance known to man. Which is why I don’t purchase it.

More importantly, as mentioned earlier, when you buy health insurance, you are pooled with all the other people also enrolled at a similar level of coverage. What you pay isn’t based on what you spend or are likely to spend but what the group as a whole does. As this group continues to profligately waste away their health, substituting expensive medication and specialist visits for better living, you are forced to share costs with them. For some people, this is pretty sensible. Those with a family history of chronic conditions, those with young families, and those who simply don’t care to take their health into their own hands are pretty well served by the traditional model of health insurance. Yep the premiums are pretty high, but so is your healthcare utilization. As an example, there’s a guy I know in his late 40s who has well-managed diabetes, taking metformin, niacin, omacor, and one other diabetes drug. His family’s health insurance comes to about 7200 a year, but when you subtract all the expenditure for diabetes that would’ve otherwise come out of pocket, the balance is only about 1200 a year. That covers routine visits for his wife and kids, emergencies, and any further expenses he or they might incur. Including his wife’s recent expensive cervical fusion operation. Which is actually pretty reasonable when you think about it.

Contrast that with me a young 24 year old with no wife, no kids, and conditions beyond the RSD. I get an MRI every year to watch for further deterioration of a very ugly symptomatic herniated T8/T9 disc and some less ugly less symptomatic cervical discs (thanks to the RSD), the occasional specialist visit when there’s an issue I’m not able to manage on my own in the weight room, and 32 dollars worth of mobic and cyclobenzaprine a year (a lot of which ends up thrown away). Even with my condition, my expenditures are never more than 1500 dollars a year. How much sense would it make for me to enroll in the 3200 dollar school health plan that doesn’t cover the most important part (MRI) anyway? Not a whole heck of a lot when I could pay the much more modest sum for critical care insurance and drop the occasional dollar in a Health Savings Account. Especially given that, in the event that I do develop diabetes or heart disease (unlikely given my nonfasting total cholesterol of 150, perfect FBG, and 15 hrs a week in the gym) the critical care insurance will pay me a rather large lump sum right then and there.

The truth is that when you buy into comprehensive health insurance, you buy into a total package that involves healthcare as a part of your lifestyle, rather than something to be used in an emergency or disastrous situation. This is especially true in today’s environment as more and more people develop ‘chronic conditions’ through their own way of life. Those who choose to live right and live well simply do not need this level of coverage. Or at the very least should be able to take advantage of pricing contingent upon how they manage the risk factors under their control.

As Americans, we should be able to choose the level of coverage we desire in keeping with the way we live our lives and a rational assessment of our risks. We do so with our cars, choosing high deductible liability insurance on beaters and low deductible comprehensive insurance for our BMWs. Why not with our bodies? My car insurance offers a 10% discount for defensive driving classes, and lowers my rate every year I don’t have a speeding ticket. Why should I not be offered the option of cheaper health insurance that acknowledges my efforts with a discount for eating right and going to the gym, or that would first require I shed my omental fat before going on medication for mildly elevated blood pressure, or eat better and exercise more for low HDL/high LDL? That’s what insurance is all about? Assessment and reward for risk reduction.

Taking it a bit further, let’s say a 28 year old walks into your office at about 220lbs. He used to be a linebacker in high school and tried out for college ball but didn’t want to deal with the demands of daily practice. Now his idea of physical activity is keeping up with his alma mater on ESPN. Routine health visit reveals mildly elevated LDL, mildly decreased HDL, BP at 148/90 (x3, whatever, leave me alone), complaints of GERD, and mild somatic symptoms of depression suspicious for sleep apnea. Now, ’standard of care’ for this guy would be a low dose statin, a diuretic or maybe an ACEi/HCTZ combo, PPi, and CPAP and/or sleep study. That’s a fair amount of intervention right there. Now, I know that we give lip service to lifestyle and prevention, and he’d leave with a stack of pamphlets along with his scrips in real life, but what if we put our money where our moth was? What if we said “tell you what, I’ll schedule you to talk with a nutritionist, who can beat into your head the importance of essential fatty acids, reduced simple sugar intake, high quality protein intake, breakfast, and 4-6 smaller portioned meals a day. Then you can meet with a CSCS (certified strength and conditioning specialist) for another hour, who will explain to you how to jump on the stairstepper for 30 minutes 4 times a week on the ‘hill’ or ’strength’ or ‘fat burner’ program, and supplement that with weight training. You can come back in three months having lost 15 lbs and I’ll re-evaluate you then.” He comes back in three months with his BP problems remarkably having disappeared and his lipid profile drastically improved (although his LDL could use a little more work), and his sleep troubles dramatically alleviated. We start him on a PPi. Now let’s say he doesn’t take care of the factors in his control and comes back. “We’ll treat you. That’s what we do. But if you’re not going to put the time and effort into taking care of your body, you can pay a bit more of the costs of your medication.” Now, let’s say he DOES put in some effort, loses some weight, and seems to be committed to a healthy lifestyle, but the problems continue. “You’ve done your part. You should be proud of yourself. And I know it didn’t help with all of the problems you have, but believe me, it will pay dividends down the road. Here’s your scrips. It’s a pleasure having patients like you.”

Now let’s say a mildly overweight female in her mid forties comes into your office complaining of low back pain, fatigue, and has a webmd article with all her symptoms of fibromyalgia helpfully highlighted. Her obese husband’s come along because his knees ache something fierce these days. You notice that she stands ‘bonily’ (no official medical terminology for it), slouching and seeming to carry all of her weight on her bones and joints, not in her muscles. Guess what? Off they go to the nutrionist and exercise physiologist. Maybe a physical therapist as well in her case. And given the high comorbidity of CFS and fibromyalgia with depression, it might not be such a bad idea to have her see a psychiatrist for further evaluation. Send them off with some mobic and wish them the best of luck. See them back in three months before you pull out your list of orthopedists and pain specialists you refer to. Fibromyalgia, low back pain, and arthritis are expensive conditions and largely have to do with deconditioning of our postural and girdle muscles. Getting our muscles back in working order is the most effective intervention we can make with regard to these increasingly prevalent ailments. Depending on how much damage has already been done, we may not be able to avoid more costly and invasive procedures, but we may be able to delay them.

Rational decision-making is based on freedom of information and accurate assessment of costs and benefits. The current healthcare paradigm in which the individual costs of aspects of healthcare (actual cost of healthcare premiums–not just personal contribution, true cost of drugs, PCP visits, specialist visits, and procedures) are concealed from them and in which they are not allowed much choice in the degree of coverage they want. The healthcare equation is one of time, effort, and money. Choosing the level of coverage you would like needs to reflect your assessment of personal risk, as well as the degree of time and effort (and a little money), you are willing to invest in your own health. The more time and effort you are willing to invest in your own health, the less money you should have to pay for your healthcare coverage and co-pays. Conversely, the less you are willing to invest in yourself as the agent of your own health, the more you have to be willing to invest in the healthcare delivery system.

The true crisis in healthcare from where I’m standing isn’t the increasing load of diseases and conditions in our population, nor is it the increasing costs of healthcare. At the root of both of these things is the dereliction of duty to self that patient, doctor, industry, and government have been party to. I’ve said before that my goal as a physician is to be useless. I really detest preventable chronic disease. And I want to live in a world where as few of my patients have them as possible. I want to help my patients do everything in their own power to stay healthy, intervening only when it becomes necessary. The current rhetoric about healthcare, and the current structure of healthcare coverage and payment, is such that it only serves to reinforce the alternative view, one in which bad health is something that happens to people, rather than something we can in large part prevent and alleviate on our own. We must make lifestyle management a part of the healthcare cost equation. And we must allow patients to reap the benefits or bear the costs (at least in part) of their own discretions. Insurance is about taking care of the factors that are out of our control. This is why the concept of insurance was developed thousands of years ago and the concept that health insurance especially needs to return to. If anything is to be done about the healthcare problems facing us today, it must be done by returning to a patient-centered focus. A focus in which the American public is made the arbiter of its own destiny.

*NBTism - Next Big Thing Ism. Using a new drug just because it’s new. Even if older drugs in the class are just as effective with little or no increased incidence of ADRs. See PPIs, BP medication, antibiotics, and DM2 drugs.

…Actually measuring it accurately. This goes for research as well as in clinical practice.

This is a huge pet peeve of mine. Possibly because I was trained in a much more rigorous science before I started on my way in the medical profession (third year medical student). Also possibly because I’m kind of a healthy living nut. And equally as possibly because I’ve been ‘overweight’ my entire adult life despite wearing pants with a 32″ waist. Hard to say really.

The point is that obesity is a serious problem. Not just when it comes to major causes of mortality like heart disease, stroke, and even cancer and dementia, but also major morbidities–ones that often further predispose you to the above-mentioned mortality risks–like arthritis, spinal dysfunction, diabetes, peripheral vascular disease, and recurrent infection. There’s also little question that excess weight substantially reduces quality of life if nothing more than for the simple reason that it’s harder to move.

There is no doubt that fact, and the escalating proportion of the population that fits this definition is an even greater concern. But we actually don’t know and can’t know how serious a problem it is as long as we continue to use the BMI (actually an approximation thereof) as our method of categorization.

The Problem with BMI

BMI is a population-level measurement and has been proven time and time again to be of little to no validity when applied to the individual. Granted, if someone has a BMI of 17.5, they probably are substantially malnourished, but it still shouldn’t be the criterion we use to differentiate anorexia from bulimia, for instance. And if someone has a BMI of 40, chances are they are indeed carrying dangerous levels of body fat and have metabolic syndrome, if not overt diabetes and atherosclerosis. But in between the BMI is nothing if not lacking in precision.

The formula for the BMI is quite simple and is nothing more than our weight divided by our height squared. Yielding units of kg/m^2. And here we have the first problem. Any measurement system we use should be based on actual physical characteristics. The only physical characteristic that would naturally be expressed in terms of m^2 is our surface area. This would actually be a substantially more pertinent (although still limited) calculation. Body Surface Area is a pretty useful quality and finds application in everything from bioenergetics to exercise physiology to pharmacology. A measurement that used BSA and weight would give us an idea of body density, which is the basis for the more accurate body composition tests we have such as immersion. But since density at a given body fat percentage varies based on height (i.e. a 5′ tall person with 7% body fat will have a different density than a 6′ tall person with 7% body fat), a Bodymass Density Index (which Height/BSA would be), still wouldn’t be the most useful thing in the world.

The next problem with the body mass index is that it really doesn’t look at what kind of mass you’re carrying.

It’s a population level statistic and is more of an epiphenomenon of the fact that people are fatter today than they used to be than anything else. In other words, the only reason the BMI tends to work is because in society at large heavier people tend to be fatter. It’s an incidental finding. Amongst my gym buddies, Ken, a 230lb behemoth, sits at 6.5% body fat (based on statistically valid caliper testing). At 5′11″, he’s ‘obese’ according to BMI, yet just about anyone reading this should be envious of his low body fat content. At 5′11″ and 195, I’m only ‘overweight’, but I would bet any amount of money that I’m the one with a higher body fat percentage. And, even though my love handles have been my constant companion since I was about 14, I carry less body fat than most people who weigh 10lbs less than I do or more.

On the other end of the scale, researchers have had to coin the term ‘normal weight obesity‘ to identify those individuals who are not caught by the BMI screen and yet carry a substantial amount of body fat. Using a cutoff of 20% bodyfat for men and 30% for women, Mayo researchers found that over half of the sample of people with BMIs from 18.5-24.9 qualified as ‘normal weight’ obese. Metabolically, they appeared for all intents and purposes similar to those with a BMI over 30. The obesity problem thus isn’t restricted to those with a higher BMI, not by a longshot.

From a research standpoint, we can pretty much invalidate most of the ‘obesity’ research that has occurred thus far, at least as it relates to health risks and etiology. I haven’t been able to find a study looking at ‘normal body fat obesity’, but given that at 5′11″ a person can only weight 178 while still being considered ‘normal’ (which really isn’t very big), I suspect that a substantial proportion of people considered ‘overweight’ and even ‘obese’ by BMI are actually well within healthy limits for body fat. One bit of (slight) corroboration that I’m aware of is a study I found some years back indicating that increases in BMI among adolescent males were linked to decreasedbody fat and increased physical activity.

Current epidemiological and population-level research in obesity is thus lumping together disparate body types and compositions into its various categories. A full half of the ‘normal weight’ group carries an unhealthy amount of body fat, while a good-sized portion of the ‘overweight’ group is actually quite healthy. The major effect is to understate the health risks associated with unhealthy levels of body fat. Other potentially important factors with regard to chronic and major illness, morbidity, and mortality could easily be missed as well, such as whether llghter individuals with high body fat are at greater risk for health problems than heavier individuals with otherwise similar amounts of body fat (perhaps accounting for the occasionally mentioned ‘protective effects’ of body fat), or whether heavier individuals with low body fat are at increased or decreased risk for chronic medical conditions compared to lighter individuals of comparable body composition.

And, again (the third time I’m mentioning it I think), as BMI doesn’t hold for individuals anyway, we find ourselves hampered when it comes to translation of research into practice. It’s literally comparing apples to oranges. There is no way to put the information BMI-based research gives us into practice when it comes to screening and treatment.

The Answer?

Measure body fat. Recent attempts to popularize waist size instead of weight are a step in the right direction. But waist size is still an imperfect proxy. While unlike the BMI it is instantly translatable from research to practice, it still overlooks other possibly important body variables such as total lean body mass.

Well, immersion (hydrostatic) body composition tests are quite obviously impractical. The equipment, facilities, cost, staff training and expertise, and patient discomfort/inconvenience are prohibitive. But the 7-site skinfold method is accurate within 2% or so, training is easy, it’s fast, and it’s cheap. It might add a minute or two of time to patient/subject processing, but the dividends it pays will be tenfold.

Conclusion

Moving to skinfold tests to measure bodyfat in research and clinical practice is the wisest step we can take in understanding, preventing, and combatting the effects of obesity. It is the simplest solution to improved understanding of health and disease as well as more effective targetting of at-risk patients.

One benefit of body fat percentage testing which I’ll only touch on briefly is that it also provides us the ability to measure lean muscle mass. Muscle is an oft overlooked entity when it comes to medicine at large. We look at our patients’ bones, joints, visceral organs, endocrine systems, and brains, but nary a glance do we lend to one of the most amazing and adaptive tissues in the human body. Which is concerning, given that it makes up roughly half of our total mass.

Lean muscle mass is a pretty important variable unfortunately ignored for the most part in research and in practice. Exercise physiologists have known for decades the benefits of lean muscle mass and medicine has just started to take notice of its role in areas from prevention and alleviation of arthritis, to decreased spinal, neck, and back problems, to improved daily functioning in the elderly, to diabetes resistance, and lean body mass may even have a protective effect with regard to dementia–at the very least providing an improvement in symptoms and slow in the rate of cognitive decline.

Whatever the case, in order to properly understand, prevent, and treat obesity and obesity-related illness, we must be able to accurately assess its extent both within the population and in our individual patients. The body is too complex to be defined by a single number, be it BMI or simply weight. And in order to best understand the human body in sickness and in health we need to move away from such simplistic measurements.

Sun Tzu advises us that ‘If you know the enemy and know yourself, you need not fear the result of a hundred battles.” High BMI is not the enemy. And we are not our weight. The enemy is body fat, and body composition is ourselves.

Target weight or unhealthy BMI, either concept is wrong. Rather we should seek a target body and mind, and to such an end we should endeavor to use the most enlightening tools at our disposal, especially when the effort is so small and the reward so large.

For just about any other kind of health problem, we talk about how lifestyle (diet, exercise, etc.) plays a huge role in the etiology of disease. Lifestyle changes can prevent disease, they can slow its progression, and in some cases even reverse it, depending on what we’re talking about.

Diabetes, cancer, heart disease…all are illnesses that affect a substantial portion of the population. And in each of these cases, a significant amount of time, effort, and money is allocated toward learning how to reduce the risks of developing such debilitating conditions. Furthermore, as a quick perusal of the ADA and AHA websites show, lifestyle modification is a crucial part of the strategy for managing these health problems. Indeed, as time goes on, doctors are emphasizing the fact that all the drugs in the world cannot make patients healthy if they make unhealthy decisions.

They claim that 47% of adults will suffer from a diagnosable mental illness during their lifetime. I take issue with the label ‘illness’ as that implies a degree of severity and irreversibility that simply isn’t the case. They also claim that 23% of us will suffer from clinical depression. By contrast, only 10% of the population aged 20 or older has diabetes.

Psychiatric problems (illness or not) can be just as deadly and debilitating as any other medical issue. Why then is there little or nothing in the way of preventive education? Why then do primary care physicians prescribe antidepressants and psychostimulants often without so much as a referral to a therapist?

We are surrounded by messages telling us how we know if we ‘have depression’ or ‘have ADHD’, and what drugs to ask our doctor for. But have we ever been told how to prevent ourselves from becoming clinically depressed? Have we ever been shown how to deal with depression, ameliorate our anxiety, or learn how to focus better?

I find it hard to believe that unlike diabetes, unlike heart disease, unlike cancer there is nothing we can do to prevent ourselves from suffering from mental health problems. Indeed, the fact that some people appear far more resistant to depression and anxiety than others in similar circumstances, combined with the relatively weak heredity of such psychiatric problems, would seem to indicate that mindset and worldview play a substantial role in resistance to mental health problems. And, even more convincingly, depression is on the rise in this country. Which would point to something we are doing rather than something inside of us being the culprit.

Relapse rates for those treated with antidepressants alone are considerably higher than for those who received combination therapy or only psychotherapy; in fact, only about 1/3 of those who take anti-depressants alone see a full resolution of their symptoms while 1/3 don’t respond at all. Da Vinci, Michaelangelo, Edison, and countless other accomplished people fit the textbook definition of ADHD, yet never took a pill for their ‘condition’.

Simple logic dictates that if systemic disease can be prevented or at the very least mitigated by behavioral modification, then certainly mental health problems would too. Scientific evidence backs this idea up quite firmly. And yet it would seem that they’re far more interested in telling us we have a psychiatric illness, then telling us what we can do to prevent being so labeled or how to fix it.

I guess you could call it a benefit of living with your parents. Mom knocked on the hovel’s door where I was busy avoiding studying and told me to come watch a 60 minutes segment on the treatment of depression through deep brain stimulation.

I think she does this just because it’s funny to see me in a rage. Cursing, throwing things (like my 8lb miniature pinscher), and semi-coherent rants equally populated by erudition and epithets characterize these award-winning performances. I’ve been told that at the climax of one of these fits, no one’s sure if I’m going to stab whoever I’m screaming at or bludgeon them to a more symbolic death with logical debate.

I get annoyed with the perception of mental healthcare (both laymen and many practitioners), not the least because like leftists they seem unable to think of long-term effects. In the case of laypeople, it’s because they haven’t been educated enough. Not exactly their fault. When it comes to practitioners, they simply have no excuse.

Now, I am not criticizing these particular clinical investigators. I have only this news report to go off of. And if they were up front with their patients on how brains work and the potential side effects related to this particular procedure (not just surgery in general), I have NO beef with them as far as ethics goes. Theory on the other hand, I do.

These doctors are using a technique called Deep Brain Stimulation of a certain area of the brain that has been found to be overactive in people with intractable depression: Area 25 (part of the Anterior Cingulate Cortex which is itself part of the Limbic System).

The fact that they’re stimulating an already pathologically overactive part of the brain should be a huge red flag that dealing with the brain is not quite as simple as action–>reaction. By stimulating it, they actually tone it down through an induced negative feedback process. Which I’m not going to explain in full because I’m lazy.

What they’re doing is theoretically sound–in the short term. The question in my mind is the longterm stability, efficacy, and safety of such a procedure.

Virtually everything in physiology revolves around the concept of homeostasis, or maintenance of a constant environment. There are several great examples of this. One being the baroreceptor reflex which attempts to keep blood pressure fairly constant. If the blood pressure stays abnormally high long enough, eventually the receptors stop reacting to it. The reflex is reset at a higher blood pressure because the neural receptors have filtered it out as noise. And now you’ve got a chronic hypertension problem.

A slightly different thing happens with the hunger-controlling protein leptin and its positive correlation with body fat percentage. Eventually, body fat percentage can get so high that leptin release can no longer increase. In these individuals not only is there a mental disconnect between eating and satiety, but a physiological one as well.

The patient who they interviewed in this segment talked about how everytime they increased the frequency and strength of stimulation, she was better for a while, and then fell right back into the pit of depression. She was considerably better off than before, but was still significantly depressed. Is it possible that her Area 25 simply adapted to the stimulation after a while and went back almost to the way it was, just as in the barorceptor reflex?

But they also showed a patient they consider their greatest success story. She had the same overactive Area 25, but has been nearly symptom free for months now. The difference in her face before and after is just amazing (as it is in the other lady for that matter). Could it be that her problem was like the leptin-body fat disjunction? With her Area 25 simply becoming too overactive to be compensated for? It would explain why she reacted more permanently than did the other patient: the stimulation returned her Area 25 to a level where her brain could compensate.

The fact that neither patient is adequately described by the same physiological model is our first clue that we still dont’ know exactly what’s going on and that depression may be considerably more complex than just an ‘overactive brain area’ or ‘chemical imbalances’.

But what scares me more is that neural tissue is some of the most sensitive stuff in the body. It pretty much dies if you look at it funny. Which kind of sucks because nerve cells, like muscles can’t regenerate; you’re born with the neurons you will die with. And one of the well-known factors in this is excessive and/or unnatural stimulation. This is the etiology of meth psychosis, the ‘holes in the brain’ in chronic ecstasy use, and drug-related Parkinson’s. Many of these substances work by stimulating neurons to release more of certain neurotransmitters (norepinephrine, serotonin, and dopamine). Chronic use causes these sensitive cells to die. Just as higher baseline production of insulin in those genetically predisposed to Type II diabetes eventually results in the pancreas burning out and an inability to produce full amounts of insulin later in life.

The brain represents one of the most complicated feedback and control systems many will ever study. Fewer still will take the time to think about all the different ways the brain reacts to external and internal changes before they make the simple declaration that something ’causes’ something or something ‘cures’ something. Short term and long term effects are often completely opposite. What looks like one thing in two patients could easily be two different things presenting the same way. And changing mood through SSRI’s doesn’t result in a normal looking brain on PET but an even more abnormal one.

The complexity of this system causes me to have the opinion that most of these pathologies are rooted in the persistence of certain thought patterns. If they last long enough, they can reset the brain as in the baroreceptor reflex. If they get too strong, they can escape their feedback loop, as leptin does. But what we see in our initial workup, on the MRI or the PET must be treated as a symptom. Treat it, because it needs treating, but remember that the actual cause is at least one step removed from whatever you’re looking at.

First science post in a long time. Expect more though. Because I feel like I’m in a political rut.

I get more than a little frustrated when doctors and fellow medical students tell me they don’t see how evolution has any bearing on the practice of medicine. Perhaps it’s because they’re taught to think of the body as a machine that on occasion malfunctions and needs to be repaired, and so find themselves inclined to think of Paley’s watch rather than Haeckel’s famous theory. Perhaps it’s because they view biology as a means to an end rather than the end in and of itself. Whatever the reason, Dobzhansky’s most famous utterance is lost upon far too many of them.

Learning
A knowledge of evolution makes understanding several subjects considerably easier. This applies to embryology perhaps more than any other. As a tutor for the dental students at my university, I’ve found phylogenetic comparison an invaluable teaching aid. I’ve also found it immensely frustrating since, being in Oklahoma, I have to preface it with “I don’t know if you’re a creationist or not, but this is an evolutionary example that helps me understand things.” When helping students to understand why the sclerotome of the paraxial mesoderm forms only axial skeletal elements but not appendicular (limb) bones, I invoke the humble lamprey. Possessed of the simplest body plan, the poor creature lacks both limbs and a true jaw. I tell them “The sclerotome is pretty old stuff, it’s only got enough material to produce a lamprey skeleton.” Vertebrae, ribs, and a skull encasing the brain and eyes. That’s about it. Jaws, ‘faces’, and limbs, being newer vertebrate features, have a different embryological derivation. And a lightbulb goes off. “Paraxial=lamprey”. Stupid simple.

Staying with embryology just a few moments longer, the development of the kidney is a rather confusing process. The embryo/fetus actually develops three different excretory systems in succession, the latter two of which are functional at various points of development. First come the cervical nephrotomes, then the mesonephros, then the metanephros. This developmental process is an elegant (and possibly the finest) example of the idea that ontogeny recapitulates phylogeny. And because of this, a sprinkling of evolutionary context can help to make sense of this process well enough for a student to keep things straight.

Perhaps the most fun use of evolutionary perspective comes when learning about physiology. Everything in physiology revolves around homeostasis. Maintaining a constant internal environment. For the most part, complexity of a given taxon is directly proportional to its ability to maintain its internal state at a constant rate. Mammals are perhaps the finest example of this ability, but all, from the simplest ball of Volvox to the lizard basking in the sun show some aptitude for this. And as to the nature of this internal state they’re trying to maintain? Blood bears a remarkable (or perhaps expected) resemblance to seawater in many respects. And this has prompted several of my physiology teachers to describe us as “a collection of cells that figured out how to take the sea with us.” Much like Wernstrom’s goldfish and his reverse scuba suit.

The greatest vindication of the use of evolutionary history as a teaching aid is the fact that although these represent extra–what mainstream physicans would less charitably call extraneous–information, they nevertheless make the testable material easier to understand. In short, the extra learning investment is more than returned.

Looking Forward
Evolutionary thinking also gives us a more stable platform from which to study the human body in sickness and in health. Understanding that the human body is an evolved construct allows us to better understand exactly what ‘normal’ is, and what conditions may bring on disease.

Anatomically and genetically, humans haven’t changed all that much in the past 100,000 years. Yet our environs and our lifestyles have shifted to the point that our current circumstances have no resemblance whatsoever to our past lives. More importantly, as technology, healthcare, and standards of living have improved, we are less and less likely to die before reproducing no matter how feeble or infirm.

What this means is that we have to treat the body as evolutionarily static at least from the birth of modern H. sapiens, and perhaps even as far back as H. heidelbergensis. And although I am somewhat critical of the view of the body as a machine, it remains a useful framework within certain limits. The heating element in your water heater would quickly warp if powered up in open air. And the coil on your stovetop wouldn’t function under water. Their failure under such circumstances is not an indicator that they are defective, but rather that they were forced to operate outside their design parameters.

I hate to use the word ‘design’ in such a context, but preventive medicine hinges upon our ability to ensure that our bodies are not placed in situations they haven’t evolved to cope with. Diet, activity patterns, and exercise are just a few of the areas in which we differ from earlier examples of our species. How does this deviation affect our health? In the realm of genetics, sickle cell anemia is probably one of the most well-known examples of the intersection of evolution and medicine. A potentially beneficial allele in one environmental context becomes nothing but a nuisance at best, lethal at worst in another. Type II diabetes is another example.

My personal agenda revolves around the basic proposition that the brain’s purpose isn’t whatever some psychologist claims it is, but rather that it is wired and coded with software that is designed for a certain environment. It is not a blank slate but an evolved construct optimally suited to certain physical and social contexts. When placed in a different social or learning structure, it can easily go haywire.

The latest area of medicine I’ve seen a place for evolution in is cancer. This might be because we just finished the unit on neoplasia in pathology class and I’d been studying it 24/7 for the past couple weeks. But everything about the pathogenesis of cancer hearkens back to lessons I had in undergrad on selective advantage, differential reproduction, and natural selection. Without getting into too much detail, cancer is essentially a progression of genetic changes, each of which allow these cells to escape the restraints that prevent normal cells from proliferating and spreading unchecked. The neoplastic cells that beget a tumor were often present 10 or 20 years before anything was clinically evident. This is because the immune system ruthlessly destroy those cells that appear genetically different from the host. Like multi-drug resistant bacteria, those neoplastic cells exist in an environment that consistently selects for the ones that evade detection, escape destruction, and reproduce faster than they can be killed. The ability of these tumors to continually reappear despite the immune system’s best efforts, and in many cases from apparently successful chemotherapy should thus come as little surprise when thought of this way. We are in fact selecting for those mutant genes that confer the ability to escape normal therapeutic and preventive methods.

We, our genes, our physiology, and our behavioral patterns evolved in one environment. They are a product of that intimate interaction between the organism and its surroundings. Changing the surroundings not only changes the nature of the interaction, but may substantially affect the fitness of said organism. While nothing so dramatic as the explosion of a polychaete worm when placed in a freshwater aquarium, there can be little doubt that much of the ’cause’ of human illness may not be rooted internally at all. Understanding the difference between our current environment and the one we evolved in will play an ever greater role in the prevention and treatment of disease.

Conclusion
Medicine has much to learn from evolution. It can provide us a foundation from which to better ground ourselves. And a scaffolding from which to reach for the sky. No other facet of the biological disciplines has remained as recalcitrant to simple Darwinian concepts as this field, and perhaps it’s time we were brought kicking and screaming into a mindset most of our colleagues found in the early 1900’s.

I’m not a fan of determinism. Especially when it comes to medicine. Partially this is because I’m just stupid and naive enough to think of medicine as a calling and not just a job. And I, personally, would only be happy if I never had to refill a prescription or even see a given patient ever again after 6 months. Of course, free will is also a crock when it comes to medicine. People are predisposed to certain conditions by dint of genetics, environment, and other factors. But predisposition and cause are two very different things, something many doctors either don’t understand or willfully ignore. Patients like it too. “It’s not my fault I’m diabetic, it’s genetic.” Certainly feels a lot better than “I should’ve paid more attention to lifestyle.

I’m sure most of my readers have heard about Ad36, an adenovirus similar to what causes the common cold. And they’ve heard about how it “makes” you fat. In a small study, they did find that 30% of obese people carried this virus, versus only 10% of others.

One thing I want to mention is that Ad36 causes paradoxical obesity. You’re fat, but you aren’t necessarily an unhealthy fat. You don’t necessarily have the high cholesterol, triglycerides and insulin problems.

But whenever someone throws percentages at me, I know that there’s another way to look at these things that can put it into a better, less alarmist/determinist, perpsective.

What they did was talk about the percentage of people of a given BMI category that are infected. But we could turn it around and look at the percentage of infected people that are obese. Roughly 30% of the country is obese, 70% not. When we compute everything out, we find that roughly 16% of the country is infected with Ad36. Of them, roughly 56% are obese, 44% not. For a virus that ’causes’ obesity, it sure seems to be kind of hit or miss.

I’ve hit this issue before. But it’s in the news again, so I thought I’d return to it. For a little background, you can see a piece I wrote or a highly recommended, if slightly older article written by a real doctor. Sorry for the lack of links. I’ll throw up a link list sometime in the next few days.

When Michael Reagan stood up at his father’s funeral and cried about how Embryonic Stem Cells could have saved the man who ended the cold war, I cried a little myself. I cried because I wish I was old enough to have better memories of a president who was by most accounts an amazing statesman and just a great man all around. I cried because it was wrong for the man’s own flesh and blood to use his father’s death as an excuse for political posturing. But mostly I cried because every time someone stumps for the new panacea, I see development of a real cure farther and farther away.

I’ll start by saying that my political position is that despite being pro-life, I have no moral qualms with harvesting new ESC cultures from cord blood or discarded embryos. In the former case, there is simply no moral quandary; the cells weren’t taken from an embryo/fetus/bay. With regard to the latter case, the operative term here is discarded. Any objections one would have to harvesting stem cells in that case would also apply to organ donation in adults as far as I’m concerned.

My scientific position is that ESC’s make for excellent models but bad therapy. ASC’s on the other hand are the exact opposite. Each have their place in the biomedical sciences and medicine. Embryonic stem cells are comparatively easy to harvest, sustain, and grow in culture. They’re also capable of differentiating into more kinds of tissue than any given adult stem cell. In addition, ESC lineages are standardized (currently 19 of them. Should be more), meaning studies are more repeatable. Adult stem cells, on the other hand are not as amenable to laboratory manipulation. They’re harder to get to (although we’re finding more accessible places where they exist), they’re harder to sustain, and they’re much harder to grow in cell cultures. On the other hand, despite tiny budgets and little attention from funding bodies or the public at large, ASC researchers have had much more success in therapeutic applications in animal models and humans alike. Even at a theoretical, freshman biology level, the advantages of ASCs in therapy are fairly obvious.

Embryonic Stem Cells

A recent issue of Scientific American highlighted the similarities between ESC’s and cancer cells (which is one of the objections to the use of ESC’s as therapy). ESC research may lead to greater understanding of the etiology (development) of various cancers. And more importantly, since when we were embryos our stem cells didn’t go tumor on us, we may be able to reverse engineer the process by which ESC’s are controlled. This could very well lead to better cures and preventive treatments when it comes to cancer. ESC’s are also a good deal more pliable than ASC’s (another problem when it comes to therapy). Which means you can do more with them in a laboratory setting, particularly when it comes to understanding developmental biology. ESC’s give us a convenient model with which to study proliferation, differentiation, and apoptosis. They’d be useful in studying how things go wrong in human embryonic development as well as how things go right. As well as in understanding the nature of the switches that turn these cells on and off and how to operate them. This is stuff we’ve been doing for decades, but thus far only with animal embryos. The moral implications of raising a human embryo for the purpose of experimentation are pretty grim. ESC harvesting methods are much more morally neutral while allowing many of the same benefits.

Of course, what makes ESCs so suited as models is what makes them so poor at therapy. Which is something the ESC researchers conveniently forget to tell the press and the public. After high school, I worked in a cell biology lab with CHO cell cultures. CHO stands for Chinese Hamster Ovary. No ordinary reproductive cells, these are all descended from an unlucky rodent’s bout with cancer. I always found it interesting that what made it such a useful laboratory model is why it killed that poor little pet. Like cancer, ESCs are immortal. Like cancer, a lot of the regular processes that differentiated cells go through are shut down. Like cancer, ESCs love to grow. Getting an ESC to stop growing once it’s in an adult body has proven to be a difficult proposition in animal models. Getting an ESC to turn into the kind of cell you want is also tough. And assuming you’ve got past all those roadblocks, you now have to deal with immunocompatability issues. When you get an organ transplant there is a pretty high risk of rejection, no matter how close a match the new organ is. It isn’t you. Your immune system knows it isn’t you. And it wants to kill it off. The immune system is a marvelous and sophisticated system that was designed for the sole purpose of killing off foreign cells. If you want those donor cells, tissues, or organs to stick around, you have to cage up that immune system, leaving yourself open to the depredation of other foreign cells. In other words, taking immunosuppresants for the rest of your life is not exactly fun. ESC researchers don’t mention to you that these problems apply to ESC therapy as well, do they? The one big success I’ve seen with them is in the nervous system. Which is somewhat expected. The nervous system is one step removed from a lot of other bodily processes, including circulatory and immune processes. Not to mention the fact that glia (support cells in the brain and nerves) secrete a chemical that actively inhibits nerve cell division and proliferation, meaning less likelihood of tumors. The one big benefit to ESCs compared to ASCs is that because they are less constrained, a single ESC culture can be turned into many different types of tissues, whereas any given ASC colony is significantly more limited.

Adult Stem Cells

What about adult stem cells, surely they can’t be any better, right? Not as models, no. ASCs are by their very nature dormant. That’s part of why they’re so hard to find and why people weren’t even sure they existed until recently. They’re hard to culture and hard to ‘turn on’. And because ASCs are at a later stage of differentiation than ESCs, they can turn into fewer types of cells. Meaning that it might take 2 or 3 different ASC colonies taken from different parts of the body to create all the kinds of tissue you can with just one ESC colony. ASCs can also be rather hard to get to: the hollows of your bones, deep in your brain, embedded in your heart muscle. Not a whole lot of people are going to volunteer for major operations just so some guy with no social skills in a white coat can play with test tubes. And, even if you could get people to do that, you’d still have the problem of lack of standardization. A researcher using stem cells he harvested from my bone marrow could do one experiment and get completely different results from another researcher halfway around the country who used your stem cells, not because the experimental process is unpredictable, but simply because you and I are different, and so are our cells.

Again, these weaknesses as a model translate to strengths as therapy. Imagine that you are told you have to hold a gun to the head of your best friend and you have your choice of two trigger types. One gun doesn’t go bang as long as you pull the trigger. Release it and you’ll be covered in brain stew. The other gun is much more conventional. If ESCs are the former, ASC’s are the latter. I’m pretty sure which one I would choose. While ASCs can be hard to get to, more accessible sources (that don’t require surgery) are being found even as we speak. These same studies are also finding that ASCs are easier to culture and are perhaps more flexible than was once imagined. At any rate, a situation in which one person has multiple degenerative disorders each needing a different ASC is bound to be rather rare. And the implications of self-harvesting for therapy are pretty obvious. Unlike ESCs–which are essentially transplants–ASCs are you. They’re your DNA and your tissue. Instead of organ transplantation, the process is more analagous to a scar fading to nothing over time.

Conclusion

Both ESCs and ASCs have much to offer us in understanding and treating disease, and they do so in a complementary, rather than competitive manner. Of course, research is highly competitive, and so whichever works better in a laboratory setting is the more likely to be funded. And it’s true that ESCs have greater potential to increase our understanding of cell biology because of this. But treatment doesn’t necessarily require understanding. When Fleming invented Penicillin he had no idea that the compound contained within put holes in bacteria cell walls, causing them to burst open. He just knew that the stuff killed bacteria. When Edward Jenner invented the smallpox vaccine, he probably had very little idea of how immune systems worked, he just knew that if you gave someone cowpox (which isn’t deadly) they woudln’t get smallpox (which is). Understanding can improve treatment, which is why it’s important. But there’s no harm in getting the ball rolling, which is exactly what we’re refusing to do by focusing on the politically expedient and the glamorous (if laboratory biology can be glamorous).

Adult stem cells offer us the potential to literally heal ourselves. To quote some old dead guy, ’tis a consummation devoutly to be wished’

The medical marketplace is one of those rare situations where the idea of government oversight has merit up to a point. An efficient market depends on the consumer being both informed and rational in his choices. This obviously requires familiarity with the performance of the product (success rate, side effects, etc.) as well as an understanding of how the drug works. This is a bit much to ask of your average consumer, considering all of the education and training required to make a doctor or a pharmacologist. It’d be a textbook case of a highly inefficient market with a great degree of misallocation of resources. In other words, patients would go broke as they died while pursuing ineffective treatments.

Is a government agency like the FDA the best solution to this problem? I can’t really say. But I think they’re a valid solution. The problem comes when they move away from that role in improving patient information to actually dictating which meds a patient can and cannot use and for what they can use them for.

FDA Approval
The ridiculously long clinical trial process is designed to determine how effective a given drug is as well as what, if any, the major side effects are. Based on this the FDA then makes a rather arbitrary decision as to whether or not the costs outweigh the benefits. Strangely enough, moneymakers like antidepressants, ADHD drugs and the like are allowed considerably higher thresholds than treatments for things like lupus, multiple sclerorosis, and other debilitating diseases.

The clinical trial itself is a good thing: It improves patient information. FDA approval is not. What the FDA deems ‘unacceptable risk’ might be far different from what an individual patient may think. Tysabri, a treatment to prevent relapse in Multiple Sclerosis, is a perfect example of this. 3 of the 1200 clinical trial participants developed a rather rare brain infection and subsequently died. These are not odds that the FDA likes. However, MS is quite a debilitating disease, and a patient might feel completely differently from a bunch of healthy people in white coats sitting far away from the pain, the debility, and the hopelessness.

Off-Label Drug Use
Another peculiarity of the FDA approval process is that a drug isn’t merely approved as ’safe’; it’s approved as ’safe and effective’. Which is a horse of an entirely different color. The FDA doesn’t approve drugs, but rather approves the use of a given drug in the treatment of certain conditions.

In other words, if your new wonderdrug has a second potential use? Guess what? Another trial, another 5-10 years before people at large can actually use it. Even though it’s already been deemed safe.

This is particularly problematic given the nature of the human body. Take Viagra for instance. Bob Dole may use it for one thing, but it has great potential in treating pulmonary hypertension and other cardiovascular problems involving constriction of your blood vessels. Although there are other meds out there, they often take a ‘bigger hammer’ approach and in many cases are incompatible with either the patient’s condition or their other drugs. Viagra, on the other hand, is quite a bit more gentle in its effect.

It’s an interesting thing about medicine in that the core of our knowledge hasn’t changed. I use the same textbooks in physiology and pharmacology as my mother did 30 years ago. They’ve been updated in the ensuing decades, but I bet I could get the same letter grade using her ancient version as mine.

A drug is approved for treatment of one illness because it has a certain effect on the body. If this effect is known to be useful in alleviating other maladies, then why must I be hindered in using it in order to treat my patients, simply because of the FDA’s shortsightedness?

Conclusion
The FDA’s biggest sin is micromanagement. As an overarching organization, it can help both patient and doctor make informed treatment decisions by bringing to the fore otherwise unobtainable data on drug performance (and more importantly harmful side effects). As such, it can liberate an imperfect market and allow better allocation of medical and economic resources.

However, when the FDA decides to make the decision for doctor and patient it not only limits their freedom, it compromises the patient’s health and the doctor’s ability to change lives. At least once in my medical career, I will literally hold my patient’s life in my hands. I will be what stand between him and an untimely death. The idea that some suits in Washington can tell me what I can and cannot do in such a situation is absurd.

Every patient is different; the etiology of their disease, its progression, severity, and how it impacts the patient’s life qualitatively. For one man with a relativeley mild case of Multiple Sclerosis, a 1 in 400 chance of dying may not be worth the risk. For a woman who finds herself in a wheel chair, losing sight, losing dexterity, losing her self, she may choose differently. Perhaps to her a year of relative freedom is worth more than 5 years of increasing debility. Who has the right to take that choice away from her?

Radio sucks. Ergo, it got stuck on Tammy Bruce during my iced tea run. She was going on about how the guy who woke up from the coma changes everything about the Schiavo situation. I was going on about how she’s a stupid [censored]. Apparently the conservative world needs a quick lesson in neurobiology. So here we go.

This is a nerve cell (neuron):

(from http://faculty.washington.edu/chudler/color/pic1.html)

Notice that there’s a big fat part at the top. That’s the cell body. That’s where all the machinery that makes the cell do its thing is. That’s where the DNA, the mitochondria, the ribosomes, all of that are. These provide the instruction set, energy, and proteins, respectively.

Now the long part is called the axon. It’s basically a biological combination of an electrical conduit and a subway tunnel. It’s essentially a passive structure. Nothing starts in the axon, merely passes through it.

At the end are the synaptic terminals. This is how the nerve cell sends a message to the next nerve cell in the chain.

Looking back to the top of our picture, the yellow branch-looking thingies are what receive the signals sent by the synaptic terminals.

Ok, now that we know all about that we can discuss how nerves respond to injury. Nerve cells, along with muscle cells, don’t keep proliferating and dividing in adulthood. They’re done. This is why after a heart attack you have reduced heart function. Once those cells die from lack of oxygen, nothing can grow back to replace them. This is also why in stroke patients, even after they recover function, it’s rarely as good or as natural-feeling as it used to be. The injured area doesn’t regenerate, other cells just learn to pick up the load.

But while we can’t make new nerve cells, injured nerve cells can regenerate. This is why finger re-attachments work. They can even take the relatively useless sensory nerves that pass over your collar bone and put them into your face to replace damaged or congenitally absent nerves there.

It’s important to note that a neuron can only regenerate if its body is intact. As I mentioned, all the machinery is in that body. Without that machinery, there’s no way to repair the damage. If it’s the axon though, the nerve cell’s body can repair it, although it may take years.

The difference between a coma and a persistent vegetative state is that in a coma, generally the cells are all there (well most of them anyway), it’s just that the axons are all screwed up. Generally as a result of blunt force trauma. In a PVS on the other hand, the cells themselves are dead. Hence the term braindead (the old non-PC term for PVS).

In a coma there is generally brain activity because the cells themselves are still alive. It’s just scattered and disorganized since the wires are tangled and snapped off. Axon growth is inhibited by several chemicals in the brain (that you don’t see in the peripheral nervous system) which is why regrowth can take months, years, even decades…but at least it can potentially actually happen. In a PVS there is nothing. There are no cells to fire. There are no cells to regenerate themselves. There is no chance of recovery.

Terry Schiavo’s brain was gone. This guy’s wasn’t. I don’t want to get overly philosophical here, but if the brain is the seat of the soul and the brain itself is no longer functioning, I really can’t consider it taking her life. Terry was a vacant body, this guy was not.

Sorry it’s late. And sorry I haven’t been psychblogging more frequently. Been really busy both on the blogosphere (CAID, Homeland Stupidity, and Liberty Papers) and in real life (two jobs, conferences, geriatric dog, etc). I’ll step it up a bit. Anyway, because I suck, I’m reminding you that we are looking for hosts who don’t suck. If you’re interested, give me an email with what works. Next Carnival will be June 13 over here. But the 27th on is completely open.

Dave over at Dare To Dream takes a really comprehensive look at the prison system and recidivism. The piece covers elements in the equation all the way from cradle to grave. Highly recommended.

The esteemed Dr. Sanity discusses the Sanction of the Victim, in which the very forces that work to correct societal problems are the ones blamed for it:

Only by withdrawing the “sanction of the victim,” –i.e., refusing to be manipulated in this manner–refusing to give aid where there is scorn and not even grudging gratitude; refusing to shoulder the burden of all as they beat us upon the back and tell us to go faster, do it better, and jump higher; refusing to pay their debts; fix their problems; or protect them from their own, deliberate, suicidal behavior–only then will the looters and the parasites be forced to recognize reality.

In Recourse to Authority, ShrinkWrapped discusses how the internet has affected mental health in ways both good and bad.

The Good:

I consider it a major benefit that my patients must take responsibility for their decision and not simply rely on my authority in areas that affect their lives.

I’d have to agree, I’m not much for authority. And I think that the idea of an authoritarian mental health professional is kinda contradictory to the goal of helping your patients to reach self-fulfillment.

The Bad:

We used to be able to rely on our news gatherers to tell us what is going on in the world. We used to be able to rely on scientists to make sense of confusing information. We can’t do that anymore and it is unsettling, confusing, and disorienting.

Assistant Village Idiot brings us a conversation he had with a psychiatrist with Bush Derangement Syndrome. Normally, I don’t much go in for the ‘psychology of politics’ thing, but I thought this was a rather good example of how rationality in humans is highly context-dependent. While the basic position may or may not be irrational, the psychiatrist’s reasoning sure as heck is.

My own submission blurs the lines a bit as I talk about my own experience with chronic pain and injury and its relation to my empathic abilities in Schizoid Tendencies Are A Two-Way Street.

Dilys talks about why some people may prefer not to be happy, thinking that it’ll give them power over others. And discusses that while this may work in the short run, it’s a bad long-term strategy.

Joe Kissel brings us an entry about handheld machines that can aid in entering relaxed or meditative states using only blinking lights and simple tones. It highlights, among other things, the powerful animal ability to impute complex patterns onto relatively simple stimuli. I’d note that sitting out on the field watching fireflies and listening to the crickets chirp often has the same effect on me that these machines do for him.

Unicovia accuses the media of doing exactliy what Dilys was talking about. Namely, that their entire business model is based around only presenting the bad, no matter what good is happening.

Peter Kua of Radical Hop brings us an inciteful discussion about fear; when it is justified and when it’s just holding you back.

I confess that I’m one of those personality test junkies. The Spark, Psych Central, Similar Minds, love em. Don’t know why, half the time the tests spit out blatanly false profiles. Still, it’s fun. And in the case of the more psych-oriented ones, sometimes scary.

For one thing, I routinely come up as extremely schizoid and schizotypal. While those characterizations are generally true, I fail to see how they necessarily reflect anything wrong with me.

At the most basic level, each of us is an individual. Each of us is our own person with our own hopes, dreams, preferences, and temperament. While schizoid and schizotypal tendencies could potentially signal personality disturbances, what they actually measure is how well you fit in. And if ‘not having the personality some shrink wants me to’ is now a disorder, I have a serious problem with that. There needs to be a little more theoretical and empirical justification than that.

As Tim Flynn, the guy who runs Similar Minds points out,

don’t think Schizoid personality is a valid disorder, some of the smartest people in history were schizoid because they occupied a remote end of the intelligence bell curve. Schizotypal personality can encompass highly original thinkers as well as totally insane people so I think it’s a flawed type. I think the remaining eight disorders are generally valid.

I would think much of my readership understands from personal experience exactly what he’s talking about right there. Lord knows I do. I’ve also found it pretty easy to deal with, though. Probably because I went to public school where smart kids would get the crap beaten out of them for not fitting in. And because you can be as creative as you want to be no matter how little creativity your friends and acquaintances display.

No, what I’ve really found boosts my schizoid and schizotypal tendencies into the stratosphere is the chronic nerve damage I’ve been living with for the past 9 years. You’d never know it to look at me that I suffer from a rather painful atrophic nerve condition. Which is part of the problem. I’ve coped too well. Which seems weird until you think about it for a bit.

As I said earlier, schizoid and schizotypal tendencies aren’t a reflection of anything internal, but rather how you interact with and compare to external society.

Tim defines schizoid personality disorder as where an “individual [is] generally detached from social relationships, and shows a narrow range of emotional expression in various social settings.” I’ve often heard it simplified as a lack of empathy or understanding for what’s going on in other individuals’ heads.

And the thing about empathy is that you have to–at least at some level–have a handle and an appreciation for what another is going through. ‘Normal’ people simply can’t understand my kind of pain at all. Imagine that you’re in so much pain that when you take the highest recommended dose of muscle relaxants you actually sleep less than eight hours because the sleep is that much more refreshing. Can’t do it, can you (those of you who aren’t royally screwed up)? Which means if we were looking at your personality using me as a reference point, you’d be the schizoid one.

Flipping it around, because I’ve built a pretty damn impressive pain tolerance up (to the point that much of it happens subconsciously), when people freak out about painful injuries/conditions, often enough I have to work very hard to bite back scorn and ridicule. Dredging up empathy? Yeah, right.

As an example, skinning your knuckles, stubbing your toe, scraping your knee, or getting a splinter are all things that suck.. When I think about it dispassionately, I’m able to admit that when such things happen to me, my brain is indeed filled with the frantic firing of C-fibers and my body does indeed tingle, burn, and throb. But in real day to day life, that kind of thing often flies so far under my radar I don’t realize I’ve hurt myself until I bleed all over something.

This can make things quite uncomfortable for me when something like that happens to someone else. As everyone else is rushing around screaming for bandaids and alcohol, I’m wondering what all the fuss is about. This apparently means I have a disorder.

Of course, a funny thing happens when we start talking about people who are really physically screwed up. I’ve found I’m considerably more affected at an emotional level by their plight than most are. Which has to do with the whole empathy being dependent on personal experience thing. When you see one of those stories or meet one of those people, you often think to yourself “I can’t imagine what that must be like.” Because of my peculiar position, I often can. Using someone who’s really crippled as a reference point, the ‘normal’ person becomes even more schizoid, whereas I start to approach normality.

My big cautionary tale here is that all ’schizoid’ means is ’statistical outlier’. Could there be a psychological problem there? Sure. But there doesn’t have to be. Sometimes the reason you can’t relate to other people is that they can’t relate to you. And if that is the case, what the mental health professional needs to worry about is considerably different. People are social creatures, and like all social mammals, we derive much of our psychological strength from others. My worry as a therapist would thus be making sure these people are able to cobble together an ad-hoc support structure given the fact that sociality won’t work as well for them as it does for others. This is one of the reasons I want to work with kids with chronic illness. No, I don’t know how much it sucks to be them, but I have a much bigger clue than most do, and I’m hoping I can use my own experience to give me a better window into their minds and thus better serve them. If we begin treating schizoid characteristics as the problem instead of just a signal of the problem, we risk making psychology as much a matter of conformity as it is about mental health. And that scares me.

New post up at Homeland Stupidity:

The American Medical Association has been proposing one protectionist or statist piece of legislation after the next, and while their motives are just as impure as ever when it comes to challenging the growth of retail-store healthcare services, as Dr. Thomas Davis points out, these retail-chain clinics aren’t the free market supporter’s wet dream that some would have us believe.

The basic point is much the same one I used in my critique of market anarchy. In this case, the big sticking point when it comes to a completely free medical market is perfect information. Or more specifically the lack thereof. I can’t think of any other market quite so large where consumers understand so little about the products and services they purchase. It’s not a matter of elitism, just a recognition that medicine is a highly complex field requiring a lot of specialized knowledge. And it definitely isn’t a function of intelligence *cough*.

My biggest proof of this? The fact that chiropractors remain highly regarded, no matter how far into quackery they descend. I’ll admit that due to sampling bias, I only hear the worst stuff. I hear the nonsense about how a bent spine can cause heart arrythmias. And, as a couple of spinal surgeons I’ve known have said: “I love chiropractors. Without their former patients, I wouldn’t own that home in Europe”. And I know the truth about their less-than-scientific education. They are just one example though, big pharma’s manipulation of both consumer and doctor ignorance being a much bigger instance of imperfect information.

I think that licensing and credentials have a vital role to fulfill, one that can only be strengthened by competition. If such agencies competed to field higher quality doctors and practitioners, the result would be that simply by looking at a doctor’s brand you would have a good proxy for his quality. Likewise, I think competition would stimulate a more effective symbiosis between NP/PA’s and doctors. Currently they operate quite antagonistically, with NP’s and PA’s seen as a threat to the primary care doctor’s practice. Sometimes you don’t need the 11 years of training and education a PCP has, but then again sometimes you do. If you could go to one place–and make one appointment–for both, everyone wins. And I think a more free marketplace would allow clinical PharmD’s to assume a role more commensurate with their education (they know a lot more than they’re given credit for).

Choice is important, and I think that opening up the marketplace can only be a good thing. Just don’t throw the baby out with the bathwater.

Good group of posts here. I’m going to host the next two but from number 5 onward, I’m opening it up. If you’re interested, let me know. Preference will be given to those with lower readership. The 1st carnival pulled in somewhere between 500 and 1000 hits due to linkage from the heavy hitters. It’s a pretty good way for some of the lesser knowns out there to be seen by others. Also, the TTLB community should be up and running by the next edition.

Now on to the submissions…

ShrinkWrapped presents Unintended Consequences, “Accidents”, and Unconscious Processes:

When a patient consciously intends a particular outcome and a different, unhappy outcome occurs from their action, it is always vital to investigate whether or not the unintended consequence was an accident or was unconsciously determined.

Assistant Village Idiot brings us an egregious example of over-thinking the nature and complexity of a patient’s psychological problems despite a minimum of contact and testing in Psych Testing Hall of Shame. After reading it, I don’t even know what to say. It’s my firm belief that most psych problems are rooted in relatively simple experiences, whether past or present. Not everyone has a psych problem worthy of a Jungian treatise. Sometimes–most of the time–they’re just over-extended.

Roy over at Shrink Rap asserts that Freud set back psychiatry by over a century. He contends (rightfully) that Freud singlehandedly pushed us away from the brain-centered perspective it had in the early 1900’s to ’so how does that make you feel?‘.

Personally, I think the current neurochemistry-centered models are entirely too simplistic, and if anything more harmful than Freud in that they ignore the beautifully complex and plastic nature of the brain.

Which happens to be a great segue into mentioningmy own submission for the carnival. I talk about the similarities between the mind and muscles, and how adopting a mind training and injury treatment approach could eventually mean less mental illness as years go by. A sprained elbow is rarely indicative of an underlying pathology or disorder. It’s much more likely to be the result of poor training, overuse, or improper technique. Same applies to a person’s psyche, in my opinion.

Joe Kissell over at Interesting Thing of the Day describes one of the more peculiar phenomena of the mind. Synesthesia is when a stimulus in one sensory modality is perceived in another. Hearing the color blue, or seeing cold. Interesting stuff.

From Dare To Dream comes yet another example of the press jumping on research findings before they’ve been properly vetted by the academic community…not to mention unwarranted assertions by study authors. This instance involves a possible link between childhood trauma/sexual abuse and schizophrenia.

Piebolar bares her soul to us once again, giving us a view into the mind at the other end of the therapeutic relationship as she describes the changes that have come over her since beginning neurontin. I wish her the best of luck in her journey, as I’m sure all who read her entry do.

Cerebration asks if blogging may be unhealthy. It all depends on how you approach it, I think. A blog could be cathartic, allowing you to literally see what’s going on in your own head. Or it could merely be a reinforcer, serving to intensify unhealthy though patterns. *shrug* This is why I’ll be in school and training for another 8 years and why no one should listen to my advice as anything more than a layperson’s. Cerebration also points out a couple articles that might be useful to those in need of a psychiatrist.

Peter Kua of RadicalHop.com brings us The #1 Way to Eliminate FEAR: Chant This Mantra Daily!.

Generative Transformation presents The 3-fold Path of Wisdom. It’s a discussion of the path to wisdom and how all the worldly constructs we surround ourselves with can hamper our spirituality.

How To Produce An Acute Schizophrenic Break, posted at Spiritual Recovery, discusses some of the ways in which schizophrenic breaks are similar to various religious practices, as well as to simple loss in the ‘real’ world. I had to poke around for a bit due to the buddhist allusion and saw some pretty interesting stuff. It’s a blog about a schizophrenic and her recovery.

By the time most of you read this, a new post should be up at Homeland Stupidity. I’ll link to it when I can get to a computer after it’s up.

Markos Moulitsas of Daily Kos fame has declared that he’s a ‘libertarian democrat’. A meaningless assertion (although a libertarian-leaning democrat can exist, and I know several). Kos uses the right words, but twists them completely out of shape to the point where they mean about as much as my assertion that I’m white (see picture on left). “Greater Freedom Through Increased Legislation” is his rallying cry. Which doesn’t make a whole lot of sense on the face of it, and makes even less after you get past the surface.

Now the AMA is playing the same game. Insisting that ‘personal responsibility should be required’. Now, I’ve been using those two words since I was about 17. So roughly 300 times longer than the AMA, who seem to have first invoked it about a week ago, after decades of pushing legislation through ‘for the public’s own good’. And in all my reading and discussion of such an idea, I never realized that you could legislate and force personal responsibility. That would be like saying my dog has personal responsibility because she doesn’t pee inside, tear stuff up, and stays off the couch. Obedience is a bit more like it.

It’s a game these guys have been playing since FDR redefined ‘freedom’ as ‘comfort’ in common parlance. It’s a game played by the douchebags at People for the American Way, the entire Democratic Party, and, well, virtually everyone in the business of expanding the role of the state and minimizing the role of the individual in day to day life. They use the words our forefathers bled and died for. They phrase things to make it sound as if they aren’t building a cage (albeit an initially comfortable one) around us. And the sad thing is, all too many of us buy it as 70 years ago our grandparents did with FDR’s socialism, hook line and sinker.

It reminds me of a great Blues Traveler song: The Hook(click for music video). It was about the 500th time I heard the song that I actually listened to what he was saying. First, I laughed my head off at their wit. And then I laughed at my stupidity for singing along without realizing what I was singing. And all these years later I nod my head in understanding at what’s happening to us:

It doesn’t matter what I say
So long as I sing with inflection
That makes you feel I’ll convey
Some inner truth or vast reflection
But I’ve said nothing so far
And I can keep it up for as long as it takes
And it don’t matter who you are
If I’m doing my job
then it’s your resolve that breaks

Because
the hook brings you back
I ain’t tellin’ you no
lie
The hook brings you back
On that you can rely

There is something amiss
I am being insincere
In fact I don’t mean any of this
Still my confession
draws you near
To confuse the issue I refer
To familiar heroes from long ago…

Sometimes it’s scary that songs can be so on-point when they were never meant to be.

Introduction:
I’ve talked about how the brain reacts a lot more like muscle than it does like hormonal or other physiological systems. And I’ve mentioned that I tend to think of most mood and affective problems more like injuries than illness. But I want to spend a little more time on the idea of mind-as-muscle and how it ties in to developing a more realistic model of diagnosis and treatment of ‘minor’ psychiatric problems.

I’ve often heard it said that the mind is what the brain does. And moving weight (actually, producing torque) is what muscles do. But there’s a lot more to lifting weights–especially if you’re cross-training for a sport and not just ‘getting big’–than just slinging lead. It’s much the same way for the mind. Good genes are of course important for building strength. Bone density, tendonal elasticity, muscular growth potential are all things that are in many ways limited by genetics. But a few strands of DNA are hardly the whole story. Building a body capable of moving a lot of weight at rapid acceleration for long lengths of time requires a proper training regimen. And this prescription can help people with not-so-good genes achieve some pretty stellar heights themselves.

Diagnosis And The Power Of Words:
I’ve never met a man who never trained who could bicep curl a 50lb dumbbell. And I’ve met plenty of men who, though more than strong enough, injured the hell out of themselves attempting such a feat. Could you imagine if a doctor told the first that he needed steroids? And if he told the second that it wasn’t his fault, that he suffered from a joint imbalance?

It just wouldn’t be done would it? The doctor would say to the first man that there was nothing wrong with him, he just had to learn how to develop his musculature, and to the second that he had to learn how to use his body.

But when it comes to the mind, the very first thing that many mental health professionals turn to is the DSM-IV TR, and they ask themselves “What kind of disorder does this guy have? What kind of disease? What kind of treatment should we pursue?” Loaded words, every one of them. There are fortunately still mental health professionals who after such a rummage through The Book wouldn’t immediately turn to the prescription pad, but rather to the therapist’s couch. Still, the words we associate with psychological issues–ones of illness and of defects–set the tone from that point on. Which is why I make it an issue to refer to them as issues, problems, or injuries.

Now, I’m not a very PC guy (if you hadn’t noticed), but words can be important. Particularly those that have to do with a person’s health. The labels ‘disease’, ‘incurable’, ‘chemical’, and ‘genetic’ aren’t very empowering; they make a patient feel like there is very little in his power. None of that compares very well with a skinny kid being told he needs to change his diet and put in a little time, but soon he too can be benching 300 lbs, as long as he really wants to hit that goal.

The Importance Of Proper Training:
Every fall, like clockwork, college freshmen join the gym and start lifting, wanting to get huge to compensate for their lack of confidence in themselves and who they are. And every fall, with increasing frustration, I drop my own weights to stop the idiots from killing and/or maiming themselves. I then give them the two minute lesson on exercise nutrition, and another two minute lesson on planning an effective workout to increase your strength at a decent, but safe, pace.

The mind is a lot more complex, a lot more fragile, and a lot harder to strengthen than your average shoulder joint. Yet most of these kids received a good deal more instruction in my short-tempered canned rants on the latter than they ever had on the former. So, if they became depressed, anxious, or otherwise upset, I’d think the default position would be that they were inadequately prepared and/or trained to deal with the world and the goings on inside their heads.

From the first day of orientation at university until the day I graduated, I was a regular at the gym. And you know, I never saw most of those kids for more than a few months. Which honestly, was probably a good thing. Most of the ones that did stick with it were textbook cases of the whole Male Distorted Body Image Disorder thing:

Guy: “I’m soo tiny.”
Girl: “Guy is cute, but he’s too big. Almost grotesque looking.”
Nick: “Dude, you’re more than big enough. Trust me, girls do not go for that kind of thing.”
Guy: “Yeah they do!”
Nick: “You just heard her say that they didn’t!!!”
Guy: “Well, yeah she says that. But she means I need to get bigger.”
Girl/Nick: “Moron”

Anyway, now that I’m completely off point (but have hopefully brought your attention to a VERY big problem among males), I thought I’d say that one of the reasons I think these guys failed so often was that they were after something that weights couldn’t give them. They wanted self-esteem, they wanted self-acceptance, they wanted to fulfill an image that they’d produced of their ideal selves.

And I think when a lot of people come in the door of a therapist’s office, they’re after something that a strong mind won’t necessarily give them. They want to be happy (which isn’t exactly the word I’m looking for). While there’s certainly nothing wrong with being blissful, it’s not exactly what I’d call a natural state of being. But sounding like Eeyore in the depths of your resignation isn’t exactly right either. What people should be after is a happy medium…a state of mind that I think the word ‘contentmen’ captures pretty well. To me contentment isn’t just about affect (happy), or philosophical acceptance (resignation), but about an emotional and cognitive mindset that allows you to roll with the punches. It’s about training a mind that’s strong enough to get you through the low points in life and flexible enough to keep you from breaking when you go through it.

Muscles aren’t supposed to be big. They’re supposed to be strong. They just happen to get big doing it. A mind isn’t supposed to be invariably happy, it’s supposed to help you get things done, something that only really happens if you’re content.

Strong Is Only One Step Away From Brittle:
Even though I approached lifting with a good deal more preparation and sanity than did most, I was still susceptible to adrenaline-induced lack of judgment, overtraining, and–especially in the damaged arm–sprains, strains and twists. If I did see a doctor, she wouldn’t declare that I had a cartilage defect or a musculoskeletal disease that causes my brachialis to sprain when I’m skullcrushin 165. She’d tell me I was an idiot, no one had any business using weights that large, and then she’d put it in a splint, cast, or sling as necessary. After hitting me again, for being a doofus (this is what you get for using docs you’re related to), she’d then tell me not to come back to her office if I hurt it again lifting.

Strong people break too, they’re just a lot less likely to. And when they do, chances are that they don’t have a disease, don’t have a disorder, but simply pushed themselves farther than their conditioning went. They need to be treated that way. Figure out just what pushed them there. And if it can be removed, remove it. If it can’t, make an action plan to deal with it. Maybe it’ll involve a couple weeks or months of pills, maybe it won’t. But the patient will think of it as transitory.

Conclusion:
The main point of this piece is simply that we must treat the mind in a way that reflects both its biological nature and its more abstract psychological workings. If my 7th grade swimming coach had looked upon the 5′ tall 74 lb kid and simply said ‘Well, he’s a skinny wimp, never amount to anything much’, he wouldn’t have been able to turn me into a state level swimmer within the year. He certainly wouldn’t have believed that that scrawny creature would grow almost a foot taller and nearly triple in weight (mostly muscle…mostly lol). If we don’t recognize that the vulnerable patient in front of us can become a resilient, self-willed individual whose strength of character we’d be envious of, we won’t ever learn to ‘cure’ psychological problems. And if we don’t recognize that sometimes the stronger you are, the harder you break, we seriously risk not being able to rehabilitate these individuals.

The man you see on the street is rarely as muscular or athletic as he could be. The same is just as true of his mind.

This one ain’t mine, but damn is it good:

Socialized medicine…all the speed and efficiency of the government with all the compassion of the IRS

Sounds a lot like Canada and the UK, come to think of it…

The thing about socialized medicine is that it ultimately becomes a rationing system with the federal government holding the purse strings. The worst, and most destructive part, is that it rations on both the supply and demand ends. Government wouldn’t have to compete–as employer of workers and doctors, consumer of pharmaceuticals, and provider of both–since it’d be the only source either way. The only thing it would be concerned with is the bottom line; it’d spend as little as it could all around with little regard for quality or efficiency (those being primary products of competition). People, both healthcare workers and patients, would thus lack incentive for prudential use of resources and maintaining a high quality of care. It basically turns healthcare into a commons. And like all such situations, the end result is erosion and destruction. Fewer new drugs, lower quality doctors, and worse availability of both.

I wrote earlier about the doctor-income problem here.

Via Hoody (read his post first)

I’m going to ignore most of what she said, most of the political issues, and most of the controversy. Instead I’m going to scream, yell, and break things because of her attitude toward doctors.

According to this tart, I should have to prescribe whatever she wants, like I’m some kind of vending machine.

So let’s get this straight. I go through 12 years of schooling and training to become a full fledged doctor at 30 (and I’ll be young at that). I end up in debt up to my eyeballs. I lose the best years of my life, years that should be spent finding the girl of my dreams, marrying her, and raising a family. Years that should be spent pursuing my passions while I’m full of youthful vigor and have a fresh mind begging for inspiration. I’ll have to deal with all the crap that goes along with the medical profession (I’m probably one of the few Indians you’ll ever meet whose parents didn’t want him to become a doctor). And on top of that, I’m supposed to compromise my own morality because someone refuses to accept the risks involved when they undertake a process that when all is said and done is designed to make babies?

People like her, and statements like that, that doctors should be FORCED to prescribe what their patients ask for, even when morally questionable, are proof positive that leftists are the most selfish, childish people on the planet. And that they will run roughshod over liberty for the sake of their own comfort. They talk of freedom of choice, accommodation of all viewpoints, and respect for all cultures, but apparently not the culture of this Hindu future doctor, or anyone who’s pro-life for that matter. They would have me become a slave.

And do you know what their defense will be? “Well, it’s your job.” No, I don’t know if they’ve read the modern hippocratic or not, but here’s a good quote for them:

Most especially must I tread with care in matters of life and death. If it is given me to save a life, all thanks. But it may also be within my power to take a life; this awesome responsibility must be faced with great humbleness and awareness of my own frailty. Above all, I must not play at God.

For all of science’s sophistication, it has yet to be able to define the point between fertilization and parturition at which the embryo becomes ‘human’. It’s an opinion. To force a doctor to take what is in his eyes a life, just because in your eyes it’s a choices is the ultimate in arrogance. It’s the height of self-centeredness, of lack of tolerance, of an inability to see the other side.

And they wonder why I rail against ‘positive liberty’ and scream that we’re heading down the road to serfdom.

Linky

Before we go much further, I just want to point out that we’re talking about teenagers. There is no more tumultous, melodramatic, crazy, unbalanced time in a person’s life. Internally, as hormones rage and social emotions develop whole new levels of complexity, and externally, as people attempt to define you by the girl on your arm, the clothes on your body, the people you hang out with, and the way you talk. In other words, if there was one period in your life where psychiatric problems would most likely be due to an inability to cope, it’s this period. This is the one period that, more than any other, where therapy can have the strongest and most long-lasting ameliorative and preventive effects.

The probe uncovered a troubling trend of physicians taking liberties with their own clinical guidelines, often bypassing psychotherapy as a component of first-line treatment. Instead, the study shows, in the years 1995 to 2002 they increasingly relied solely on the drugs that were supposed to support, not supplant, counseling.

This quote really says it all, as far as I’m concered. They are trying to replace therapy with meds, which will be to the detriment of every one of these kids. In most of these cases something is making them depressed. It would be to these kids’ benefit to understand what that thing is and why they’re letting it bother them, instead of waiting until they’re 35 to go see a therapist and talk about their awful teenage and college years, and finally figuring out what it was all about, wouldn’t it?

the guidelines of the American Academy of Child and Adolescent Psychiatry call for trying talk treatments first in depressed children and, in the most severe cases, combining pharmaceuticals with psychotherapy. Part of the reason for this recommendation is to increase the odds the physician will monitor the medicines’ effects and ensure patients’ compliance.

But what the Stanford team found was that while office visits by depressed teens more than doubled over the seven years studied — soaring from 1.4 million in 1995 to 3.2 million in 2002 — the use of psychotherapy in that period sank from 83 percent of the visits to 68 percent. At the same time, reliance on drugs increased from 47 percent to 52 percent of the cases.

That may not seem like such a big change — until you consider the dramatic increases in the diagnosis of depression in children and realize the actual number of youngsters on anti-depressants more than doubled during the period studied, the scientists said.

What’s more, as the drugs took center stage, they shoved talk therapy to the back burner, they said. So much so that it was forsaken altogether in between 42 percent and 52 percent of doctor’s visits by anti-depressant-using children, the Stanford team reported.

Not a good thing, especially because in our culture of therapism, psychiatrist visits are likely to only increase, meaning more kids put on robot pills instead of being helped with their social and psychological issues.

bah!

Interesting

Most people know that the appendix is a vestigial organ, a remnant of an intestinal system that in our ancestors was much, much larger. Plant material, particularly leaves, is hard to digest. Mammals can’t even do it if it weren’t for gut flora (bacteria) that breakdown the cellulose and other fibrous tissue for their own energy needs. Once broken down into smaller, more absorbable and digestible products, we can use it. But even with the aid of the bacteria, it’s still not particularly easy. So animals that rely on high fiber plant diets for their sustenance tend to have long intestines. The length means there’s more bacteria to do the initial breakdown, and more surface area to absorb the remnants. You can contrast this with meat eaters. Meat is much more readiliy broken down and absorbed, which is why carnivore guts are a lot less complex and a lot less large.

Just think of the complexity of the ‘four-stomached’ cow versus the simple, almost straight-line gastrointestinal path of the cat. All primates rely heavily on fruits and leaves in their diet. Humans, believe it or not, aren’t any different in this regard. Most of our calories should come from non-meat sources. But we don’t place anywhere near the emphasis on folivory that say colobines (leaf-eating monkeys) or even other apes do. So we dont’ need that much gut. Unfortunately, because of the way natural selection works, we end up with a useless remnant that only serves to make us sick.

But is it really completely useless? Chris Wanjek points out that it isn’t quite the layabout we’ve made it out to be:

Biologists in the early 20th century surmised that the human body had over 100 useless parts left over from our more ape-like lifestyle a few million years ago. The parathyroid was one such organ, now known to regulate calcium-phosphorous metabolism. The appendix was another…

As quickly as 11 weeks after conception, the appendix starts making endocrine cells for the developing fetus. Endocrine cells secrete useful chemicals, such as hormones, and the appendix endocrine cells secrete amines and peptide hormones that help with biological checks and balances as the fetus grows.

After birth, the appendix mainly helps the body stave off disease by serving as a lymphoid organ. Lymphoid organs, with their lymphoid tissue, make white blood cells and antibodies.

While this is true, the appendix’s endocrine cells don’t secrete any different hormones than the rest of the gut. And while it’s full of lymphoid tissue, so is the rest of the gut as well. I know this because I consistently failed to identify them properly on our histology final. And while it may or may not provide a better ‘training ground due to various aspects of its organization…

The dirty gut is a good training ground for young white blood cells. The appendix, with its sac routinely collecting and expelling foodstuffs, exposes the white blood cells to myriad bacteria, viruses and drugs passing through the gastrointestinal tract. This way, the white blood cells learn to fight potentially deadly bacteria, such as E.coli.

…I’m not sure just how important that really is to overall immune function.

The gut is a highly specialized and complex organ system. It has its own separate nervous system, an amazing range of hormonal functionality, forms an important part of the immune system, and, of course, digests our food. The appendix has lost the latter function, but retained the rest. Which doesn’t necessarily make it an important part of the body, just means that it’s only truly vestigial in one respect.

But he does bring up some interesting uses for the appendix when it comes to reconstructive surgery:

In the not-too-distant past, zealous doctors would remove the appendix during other types of surgery—to get it “out of the way” just in case it would some day become infected. The philosophy was: The appendix is useless; I’m already elbow-deep into this person’s gut; why don’t I just snip the appendix now.

But no more.

Doctors now realize they can use the appendix for reconstructive surgery. In one type of bladder “replacement” surgery, doctors take part of the intestine to form a bladder and use the appendix tissue to recreate a sphincter muscle, which can contract and open the bladder when urinating. Similarly, the appendix is used as a substitute ureter, a tube that carries urine from the kidneys to the bladder.

Good stuff.

Yup.  Just ‘Why Fat People’.  Why do they exist?  Why is it so hard for some to lose weight while others have trouble gaining it?  Well, quite frankly it’s because the human body is an evolved construct.  It evolved under certain circumstances and is best adapted to a certain pattern of activity.  It’s been tens of thousands of years since we left that adaptive zone, more or less, but our bodies haven’t changed all that much.  Partly this is because unlike other animals, we left that adaptive zone by way of technology instead of changes in our bodies.  From about 1.8 million years ago with the rise of Homo ergaster through around 60,000 years ago (the Middle-to-Upper Paleolithic), hominid technology; what little there was, was pretty crude.  Instead of taking us beyond the capability of other animals, it merely allowed us to break even with the carnivores.  You see, as monkey playing wolf, we didn’t have sharp teeth and claws.  Our primitive wooden spears, hand axes, and cutters served as prostheses.  But, as Neandertals dwindled and modern humans expanded their range, newer, more advanced tools came to the fore.  These novel tools did take us beyond the capabilities of other omnivorous mammals.  It made hunting, gathering, virtually everything involved in living easier.

That technology is one of the reasons our bodies haven’t had to change that much.  We’re simply less likely to die from things that would kill other animals.  A wolf that can’t run fast won’t eat.  A man that can’t run fast can just hurl a spear.  And, because that technology acts as a prop, it’s allowed us to accrue all sorts of genetic and developmental baggage that makes us in many ways less healthy than we were 40,000 years ago.  From the hafted tools our umpteen-great grandfathers used to the computers many of us spend most of our time on, technology has made us fat.  What follows is partially science, partially scientific-informed speculation.  In other words, while a lot of what I’ll be presenting is fact, a lot is only likely, or merely plausible.

The most important thing to understand about the human body is that it’s an evolved construct.  By this I mean it’s a pretty jury-rigged affair when all is said and done.  A complex and marvelous mechanism, but shoddily put together nonetheless.  Anyone who’s studied Engineering Control Theory would be appalled by the lack of logic of the body’s mechanisms of homeostasis.  What I mean by this is that things that are clearly inter-related from an external perspective aren’t necessarily from an internal perspective.  The relationship between food intake, energy expenditure, and body composition is one of the most counterintuitive, complex, and just plain retarded systems in the human body.  Which might explain why weight control is one of the most difficult things for us to do.

Diet Composition 

It would make sense that we eat more food when we expend more energy, food being the primary source of fuel for us.  And, that’s a relationship that tends to hold true.  The converse would also make sense, that we eat less when we do less.  Unfortunately that isn’t quite the case.  Our hormonal control systems for appetite and activity are separately maintained, with different ’set points’, different degrees of sensitivity, and different timelines of adaptation.  While they do talk to each other, think of them as a long distance relationship rather than a codependent couple.

First, let’s start with food intake.  Clearly, how much you eat is a part of the weight equation, but its role is often far overstated.  There are a lot of fat people who eat too much.  There are also a lot who don’t.  And, we all know the rail thin guy or girl who eats 4000 calories a day and can’t put on a single pound.  Clearly, food isn’t the be all end all.  When I hear about friends who spent weeks, months or even years on one of those super-restrictive 1000-or-fewer calorie diets, I cringe with sympathy.  They were misled.

Diet is extremely important to weight loss and maintenance, but not so much the amount as the composition.  In fact, low-cal diets can make weight loss harder than if one were to go by a regular 2000 calorie daily regimen.  We must ask ourselves what hominids evolved to eat.  They are descended from monkeys, which means largely fruit-eating (and occasionally insect, lizard, and egg eating) mammals.  Other apes and a couple types of monkeys are known to scavenge and hunt occasionally (1-4% of their diet by weight).  So there’s little doubt that hominids were doing at least that.  And, there’s very good evidence that hunting and scavenging became a much more important (some would say dominant) aspect of their lives well over one million years ago.  Hominids in this respect were probably a lot like the wild social canids (wolves, jackals, etc) in their omnivorous nature.  A typical temperate or tropical canid diet can be 40% or more plant product by weight.

And then we can look at intestinal length.  The longer the intestine, the more comes from plants.  Cows have looong intestines.  Monkeys and most apes have shorter ones.  Humans are shorter than other primates.  Canids are shorter than the above.  And cats are shorter than the rest of these guys.  In other words, we’re very much in the middle.  We’re not carnivores, we’re not frugivores.  We’re omnivores.  We need a lot of sugars from fruits and other plant parts.  And we need a fair amount of protein (from meat, generally).

Which brings us back to the importance of diet composition.  Humans are limited not by their fat intake (for the most part), but by their carbohydrate and protein intake.  You need carbohydrates to fuel the body.  They’re what we’re most efficient and fastest at processing.  Fat has more energy per gram, but it’s harder for us to start using it.  Just think about that intestine length.  We need a lot of sugar in our diet.  And we need protein.  Although protein can be metabolized as an energy source, mostly it goes to repair, rebuild, and renovate the body.  Exercise, metabolism, basically everything we do causes our cell machinery to wear down a bit.  That machinery is made up of proteins.  Keeping ourselves in top form requires enough protein building blocks coming through our digestive system to undo that damage and a little extra to build bigger and better machinery.

Just about the only thing muscles and the brain run well on are carbs (other parts of the body, like certain organs, do better with fats).  Starving your body of them will only destroy your body’s ability to do any work at all.  And without protein, you’ll basically find yourself falling apart from the inside out.  Some of the stuff I’ve seen and read about what happens in a vegan’s body is nothing short of shocking.  Same can be said for those who get most of their calories from meat and none from vegetables.

Old-school hunter gatherer hominids probably burned roughly 3000-4000 calories a day of food.  We can estimate that based on what modern hunter gatherers expend.  That’s what the human body expects to come through it.  Any less than that, and you’re operating in fuel starvation mode.  Any more than that and you’re flooding the system with more than it wants.  In starvation mode, your body shuts certain things down to conserve energy, and decreases the ability of other parts to exert themselves.  In other words, it’s not burning as much as it used to, at least partially negating the effects of caloric reduction.

What’s more, because as I said, activity level and diet don’t perfectly correlate, the super-low calorie diets can shut down so much of your body’s machinery that you actually put on fat because the reduction in energy expenditure has dropped more than the reduction in energy intake.  And that’s just talking basal, cell-level, non-activity-dependent expenditure of energy.  Of course, caloric reduction also affects one’s ability to undertake activity and thus expend energy, which brings us to our next major topic.

Activity Levels 

As I said in the introduction, our activity levels and behavioral energy expenditure are considerably lower than they were in the prehistoric days.  I used to get in one to two ‘antisocial’ days when I was in graduate school.  On these days I used to strap on a backpack holding roughtly 60lbs of granite and walk 20-25 miles through the streets of London.  Beyond giving me a much needed chance to unwind and lose myself in physical exertion, it gave me a taste of what daily life would be like for an early hominid.  Based on archaeological remains, we surmise that hominid groups would travel anywhere from 10 to 30 miles in a given period.  Furthermore, these finds lead use to believe that they butchered their prey away from their campsites, meaning that, like little old me, they were toting a load for at least part of the journey.  I was also a pretty good model because at 5′11″ and about 200lbs I was more or less a walking facsimile of Homo heidelbergensis, the first of the hominids with brain sizes about like ours.

These were 4000 calorie days.  But the interesting thing was that not only was I eating a lot on the walking days, I was eating around 3300 on the non-walking days.  And not gaining weight.  Now, leading a much more sedentary lifestyle with little or no exercise (just like I was 5-6 days out of the week in London), I’m down to 2600-2700 calories a day at a steady 210lbs.

Basal Metabolic Rate

Strange you say? Not especially once you think about it.  It all has to do with arousal.  I don’t mean the dirty kind, or mental alertness, but the readiness of your muscles and supporting tissues to leap into action.  Immediately after blasting through a set on the bench at 100% intensity, you’ll probably notice that your muscles are warmer.  Your muscles are metabolizing more sugar, doing more work, and in consequence, releasing more heat as a waste byproduct.  Your ability to do work is dependent on the level of this metabolism.  The more carbohydrates your muscles are turning over, the more you can lift.  Now, getting your muscles primed and ready to do 100% intensity can take a while can’t it?  That’s why we warm up.  We’re increasing the level of metabolism in our muscles before we actually start doing work with them.  But even when we’re just sitting there doing nothing, our muscles and other tissues are metabolizing substrates, burning energy.

This is our basal metabolic rate.  Your BMR depends on a number of factors ranging from genetics to diet composition (more sugar, higher BMR, to a point).  Another factor it depends on is how warmed up you are when you’re doing nothing at all.  You can think of this as priming.  Different people have different levels of priming, some of it genetic, some of it having to do with expectation of activity (not activity level).  I’m naturally pretty well-primed.  My warmup tends to be flexing and shaking a bit and then getting right to it.  Which is why with less than an hour of real exercise a week, I still eat close to 3000 calories a day.  Other people aren’t quite so lucky, but even they can change their level of priming based on the body’s unconscious expectation of activity.  This is the reason I ate more even on my non-walking days back in England than I do now.  My body was under the influence of both my genetic priming, and my activity-based priming.  My body expected to be worked hard and was maintaining a higher level of readiness, which of course burned more energy.  Think standing to attention versus at ease.  Both you’re completely stationary, but one’s much easier to maintain than the other.

Conclusion

I’m going to tie all this together with a car analogy.  Cars have an air/fuel ratio they like to maintain.  For cruising it’s generally about 14.7:1 air/fuel by volume.  Less air and you’re lean, more air and you’re rich.  Both result in loss of power and efficiency.  If we think of dietary composition the same way, too little carbohydrates and too little protein can be just as damaging.  It’s important to maintain a good ratio to keep the car operating at a good level of efficiency.

Now, while all cars do best with a single air fuel ratio, the total rate of flow they do best with can be worlds apart.  The rate of fuel flow my Mustang has the best fuel efficiency at comes at around 77mph.   Whether the rate of fuel flow is higher (faster speed) or lower (slower speed), my Mustang gets worse efficiency.  It’s much the same for people, eating less can be just as bad as eating more; under either condition, our ‘rate of fuel flow’ causes us to be in a suboptimal position.
I don’t know how many of my readers have ever drag raced, but there’s a thing you do called power-braking.  When you’re at the tree (the lights that tell you when to go), you put your left foot on the brake, pressing down harder than you would at idle.  Then with your right you gas it.  Depending on the car, the brakes, the horsepower, and the tire, you try to get to the highest RPM’s without either your tires spinning or your car moving.  You’re not going anywhere, but you’re burning a lot more fuel than you do at idle.  Why?  Because when the green hits on the tree, and you let go of the brake, you’re that much further into the efficiency zone of your engine.  Priming.

Air/fuel ratio.  Fuel flow rate.  Idle RPM’s.  “Work smarter, not harder”, as Uncle Scrooge from Duck Tales was fond of saying.

I call BS. The study does say that they can guage our testosterone levels from our faces. To which I say of course. That’s kind of a ‘duh’. Signalling theory predicts that various aspects of our bodies serve as visual markers of aspects of our internal condition, particularly with regard to reproduction and health. Examples include the link between waist-hip ratio and fertility, and facial symmetry as a signal of health and a bountiful juvenile growth period.

Beyond determination of basic secondary sex characteristics (external genitalia, body hair, fat and muscle distribution, boobies, etc.), estrogens and androgens also affect the degree to which we express those things. “He has chiseled features,” or “she has a jaw like a man,” are cases in point where testosterone is concerned.  Guys with baby faces and girls that don’t have hairy arms are examples of low testosterone.  Or, take a look at the faces of pro wrestlers who aren’t fat like John Cena (i think that’s his name).  Their faces almost look like caricatures of male-ness because nearly everything they do has a stimulatory effect on testosterone release.

But this part:

“Women’s ability to estimate men’s interest in infants from face photographs is perhaps the most novel finding to emerge from the study,” researchers wrote in British journal the Proceedings of the Royal Society B: Biological Sciences.”

This I find a little more sketchy.  Testosterone has little to do with paternal care from my readings (and this is what I research, albeit at the wild animal behavior level).  Instead what matters is prolactin levels.  Obviously from the root stem we get that its a hormone involved in milk production.  But it’s also vital to the initiation, maintenance, and focus on parental care in both males and females.  Good dads in the animal kingdom have high prolactin levels.  And considering that some animals with very high prolactin levels also have high testosterone levels (alpha male capuchins, wolves, and, well, me), I’d think that we can safely say there isn’t that much correlation between the two.  And because prolactin levels only increase when babies are around, there’s little reason to believe that it affects appearance in a way that could be guaged by the study.
This is speculation but what I think we’re seeing is a secondary cultural effect.  Our culture has created an expectation that males with high testosterone are whores with little interest in long term relationships (especially at the college level).  And in consequence, low testosterone males have chosen the alternative mating strategy of appearing to be nurturing and caring.  Having recently left undergraduate study, I can attest that this does indeed seem to be the case.  Not only do males feel like this is the way they should behave, females assume this is how males will behave as well.

Being a big aggressive looking male, most people assumed I was a manwhore, where nothing could be further from the truth.  And to this day, most people laugh or look in disbelief when I tell them with 100% certainty that I want to be a child and adolescent psychiatrist.

Like I said, I see plenty of high testosterone aggressive males all over the animal kingdom who are great fathers.  In fact, low testosterone males in a lot of taxa actually choose the ‘hit it and quit it’ method when it comes to making babies.  An example are orangutans. The big 200lb honkers with the big old fleshy cheekpads are the ones with high testosterone.  While they aren’t particularly good fathers, they do at least stay around the females they mate with.  There are other males, though, who have low testosterone, so low in fact that they pretty much look like females.  They’re the sneaking type, even going so far as to rape the females.

It happens in fish too, who actually can be good fathers.  The big aggressive males make a nest, fight off all comers, and take care of babies.  ‘Sneaker’ males are about the same size as females and don’t fight or defend territory, instead they try to fertilize eggs laid in a big male’s nest before he has a chance to.  Again, they don’t parent.

Where am I going with this?  Nowhere special.  Just making the point that although my dispossesion is a bit like Marv from Sin City, I love kids.

Interesting new treatment. Basically they implant a device that stimulates your vagus nerve at periodic intervals. The vagus has all sorts of connections all over the place, from your voicebox to your heart to most of your digestive tract. Interestingly, a lot of vagus nerve terminals release serotonin as their neurotransmitter, just like the brain neurons implicated in control of mood and depression. What that has to do with anything? I couldn’t tell you. Most can’t at this point.

This is going to come as a surprise, but I’m not summarily giving the Indian Cowboy stamp of disdain to this somewhat drastic procedure. This is for two reasons:

1) It’s only indicated in people for whom nothing else works.

2) The lead times between procedure and onset of relief on this are significant and long enough that it’s unlikely to be abused.

With 300 million people in this country alone, there will be organic, idiopathic causes of brain disease. It’s just a fact of life. While I think the number psych treats this way is significantly overstated, they do exist, and we need to be able to do something for them. This is the kind of stuff that is perfect for them. It actually rewires these peoples’ brains to respond like a healthy person’s.

With most therapies, whether behavioral, pharmacologic, or ECT, we tend to see improvement 3-12 weeks after starting. However with VNS (Vagus Nerve Stimulation), the lag time approaches 1-2 years. I’m going to turn to the articles to give you a better understanding of what’s happening before I add in my own thoughts

Article 1:

Patients in the study generally responded around 12 to 24 months after beginning the treatment. Dr. Charles Conway Saint Louis University presented his research results Thursday at the annual meeting of the American Psychiatric Association.

The most surprising finding from the study, conducted by Conway and physicians from Washington University in St. Louis, were the long-lasting benefits of the treatments.

“There are a number of subjects who have gone into remission and stayed in remission for the past four or five years,” Conway said.

Very promising. It’s the nonresponsives and the ones who turn to pharmacology who tend to have the highest rate of relapse, as he said. Which means they tend to do the most damage to themselves and their families in the interim. It’s very encouraging that we now have a way to treat those who we’re just unable to get through to.

Conway studied the neuroimages of the patients undergoing the treatment. He noted that the brain reacted systematically to the vagal nerve stimulation, and by the end of the two years patients were experiencing a significant decrease in activity in the prefrontal region, which is more active in patients with depression. The studies suggest that the brain is experiencing long-term changes.“The areas that are going activation and deactivation are all areas we know to be involved in depression,” Conway said. “What appears to be happening is further in the treatment it’s almost as though there is some brain adaptation to the stimulation.”

And let’s flesh it out a bit with a quote from Article 2:

When Dr. Conway examined the neuroimages of four patients 24 months after they began receiving vagal nerve stimulation, he found brain activity that was similar to what doctors see in patients who have received ECT. “There actually appears to be decreased activity in regions of the prefrontal cortex, which is very much parallel to the findings of treatment response in ECT, and the opposite of findings seen in medication-response to depression.”

He found unexpected action in the prefrontal cortex of the brain that is similar to brain activity in depressed patients immediately after they have received ECT and before its effect wears off.

First, I have to snigger at the remark Dr. Conway said, about medication-response to depression looking opposite of a healthy and an ECT brain. Told you they were just covering up the real problem.

Anyway, ECT is generally considered the most effective treatment for depression. After it, your brain looks normal under a PET scan. It’s just that it doesn’t last long. What they’re finding is that after you wait that average of 21 months (which kinda sucks) your brain looks normal, just like it does immediately after an ECT. Which is another part of the reason I don’t mind this so much. It’s making your brain look normal, instead of covering up one abnormality with another drug-induced abnromality (see previous paragraph).

Now, the most interesting thing about all of this is the difference in times between most psychiatric therapy and VNS. The VNS time of 1-2 years instantly make me think of recovery of function after a stroke. It’s an almost perfect fit. In other words, VNS looks like a neuroanatomical, self-healing cure. Instead of a neurophysiological, self healing cure we tend to see with CBT, acceptance therapy, or drugs. The difference is that in the latter, we’re not looking to change the way the nerves connect to each other, just the way they function and fire. In the former, the brain is literally rewiring itself. This is why when a person has a stroke and loses the ability to speak, he can re-learn using different brain areas. I’m not 100% sure that’s what’s happening with VNS, but I’d put a small flutter on it.

Pottering around blogcarnival.com revealed no carnivals dedicated to psych. Which is unfortunate because there are a lot of psychbloggers out there. Many of whom get plenty of traffic. I’m bored and my summer job don’t start for a couple more weeks, so I figure why not start one. Plus, I have Dr. Sanity’s approval.

I couldn’t think of how to say that this carnival is intended to be a pretty open and encompassing affair so I stole and lightly massaged some verbiage from The Tangled Bank’s homepage…

This is an egalitarian activity. You do not have to be a Ph.D., you don’t have to write articles with ten-syllable words, you don’t have to discuss esoteric details. All you have to do is express some enthusiasm for [psychology and psychiatry] or encourage study of the same.

Got an interesting post about Cognitive Science? Want to discuss your personal experiences with mental illness? Do you want to talk about the failures of current psych theory (a favorite of mine)? Or about a problem with the status quo in the mental health profession (another favorite of mine…even moreso for Dr. Helen)? Maybe you want to talk about the psychology of individuals who believe in certain ideologies (that’s Dr. Sanity’s big thing. You could even discuss ‘discredited’ theories like those of Freud and Jung (which still have some merit in understanding the mind, even if they are of little therapeutic value). Heck, I’ve got a post or two about the Axis II psychological disorders my dogs seem to suffer from every now and then. Even silly tongue-in-cheek stuff like that is good too.

Point is, it’s all good. If it has to do with psych, it’s well-written, and it’s an actual commentary from your point of view rather than simply a link and a quote with a quick “I like this”, then send it in. Should Fun times will be had by all.

I’ll be hosting the first one on Thursday, June 1st, so get your links in to me by about 6pm the Wednesday before. Feel free to send multiple submissions, since I have no idea how popular this will be these first few carnivals. That may change if we get to be anything like the size of Tangled Bank, Skeptics’ Circle, or Grand Rounds. We’ll start out bi-weekly and if it looks like it’ll work we might move up to once a week. Once it’s off the ground I’ll open up hosting opportunities to those who are stupid enough to take on the work.

You can either submit by sending me an email at:

indiancowboysblog@gmail.com

Or by using the Blog Carnival Submit Form.

Let’s have some fun with this.

These are almost getting formulaic I know, sorry. I’ll stop when the scientific integrity starts, k?
linky

One thing that this new article makes really apparent is that these so-called psychiatric disorders often present with the same symptoms, especially in children.

“Many symptoms of depression also present with other psychiatric disorders,” noted Dr. David Fassler, a Burlington, Vt., child and adolescent psychiatrist, clinical associate professor of psychiatry at the University of Vermont and author of “Help Me, I’m Sad: Recognizing, Treating, and Preventing Childhood and Adolescent Depression” (Penguin, 1998).

“For example, irritability can be a sign of depression or anxiety or attention deficit or bipolar disorder or a reaction to a learning disability, so a proper diagnosis is critical,” he said.

In a further entanglement, numerous conditions with overlapping characteristics often coexist, making the symptom sorting all the more tricky, even for professionals.

“The symptoms of the four most prevalent mental-health conditions (ADHD, anxiety, bipolar disorder and depression) are not always easy to tease apart, especially in children,”

See this is what I’m talking about. Four different ‘disorders’ each with four different recommended biochemical treatments ranging from medical methamphetamines to the pharamacological equivalent of ecstacy. But they all look the same?

As many as two-thirds of depressed children also suffer from other oftentimes look-alike disorders. Untangling these so-called comorbidities hits a snag on the chicken-and-egg quandary: Which came first and is one the cause, effect, neither or both of the other?

And here Ms. Wasowicz hits the core of the issue; the real reason I won’t shut up. Comorbidities really crack me up. They talk about the comorbidity of depression and chronic illness a lot. Which is exactly what I’ve been trying to say. Depression is caused by thoughts. If you’re chronically ill, easy to think bad thoughts. Ergo, easy to get depressed. Not hard to understand. Knowing that, which is better? Drugs, or attempting to talk with this clearly distressed person who’s not in the best of health about their fears and their qualms?

Inconsistencies like this are why I think many psychiatric disorders should probably be thought of as ‘psychiatric injury’ instead. More often than not, there is an initial insult. The irritability, change in sleeping patterns, defiance, all of them are merely part of a response. Certain sets of symptoms are gathered together into neat little bundled and called ‘disorders’ or ‘disease’. These symptoms are then treated. Now, even before I got to med school I learned that it’s important to treat the root cause of a disease rather than merely the symptoms.

It’s important to note that since there is little to no causative evidence that ‘anxiety’ causes ‘anxiety-type symptoms’ or ‘depression’ causes ‘depression-type symptoms’. Which means when we can’t tell the difference between the two (as was discussed more heavily in the article), we decide which is which based on what medication they respond to. Which sounds eerily similar to what goes on in the recreational drug world. People all have ‘their drug’, something that just makes them go ‘click’, something that they just feel completes them. You’ll meet hyperactive people who use marijuana to calm them down. Or similar people who use meth to get even more hyper. Or you might a calm person who does downers because ‘that’s their thing’. On the other hand, he might turn into a totally different person on PCP, and that might be what he looks for. In other words. Similar personalities, different drug/responses desired.

One of the worst thing a surgical oncologist can do is not cut deep enough. Leaving behind a part of the tumor is usually pretty bad news for the breast cancer patient, indicating a likelihood of metastases and lower survival down the road. Similarly, I continue to fear that we don’t go deep enough when rooting out the causes of psychiatric problems. It’s easy to say ‘He looks anxious. Let’s call it Generalized Anxiety Disorder and figure out which street drug works best.’ It’s a lot harder to say ‘I wonder why he’s so anxious; let’s find out, and if he needs something to keep him calm meanwhile, we’ll put him on something temporarily.

I walk with a pronounced limp a fair amount of the time. If the doctors looked at my leg the same way psychiatrists treat the mind, this is roughly what would have happened:
“Doctor, I’m limping.”
“You have Generalized Limping Disorder. It’s a serious medical condition caused by the fact that your leg hurts.”
“So you’re telling me I’m limping?”
“Yes, but more officially.”
“Ok, so what can we do about it.”
“Well, here’s some Oxycontin”
“What about fixing the limp.”
“Nawwww. You’ll feel all happy and loopy on the opiates.”
“Ok”

Now, what the doctor should have done is try to fix my limp first and only if he couldn’t should he have told me to drug myself to my eyeballs.

I’m going to limit my typical tirade against anthropocentrism to three sentences for the sake of brevity and boredom prevention: Human brains did not evolve in a vacuum; as neuroanatomists have noted for close to 200 years, there are scarcely any differences in kind between the monkey brain and the human brain, merely differences in degree. People act surprised at the fact that other animals have emotions and the ability to infer. Which is why psych is such a radioactive pile of cow dung; it has a flawed view of just how deep the roots of our cognitive and emotional attributes go and why they came to be in the first place.

Ok, done. And yeah, I guess I cheated by using semicolons, making it five sentences not 3. But my blog. My bandwidth. Deal.

This is not a problem I have. Luckily for me, I wasn’t raised in an epistemological framework of unjustified humanism (whether religious or atheistic in nature), but rather was taught to appreciate the commonalities of all living things. Especially monkeys. Not only that but I’ve had a lot of face time with them. I’ve been tricked, outsmarted, beaten, berated, bitten, and generally abused by several species of monkeys originating from three different continents. I have no doubts as to their intelligence or as to the fact that they think just like we do, just in a less sophisticated manner.

A new study from Harvard researcher Dr. Marc Hauser highlights the ability of monkeys to make inferences about situations they’ve never encountered before.

Monkeys keep turning out to be smarter than people think they are. Researchers have shown that they can count to four and are aware of differences between languages like Dutch and Japanese, even though they don’t known what is being said. Now, Harvard psychologists find that monkeys can draw correct conclusions about novel situations. For example, shown a white towel that turns blue, a blue knife, and a glass of blue paint, they can figure out that the paint not the knife is responsible for the change in color.

“Our studies reveal a striking continuity between humans and monkeys in their capacity to draw causal inferences without the help of familiarity with the events or situation,” says Marc Hauser, a Harvard professor of psychology. “This ability highlights the richness of the monkey mind in terms of its understanding of the material world.”

Thank you, Dr. Hauser. And I mean that wholeheartedly. Both scientists and the public need to understand that there isn’t very much that makes humans unique, not because I’m one of those ‘human rights for great apes’ freaks, but simply because we can’t develop a conception of who we really are unless we understand just how we’re related to others.

Anyway, moving on to the experiment itself:

Next, they saw the glass of water and two halves of an apple. Following this, a knife was lowered, and two apple halves seemingly became a whole apple.

To a human, even an infant who had never seen such things before, the last two apparent happenings would never really happen. Can monkeys infer the same outcomes? Evidently, the answer is “yes.” They looked longer when a glass of water appeared to cut the apple than when a knife seemed to do the same. The longer look signaled disbelief.

Surprisingly, they didn’t fail. Without ever having seen a glass of water and two apple halves, or a blue knife and blue and white towels, the monkeys inferred that water cannot cut fruit and knives can’t change the color of towels.

And that’s the key here, just by looking at the objects, the monkeys were able to figure out what their actions were. Inference at its finest.

The experiments, then, answer a key question about human versus monkey intelligence. Is the capability for figuring out what is possible and not possible when you see something for the first time uniquely human? For Hauser, Spaulding, and a lot of scientists who read their report in the May 2 issue of the Proceedings of the National Academy of Sciences, the answer is a resounding “No.”

“Humans are not alone in their capacity to draw causal inferences from limited experiences,” the Harvard researchers write. “This capacity is part of the evolved psychology of rhesus monkeys and most likely other animals as well.”

Which really says it all, I’d head to the article itself since it ends with a great David Hume-bashing ending. I’m not much of a fan of philosophers either (although I’m a fan of philosophizing), like the psych establishment, they seem to have an allergy to the real world.

The saddest thing about this whole business is that people like Dr. Hauser have to go out and prove something that should simply be assumed based on parsimony.

I’ll end this by saying that, as I’ve mentioned before in my psych rantings, unless we understand the selective forces that led to the differentiation of the primate brain from those of other mammals, and the forces that led to the gigantic increase in encephalization between hominins and other primates, we won’t really understand what the brain was designed to do. And if we don’t understand that how the hell can we know when something is actually wrong with it?

Introduction
What a lot of people forget or just don’t understand is that unlike the traditional ‘computer/problem-solver/integrator’ analogy, the brain is highly context-dependent. The way it reacts to the outside world, and in fact the way it perceives it, is highly dependent on both exteroceptive (the world outside) situations and interoceptive(mood, motivation, etc) responses. This is a function of the limbic system. Which is one of the most fascinating parts of the brain.

It’s one of the weaknesses of most facets of psych that they don’t take into account how the wiring and reactions of the limbic system can radically change the way we think, without us even knowing about it. I’m not going to get hugely detailed today because I have a final in four hours, and because that would bore everyone, including me.

Instead, I’ll give a quick and dirty overview and integrate it with a story about my ancient dog that illustrates my main point dramatically.

Neuroanatomy of the Limbic System
First, a few pictures.

(From the wiki page I linked to earlier–Limbic System in red)
This is a real simplistic image, but it allows us to consider the gross brain anatomy and introduce a couple of evolutionary considerations.

The yellow, blue, and green areas collectively make up the brainstem. Each of them has a different function: the yellow and blue areas are called the medulla oblongata and the pons, respectively. The green is called the cerebellum. The yellow and blue areas are arranged basically like the spinal cord on steroids, and handle a lot of the basic aspects of physiological maintenance. They do the breathing and the intestinal movement and the heart and all that. You can actually cut off or destroy most of the brain structures above them and still have a live animal…just one that can’t do anything (essentially a coma). The green area is completely different from these guys. It handles coordination and making sure your movements are smooth, certain, and accurate. People with strokes often have this area affected, which is why they might shake when they move (intention tremor), have trouble walking (ataxia), or be unable to adjust their movements in the middle of an action. The brainstem is about as basic as a brain can get: You can live with it, but not really do much. Some of the non-vertebrate chordates seem to just have a brainstem and nothing above it.

The tan part of the brain that’s surrounded by the red limbic system is what’s called the diencephalon or sometimes the basal ganglia. This area of the brain serves as a relay station between the tan stuff outside (the cortex–stuff that does the ‘thinking’) and the ‘lower stuff’ below. Basically, it filters and gets sensory information to the right place to perceive it; it also modifies the info just a bit. And after the cortex is done sensing, integrating, and responding, it takes the cortex’s signal, processes it again, and sends it to the right places in the brainstem and spinal cord to get the motor response we want.

The basal ganglia are pretty complex and can do a little behaving of their own. ‘Motor programs’ such as throwing a punch or walking are found there. It also helps with keeping your head on straight. Two degenerative diseases that affect the basal ganglia are Huntington’s and Parkinson’s. Huntington’s preferentially attacks a basal ganglia nucleus called the caudate, which is important for cognition. This is why Huntington’s patients develop dementia in addition to the chorea (involuntary movements). Parkinson’s, on the other hand, attacks the Substantia Nigra, which help in the initiation and cessation of movement. This is why Parkinson’s patients shake when they’re still, but have a hard time moving on purpose; it’s like a faintly heard radio station. The static is almost as loud as the signal.

The limbic system is one of the phylogenetically oldest parts of the cerebral cortex; even the way it’s constructed at a cellular level is more primitive than the rest of the cortex (but more complex than lower structures). The oldest part of the limbic system is called paleocortex or archicortex, while the newer parts are called allocortex. All vertebrates have well-developed limbic lobes, but many don’t have much–if any–of the cortex surrounding it (the outer tan stuff). This is why goldfish seem so stupid. And why rats are less complex than cats, which are less complex than monkeys. Less of what’s called neocortex.

Archicortex has 3 layers of neurons that interact with each other in a complex network. Allocortex has 3-5 layers that can be kind of indistinct. And neocortex has 6 well-defined layers. Your emotions start in the paleocortex, move through the allocortex and then on into the neocortex. We’ll look at that in detail after a couple more pictures…

Here’s a schematic of how these structures talk to each other:

(click for larger)

And here are a couple of drawings:

(click for larger)

(click for larger)

This last one is probably the best. It not only shows the structures but how they connect.

(clicky)

Stuff comes from the sensory cortices (the unshaded cortical parts toward the back and sides of the brain) into the Hippocampus (the archicortex) and Amygdala. Sensory information travels to the hippocampus and amygdala through the parahippocampal cortex (allocortex)The hippocampus is the organizer for sensing and remembering details about the outside world (exteroceptive information) while the amygdala handles emotional context (interoceptive information).

Together, they send information to the anterior cingulate gyrus (which is part of the neocortex) through the thalamus which is part of the relay system we talked about earlier. The cingulate gyrus then projects back to the hippocampus and amygdala through the parahippocampal cortex. Making Papez Circuit.

Confusing, but what it all boils down to is that the hippocampus and amygdala are what help us store memory, recognize similar situations, and, in the case of the amygdala, tell the brain how to feel about that. The emotional side of things is what we’re most concerned with today, so we’ll talk about the amygdala a bit more. The anterior cingulate cortex is what turns the amygdala’s emotional response into a guiding behavior for the frontal cortex (the part that does the thinking). The anterior cingulate is important in motivation; lesions to it result in people that understand that something scary is happening, but don’t respond to it. The amygdala also projects to the nucleus accumbens. If you’ve ever read about the neurobiology of addiction you’ve probably heard of this structure. It’s the one that dopamine activates. It’s our ‘reward center’. So together the areas the amygdala projects to provide motivation (anterior cingulate) and reward (nucleus accumbens). One encourages you to do something, the other one congratulates you on achieving it.

These areas in turn project to the frontal cortex, the area we think of as the seat of cognition, personality, and consciousness. In other words, any time you think about anything, your conscious thoughts are being unconsciously modified by the limbic system. This is evolutionarily important because it allows the brain to be efficient and speedy. It makes sure you’re more motivated to do things that’ll help you avoid dying or help you make more babies. It rewards you for doing something that doesn’t get you killed or helps you so you’ll do it next time.

Instead of spending equal time dealing with things in the environment, it lets you ignore crap like dirt and leaves and focus on the jaguar approaching you and the pretty little thing that just smiled at you. But, of course, it does all this without actually letting you know.

The Story
My dog has been going through a rough patch. Breathing heavy, coughing up a little phlegm. Didn’t touch her food all day yesterday. But she ate everything else she was given; fruits, pudding, bread, whatever. Mom was freaking out. Dad was worried. I was at school taking a test and knew nothing of her going off her feed. So I get home, see the full bowl, and then I started freaking out. Called mom. She told me the dog had something to eat.

So I figured she had a viral infection. Would explain the phlegm and the thirstiness and the heavy breathing. And if you’ve ever had a lingering respiratory viral infection (like RSV), you might have noticed a change in your sense of smell, even if your nose wasn’t plugged up (anosmia). We have really bad noses but really good tongues. Dogs are the reverse. Flavor is mainly to do with your nose, believe it or not. So with her nose all blocked up, that food wouldn’t mean much to her.

Little brown pellets are just little brown pellets. They go through the hippocampal (exteroceptive) system but completely fail to activate the amygdala. The amygdala doesn’t tickle the cingulate, so the frontal cortex doesn’t care too much either. So my dog has no interest in a food that to her aging eyes looks just like gravel. That slightly off-putting odor, on the other hand, sends her into a frenzy. She remembers eating it with fondness as the amygdala grabs interoceptive memories of her nucleus accumbens rewarding her for eating. Her cingulate gyrus motivates her to go right after that food. The motivational memory was tied to the smell, and only the smell.

But that doesn’t explain the fact she’d eat her various ‘treats’. Well, actually it does. To a dog, when their master gives them something from his hand, it’s literally a reward. And that nucleus accumbens fires right up. So Shelly has generalized taking food from my hand to mean she’s going to be rewarded when the food hits her taste buds. Her amygdala and hippocampus together recognize me holding something in my hand and holding it out to her as food in my hand. Her amygdala adds the memory of the ‘reward’. It tells the cingulate gyrus which promptly kicks her frontal cortex in the pants, sending her questing after the tidbit. Of course, in her senility, usually she misses and chews on my finger first.

We’d tried everything to get her to eat. Brought the bowl to her, held her upside down and stuck her nose in it, threw it at her. At one point I was considering chewing on it like you do with a baby to convince them that Gerber’s isn’t as nasty as it looks.

I was explaining the reward and motivation thing to my little bro, when he said “Doofus, then hold her dog food in your hand like it’s a treat. She’ll start eating it then and probably keep eating.” Sure enough, it worked. Once I’d gotten her to take the ‘treat’ from my hand, the taste memories kept her motivated.

Final Thoughts
Same object, different responses. Not because my dog’s thoughts changed but because which thoughts she was enabled to perceive were different. The subconscious mind is some powerful stuff, and while we do have some control over it, we only get that way by understanding the way our brains work in the first place. The challenge of psych and mental health research in the coming decades is to understand how to work with these subconscious processes as much as any conscious ones. Cognitive Behavioral Therapy is all fine and good, but if the problem isn’t necessarily cognitive (as limbic system could be argued to be), it won’t have much of an effect.

Continuing my commentary on UPI’s ADHD series with the newest installment…

“The main point is that stimulants alone are typically not adequate, given their lack of carry-over effects once stopped, their inability to teach parents and teachers and children new skills, and the fact that combining medication with empirically supported behavioral treatments typically yields the best chance of normalization,” said Stephen Hinshaw, professor and chair of psychology at the University of California, Berkeley, and principal investigator on the Multimodal Treatment Study of Children with ADHD.

Sounds about right. Even the most selective of psychiatric meds can’t help but take a brute force approach. Worst case scenario is that they act on all neurons that respond to a specific neurotransmitter, in this instance noradrenergic and dopaminergic circuits. The more selective stuff acts only on neurons with a specific receptor sub-type. An example is found in the treatment of Parkinson’s Disease (think Michael J. Fox or Mohammed Ali) and Schizophrenia. Both involve problems with dopaminergic circuits, but they differ in the type of dopamine receptors in each. Schizophrenia treatments involve pharmacological agents which act on the D1 receptor while Parkinson’s drugs work on the D2 receptors.

The problem occurs in that receptor sub-types are shared amongst a large variety of circuits with many different functions. Many antipsychotics used in the treatment of schizophrenia have the side effect of causing random chewing motions of the mouth (Tardive Dyskinesia). This occurs because although D1 receptors are involved in the malfunctioning circuits that cause hallucinations, they’re also involved in the basal ganglia motor system. Because the drugs act on both of those circuits, the hallucinations are controlled, but the crazy mouth happens too.

ADHD drugs don’t even pretend to be selective, they just take a bigger hammer to the locus coeruleus (norepinephrine) and ventral tegmentum (dopamine) and jack up the levels. Such a gross intervention lacks the finesse and the selectivity of dealing directly with such issues as internalization of behavioral norms and academic success. I doubt that any drug could be.

Indeed, in a survey, 98 percent of specialists viewed multimodal therapy as most effective, but only 34 percent said they use it in all patients, reported Alistair Sinclair, analyst at the London-based market research firm Datamonitor, which conducted the study.

So they know about the importance of behavioral therapy, but they fail to push it. Of course, part of this lies in the fact that most cases of ADHD are treated without referral to specialists. All too often the buck stops at the pediatrician. Which is a problem, because while a pediatrician is trained in all sorts of pathophysiological processes, he’s not trained to understand the softer side of therapy and cognitive insults resulting in behavioral problems.

“Thirty years of research show ADHD drugs used alone do not help children avoid long-term outcomes that are a hallmark of the disorder — substance abuse, domestic problems, school dropout, delinquency and criminal behaviors,” said William Pelham Jr., University of New York at Buffalo distinguished professor of psychology.

Given a fair shake, his extensive research shows, behavioral therapy could cut the need for chemicals by an attention-grabbing 75 percent, he said.

I daresay it could be decreased even further. Which should always be the goal when we take such ham-fisted methods to an object as delicate, plastic, and complicated as the brain. He continues:

“The vast majority of ADHD children are treated with medication as first-line treatment by their physicians,” Pelham said. “Yet … there have been many studies of this over the past 30 years, and not one has found beneficial long-term effects of stimulants.”

“Unfortunately … many parents of ADHD children are not made aware that there is a well-established, evidence-based alternative to medication — behavior therapy,” he added. “Instead of immediately prescribing the drugs, physicians should be recommending to parents a sequential approach — behavior therapy first, and then add medication if needed.”

Which is exactly why I’m in med school instead of playing with South American monkeys…and getting paid to do it. It’s almost criminal to treat child behavioral problems the way we do. I don’t think anyone could disagree with the premise that the fewer chemicals in our bodies the better and the fewer drugs messing with our brains the better, yet medicate first and therapy maybe remains the dominant approach.

There needs to be a greater reliance on mental health professionals, particularly ones who practice behavioral therapy methods, in child and adolescent mental health. Pills remain nothing more than symptomatic treatments, ones which lack the finesse to deal with complicated behavioral issues.

Continuing my commentary on the excellent ADHD series UPI’s running on Sciencedaily, I’ll be taking a look at the newest article today.

Because I’m a demagogue, I have to draw attention to the 3rd sentence:

The treatment criteria call for moderate to severe symptoms that both parents and teachers agree disrupt home life and impair school performance.

And, because I won’t let go, I’m going to point out again that ADHD is always viewed through its impact on the teacher and the parent, rather than the child. While I’m not stupid enough to think that a 6 or 7 year old kid can tell you exactly what’s going on in their head, I’d still say that their internal state is at least somewhat important if we’re interested in their mental health.

Respected professional journals are devoid of evidence that would convict doctors of the massive overmedicating charged by skeptics, these specialists assert. If anything, they see a criminal neglect of youngsters who struggle needlessly when quick and easy help awaits in a capsule.

Antipsychotics, tricyclics, stimulants, antileptics, all drugs that have been used to treate ADHD. None have been shown to directly affect the source of the behavioral problem in the first place. The former two often causing devastating flattening of emotional behavior. And tricyclics, originally an anti-depressant now deemed too high in side effects for use in adult depression. Given what’s known about these pills, and what’s not known about how they work, some might charge that the criminal neglect lies in trying to distill the treatment of a complex psychological phenomenon down to a single little pill.

The Multimodal Treatment Study of Children with ADHD, or MTA, funded by the National Institute of Mental Health, indicated pharmaceuticals trump non-drug options for speedily alleviating the core symptoms of hyperactivity, impulsiveness, inattention and aggression. But it acknowledged more than a pill is needed to address such overarching problems as arrested academic achievement, poor social skills or conflict at home or school.

Yup, psychoactive drugs are good at forcing gross behavior into the mold one wants (i.e. symptom treatment). What they’re not so good at is attacking the underlying cognitive and emotional sources of the behavior (you know, causes).

Those challenges appeared better served with a combined approach that supplemented medication with teacher consultations, 27 group and eight individual behavioral training sessions for parents and an eight-week intensive summer program aimed at boosting the child’s social, sports and scholastic skills.

Huh, I never thought that actually going after the behavior itself would be effective.

And, as always, the early gains of medication-based therapy tend to disappear over time. Because, as I said, the drugs crudely force your mind into a mold by playing with serotonin, norepinephrine, and dopamine. They don’t do much more than that. Behavioral training, on the other hand, gets to use the brain’s greatest strength; its plasticity. Which is why generally within a year or two, the behavioral kids accelerate right past the drug kids. One group has learned to deal with the way their heads work. The other has just had it covered up.

linky

This series on ADHD with periodic installments at Science Daily is a really fine piece of work, exposing the lack of understanding of ADHD treatment of the very doctors that prescribe them, and the seeming unwillingness of them to deepen their knowledge or address the problems with the science. Here are some of my comments on earlier installments.

on to the article:

Why, many wonder, do stimulants settle down children who already appear to be overstimulated? And why do prone-to-abuse Schedule II controlled substances not only not get hyperactive children hooked but also apparently lessen their risk of future addictions, as most studies suggest and most mainstream practitioners contend?

Here’s a hint, because they’re not really overstimulated. They’re actually understimulated. Basic ecologically-valid cognitive neuroscience here. Which is why it’s so funny that they don’t get it.

As for addiction, it’s a well known phenomenon that the slower and more controlled the release of the drug is, the less likely it is to addict. Some researchers try to argue that the decreased incidence of drug addiction among children on these drugs is proof of their beneficial effect. This is completely unsubstantiated; a chronic pain patient on controlled release Morphine is less likely to become addicted than a chronic pain patient undergoing no pain treatment. This isn’t because of some beneficial psychological effect, but simply because you tend to self medicate with the street drug version ; which because of the rush is much more addictive. It’s simply because the doctor gets to the patient before the drug dealer does.

Researchers say the compounds appear to help suppress certain behaviors by altering one or more of three chemical messengers in the brain, the neurotransmitters dopamine, norepinephrine and serotonin, which the prevailing, though far from proven, theory implicates in ADHD comportment. In a counterintuitive twist, the chemical change somehow leads to improved self-control — provided the dose is right, investigators say.

Too much drug, and the hyperactivity revs up into even higher gear, while attention span sputters.

In one of the first studies to probe the mystery in humans, government researchers observed in lab experiments how the stimulant Ritalin boosts levels of dopamine, the brain chemical associated with feelings of reward and pleasure, stimulating attention and motivational circuits that fire up the ability to focus and complete tasks.

And it’s not counterintuitive at all. As anyone with a basic neurobiology background could tell you, memory and attention are intimately connected with emotion, drive, and reward as even they themselves state. As one of my neuro profs pointed out TODAY, one of the things that makes 1st year medical school so hard compared to later years is that there’s less of a connection to patients, less of an emotional involvement, and seemingly less goal-driven. Which is why it’s so funny that they don’t put two and two together. These kids aren’t getting motivational stimuli from the modern classroom. Hence the low dopamine and inattention. As always, one should apply the Monkey Rule. Bad for monkeys, bad for children. Can you imagine a monkey paying much attention to the teacher in a classroom? No, total lack of interesting phenomena. Same with children. Yet, instead of fixing this lack of motivational stimuli, instead they titrate up the dopamine levels in the brain directly.

These circuits do not work at full capacity in those with ADHD, who stray off focus with the slightest distraction, the controversial theory goes. By normalizing the chemical levels, Ritalin should get them back on the attention track, scientists speculate.

Or, you know, it could simply be that these circuits never get stimulated in the first place.

As always, the tireless Dr. Baughman offers his contrary opinion (I’m a fan if you hadn’t figured out by now):

“There is no psychoactive drug that does not injure the brain short- and long-term and impair perception, learning and adaptation. So a drug abolishes ADHD behaviors, conduct disorder behaviors, oppositional defiant disorder behaviors. They do nothing but abolish,” neurologist Dr. Fred Baughman, a long-time critic of the use of psychiatric drugs in children, wrote in an April 18 infomail sent to his Website subscribers. “When is the child to learn to control these behaviors with the normal brain God gave him?”

Are there children that truly have a brain pathology and need medication? Probably. I’ve never met an ‘ADHD’ kid who fit that bill though. The challenge of psychiatrists is to explain why they use one treatment for ‘gifted’ kids and one for ‘ADHD’ kids.

The ‘gifted phenotype’ is virtually inseparable from ADHD in terms of classroom behavior. But ‘gifted’ kids have an IQ of over 120. Despite showing a similar lack of excitement in the dopamine pathways, it’s taken for granted that these kids have a fully functioning dopamine reward system; it’s just not being stimulated.

Conventional wisdoom then proceeds to pull a 180 on ‘ADHD’ children, saying that their dopamine reward system is broken. Of course, they don’t test this, they can’t show a pathology, they can’t show any difference between these children and ‘gifted’ kids except IQ. Which, as far as I know, hasn’t been shown to correlate directly to attention. There are many kids with an IQ of over 120 that don’t display the ‘gifted phenotype’.

Holes abound everywhere, holes they haven’t been made accountable to fill. Illogical assumptions are made, and are allowed to form the foundation for current psychiatric theory. Brain chemicals are clamped at certain levels, abolishing the basic plasticity that gives us personality, individuality, and flexibility. Those who don’t act as teachers, parents, and society would wish them too are simply prescribed into submission. Those who don’t feel what they want to feel simply prescribe themselves into artifical moods.