Part VII Jeffrey Bland Bastyr Lecture June 2009

And then more recently in this era, we have one other person whose picture I didn't show you, but I will now. Dr. Bruce Haines, who was a Linus Pauling student who became the head of biochemistry at the University of California, Berkeley and is now 80 some years young in carrying the flames, still doing active research and publishing, has a whole research group at Oakland Children's Hospital, professor emeritus from Berkeley. And he wrote the seminal article that really codifies all of his work over the last 70 years that appear in the American Journal of Political Literature. This is an article that all of us in the field wish we would have written, but he was granted the person to write it. This has 650 some references in it. Going back and asking the question, what is the public world? What is the published the world's literature that supports from good science the role of increased value from vitamin intake beyond that of the rdm? Looking at it from a biochemical perspective, this orthomolecular perspective. And he goes on to say, as many as one third of mutations in a gene result in the corresponding enzyme having an increased Michaelis constant. That's the way biochemists kind of assess the binding efficiency of a coenzyme to an enzyme. So this Michaela's constant. And so you say, can you vary the Michaelis constant, the binding of a vitamin to its coenzyme through the genes? And the answer is yes. And so to get you either change the genes or you, you just give more of the message until it finally sticks. The analogy I use as a boy when I was a baseball player was catcher. And the thing about being a catcher, where you wanted your glove to be perfect, have a perfect pocket, right? So when that ball got anywhere near the pocket, it would stick. You didn't want the ball bouncing out, right? So as a young boy, I can remember putting linseed oil in my catcher's net, putting my baseball, my heart ball in there, and so sleeping on it, right? Because that's the way you really make the pocket strong. So that's like orthomolecular medicine. How do you get the pocket to bind to the baseball? You just keep hitting the baseball into the pocket harder and harder. How do you increase the rate of hitting? By increasing the concentration. Take more of it. That's the concept, right? So the need for an individual is based on their genetic uniqueness. It's not based upon a standard on the back of certain. Am I making sense here or am I losing it? So lastly, let me just tell you how this all really works. So we have these well defined genetic illnesses that everybody knows is just the bad luck of the draw of the genes. One of those which is so common in live births in the United States. And we have in our neonatal units a test for in the diapers is called phenylketonuric. Right. So if a phenylketonuric child who cannot metabolize the amino acid phenylalanine has this condition in their first urine that'll go into their diaper will be the unmetabolized phenylalanine. And there is a dye in the diaper that will pick that up and make it look colorful. So it's a diagnosis of that condition. So, so why? Because if you keep that child then on a phenylalanine enriched diet, a normal diet, they will deal with retardation and early death. So the treatment for this condition is to remove phenylalanine from their diet to the extent possible, which generally means a medically prescribed diet using a medical food that's got no phenylalanine. Are you following so far? Okay. And it's very difficult for the parents, obviously, and the child's approach pretty. Use the word bland. Pretty bland diet. So if you could find a better way to do that, an easier way, it would be nice. So now let's use orthomolecular medicine. So the concept is phenylalanine can't be converted into its downstream product, which is called tyrosine. The enzyme that does that in the body is called phenylalanine hydroxyl. Am I okay so far now does that enzyme work all by itself? No, it has a coenzyme that facilitates its activity. And what is the coenzyme for phenylalanine hydroxylase? Tetrahydrobioptra, one of the folic acid derived related materials, tetrahydrobiot. So now you might ask the question, if what I told you is at all correct about or orthomolcular medicine mean increase the concentration to drive a sluggish equilibrium to completion to get normal function based on advertising genes, could you then give higher doses of tetrahydrobioptarin and treat phenyl ketoneria? And what is this particular summary in the New England Journal of Medicine? I want to emphasize I've not gone to a tertiary grade journal talking about the stage, standard of identity and good medicine. In this paper they show tetrahydrobioptran supplementation led to responsiveness in patients with mild to moderate pku reducing the need to restrict phenolity in the diet, normalizing their physiology. Why? Because it does this. It promotes the conversion of phenolity into tyrosine by activating the inside. That's not defective, it's unique. Right. I want to emphasize, once you start to talk about defective enzymes, you start talking about flaws. Well, I'm telling you, every one of us has flaws. If we're going to use that as a definition, I would like to say every one of us has uniqueness because in the right place, what one might call a flaw is really a strain. I like to use that relative to my obnoxious personality in the right place, my obnoxious personality is really an asset. I just have to know when to use it. So that's really the kind of construct of this whole model. So then Dr. Ames follows up on this and says, what does this really mean? It means something about the difference of adequate health and optimal health. That's the really key kind of driver here. If all we're trying to do is Prevent scurvy, very, very 03 omnia rickets, quashboard marasmus, we don't need a whole lot of these nutrients. But if we're trying to drive to optimal function, compress morbidity, extend functional health, then we're going to ask a different series of questions and we're going to be more personalized in our treatment of that patient. And we're not going to use 70 kilogram human beings in the back of cereal boxes as our guide. We're going to use that patient and their history as the guide, and that means their individual health history, their family history. So he goes on to say, many common micronutrient insufficiencies based upon specific genetic constituents cause mitochondrial decay with oxidant leakage leading to accelerated aging and neural decay, meaning things like Alzheimer's disease. It's not just age alone. In fact, I'll close with the following statement. I have looked at the literature extensively. I've talked to gerontologists. I've been on the search for years and years to ask, has there ever been a study published in animals or humans that demonstrates that any disease is caused by aging? Now, let me make sure I understand what I'm saying. You understand what I'm saying? I'm not saying is associated with aging. We know that's obviously true. I'm saying is caused by the mechanism of causation of that disease, is a consequence directly of something related to aging. And the answer is no. It's still equivocal There has never been a demonstrable group in animals or humans that a disease, heart disease, cancer, diabetes, is caused singularly by aging. So there's a lot of variable in the equation, and it's that variable that constitutes the new medicine. It is really what Archibel Garrad is talking about. It's really what happened when Jacques Cartier and his sailors got locked into the ice in the St. Lawrence Seaway. It's really what the First Nation natives knew when they told them to make that bark tea. It's really what Lynn proved in his clinical trial, small as it was. It's really what Cook introduced into his seaboard explorations that never lost a person at scurvy and became world famous. It's really why the British beat back the French and Spanish Armada and that we don't speak all the languages we probably should speak on and on and on this model. How much do you have to radiate the light to create a social change? That's going to be your job. That's what you're training yourself for. What an opportunity to leverage this information and create this champion. Thanks very much.

We can open it up for. I want to be respectful of Dr. BL's time, but if you guys have some questions, we can take a few minutes to.

Please. Thank you.

So I'm just sitting here the whole time thinking, well, how do I find out what my math looks like? Like, do I just throw it on the bottom of my.

That's a very good.

In my mouth.

Or is it just.

I mean, is there a way. I'm assuming it has something to do with the.

That's a really good question. So the first and simplest and low technology way to get the answer, which is the way to strive for, is good clinical observation, judgment in a nutritional assessment, which is what I'm sure you are learning through your curriculum. How you visualize a patient in their presentation with the eyelids and the cheviosis and the dermatitis and the. All the various things that you go through, the luster of their hair, the color of their eyes, the easy bruising, all these myriad of things that crack back to a pattern that suggests certain kinds of nutritional needs.