Jeffrey Bland (PhD) presents a historical and conceptual lecture linking the rise of the vitamin/supplement industry and preventive-medicine movements (mid‑20th century figures such as Adele Davis and early organizations) to evolving scientific ideas about genetics and environment. Bland highlights Linus Pauling’s 1949 work on sickle cell as an early use of the term “molecular disease” and uses numeric examples (fetal vs. sickle hemoglobin ratios) to argue that gene carriage is not determinative—environmental/modifier factors can change phenotypic outcomes. He also raises modern examples (BRCA1/2 penetrance) to show that modifiers, not only genes, shape disease risk and medical decisions.
Questions this video answers
Over 100 million copies.
After World War II (late 1940s).
Milder forms: ~40% fetal hemoglobin to 60% sickle hemoglobin; more severe forms: ~50:50 (or shift toward greater sickle proportion).
"Molecular disease."
80% plus probability.
Chapters
Now here's the next figure. This is a woman who probably is named procedure and reputation. Some people credit her with the worthing of the vitamin supplement industry. Adele Davis. Most people who are book authors would love to have but just a small fraction of the sex she had in her books that were published in the course of her life. Her book sold over 100 million copies in the 50s and 60s. 100 million copies and changed the paradigm. So what was her concept? I knew Adele Davis as well. Very interesting woman, to say the least. She was a registered dietitian turned rebel. And she grew up down in the beaches of Southern California with Gaylord Hauser and the people that really were the blackstrap molasses, yeast and yogurt and whole grain and wheat germ group that were exercising in Venice beach every morning and were this whole vitality movement. And so she became a group of doctors in Southern California, including Weston Price and Robert Pottinger, if you're familiar with their names, to talk about these issues and how to Vitamin supplements. I want you to recall vitamin supplements as an available commodity did not come until after World War II. So we're talking about the late 40s in which vitamins were even available in supplemental form. So that's the dawn of the health food industry. And that's why for me, being a birthday in the 40s, I think I was just born at this interesting time to see this transition when we didn't have it before. We didn't even have supermarkets when I was a kid. You had to buy stuff every day like you do in Europe often. And then supermarkets came in when I was in elementary school. So there was a whole transition in food habits and nutrition supplementation just starting to evolve. So now this is a classic photo. This is a photo I dug out of my archives 1974. And this was one of the first meetings of the International association of Preventive Medicine. Susan, my wife and I were members of this organization way back when, in which this was the first kind of doctoral organization in the country to try to enlist these concepts of Williams and and Pauling into medical practice. And it was made up of several thousand, and I would call them avant garde, you know, early adopter type of practitioners. So this is a picture actually of the other Helen Pauling, who is Elinus Pauling and Roger Williams at the inaugural meeting of the International Academy of Preventive Medicine. And interestingly enough, that meeting spawned them a chapter of the international academy that became the Northwest Academy of preventive medicine in 1975. The Northwest Academy of Preventive medicine headlines falling here in Seattle for its inaugural meeting. And I became the president of the Northwest Academy of preventative medicine in 1977. So we were kind of like chartered to do this up here in the Northwest, which became a place that a lot of the docs, by the way, this time naturopathic medicine in this area was working under a grandfathered licensure with no college. That was really vital. In 1977, I went down to Northwestern College of Naturopathic Medicine with a group of people to resurrect their program. And then in 1980, obviously Vaschur started. So this was a whole interesting period of kind of emergence of this field during this period of time. So here is Linus Pauling's contribution. Linus Pauling talks about the inheritance of sickle cell anemia in this landmark paper, series of papers actually that appeared in Science magazine in 1949. The ability of red cells to sickle is observed to have genetic basis. But no one knew what the genetic basis of sickle cell anemia was until Linus Pauling and his postdoctoral student Harvey Attano made these discoveries that were published in the same issue of the Lancet in which he says the fact that sickle patients with mild forms of sickle cell disease have red cells that contain two forms of hemoglobin, one is called fetal hemoglobin and the other is called sickle hemoglobin in the ratio 40 to 60 rather than 50, 50 found in patients with more severe forms of sickle cell anemia might be accounted for by the fact that there are a number of genes that regulate the production of this sickle hemoglobin. And those gene expression patterns are probably related to environmental factors, meaning not every sickle cell of ED patient that carries that gene has the same kind of disease. Some very severe with a lot of crises, some go through a fairly mild disease. And they're environmental modules you talk to, principally an African American disease are seen more frequently in that genetic lineage. You talk to them, they'll say if I'm stressed, I don't sleep right, I don't eat well. My much more susceptible to have a crisis, a sickling crisis. So it's interesting to note that cr fetal hemoglobin genes that are not sickle to the sickle cell anemia, the baby is not sickle. What happens is they become sickle as they develop adult hemoglobin postpartum. But there's still sickle hemoglobin available in their genes that can be modulated by Expression that dilutes out the sickle hemoglobin. And a small change from 40, 60 to 50, 50, meaning 60% fetal and 40% sickle, to 5050 can mean the difference between crisis and number. And the environment can modulate that. Now this is a major paradigm shift in medicine, by the way. I would say if I gave this talk right now to a group of highly trained, competent medical practitioners, most of them would say they've never heard this before. This is like really remember the illumination. How far deep does the light go? Not deep enough yet to make the shift. Right. That's the point I'm trying to get to. So why is this a big deal? Why am I making this light so dramatic? I'm making this dramatic to try to get you to understand that our genes, even in cases of genetic type lineage, like sickle cell anemia, are not the full determinant of our phenotypic health outcomes. These other variables modulate their expression patterns. And this is why in this article, Dr. Pauling used for the first time in the medical literature the term a molecular disease. A molecular disease tracks to genetic variability, biochemical individuality, genetic probing disease, all the way back to a large bob rod with inborn errors of metabolism. So now I ask the question, when we use the term inborn errors of metabolism, is that some form of discrimination? Maybe it's inborn uniqueness of metabolism because the people that carry the genes for, let's say, sickle cell anemia, we're talking about that, let's use that as an example. Are people that were selected for in equatorial Africa to be resistant to what, malaria? Right. So it wasn't a defect in their genes. It was a selective advantage in the condition that they found themselves by calling these genetic metabolism diseases of infancy. It already stigmatizes, doesn't it? It's like a box you can't get out of. We do this in our language all the time. We say that autistic child as if we knew what the heck autism really is. We don't. It's not a single disease. It's a demonstration of a presentation of behavior. It's not a disease. But we label that child as a disease. And they will become that disease, won't they, for the rest of their life? Because they will be treated that way, counseled that way, managed that way. Their parents would think of them that way. It's a form of discrimination. And medicine does this by labeling people with things that appear like you can't escape. Let me use an example, BRCA 1 and 2, a lot of women in this audience, you're all familiar with these breast cancer genes, right? We know the data says that if you have a double allele of BRCA1 or 2, that you will have 80% plus probability of developing breast cancer in your life. And so women are counseled to have prophylactic breast removal if they have this history of. There's a series of rules, right? The criteria that have to be fulfilled. That's a pretty significant decision to make to have your breast removed prophylactically. So I was. And you know, the woman who discovered. Are you familiar with the woman who discovered the BRCA 1 and 2? She's a university of Washington geneticist. I mean, a remarkable woman. She had dropped out of graduate school during the 70s to do peace marches against Vietnam. She's just really a very, very compelling, humanistic, brilliant person. And so she was at a seminar and I was presenting this data for this. Brilliant. And I asked a question, I said, you know, it's true that 85% of these women end up. But what about the 15% of the women that have the same genes that don't get. And her response is, that's exactly what is most interesting to me. What are the modifier factors that regulate the promoter regions of those genes that ultimately cause them to turn on or turn off their functional capability? If we can harness that, we can't change the genes yet, but we can change maybe the environment. So these are very interesting new questions. Aren't they illuminating through the crowd?
