Minarik, Jules Hirsh, Boston discussed on The Peter Attia Drive
I came to New York actually after looking around in the Boston area for someone who could mentor me in this kind of activity, and it turned out there. I mean, there's some interesting stories about that. But the advice that I got from the people who are not in a position to help me in the way that I thought I needed help was that I might consider going to the Rockefeller and working with the physician scientist named Jules Hirsh who would time was very interested in the biology of adipose tissue from a number of perspectives, and I had actually communicated with Dr Hirsch in the literature by commenting on some of the work that he had done with regard to add up sites and signals that might come from adipose sites that affect potentially food intake and body weight. This was an area that he was quite interested in and I. I was to based on some of the thinking I had done about it while I was in the training in Boston. And he, and I actually had a communication in the literature on some of the work that he had done, and I went actually to visit his laboratory, and while I was in New York for an entirely different reason. And it was very shortly. After that that I move which is another great example of the types of common threads, we see in great scientists whether they be scientists or physicians I and his which has mentorship right again. Every person I talked to who's done something remarkable in science can point to mentors a mentor or mentors. And obviously for you Jules was probably the most important mentor. I'm guessing that's right. I had very important other mentors in the area of clinical medicine and the one who trained me and indoor chronology individual again of physician, scientists more clinically oriented name. Jack Crawford himself was. Very interested in the role of body fat and its interaction with other physiological systems in the body, most notably onset of puberty, and it was he actually put me in contact with another scientists at Harvard name rose Frisch who also was very interested in why for example, young women who lost weight as a result of anerexia or more commonly in her experience dude of very vigorous physical training for things like distance running or bicycling swimming became a Minarik. In other words, there period stopped and rose was very curious about why this was and whether there was a communication between fat and parts of the brain regulate the Kanada axis, which is the hypothalamus again. And I remember having many conversations with rose about where the signal might becoming from. She thought it actually might be coming from. Adipose tissue at sites in the bone marrow. And it was always encouraging me to study bone marrow. As a source of whatever this signal might be. So what year did you arrive at Rockefeller, nineteen seventy eight at that point in time was the adipose tissue was at a post cell where they it was this regarded as an inert sort of storage depot for fatty acid, or was it considered an endocrine organ, like what was the state of thinking about fat at that time the view of the role of adipose tissue was very strongly in the direction of the sort of former characterization that you made which is that it was a passive depot for fat. In the form of storing free fatty acids as triglycerides, so that they were hydrophobic. So that you could pack a lot of calories into organ or into cell without having a lot of water there. So it's very efficient way of storing energy, actually, as you know to probably around nine calories per gram. And its role as a signaling device or an integration. Organ was really people were thinking about it. But there was no firm evidence in this regard, other than I think the increasing sense that the size of the adipose mass was doing something to the levels of circulating insulin that somehow insulin rises when the fat mass rises the mechanism or the release of the other way around was clear where which direction so at the time, I think the view was pretty much as fat mass increases the concentration of insulin rises to to meet the consequences of so-called, insulin resistance, which occurred not only in adipose tissue. But maybe more importantly in liver and muscle..