Peter Schmidt, From Math to Neuroscience

 

92-168 Peter Schmidt

SPEAKERS

Peter Schmidt, Will Bachman

 

Will Bachman  00:02

Hello and welcome to The 92 Report conversations with members of the Harvard and Radcliffe class of 1992 I’m your host, Will Bachman, and I’m delighted to be here today with Pete Schmidt. Pete, welcome to the show.

 

Peter Schmidt  00:16

Thank you

 

Will Bachman  00:18

So Pete, tell us about your journey since graduating from Harvard,

 

Peter Schmidt  00:23

Sure. So I’ll start with senior year. We, we are in our senior year. We were going through the coming out of the Iraq, Iraq one and the all the news was about the jobless recovery, that we’d had a sort of recession, and I, as a senior, was very nervous about trying to find a job, and so I thought, oh, I can just go to graduate school. And so that was really how I wound up going to Cornell the study really so I studied what was called biomechanics. But it’s not really bioengineering. It’s mechanics, in the sense of of classical mechanics or quantum mechanics applied to biology. It’s the mathematics of biological systems. And I did work studying, how do you mathematically model a clinical trial? Because as a when I was graduating, I thought, well, I could do work in computing, or I could do work in biology. And I thought, well, I don’t know where computing is going to go, but biology will always be here, so I’ll work with biology. So I went to graduate school, studied mathematics and computing as applied to modeling clinical trials in orthopedics. I got a fellowship in New York doing at a orthopedic hospital, I did some work on total joint replacement, and then I got out and found my way through a circuitous path to neuroscience. And I spent starting I really got involved in neuroscience in about 2009 I led a bunch of clinical research. From there, I wound up I worked for a nonprofit for a while. I left there to be the vice dean of a medical school, and I left that to get directly into running clinical trials, and that’s what I’ve been doing since the pandemic is, is nonacademic work. I have an appointment at NYU in neurology, but I’m really focused on drug development, and I’d love to be involved in some way when we first develop a drug to change the course of Parkinson’s disease, and that’s sort of what I what I hope to do now is think about what we can do better in Parkinson’s disease, and be involved in that.

 

Will Bachman  03:13

Why? Why Parkinson’s in particular?

 

Peter Schmidt  03:15

Parkinson’s Disease is a super interesting disease that has terrible effects on a lot of people, but it’s a very it’s a tractable part of the brain. I’m essentially a mathematician from my PhD work, and I like to have things that I can think about in my head. And the cortex is very complicated, and you really need a lot of models. You know, you need to map out cortical networks. You need to think about very complex structures, but the Parkinson’s disease affects part of the brain called the basal ganglia, and you can model in your head what goes on in a basal ganglion. So you can just sit and think about it. And I enjoy that, and sit and think about neuronal signaling in the in the sort of lizard brain structures, and how at different levels, things are affected. The work I did in my PhD, we thought about, I did a lot of modeling of bone, and we thought about, how does bone work at the cellular level, and then how did those cellular impacts structure change the structure of bone? And so I that was my pattern of thought that I worked on in my PhD. And now I like to think about, how does the small scale, how does the micro How does understanding the microstructure help us understand the macro structure, and that the basal ganglia is a nice place to think about that.

 

Will Bachman  04:52

Okay, well, tell us. Tell us a bit more about the basal ganglia. What and about Parkinson’s? What? What? What? Is wrong in Parkinson’s and what, what are some of your ideas about what might be like past to investigate?

 

Peter Schmidt  05:06

So there’s a great sort of pattern of, there’s a great example of a pattern of thinking that that is a challenge for society in in Parkinson’s disease, and that really breaks down to the struggles we have in determining whether a question is a question of science or question of engineering. And the way I break that down is a question of science. We don’t know the answers going in. We are kind of, you know, there’s a question, there’s something, there’s a structure or a function that we don’t understand. And then we need to go in and think about and think about, well, what does actually happen? And we need to be open to whatever the answer is. And engineering is where we say, well, we know how these pieces work, and if I assemble them in the correct way, I will get a solution to this problem. And if I can’t get from get between the two banks of the river with this pile of steel and bolts, then I need to think harder about how to engineer that, because I know there is a solution to get across that river. And so a lot of times, people assume that we that they know the answer, they know that the answer to the problem in advance, and they just need to build the structure that crosses the gap. And if you look at the some of the way the scientific community is reacting to, for example, things that are going on at the Department of Health and Human Services right now, there’s a there’s a sense we know what vaccines do, and we just need the evidence to prove it, and there’s a sense we know what the effects of of engineered foods are, and that we just need to prove that. And that problem has affected neurodegenerative diseases like Alzheimer’s and Parkinson’s too. In the early 2000s people thought that there was that the solution was going to be stem cells, and that we were going to be able to put cells into the brain and they would repair defective networks. And then the current thing is focus on extracellular proteins, so we’ll be able to put a drug in and it’s going to destroy the proteins that are outside of the cells, and that’s going to cure Parkinson’s. And you know, Alzheimer’s is where their drugs approved with this mechanism, and people are working on drugs like this for Parkinson’s too, but that presupposes that we know that those protein, that those extracellular proteins, are actually the cause of the disease. And there’s a scientific question that we’re jumping past, which is, what is the role of those extracellular proteins? And we need to go into that understanding that we don’t actually know the answer to that. So that leads to sort of two interesting anecdotes, I think if, if you go back to the idea of extracellular protein, 1990s a Stanford professor discovered won the Nobel Prize for discovering pre and diseases, so things like mad cow disease and scrape he studied scrapey and cheap. His name will come to me as I as we go on. And so he won the Nobel Prize. And then he got on the speaking circuit, and he went around all the people with neurodegenerative diseases, and he said, Look, your disease has characteristic protein. So mad cow disease or crudesfeld Jakob disease, there they have a characteristic protein that is the pre and protein. And so you would say, well, in Alzheimer’s disease, you have a characteristic protein, a beta and and also tau is implicated in in Alzheimer’s and in Parkinson’s disease, we have alpha synuclein. He said, You guys have a characteristic protein that you need to look more at that protein. And he was very smart and a very compelling speaker, and so all of us in the field said, Oh, gee, we need to look into that. And that led to a bunch of initiatives focused on those proteins. And it led to us discovering that a lot of these proteins would build up. And you. In this extracellular space. But we never stopped and said, Why are those proteins building up? Why aren’t they going through the normal cellular synthesis and destruction life cycle of a normal protein? And maybe it’s the failure to destroy those proteins inside the cell that’s the disease, and their accumulation outside the cell is just the exhaust of the disease, the byproduct, the waste, and so the but we got this ball rolling and saying, This is going to be the solution. These, these protein targeted therapies are going to be the solution. And now we have a number of drugs that have had questionable efficacy. Now there’s a there’s some drugs like lecanemab from Biogen, that is, that does actually give you a benefit in parking in Alzheimer’s disease, probably slows the disease by about 25% 20 to 25% but it doesn’t stop the disease, and it doesn’t reverse the disease. It doesn’t, you know, neurons don’t recover from it. So what’s probably going to happen is we’re going to exhaust this pathway, and then people are going to say, well, I need something more, and we’re going to start looking at intracellular proteins. But the challenge we’ve had is that people gravitated to this one solution without, you know, and they engineered a drug to attack that solution without answering the scientific question, what is the relevance of this extracellular protein? And so we need to go back and do more science. And that science is happening. It’s just not getting into the drugs are slow in progressing through the pipeline, whereas we’ve already gotten these and in Parkinson’s disease. So we, what everybody wants is, can we, can we restore lost cells? And there are a lot of people who are saying, can we, if we could restore lost cells in the brain. We could, we could stop aging. You know, the the big limit on aging is that, since we’ve stopped smoking and identified nutritional issues and things like that, and gotten very good at cardiac care. Now, our bodies are often outliving our brains, and our brain is the biggest limit on longevity. And so, you know, people say, well, now what we need to do is figure out how to make the brain live longer so that we can all live to 150 or 300 years old, or however old we want to make it. And the challenge there is that so people think, Well, maybe if we could just stick cells into the brain, they could fill in gaps in the network. But the brain isn’t like a muscle. You can’t if you exercise it, it doesn’t recruit new cells to the brain. The brain is that it’s a amazing, lazy organ. It always wants to find the shortest pathway to do things. We always want to find the lowest energy activity. I’ve been giving a lecture lately about about on how we can use high energy tasks for the brain to identify things that we might want to augment with AI. So how can we use AI? How can we understand the place where AI would be would supplement human intellect in a way that lets us be strong in the places we’re strong, and lets the brain be and lets the AI serve the other issues and so. And the way you identify something that’s hard for the brain to do is by the energy, by the time and energy use, anything that uses a lot of energy. You know that over time, people are going to get tired of it. And this goes back to a study that was done in the 90s with an Israeli parole board, where they found that your highest chance of getting parole was to have your case seen first thing in the morning, and your second highest chance was first thing after lunch. And basically, they found that if you were the last case before lunch or the last case before the end of the day, you had zero chance of getting parole. And because our brain, even without without any consciousness of it, our brain. Get tired of making difficult decisions over time, so we need to focus where we’re going to put that energy, and so the our brain always wants to find the shortest pathway, and the hardest things for us are things like ambiguity. So there was a study that illustrate, to illustrate this, where somebody said, I’m going to show you. I’m going to I’ve got two urns. In one urn, I’ve got 50 black balls and 50 white balls, and in the other urn, I’ve got 100 balls, some are black and some are white. And so you go to a person and you say, I’ll bet you $1 that the next ball I pull out of one of the urns will be black. Will you take that bet? And which urn will you bet on? And they say, Well, I I’ll take that bad, and I’ll bet on the urn with 50 black balls and 50 white balls. And then you say, Well, what if I change that to a white ball? And they say the same thing. They don’t. They don’t. They know that either the odds are equal or they’re going to be in favor of black or in favor of white in the UR, you know, in the urn, where we don’t know what’s in it, but they will always choose to make the bed against the urn of known consistency, because our brains prefer risk to ambiguity. So if you’re asked to, so we’re much better off using an AI tool to you tool to to screen and and identify risk situations within a data set, and then let the human evaluate the risk than we are, to give a person A huge data set and, say, figure out what, where this figure out what the solution is. And it’s because we’re always coding shorter and shorter pathways. We’re always trying to figure out what’s the shortest cognitive pathway to come to a solution. And ambiguity is an energy intensive food brain. So go ahead.

 

Will Bachman  17:22

Yeah. Okay, so you’ve had really a number of stops in your careers, like different stages of your career, some that you’ve jumped over pretty quickly, like you were you said, I think Vice Dean of a medical school,

 

Will Bachman  17:38

yes.

 

Will Bachman  17:39

Tell us about that experience.

 

Peter Schmidt  17:43

So I was, it was a very interesting situation. I was at the I was at East Carolina University. The dean was a friend of mine who was Parkinson’s researcher, formerly the vice dean for research at Duke, was brought in as dean there, and he wanted me to come in as Vice Dean, really the Chief Operating Officer, so I oversaw clinical care and research in the medical school. And then there was another Associate Vice Dean, you know, associate dean who oversaw medical education. It was super interesting. One of the the East Carolina University has as its mission, state mandated mission to oversee, to over to train African American physicians to serve in communities in North Carolina, and we got highly ranked for diversity and for for training physicians who went on to serve in underserved areas by US News, but I was there during the first Trump administration, When it was an issue, but not the issue, not the level it is now. And we would talk about, well, what is the how do we defend a state mandated mission to to have to train a diverse workforce? I get a through, and we got the medical school reaccredited with no comments,

 

Will Bachman  19:32

I’m sorry, Peter, you cut out for just a second. Go back to you said the question of, how do we deal with the state mandated mission

 

Peter Schmidt  19:42

to so we had this, you know, there was in the first Trump administration, there was clearly pressure about diversity missions. It wasn’t at the level it is today, but there was clearly pressure we didn’t worry that we would. Would be subject to the end of the that there would be an indictment or, you know, federal lawsuit against us. But we did understand there was pressure about it, but we had this, you know, state mandated mission in North Carolina code saying that we were that part of our mission was to train African American physicians to serve communities in North Carolina. And we were having the pressure from, you know, and there was the obvious pressure from the administration, and so we would regularly discuss that with the school attorneys and figure out it was very pragmatic. It wasn’t, you know, there wasn’t this, like we were just trying to get through the day, each day, you know, with all these challenging pressures, just trying to figure out, well, how do we get from here through the next, next period? But it was very interesting to be involved in that in a professional setting, not thinking about it as as a political topic, but just this is what we’re here to do. This was our mandate, and we need to do it

 

Will Bachman  21:26

right. Tell

 

Will Bachman  21:28

us about running clinical trials and being involved in that space. Tell us a little bit behind the scenes of what goes on in a clinical trial that those of us not in that field might not be aware of.

 

Peter Schmidt  21:40

So there’s the the there’s the the the old military saying, you know that amateurs talk about strategy, professionals talk about logistics, and the success of a clinical trial is five to 10% science, 90 to 95% logistics. How do you make sure that the so you know? How do you recruit subjects? How do you keep the how do you bring people in so that you’re you’re fulfilling your mandate to recruit the 300 subjects that the drug company wants enrolled. How do you how do you make sure that that you’re going to that they understand you’re going to achieve that? So I love to work with academic medicine. I work in academic medicine, I maintain a connection with with academia. But universities are very slow. University administrations can be very slow. So if you’ve got six months to recruit subjects into a trial, you’re not going to recruit the first subject at a place like Harvard Medical School, you know, Mass General or breath Israel Deaconess, in six months. But once you get them started, they have a huge volume of patients, and so they recruit very quickly. So people have a very hard time thinking about problems of more than one variable, and clinical trial recruitment is a two variable problem. It’s time to start, and then recruitment rate once you’ve started. And so a lot of clinical trials are dominated by very small private clinics who have very fast moving ethics boards, you know, who don’t spend a lot of time asking for additional information, and who’ve got contract, who’ve got attorneys who will approve any reasonable contract, and And then you go to a place like Mass General or UCSF or, you know, an elite medical school, and everybody wants to weigh in. Everybody wants to review the study. They want to think about, is this going to make sense? Is this ethical for our for our patients? And it takes months and months to get a trial going at a place like that, but once you get them started, they might have 10 neurologists seeing Parkinson’s patients on a, you know, every Thursday. And so that clinic is going to be full of people who are potential recruits and and they will get, they will recruit very quickly. And then also, if you’re a drug company, it’s really valuable to have elite academic leaders who work with residents and fellows running your trial, because then there’s going to be somebody, you know, they’re going to be new doctors coming out who remember

 

Will Bachman  24:59

that.

 

Peter Schmidt  25:00

Oh, yeah, this trial went on, and I think it went pretty well, and it’s very good for commercialization once you once you get there, so you have to kind of work with your drug company and say, I understand, you know, it’s been four months, and Mass General hasn’t gotten us any subjects yet. We’re still waiting on contracting. But once you get through that, once you can get to that point where they’re recruiting and they bring in five subjects a month, or, you know, some large number of subjects a month, because you’ve worked with them, and you got a relationship with them, and they know that they’re that, once they get approval, they’ve got to deliver, then you get an excellent trial. And there are a lot of drugs that will come out where they’ve only run their trials, in these private clinics that private research, only clinics, nobody knows the drug. Nobody in clinical practice knows the drug, and so you get approval. So first of all, you go in front of the FDA panel, which has a whole bunch of Stanford and Harvard and Yale physicians sitting in that panel, and they don’t know, or they may actually not, particularly like your lead investigators. And then you get, you know, if you get to approval, then you’ve got all these people, then none of the the physicians who are out there thinking, I’m going to set up my practice. I’m going to see a bunch of new patients. They don’t know your drug because they it wasn’t run at the training site. So in a lot of neurology trials, what they want to target is the new the you know, the De Novo patients, the newly diagnosed patients. And what a lot of people don’t realize is that in academic medicine, a physician who’s been in practice for 15 years has a lot of patients who are 15 years into their disease. Course, because they’re really good doctors, and they treat their patients well, and their patients survive and they stay. And so if you want newly diagnosed patients the greatest concentration. So when you’re just hired, you start

 

Will Bachman  27:33

that sentence again. You cut out Sid, so if you want newly diagnosed patients,

 

Will Bachman  27:38

so

 

Peter Schmidt  27:38

if you want newly diagnosed patients, you need to go see if you need to work with a new you need to work with a young physician, somebody who’s just out of training. Because when the new patients call and say, I need to see a doctor that who, that’s who has open appointment slots, and so most physicians, as they age, so do their patients. And they get one, you know, they get some new patients here and there, but the big body of new patients is going to be with the new doctors. So if, if you want, so you need young physician. If you’ve got a drug that’s coming out that’s most effective in a newly diagnosed Alzheimer’s patient, you need young doctors to be prescribing that, because that’s where you’ll find the most newly diagnosed patients. The senior dots have all the patients who their great care has carried for enhance the survival. They’ve they’ve lived longer, they’ve had better lives, but they have these you know, if they’ve been in practice 20 years, you’re not going to have a 20 year Alzheimer’s patient, but their panel is going to be full of people who have been in there a long time.

 

Will Bachman  29:04

What are the kind of decisions or choice architecture that these physicians at the elite hospitals you mentioned? How are they deciding which trials they want to participate in? Like, what’s the incentive structure for them. Do they to participate at all? Is it because they get, like, free drugs, or they want to be on the cutting edge, or, you know, they get published, or, like, what? How are they

 

Peter Schmidt  29:34

them? Most of them have a particular scientific interest, so they need to pay the bills because, you know, their vice dean calls up their chair and says, you know, Dr Smith isn’t generating enough RV use, and so they need to be able to bring in that revenue. And that’s why people talk about, you know, you hear about the indirect rates and how much money is going to owe. Overhead, but that overhead is to replace the money that they would have brought in to pay to keep the lights on and the heat in their offices and things like that that they would have gotten from clinical care, but aren’t because they’re doing a trial. So they need to get that overhead money, and they need to get that funded. But most physicians in an academic setting are not picking based on who pays the most, but on a trial that’s in a particular research area of interest to them, they’ll think this drug, for the you know, this anti neuro inflammatory drug, I think it’s going to be really promising in Parkinson’s disease. And then they’ll run a bunch of anti neuro inflammatory trials, and then they’ll, you know, wind up knowing a lot about it, and pharmas got to talk at a conference about our trial. And, you know, there are, there are a bunch of indications that get a lot of engagement. So I’ve worked in Huntington’s disease. The physicians who treat Huntington’s Disease get very passionate about it. If you’re the child of a person with Huntington’s you have a 5050, chance of having the genes that puts you at risk. And so there’s a lot of family engagement in Huntington’s and that it becomes very meaningful for a lot of Huntington’s docs to focus on Huntington’s. Think about what can we do to give the best lives to the children of our patients, you know, for our patients today and for their children in the future. So you really see a lot of passion in Huntington’s. See a lot of passion for people who get involved in a lot of diseases, but Huntington’s is one where you really characterize it. And you know, you’ll see the same thing in like cystic fibrosis, the physicians who treat the pediatric pulmonologists who treat cystic fibrosis, and who then, because they’re specialized in CF, they they are trained as pediatricians, but they stay with their patients into their 40s and 50s, because they’re the ones who know the disease. That’s a very engaged and interested group.

 

Will Bachman  32:32

I guess you know, people who are not closely connected with the pharma industry might be surprised that the pharma companies themselves don’t run the clinical trials and that it’s run by or May, they don’t always do it. They often will outsource it to clinic.

 

Peter Schmidt  32:51

So that’s changing a little bit. So over the last you know, since we were in college, when we were in college, there were a lot of things that were like, you know, penicillin was, is a molecule that’s produced by bacteria and was discovered and turned into a drug and given back to those found in nature. You know, aspirin and cannabis are plant products that we’ve distilled down and made them into something that we give to people therapeutically or recreationally. But since about 2000 since the genomic revolution, there are a lot more drugs that are discovered in in the lab, in a petri dish or in an animal model. There are a lot more things where we identify a target and an animal, and then we make a molecule that targets that, and then we think I’ve discovered a way to treat a disease. And so what’s happened with that is you produce a drug, but and you think, well, this will be for Parkinson’s disease, or this will be for epilepsy, or this will be for diabetes, and then you discover it has alternative uses that, and sometimes those come up in when you’re in early in human trials, you know the GLP one agonists that are all the rage right now were first discovered in Gila monster saliva, and then a drug called exenatide was the first drug that that used that molecule. And then people tried to figure out how to make longer acting versions of that. And then they discovered this weight loss when it was in humans. If you were to come up with, you know, if you were to say, Well, what should we have done with GLP one agonists from the start, if you’d figured out this weight loss function and. 90s, when these were first introduced in diabetes, you’d make a lot of money back then, you know, you can make the money now. Instead, now they’re making the money but, but you could have been making that money from the start. And so a lot of drug companies are now saying, we want to own our data. It used to be that all used to be that you drug company would get some money and the CRO would essentially give them highly skilled temporary staff who would run the trial. But now people are saying, well, having that raw data and having a library of the raw data from our trials is going to be really valuable to us. So we don’t just want the output of the statisticians, we want the trial data. And so there’s a little bit of a interplay in terms of where it’s best to have what function. And if you look at what McKinsey is publishing on this, they’re very much in favor of this model, where you bring that that where the pharma keeps the data, and I think that that’s probably right. You want to be able to understand where it is. And then also, we’ve got this problem that it’s almost like, you know, if you imagine, it’s almost like there’s, there’s, there’s this organized crime that is doing some of that’s trying to run trials fraudulently. There’s been some work. There have been some reporting in science about drug trial, about Alzheimer’s trials, where some groups in Miami have brought in fake patients,

 

Will Bachman  36:46

what? And

 

Peter Schmidt  36:47

I’ve been involved in one of these trials. I did a rescue at one point of a trial where the prior CRO had allowed in fake patients. And I’ve seen this, and it was bad. This is a real problem. And it it seems like I didn’t visit the sites, but I talked to the people who did the site visits. And you know, they’ll get a storefront upstairs at a strip mall in a not very elegant area, and it doesn’t look, even look like a clinic when you go there, and then you go through the papers, and it’s clear that they were not filled out by patients, when you go and look at the source data. And so that’s another challenge, and it’s another reason why, as the data is coming in, a lot of these problems, we could have identified them at the moment the data was entered, if we’d been looking for it, but a lot of times we don’t look for it. And so there’s this pressure now also to get this tighter control on that data as it’s coming in.

 

Will Bachman  37:54

That’s That’s wild. So just making up fake patients and fake you know,

 

Peter Schmidt  38:00

I don’t know who they’re getting, but there was a idea that maybe it was, you know, unhoused individuals who are coming in and taking a pill, and then they’re doing the the pharmacokinetics. So they’ll do a blood draw after they take the pill to get the blood draw if they need to get a blood draw. But but that these are not necessarily patients with with a disease. And then a woman I know who visited one of these clinics said, you know, after they see patients, if you go outside and look in the trash can outside the door, it’s all of the drug you’ve distributed, they’re not going home and participating in the trial. They just came in to get the pain in it, so risk we need to keep an eye on, and that, that that sponsors need to be aware of.

 

Will Bachman  38:53

So we are. We’re chatting here on a zoom where we’re just going to publish the audio, but I we were talking before the show started, that you’re sitting in a freshly sheet rocked room all purple sheetrock at at a farm. Tell us about beyond clinical trials and work what tell us what else is has gone on in your life that you’d like to share.

 

Peter Schmidt  39:20

So this fall, my our youngest child went to, left for went to college. He’s the Barnard in New York and the my, we inherited my wife’s longtime family farm that’s been in her family for 200 years, and and her father died in August and left us the farm. So we’re trying to figure out how we can work on the farm. I love to i My career is always thinking so i. Like working with my hands and my off time. I do a lot of woodworking and the construction here, and we have a piece of construction equipment called a skid steer, which has four wheels, but they don’t turn. And so the way you control it is, some go forward, some go backwards, and and I’ve been it’s got a whatever attachment you want to put on it. And we’ve got about 20 my my father in law was a tractor dealer, so he got, for low cost, all the attachments that go on it. So we’ve got the auger and the forklift, and I really enjoy the forks. I’m I’m a forklift. Affection a fiction Auto, and I enjoy driving things around with forklift. We just took delivery of one of those husvarna robot mowers,

 

Will Bachman  40:53

okay

 

Peter Schmidt  40:53

this morning, and I told the guy they delivered it on a pallet. And I said, just put it anywhere. I’ll go get my forklift to move it in. And so we, I was driving my forklift this morning before this call to get my robot mower going. And so it’s a it’s fun. We’ve got, it’s got a big I now have my dream, which is both a wood shop and a metal shop. So we’ve got a wood shop and a metal shop. I brought my table saw up, and we’ve got all the tools, and we’ve got a car lift so I can, I can do work on my cars, in my in my spare time. So I’ve told my wife that she gets she’s the farmer and I’m the farm handyman. And sometimes people say, Oh, Pete, you’re the farm hand. And I said, No, no, no, the farm hand does what he’s told. The farm handyman just fixes things.

 

Will Bachman  41:53

Okay,

 

Peter Schmidt  41:55

so I don’t want to spend my off time doing what I’m told. I want to just fix things that are broken.

 

Will Bachman  42:00

And with a 200 year old farm, there’s basically unlimited number of those things.

 

Peter Schmidt  42:06

It really is. Yeah, there’s everything, everything could needs maintenance or repair. We’ve been driving by the tractor Dealer, and I’m so tempted to buy one new tractor so that we’ll have one thing that has a warranty. Everything else is just fix it yourself or put it on the lift.

 

Will Bachman  42:33

Pete, tell us going back to school. Tell us about any courses or professors at Harvard that continue to resonate with you in some way.

 

Peter Schmidt  42:44

I so when I was in, I think my sophomore year, so I got some when I was a freshman, I got grades that I had never seen in high school, and and I thought, You know what, I’m pretty okay with that. And so I always took the hardest classes that I thought, I’ll just take the hardest classes I can. So I took, I took a quantum mechanics course that I had no place being in

 

Will Bachman  43:22

it

 

Peter Schmidt  43:22

got me going, and I took, I took a bunch of classes like that. The things that really stood out I did, you know, material science class, where we did X ray interferometry of solid of crystalline structures, which was very interesting. I love the quantum I did quantum chemistry. So we looked at how, how atomic bonds formed on a quantum level. That was very interesting to me. I think the the class that I go back to the most was I took physics 15 C. So there’s, I mean, 15 B that I don’t think that was the number at the time. Maybe it

 

Will Bachman  44:14

was electro mechanics,

 

Peter Schmidt  44:15

physics, for physics majors as a friend,

 

Will Bachman  44:19

1212, A, B and C, right.

 

Peter Schmidt  44:21

Oh, but I took the other one that was A, B and C in two, in two classes. So I think it was 15 A and B and 15 B was they gave us a textbook where they were, all of the examples were, you know, cosine, omega t, sine omega t for frequencies. But all of the lectures were either the i omega t, and, you know, and you. We so we didn’t have any references that used the way that the that the lectures were given, or the and so I would go back to my notes on that for years, and probably, like my third or fourth year in graduate school, I finally understood. I finally got through all of what was covered in that class. And then I took a class in engineering that was about fits and tolerances, and it was just absolutely like, that was like, that was the thing that just absolutely resonated with me. That was the place where, if, if anybody, you know the professor, could just say, you know, Pete, can you explain this? And I would just explain that. That was so I remember that was a great one. And then my roommate, Bart Lewis, was studied folklore mythology. He’s now in banking, which, you know, is really driven by folklore mythology these days. So

 

Will Bachman  46:08

I think

 

Peter Schmidt  46:09

it was well prepared, but I took the Icelandic Family Sagas with him, and that was a really great course. That was my my only pass fail course of my entire college career. But very enjoyable.

 

Will Bachman  46:30

Tell us about fits and tolerances, something that we might not normally think about if we’re not engineers in our day to day life. What What fascinated you about that topic,

 

Peter Schmidt  46:38

fits intolerances is how you do all of this. You know, what things do you have to measure to the 32nd of an inch, and what things does it matter plus or minus an eighth of an inch? What are the things where you have to you and a lot of people like to think in terms of exact values, and they don’t understand that in reality exact So there’s an example would be, if you’re making, if you’re cutting two pieces to go together, there are three options. One is a clearance fit, where, when you put those two things together, there is a little extra room so that they’re not pressed up against each other. Whether you’re drilling a hole and putting something through the hole, clearance fit, it just slides through. And then you can have an interference fit where, when you’re putting two things together, there’s all they always hit, they always run into each other, so you can’t put the bolt through the hole. You’ve got to hammer it through, because there’s always material that overlaps. And then you can have what’s called the transition fit, where you’re trying to get it close enough. Now most people think of everything in terms of that transition fit. I want to get it exactly right, but almost nothing is optimally done with a transition fit. If it needs to be tight, then you should plan for it to be tight. You shouldn’t plan for it to be exact. And if it needs to be loose, then you should plan for it to be loose, right? So in finance, you never want at the end of the month for revenue and expense to exactly line up. You want to have a little cash left over. You want, you’ve got cushion, because if you ever wind up being a little over, it’s really bad. So it, you know it, it works in almost every world to think about. We talk about things as matching, but in reality, you almost always want to target being a little over or a little under. And you want to know which is better. You want to know which is your target.

 

Will Bachman  49:40

Thank you, Pete. And for listeners, where can they find you online if someone wanted to follow up or just continue to keep track of what you’re doing.

 

Peter Schmidt  49:49

So I think LinkedIn is probably the best place to find me these days. I check it fairly regularly, but I’ve largely gotten off all the socials i. I’m on. If you want to see if I take an interesting photograph, I post it on Instagram, but it’s mostly sort of landscapes and interesting things, not anything serious or and I don’t really go on Instagram regularly enough for dialog. But if you want to see where I’ve been and then what up do, and then Instagram, but LinkedIn is the best way to contact me.

 

Will Bachman  50:24

We’ll include those links in the show notes. Pete, thank you for joining today.

 

Peter Schmidt  50:28

Sure you.