The Mysteries of Parkinson’s, with Jon Palfreman

October 05, 2015

Brains, the means by which we scrutinize our world, are themselves inscrutable, and no more so than when things are going wrong. Just ask our guest this week, award winning medical journalist Jon Palfreman. After spending years of his life studying Parkinson’s in order to write the classic book, The Case of the Frozen Addicts, Palfreman was himself diagnosed with the very disease he built his career around understanding. Palfreman’s new book is called Brain Storms: The Race to Unlock the Mysteries of Parkinson’s Disease.

As modern medicine allows our bodies to live longer with each new generation, the search is on to find ways of preserving our brains from neurodegenerative conditions like Parkinson’s and Alzheimer’s, diseases that drain much of the value from these lengthening lifespans. Palfreman gives insight into both our understanding of the disease, as well as the latest medical advancements and further points of study in our race to understand the brain.

This is point of inquiry for Monday, October 5th, 2015. 

Hello and welcome to a point of inquiry. A production of the Center for Inquiry. I’m your host, Lindsay Beyerstein. And my guest today is Gyeon Palfreeman, an award winning medical journalist and a professor of broadcast journalism. You may know him as the producer of acclaimed science and medical documentaries such as The Vaccine, War and Harvest of Fear. He’s the author of the classic book The Case of the Frozen Addicts How the Solution of a Medical Mystery Revolutionized the Understanding of Parkinson’s Disease. He’s here to talk to us today about his new book, Brainstorms The Race to Unlock the Mysteries of Parkinson’s Disease. This remarkable book interweaves insights from the history of medicine, in-depth discussions of the emerging science of Parkinson’s disease, and the author’s own experiences as a Parkinson’s sufferer. He embraced the Parkinson’s beat full time after being diagnosed with the disease in 2011. 

John, welcome to the program. 

Glad to be here. 

Lindsay, can you start by telling us a bit about the case of the frozen addicts from San Jose that kind of started this whole odyssey for you? 

Well, this was a story I did some 25 or 30 years ago, and it’s an astonishing story. It’s a group, a group of California drug addicts froze up, unable to to move or talk. And they ended up in a psych ward or some some of them ended up in prison cells. And it presented a real mystery. They seem to have developed the symptoms of Parkinson’s disease overnight. And a very clever young neurologist called Bill Langston figured out what had happened. He first of all, he gave them Dopa and they started to move again and they could talk about what they’d done. It turned out they’d all consumed a bad batch of synthetic street drug and the drug maker in some backroom laboratory somewhere inadvertently added a toxic neurotoxic and called AMPTP, which had gone in and destroyed the same region of their brains that gets destroyed in Parkinson’s disease. And at the time, this looked great. This was going to be a terrific revolution in Parkinson’s disease research because now you could use this neurotoxin to model the disease in animals. And as it happened, it hasn’t turned out to be quite as revolutionary as all that. And that was the story which got me first involved in Parkinson’s. And it was it was a story which in some ways launched my career. I still look back on it as one of the top three stories I’ve done in a lifetime as a science journalist who was an important story for me growing up. 

My father was a physiological psychologist and he used to teach that the case of the Frozen Addicts video every year for his students. And I was just I like to watch it, too. 

Well, that’s good to know. It’s very interesting. It it’s become a sort of a classic. And you’ll find it on neuroscientist’s bookshelves that the book that we that I actually wrote to later with the Branxton, the neurologist’s. And it’s just a wonderful story. But then it was sort of ironic that there are 30 years later of all the diseases that I could contracted. It turned out to be Parkinson’s disease. 

What made you first think that you might have something neurological that needed to be looked into? What did you notice was changing about your body or your life? 

Well, I think I denied it. I mean, looking back, there were signs before long before I got diagnosed. Maybe two or three years. I remember my daughter mentioning to me that I wasn’t swinging my arms naturally as I walked. And that’s a clear sign that a lot of automatic actions that that are done by the basal ganglia sort of break down in Parkinson’s. But at the time, I just thought that was nothing. And then I had a slight tremor in my left hand. But then I my mother had had had had a tremor caused by something called essential tremor, which is a benign, non degenerative condition. And so I just said, well, I just assumed that’s what I had. It wasn’t gonna be Parkinson’s. And so I didn’t expect it. And so when the diagnosis finally came, I was kind of shocked. 

It’s a big thing to be told, because it’s so in some so dire and in some way so uncertain because you just don’t know how the disease is going to progress. 

No, it’s a horrible thing. I mean, it took me about a year to process that information. I mean, it’s it’s true what people say about the stages of grief. You have to go through. You get angry. You deny it. You seek second opinions with a disease like this, you you try and keep it secret. It’s a sort of absurd thing in retrospect. 

When you think about it, you think, if I can blend in with the world of the well, then it can’t be so bad. Right. 

And also, you don’t want people judging you or making assumptions about you because obviously they know this thing about your medical history. 

Absolutely. I mean, that’s the thing. You don’t want people to think this isn’t you anymore. But actually, what’s happened is quite profound because you you’ve got a disease, in my case, Parkinson’s. But it could be any disease like cancer because of that. The next episode of your life is gonna be different. And you have to come to terms with that. And so it took me took me a while before I was really comfortable to come out and talk about it. And I went back a bit about a year after I got my diagnosis, I spent an afternoon with the neurologist, Ben Langston, who made the documentary about the Frozen Attic, where we spent we spent two or three hours talking about all the things that all the research developments that that happens in Parkinson’s disease in the last 25 years. 

And when I came away from that meeting, I realized I had a destiny, like an opportunity, but really a destiny to use my training as a science journalist and my insights as a patient to explore this malady that Fated dealt me and to try and produce a book that would make a contribution be of help to other other patients. And that’s what I set out to do, write the book. 

So it was a way of finding meaning in this life altering calamity. 

Yes. No, William. It was a very helpful sort of thing for me to do. And it was an extraordinary experience, partly because I got to meet some remarkable neuroscientists. And pure interest of the journalism was fantastic. But but mainly because I became friends with a new community of people, of other people who had Parkinson’s disease. I mean, people who share a disease are members of a common tribe. And it’s quite amazing how instantly helpful and understanding people will be if you call them up and ask for advice. But really, what you what I noticed by getting to meet some of these people is that they had inspiring stories that courage and the things they’d done to sort of combat this disease were what ways to help me go forward with it. So there were people like there was a surveyor from England called Tom Isaacs who who walked around the coastline of Great Britain to raise money to form a charity to cure Parkinson’s Trust, which he now runs as a ballet dancer in New York called Pamela Quinn, who teaches Parkinson’s patients how to trick or trick their bodies so that they can move properly. There’s all kinds of people who just showed tremendous courage and insights, and meeting them has been one of the great treasures of the great positive aspects of this thing that’s happened to me. 

I want to talk more about their for especially the dancer and what she teaches people. But can you give people kind of a capsule summary of what Parkinson’s is in terms of its signs and symptoms? 

Yeah, so, I mean, classically, Parkinson’s has been portrayed as a movement disorder, and that’s still know, I think, a lot of what it is. So so you might you might start with a tremor in one limb and you get a stiffness, a rigidity of movement. People with Parkinson’s tend to move slowly. They can’t have a stooped gait when they walk, when they bend over their faces, lose expression and the handwriting. Can, I think, micrograph here where as you as you write a line, it gets it tends to get smaller as you write as you go from left to right. And then there’s what we call the motor disorders, the motor movement disorders, the things which are most noticeable. And that’s really when James Parkinson eating in the early part of the 19th century, he walked around the streets of north London, of east London in Shoreditch, and he could see he just noticed people who move differently from everyone else. They moved ordinary and he went up and interviewed them. And that’s how he got the basic idea for his pamphlet that the essay on the shaking palsy. But now, increasingly, we think of Parkinson’s, we think of the motor disorder or Parkinson’s as being the middle act of a three act play that really long before people get diagnosed, maybe 10, 20 years before people get diagnosed. There’s a disease going on in people’s body, sometimes throwing up suggestive signs, but not quite, you know, like constipation, loss of sense of smell. Sleep disorders, they tend to be highly correlated with people who later to get Parkinson’s disease. So if that’s the first act in the three delay, then getting diagnosis and developing the motor disorder is like the second act. And then. The pattern of damage continues working throughout the body and brain. And so later, people get in addition to motor disorders, they can get cognitive disorders and hallucinations and all kinds of bladder dysfunctions, all kinds of things which which go on to. So it’s a much more complex, systemic disease. 

But everybody goes through the middle phase and that’s really when it’s picked up and diagnosed. And that’s why it’s it’s characterized still by most people is as a movement disorder. 

Scientists are increasingly rethinking the idea that Parkinson’s is simply a dopamine movement disorder. In terms of the brain, what are some of the new things that they’re thinking about in terms of what’s going on with Parkinson’s? 

Well, the big and the big idea, and it was discovered with it, is a fascinating detective story, which is portrayed in one of the chapters of the book that the big idea was the discovery that there seemed to be a protein called alpha synuclein, which goes rogue. It misfold and sticks to other alpha synuclein proteins and forms these sticky clumps. And they they jumped from neuron to neuron killing, killing cells in their wake. And that’s how the disease spreads. And it may it might start in the nose or even the gartland, and then it spreads to different regions of the brain going to the region. In this instance, your Nager where a lot of the dopamine cells are killing off, you know, maybe 60 or 70 percent of those and then spreading to other areas like the cortex. And so this model of a sticky aminul aids and you find in the brains in autopsy and pathology, you find these things or Lewy bodies which are stuffed full of alpha synuclein, which it does seem that it’s the thing that’s associated with it. If you have too much of this alpha synuclein, you get Parkinson’s disease. And so all the effort in in developing disease modifying treatments is going into finding ways to inject into the body instead of chemicals which can dissolve this alpha synuclein. And the great, great prospect would be that you could if you gave this early enough, if you had biomarkers which would predict somebody who didn’t have Parkinson’s might be at risk for getting them five or 10 years down the road, you could stop it in principle from ever happening. 

So that’s with somebody who hasn’t got it, but also with somebody like me who’s who’s got it and who suffered already cell damage. You could you could help me. Not so bad. I didn’t get any worse. It’s bad. Different regions of the brain, because I’d be perfectly happy if I could maintain my current level of functionality. So that’s that’s the big hope at the moment. And there’s a number of agents which are going to go into clinical testing in the next year or two. 

So the thinking is that Parkinson’s in some ways, similar diseases like Alzheimer’s disease or chronic traumatic encephalopathy, where rogue proteins are kind of fumbling through the brain and disturbing and killing cells, correct? 

Yes. They all they all seem to work the same way. So. So with Alzheimer’s, their protein is they have two proteins, one called amyloid beta and one’s called count tangles. And Huntington’s disease has a protein called Huntington. And the theory is they all work the same way that that rogue misfolded proteins spread in in what’s called a pre on late way that you may have heard the word pre pre on is an infectious protein. And these these aren’t quite fully fledged prions in the sense that they can’t. And in fact, one human being from another, but they spread internally within one body and brain. And it’s a fascinating theory. And it’s it seems to me that they’re on the right track. I mean, it may make an effort to be wrong, but it seems very, very, very promising. And a lot of researchers are betting the farm on alpha synuclein in Parkinson’s. And there are even there even products which can take out more than one of these amyloid at once. There are products which can not only knock out alpha synuclein, but can knock down amyloid beta. So you’ve got the you’ve got the potential of having Pann therapies down the road, which might just offer protection for more than one of these horrible neurodegenerative diseases, because these neurodegenerative diseases are going to become more common because the biggest risk factor for them is age. The older you get, the more likely you are to get them. So people aged 90, 50 percent are going to get Alzheimer’s disease. 

So living, living long isn’t necessarily always a good thing unless you can cope with some of these problems. 

So what’s the big challenge in the book? You write about these synuclein scavenging drugs that are agents with veggies that are able to suck up so much of this raw protein, in vitro. What are some of the big challenges in terms of getting that from the petri dish into a human and having it work? 

Well, we have to get a delivery mode. So, I mean, what’s being talked about now is sort of intravenous infusion. So seven every couple of weeks or every month, you get the intravenous infusion of an agent, which would a lot of which would get metabolized and broken down. But some of. Which would find its way to the brain and would probably take out the cell at the office and you clean blobs were sort of leaving one and going into another. So they would be vulnerable to this kind of agent. And this idea could be completely true, but it might be technically very difficult to make it work. What they found with Alzheimer’s, for example, is that, you know, they’ve got a good idea that this should work. But generally, by the time they give it to the people with with moderate Alzheimer’s, the damage to the brain may be too extensive to make a clinical difference. So. So, I mean, everybody is really interested in what are called biomarkers, finding ways to predict the disease as early as possible, because then you’ve got the biggest Johnson producing a change you can detect clinically. 

There’s some really interesting stuff in the book about finding populations of people who are at risk for rare genetic variants of Parkinson’s and using them to study the natural course of the disease and opportunities for intervention. Can you tell us a bit more about that? 

Yes. Well, I mean, the office in England was discovered in a family called the Contorts. You can read this is a large Italian family which had a very rare inherited form of Parkinson’s disease. And this is true for Alzheimer’s disease. It an extraordinary, interesting cohort of people with an inherited form of Alzheimer’s disease. And in Colombia, in Medellin, Colombia. And this is this is a family where large a large family called the McKendree, where you can tell with a genetic test who’s who’s going to develop. You know, the person who’s 25, you can tell whether they’re going to develop Alzheimer’s when they’re 40. So, you know, with absolute procession, who’s going to get it? So if you could give one of these drugs to break down the amyloid beta to the group of people who you knew were going to get it under normal circumstances and you delayed that onset or you stop that onset, then you’d have a pretty good idea that you had a drug that works. And we need we need tricks like that in order to prove proving the case is is very hard unless you have sort of model populations with these characteristics. And so so that’s one area where people are looking at and then imaging is another area. If you can image if you can image the damage in the brain and show that the agents you’re putting in reducing some of that imagery, that would be some evidence as well that you were on the right track. 

It’s a really interesting discussion in the book about surgical interventions from Parkinson’s disease. Can you give us kind of an overview of what’s been tried and where we’re at now in terms of brain surgery to treat the condition? 

Okay, well, a lot of a lot of the things are surgical because you need to get them into the brain, basically based on the theory of the frozen addict, which was the development of this neurotoxin, AMPTP. The only research sought to find ways of protecting neurons, reviving neurons and even replacing neurons. And so there were a whole series of neural graft experiments done where fetal tissue knew fetal tissue neurons were put in to replace the ones that had been damaged and so forth. And this was a surgical procedure. And in uncontrol studies, what are called open label studies. They seemed to work pretty well and it didn’t work all the time. But you got some pretty remarkable results in some patients. But there’s always the problem about if you have if you have a disease that people want to get better and everyone wants wanting to get better, that there might be psychological reasons, there might be a placebo effect. And so they did a series of placebo controlled trials of this. And it’s in surgery. It’s surgery. It’s pretty hard to do placebo controlled trials. You’ve got to sort of tell people they’re getting the procedure, you know, put them through the thing. Dress up in in in the gowns and drill a hole in the head and then fill it up. And everybody thinks that nobody knows who’s got the real treatment. 

So it’s pretty high intervention even be in the control group. 

Yes, that is a sham operation. But the but the power of surgery and the medical ritual is such that it turns out to be enormously powerful. And really, when you control these factors and did placebo controlled trials, the results sort of more or less vanished. They evaporated. They didn’t evaporate completely. But basically it didn’t seem like it would work. And a similar thing was done with what we call neurotrophic factors. These are these are sort of the ways of injecting almost brain fertilizer into the brain to to help signature on revive. And that looked pretty good in uncontrolled trials. But in the controlled, placebo controlled Sham Surgery Council, they failed, too. And so I think you you have a a strong placebo effect with Parkinson’s, partly because people want to get better, but also because the brain that other experiments have been done, the brain acts like a compounding pharmacy. The brain actually can manufacture dopamine itself. And if you expected to manufacture dopamine, maybe it will. And so it’s quite extraordinary. So we have these are very hard things to prove. 

Is the idea that the placebo effect itself is somehow mediated by dopamine, so by triggering a placebo effect, you’re doing what you would want a Parkinson’s treatment to do? 

Well, yes. I mean, at least one or two of the early experiments when when people were given feline’s solution but told they were getting dopa their brains generated Alvo dopamine. Right. So, I mean, that doesn’t mean I had to come from somewhere. So it was an endogenously generated inside the body. And we know that, we know the brain can generate opiates. It has the capacity to do this because it’s like it works like a pharmacy. So all these things are very complicated. And the thing about surgical placebo effect is they can they can be quite persistent. They can last for months, even years. And so these are these are complications which have to be dealt with. And it is really amazing when you look at how how how hard biomedical research is and how disappointing it must have been for some of the people who spent literally decades working on some of these things to admit that this wasn’t the way to go. 

Was the placebo effect big enough that it was making a meaningful clinical difference in people’s lives anyway? 

Oh, yes, it was. It was. It was doing. It was doing it at least as much as although it was it was making a 50 percent improvement in in the people who it affected. It was making a 50 percent improvement in their condition. So that that was at least as big as the effect of taking L dopa. So it was it was it was clinically pretty significant, pretty robust and held up. And so. So it’s chemically real. Right. I mean, you shouldn’t think of the placebo effect as being hocus pocus. I mean, it’s real. It’s real chemical action going on in the brain. It just complicates medical research. But medical research is done trying to find out. They wanted to know whether the neuro grafting working. You know, the you can you can only leverage the natural placebo effect to a certain extent. I mean, you find, for example, that people perform better when they go into a neurologist office than they do outside and they give a better performance. And very often the spouses of Parkinson’s patients say, why don’t you want as well when when you’re at home? Right. And so that’s all to do with expectation and then the therapeutic ritual and all kinds of things like that, which you should think of as affecting our brains, our brains are responding. So there is something chemically real going on which is interesting. 

Do you think that Parkinsonian patients are more responsive to placebos than patients with other conditions? 

No, no. I just think Devant means one of the one of the things which which when they have evidence, are generated. I mean, pain opiates is another huge area where you can tell you can get people say nine solutions and tell them they’re getting morphine and they’re pain will. We’ll go away and it will turn out that they’re generating internally endorphins, natural painkillers. 

If someone is susceptible to one kind of placebo effect, I mean, either placebo super responders, if somebody responds to sailin opiates, are they then a better candidate for some other kind of placebo like sham neurosurgery? 

Yeah, yeah. Yeah, that’s right. Some people there aren’t there seem to be what are called placebo responders, people, you know, maybe 20 percent of the population that is especially responsive to possible effects. Yeah, absolutely. 

Did they find that the people who did best with a neurosurgeon for Parkinson’s, the grafts that they do tests to find out whether they were placebo responsive? 

Generally, there’s been some work on that. They didn’t do much at the time. That’s one of the experts on this is called John Stossel, who works in Vancouver. And there is some evidence that it was a subgroup of responders who who had the best effect. It’s pretty difficult to turn that into a viable clinical strategy, though. I mean, of seeking out these responders. And I think it’s kind of hard to base a robust method of treatment on deception. I mean, I I think these are all challenges which the medical profession has to deal with. 

But it seems like it’s not deceptive if you can show that there’s some empirical benefit to doing this. But in general. But you wouldn’t ordinarily do it because the risks don’t out. The benefits don’t outweigh the risks. But if you know somebody is a placebo super responder, maybe you can be confident that the benefits will outweigh the risks. 

Yeah, that’s right. But deceptions involved and there are issues about what you tell people. Right. So if the effect depends on me, me telling you I’m giving you leave a doper and I’m lying to you. Then in some in some areas that may be considered a problem, a bit of a knotty, philosophical, ethical problem. 

Can you talk about how Eldo Bo was discovered and refined as the leading medication for Parkinson’s disease? 

Right. Well, I mean, in the 50s it was the evidence began to emerge that a shortage of dopamine cells in the brains of people with Parkinson’s seemed to indicate seem to to go with the disease. And this led to the idea that you had to you might benefit a patient by replacing the dopamine. The dopamine can’t pass into the brain, come pass through the blood brain barrier by itself. So you needed to have a precursor, which was called L Dopa, which slipped into the brain and then converted into dopamine. And it was it was very, very hard to make work initially. I mean, there were some claims in 1960 that it worked, but people didn’t believe it. And then there was a double blind trial in 1966, which categorically didn’t find any benefit. And it turned out that you had to you had to use very large doses and that you had to combine it with a substance called carbide dopa, which stopped it being broken down in the body because a lot of it never made it to the brain. It’s just it’s going to survive long enough. And they didn’t get the sort of the formula and the dosing rate until about 1968. If you look at some pictures of some some films and videos from that period, it’s quite astonishing. You have people who are extremely disabled. Because in those days, somebody with a Parkinson’s diagnosis died within six or seven years and then a few weeks after taking on doper than walking around. And they look completely normal. And it was it was considered so miraculous. Many people thought that this was going to be a cure. But, of course, within within a relatively short space of time, it turned out that the old dopa produced motor complications, that after after a while, the activity of the osoba would cut off suddenly or would lead to uncontrolled movements called dyskinesia, which were disabling, too. And so there are still today, as is the single biggest breakthrough in Parkinson’s, and it makes the most difference to people’s lives because with it, people can live 20, 25 years. But it’s a fountain bargain. They still have a fairly poor understanding of actually how it works. It certainly does work, but it but it doesn’t work perfectly. And they haven’t found over the years better ways to deliver it more continuously. You take out Dalmau, right? Yes, of course. Yeah. 

Well, what does it feel like when you take it? Is there a rush to it? 

No, I don’t get much of it. Only some people they can tell when it kicks in. Like, I guess like a drug addict, you know, it comes in. But I don’t. I don’t register it personally. All I know is that I take a schedule. And if I do that, I don’t I don’t get it. Bad tremor. But I don’t I don’t I don’t have much rigidity, so I don’t tend to freeze up. So. So it’s it’s more complicated for me to know what exactly it’s doing. I try to control the amount. I don’t want to take more than I need to because I don’t I don’t want to sort of encourage the dyskinesia. So I take between three and four tablets a day. And if I if I was to stop taking it after about a week, you’d notice I’d get worse, I’d get more rigid and my face would lose expression and so forth. But on a day to day basis, it’s really like a maintenance thing. It just just keeps me at the same level. 

Some of the other patients you interviewed for the book were taking dopamine agonist cause strange side effects. Can you talk a little bit about how those drugs produce compulsions and the people that take them? 

Yes. That’s fascinating. So there is a class of drugs called dopamine agonists, and these don’t work anything like as well as how holdover, but they’re often given to people to start with because they they might sort of delay the dyskinesia. And one of the most astonishing things to see is if they do, they do lead in maybe 10 percent or 15 percent of people to these compulsions. And these I didn’t I really didn’t believe this when I first heard it. But it seems that it’s definitely true. Some people become gambling addicts and gamble away the family fortune. Some people become sex addicts. It’s quite astonishing. And I I’ve talked to people who suffered these compulsions. And even when they’ve known about the literature which which mentioned it, they didn’t think it was affecting them. It’s a pretty fascinating kind of area. 

And they would stop the drug and they would suddenly stop when they did when they when they stopped the drug. 

The compulsion tends to go away right away, immediately. 

Do you know of any people that have just decided that they’d rather take the drug and manage the compulsion? 

Well, I think I think these are pretty bad compulsions. I think managing the cases I’ve seen, they literally became gambling at his state. They they spent the family’s money, you know. 

But I was thinking about the sex addicts who might be just like, well, I always wanted an open marriage. Any of those people just decided that they were going to have a different sexual lifestyle as a result. 

Right. There are cases of people who suddenly make unwanted advances to their subordinates at work and that kind of. 

OK, so these are these are like non consensual sex acting out. This isn’t just people who are having more consensual sex. 

Yeah. I mean, this is people who have lost their normal boundaries. Right. I mean, that the compulsion forces them to do something which is either anti-social or very, very much against their own interests. 

So pretty much if somebody gets that, they have to stop taking the drug. 

Yeah, absolutely. And that’s usually what happens. 

And then they usually move on to Al Dopa sooner than they would have preferred. 

Yeah, they then don’t go back. I mean, it’s quite an alarming finding, really. 

Yeah. And it’s interesting that people have so little insight, even when they’re aware that their drug could cause them to have strange behaviors like that. 

Yeah, I mean, I think most people don’t think it can happen to them. I mean, you know, if I took dopamine agonists for a short time, maybe six months to a year, I didn’t notice anything. And I, I would have probably said it’s impossible. I’m not a compulsive personality, but that’s exactly what everybody else says. The ones who get the compulsion to write, it’s a real phenomenon. 

The people who are compulsive probably just refuse to try the drug in the first place. They know that. 

Yeah. So it is it is real and it doesn’t it is maybe affects 10 percent of people. 

That’s all the time we have. Thank you so much for coming on the show. This has been a fascinating discussion. Okay. Back to talking. Indeed. Take care. 

Lindsay Beyerstein

Lindsay Beyerstein

Lindsay Beyerstein is an award-winning investigative journalist and In These Times staff writer who writes the blog Duly Noted. Her stories have appeared in Newsweek, Salon, Slate, The NationMs. Magazine, and other publications. Her photographs have been published in the Wall Street Journal and the New York Times’ City Room. She also blogs at The Hillman Blog (, a publication of the Sidney Hillman Foundation, a non-profit that honors journalism in the public interest.