Scientists are supposed to be  the most objective among us.

It’s one of the reasons academic publications  are usually written in third person. Using “I” or “we” might suggest that people were   involved and brought their  own biases into the study.

But scientists are, in fact, people. And, despite how hard they work to reduce  the influence of their own perspectives,   their lives shape their research. Sometimes they become scientists  because of those experiences.

For example, trauma could open their  eyes to a neglected area of research. Or an unexpected diagnosis might inspire them to   look into a rare disease that  no one else is going to study. As it turns out, science isn’t as impartial as   some people like to think  …and that’s a good thing.

Just ask these five scientists who are  finding treatments for their own diagnoses. [♪ INTRO] In 2010, David Fajgenbaum was  training to be a medical doctor. He was looking forward to a life of  helping other people when they got sick. …Until his own health went downhill fast. He had overwhelming fatigue and enlarged lymph  nodes that told him something was very wrong.

As it turned out, his organs were failing. Suddenly, he needed to use his  medical training to save himself. In the prime of his life, he  found himself in the hospital   literally on the brink of death at  least four times in three years.

Nobody knew what was causing his body to fail. But eventually, he got his  diagnosis: Castleman Disease. It’s a rare immune disease  that attacks your organs.

But his version was even rarer. Fajgenbaum was diagnosed with idiopathic  multicentric Castleman Disease:   a very specific problem that is very  dangerous for very few people in the world. The leading experts on that disease  at the time were studying in Arkansas,   so he booked a trip there. …And none of them knew how  his particular subtype worked.

Which meant he had to figure it out himself. Since any good investigation needs data, he  started by gathering blood samples to analyze. Specifically, he gathered his own  blood samples that had been taken   during those years in and out of the  hospital, and he started running tests.

The results pointed to a specific enzyme  that’s supposed to help you make proteins,   grow cells, and regulate your metabolism. It’s called mTOR, and it was in overdrive. This was a huge discovery, because once he knew  that mTOR was overwhelming his blood samples,   Fajgenbaum could look for ways to  bring it back down to healthy levels.

Like by taking a drug that already exists! Sirolimus, also called rapamycin, is an  mTOR inhibitor used to prevent people’s   bodies from rejecting new organ  transplants, among other things. Considering how long it takes to create  a new drug and get that into production,   Fajgenbaum’s chances for a  long, healthy life would be   increased dramatically if this drug  got his Castleman Disease in check.

So he convinced his primary care physician to try   using sirolimus for a purpose  that it was not developed for. And it worked! More than a decade later, he’s still in remission.

After that success, he wanted to do what he  could for other people in the same situation. That’s when he opened his own research  lab focused on Castleman Disease. In 2020, his lab published an analysis  of the lymph nodes of people with the   idiopathic multicentric version of the disease.

They found that they also  had more mTOR than usual. So he’s not a unique case. At the time we’re filming this video, a phase  II clinical trial is being conducted to see   if mTOR drugs can effectively treat  more people with Castleman Disease.

And Fajgenbaum’s research reveals similar trends   for patients with diagnoses that have  a lot in common with Castleman Disease. Fajgenbaum might have started out trying to  save his own life, but he ended up founding   multiple non-profits to find other already  approved drugs that may treat rare diseases. In the last few years, they’ve advanced 14 drugs   to be repurposed as treatments  for diseases like Castleman.

Today, thousands of lives have been  saved, including his own, from this work. And the stakes are just as high  for the next scientist on our list. Chris Nowinski was just a normal guy following the  same old boring career path that most of us do.

He played football at Harvard, graduated  to be a professional WWE wrestler,   became a published author,  and finally a neuroscientist. See, during his time with WWE,  he got kicked in the chin hard   enough to give him a concussion  and end his wrestling career. He had temporary amnesia after  impact, then would get throbbing   headaches whenever his heart rate went up,  and eventually developed a sleep condition.

That kind of injury can change an athlete’s life. For Nowinski, it inspired him to  dedicate himself to head trauma. First, he spread the word in a book  about football players with concussions,   which he knew about from  his time playing football.

Then he got a PhD in behavioral  neuroscience from Boston University. He wanted to study the brains of  athletes who had experienced head trauma. But brains are hard to come by.

And the process of acquiring them was intense. He individually called medical examiners  and the families of each deceased head   trauma victim that he wanted to study  and he asked for their permission. To give you an idea of how hard that was,  on top of the emotional toll it took, he was   met by medical examiners that didn’t believe  what he was investigating was a real disease.

These days, we know it as chronic  traumatic encephalopathy, or CTE. But back then, it wasn’t  nearly as well understood. We didn’t know all of CTE’s wide ranging symptoms,   from less control over your impulses,  to depression, to progressive dementia.

And we definitely didn’t know how  multiple sub-concussive hits can   have similar effects to those big  hits that immediately throw you off. After all, you can often move on from them  relatively quickly and think you’re fine. And the effects might not appear for decades, so  they don’t always get attributed to the impact.

But with the help of the concussion  and CTE foundation, brain bank,   and brain donation registry that Nowinski started,   researchers got a lot more data and we’re  learning how common this problem is. After those initiatives, many athletes  publicly pledged their brains to research. So Nowinski no longer had  to gather them one by one.

And he could contribute to a 2024  study that analyzed hundreds of them. That study found some serious  effects of traumatic brain injury. Basically, these brains were  thinner with fewer brain cells.

And it got worse the longer brain  donors had played contact sports. In this dataset, CTE donor brains were wasted away  in critical areas, like where you store memories. It’s the kind of brain thinning seen in dementia.

And a protein that’s often less  present among dementia patients   was showing the same trend in these CTE brains. So CTE is seriously damaging people’s brains. But we’re moving in the right direction.

In addition to his research, the publicity that   Nowinski stirred up around CTE has led  to changes in the rules of some sports. Like, heads are much more off limits in  American football than they used to be. There’s still a lot that needs to happen  if we want to seriously reduce head trauma.

But the first step was  getting it on people’s radar. Medical research certainly  wasn’t on Sonia Vallabh’s radar. She went to law school.

Ask any lawyer, you don’t do that for fun. You do it because then you get to work in  a field at least a little related to law. Like, more related than running  a biomedical research lab.

But sometimes life takes you in  directions you never expected. For Vallabh, this drastic career  change started when her mom fell ill. She lost weight, her vision, and her memory.

And at age 51, Vallabh’s mother was dead. Without many clues, the whole thing was a mystery. So the family opted for an autopsy.

And the results would change their lives forever. Sonia Vallabh’s mother had  died of a prion disease. These occur when a misfolded protein in the  brain causes other proteins to malfunction,   spreading through your brain  and killing your neurons.

These diseases ramp up in a matter  of months, degrade your brain,   and without a doubt will kill you. They might even kill your whole family. See, Vallabh’s prion disease was genetic. 1 in 50,000 people has this single letter DNA  mutation in their prion protein gene, PRNP.

And they can pass it down to their children. Meaning Sonia Vallabh had a 50% chance  of inheriting it from her mother. And one test later, she learned  that she had the mutation too.

Vallabh knew that there was no cure. Meaning this prion disease would  kill her if nothing changed. So she rolled her sleeves up and got to work.

She and her husband left their careers,  earned PhDs in biomedical science,   and opened their own lab devoted  to studying prion diseases. The rogue prion protein they study is called PrP. It’s the one that misfolds and causes the  deadly effects I talked about earlier.

Usually, PrP helps your nerves send signals  by maintaining their myelin coating. But when it changes shape, it  becomes a prion and causes disease. PrP is necessary for prion disease.

But we know that mice can live  a healthy life without PrP. So in Vallabh’s lab,   they’re working on a treatment that  would reduce PrP before it goes rogue. That way, you have less fuel  around when the fire breaks out.

As a person who knows she has the genetic mutation  but hasn’t entered disease progression yet,   Vallabh thinks about the problem  differently from other researchers. She’s not waiting until  symptoms start to treat them. She’s looking for more preventative options  that keep disease from starting at all.

And her search is paying off. She has demonstrated that this approach  can work against prion diseases in mice. You don’t even have to 100% eradicate  PrP to get an effective prophylactic.

Just reducing it by 21% helped  prion-infected mice live longer. And it only took one week of  treatment to cut PrP RNA in half. So that goal seems very attainable.

Plus, the mice that had started  showing symptoms benefited, too. After a single treatment, mice  lived longer than their untreated   peers and reversed some of their weight loss. Some mice even reversed signs of brain damage!

It’s definitely not a cure yet. But this treatment idea seems to  improve longevity and quality of life. For a terminal diagnosis, early  intervention options that delay   the start of the disease and give  you back some of your life are huge.

For now, the data comes from mice. But there are several clinical  trials currently underway,   which Vallabh and her husband  built the infrastructure for. And Vallabh is optimistic that this will be a real   treatment option for people like  herself within the next few years.

In these situations, many doctors find genetic  testing hopeless because there’s no cure. But Vallabh encourages people  to seek genetic testing and   join trials to make progress toward treatment. From her perspective, knowledge is  empowering and might even change her fate.

Before we introduce the next incredible  scientist working on their own diagnosis,   it’s time for a quick ad break. Thanks to 80,000 Hours for  supporting this SciShow video! As a nonprofit, their only aim is to help  you find a fulfilling, high-impact career.

And we at SciShow love a nonprofit. …80,000 Hours is too. They've just released a new edition  of their career guide — 80,000

Hours:   How to Have a Fulfilling Career That Does Good. It explains how to plan a  meaningful career in an age of AI. With tools like that and a job board with  hundreds of handpicked roles updated daily,   80,000 Hours can help you work toward  solving our most pressing problems. On average, you’ll spend  80,000 hours in your career.

So here’s how you can try to spend that time well: Go to 80000hours.org/scishow, or  click in the description or pinned   comment to pre-order your copy  of their updated career guide. Learn what makes a high-impact career,  get new ideas for impactful paths,   make a new plan based on what you've  learned, and put it into action. Julio Saez-Rodriguez was a scientist  long before he became a patient.

He spent his life researching  the molecular basis of disease. But when he was diagnosed with a terrible one  himself, he had never even heard of the condition. This was even more surprising once  he started looking into the disease.

It’s the reason for a third of  all adult kidney transplants! It affects a lot of people! And without treatment, it can be deadly.

It’s called IgAN. IgA stands for immunoglobulin A, the  main antibody in your gooey bits:   saliva, tears, that kind of stuff. So it’s normally a good thing to have around.

But when it gets into your kidneys,  it can spark chronic inflammation,   eventually leading to end-stage  kidney disease, AKA nephropathy. That’s the N in IgAN. When Saez-Rodriguez was  diagnosed more than a decade ago,   he didn’t have many options to treat his IgAN.

But, considering his background in  bioinformatics, he had the tools to look into it. It just didn’t occur to him to study  something like IgAN until that point   because his own research was  just following the field. That meant pretty much ignoring kidney problems   because that’s not where the money  is, despite it being a major killer.

But his new perspective as a patient changed that. He realized that IgAN is actually a great  candidate for investigation through the   big data approaches that he specializes in. For example, Saez-Rodriguez created  a new tool to make sense of giant   data sets holding information about your genes.

The idea was to use different sources of things we  know, like how proteins interact with each other,   to see where those different sources  overlap and result in disease. Through this analysis, Saez-Rodriguez  and his team were able to identify 20   molecules in the body that play a role in IgAN. And when we know those molecules are  involved, we can do something about them.

There are drugs that already  exist that act on those molecules. But those drugs haven’t been applied to IgAN  yet, so the solution might be out there already! It’s like what Fajgenbaum is doing  to find drugs that could be used in   new ways instead of making new ones from scratch.

With 20 target molecules, there’s potential for   a variety of drugs to help people who  have different experiences with IgAN. And becoming a patient taught Saez-Rodriguez   that you need more information to  know which drug you should take. Before his diagnosis, he used to describe  disease in broad terms at the population level.

But now he wants to get down  to the detail of a single   individual and where they fit into the data. That’s what led him to create the IgAN atlas,   which uses big data sets to  find more targeted treatments. Researchers can compare multiple organs from  multiple patients across their tissues, genes,   proteins, microbes, and any other relevant  players to get the full picture of disease.

By compiling huge sets of molecular data,  the atlas has helped identify key cells   that scar the kidneys, map the distribution of  different immune cells in the kidneys, and even   find a gene that could be at the root of the weird  inflammation that’s so problematic in IgAN cases. And those are just a few examples of the  ways big data is tackling this disease. Overall, the atlas has compiled 24 clinical  trials that are being conducted right now.

And Saez-Rodriguez put his money where his  mouth is, because he’s enrolled in one of them. Sometimes, the career you built before being  diagnosed can help you work toward treatments. Other times, it’s the reason you  need a treatment in the first place.

Susan Michaelis was a pilot. Not what you probably imagined when I first   described scientists who  study their own conditions. But it’s what set her on her research journey.

In 1997, after three years as a commercial  pilot, Michaelis landed her plane and collapsed. No one had any explanation  for what happened to her,   but some other people in the industry  seemed to be experiencing similar things. So she set off to study what was going on.

Her PhD investigated the flight safety and health   implications of exposure to  contaminated air in aircraft. Yep, through her studies she  figured out what happened to her. It’s called aerotoxic syndrome.

Michaelis learned that toxic fumes occasionally  leak into plane cabins from their jet engines. …Even on new planes. This has affected more than 100 flight  attendants and pilots over the last 20 years. And the reports are only growing.

Now, I don’t know if this will  make you feel better or worse,   but it’s much more frequently reported  in pilots and crew than in passengers. So technically anyone who flies could  be at risk, but the risk varies. That risk comes from something called bleed air.

Basically, all airplane air goes  through the engine, by design. Unless you’re on the Boeing 787. That’s the only plane that doesn’t  send air through the engine.

Usually bleed air is filtered. But oil and hydraulic fluid can seep into really  hot places like a plane’s engine and power units. Then that stuff can vaporize and release  dangerous stuff like carbon monoxide,   organophosphates, and formaldehyde  into your breathing air.

Since planes are literally designed in  a way that could introduce this risk,   they have seals to minimize that leakage. But they don’t completely prevent it. So normal operation will  produce some contamination   in the air that you breathe on a plane.

Most of it comes from times when  the plane uses a lot of power or   changes pressure, like during taxi or take off. It isn’t the kind of thing you usually see,  and you become acclimated to the smell quickly. So it’s easy to miss.

But for some people like  Michaelis, it’s really toxic. Different people have different genetic  susceptibility to the compounds in these fumes,   which is probably why not everyone suffers the  most extreme version of aerotoxic syndrome. Some people don’t report any effects at all.

But for those who do feel symptoms,   they can range from short term dizziness and  fatigue to chronic lung and heart damage. And sometimes, the consequences can be far worse. Michaelis’s doctors believe that toxic  fumes in bleed air caused her breast cancer.

After all, there are contaminants in the  fumes that are suspected to be carcinogenic. And aircrew have higher rates  of cancer than the rest of us. What’s worse, Michaelis’s breast  cancer was a kind known as lobular.

It’s different from the more common ductal  breast cancer because it doesn’t form a lump,   so regular screening may report cancer-free status  when there’s actually a serious problem growing. And last year, lobular breast  cancer took Michaelis’s life. But not before she brought attention to  aerotoxic syndrome and lobular breast   cancer through academic publications  and campaigns geared toward the public.

Thanks in large part to her work,  the airline industry is working on   several innovations to prevent  this from happening to others. Bleed-free engine designs and air quality  sensors are the future of plane technology. Ultimately, these scientists may  have entered into their area of   research because they wanted to understand  their own conditions and find treatments.

But their work helps everyone  affected by those illnesses. Whether it’s a rare disease or one that just  doesn’t have much money behind it, lots of   challenges are being tackled by people who have a  personal interest in spearheading those efforts. And they are literally saving lives.

So it’s a good thing they  got interested in themselves. [♪ OUTRO]