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Sometime around 1907, well before the modern randomized clinical trial was routine, American psychiatrist Henry Cotton began removing decaying teeth from his patients in hopes of curing their mental disorders. If that didn’t work he moved on to more invasive excisions: tonsils, testicles, ovaries and, in some cases, colons.

Cotton was the newly appointed director of the New Jersey State Hospital for the Insane and was acting on a theory proposed by influential Johns Hopkins psychiatrist Adolph Meyer, under whom Cotton had studied, that psychiatric illness is the result of chronic infection. Meyer’s idea was based on observations that patients with high fevers sometimes experience delusions and hallucinations.

Cotton ran with the idea, scalpel in hand.

In 1921 he published a well-received book on the theory called The Defective Delinquent and Insane: the Relation of Focal Infections to Their Causation, Treatment and Prevention. A few years later The New York Times wrote, “eminent physicians and surgeons testified that the New Jersey State Hospital for the Insane was the most progressive institution in the world for the care of the insane, and that the newer method of treating the insane by the removal of focal infection placed the institution in a unique position with respect to hospitals for the mentally ill.” Eventually Cotton opened a hugely successful private practice, catering to the infected molars of Trenton, N.J., high society.

Following his death in 1933, interest in Cotton’s cures waned. His mortality rates hovered at a troubling 45 percent, and in all likelihood his treatments didn’t work. But though his rogue surgeries were dreadfully misguided and disfiguring, a growing body of research suggests that there might be something to his belief that infection – and with it inflammation – is involved in some forms of mental illness.

Symptoms Of Mental And Physical Illness Can Overlap

Late last year Turhan Canli, an associate professor of psychology and radiology at Stony Brook University, published a paper in the journal Biology of Mood and Anxiety Disorders asserting that depression should be thought of as an infectious disease. “Depressed patients act physically sick,” says Canli. “They’re tired, they lose their appetite, they don’t want to get out of bed.” He notes that while Western medicine practitioners tend to focus on the psychological symptoms of depression, in many non-Western cultures patients who would qualify for a depression diagnosis report primarily physical symptoms, in part because of the stigmatization of mental illness.

“The idea that depression is caused simply by changes in serotonin is not panning out. We need to think about other possible causes and treatments for psychiatric disorders,” says Canli.

His assertion that depression results from infection might seem far-fetched, or at least premature, but there are some data to bolster his claim.

Harkening back to Adolph Meyer’s early 20th century theory, Canli notes how certain infections of the brain – perhaps most notably Toxoplasma gondii — can result in emotional disturbances that mimic psychiatric conditions. He also notes that numerous pathogens have been associated with mental illnesses, including Borna disease virus, Epstein-Barr and certain strains of herpes, including varicella zoster, the virus that causes chickenpox and shingles.

A Danish study published in JAMA Psychiatry in 2013 looked at the medical records of over three million people and found that any history of hospitalization for infection was associated with a 62 percent increased risk of later developing a mood disorder, including depression and bipolar disorder.

Canli believes that pathogens acting directly on the brain may result in psychiatric symptoms; but also that autoimmune activity — or the body’s immune system attacking itself — triggered by infection may also contribute. The Danish study also reported that a past history of an autoimmune disorder increases the risk of a future mood disorder by 45 percent.

Antibodies Provide A Clue

The idea there could be a relationship between the immune system and brain disease isn’t new. Autoantibodies were reported in schizophrenia patients in the 1930s. Subsequent work has detected antibodies to various neurotransmitter receptors in the brains of psychiatric patients, while a number of brain disorders, including multiple sclerosis, are known to involve abnormal immune system activity. Researchers at the University of Virginia recently identified a previously undiscovered network of vessels directly connecting the brain with the immune system; the authors concluded that an interplay between the two could significantly contribute to certain neurologic and psychiatric conditions.

Both infection and autoimmune activity result in inflammation, our body’s response to harmful stimuli, which in part involves a surge in immune system activity. And it’s thought by many in the psychiatric research community that inflammation is somehow involved in depression and perhaps other mental illnesses.

Multiple studies have linked depression with elevated markers of inflammation, including two analyses from 2010 and 2012 that collectively reviewed data from 53 studies, as well as several post-mortem studies. A large body of related research confirms that autoimmune and inflammatory activity in the brain is linked with psychiatric symptoms.

Still, for the most part the research so far finds associations but doesn’t prove cause and effect between inflammation and mental health issues. The apparent links could be a matter of chance or there might be some another factor that hasn’t been identified.

Dr. Roger McIntyre, a professor of psychiatry and pharmacology at the University of Toronto, tells Shots that he believes an upset in the “immune-inflammatory system” is at the core of mental illness and that psychiatric disorders might be an unfortunate cost of our powerful immune defenses. “Throughout evolution our enemy up until vaccines and antibiotics were developed was infection,” he says, “Our immune system evolved to fight infections so we could survive and pass our genes to the next generation. However our immune-inflammatory system doesn’t distinguish between what’s provoking it.” McIntyre explains how stressors of any kind – physical or sexual abuse, sleep deprivation, grief – can activate our immune alarms. “For reasons other than fighting infection our immune-inflammatory response can stay activated for weeks, months or years and result in collateral damage,” he says.

Unlike Canli, McIntyre implicates inflammation in general, not exclusively inflammation caused by infection or direct effects of infection itself, as a major contributor to mental maladies. “It’s unlikely that most people with a mental illness have it as a result of infection,” he says, “But it would be reasonable to hypothesize that a subpopulation of people with depression or bipolar disorder or schizophrenia ended up that way because an infection activated their immune-inflammatory system.” McIntyre says that infection, particularly in the womb, could work in concert with genetics, psychosocial factors and our diet and microbiome to influence immune and inflammatory activity and, in turn, our risk of psychiatric disease.

Trying Drugs Against Inflammation For Mental Illness

The idea that inflammation – whether stirred up by infection or other factors — contributes to or causes mental illness comes with caveats, at least in terms of potential treatments. Trials testing anti-inflammatory drugs have been overall mixed or underwhelming.

A recent meta-analysis reported that supplementing SSRIs like Prozac with regular low-dose aspirin use is associated with a reduced risk of depression and ibuprofen supplementation is linked with lower chances of obtaining psychiatric care. However concomitant treatment with SSRIs and diclofenac or celecoxib – two other anti-inflammatories often used to treat arthritis – was associated with increased risk of needing hospital care due to psychiatric symptoms.

A 2013 study explored the antidepressant potential of Remicade, an drug used in rheumatoid arthritis. Overall, three infusions of the medication were found to be no more effective than a placebo, but patients whose blood had higher levels of an inflammatory marker called C-reactive protein did experience modest benefit.

“The truth of the matter is that there is probably a subset of people who get depressed in response to inflammation,” says lead author Dr. Charles Raison, a psychiatry professor at the University of Arizona. “Maybe their bodies generate more inflammation, or maybe they’re more sensitive to it.”

How infection and other causes of inflammation and overly-aggressive immune activity may contribute to depression and other mental illnesses – and whether or not it’s actually depression driving the inflammation — is still being investigated, and likely will be for some time. But plenty of leading psychiatrists agree that the search for alternative pathologic explanations and treatments for psychiatric disorders is could help jump-start the field.

“I’m not convinced that anti-inflammatory strategies are going to turn out to be the most powerful treatments around,” cautions Raison. “But I think if we really want to understand depression, we definitely have to understand how the immune system talks to the brain. I just don’t think we’ve identified immune-based or anti-inflammatory treatments yet that are going to have big effects in depression.”

But the University of Toronto’s McIntyre has a slightly brighter outlook. “Is depression due to infection, or is it due to something else?” he asks. “The answer is yes and yes. The bottom line is inflammation appears to contribute to depression, and we have interventions to address this.”

McIntyre notes that while the science of psychiatry has a long way to go, and that these interventions haven’t been proved effective, numerous approaches with minimal side effects exist that appear to be generally anti-inflammatory, including exercise, meditation and healthy sleep habits.

He also finds promise in the work of his colleague: “Like most cases in medicine, Charles Raison showed that anti-inflammatory approaches may benefit some people with depression, but not everybody. If you try on your friend’s eyeglasses, chances are they won’t help your vision very much.”

Bret Stetka is a writer based in New York and an editorial director at Medscape. His work has appeared in Wired and Scientific American, and on The Atlantic.com. He graduated from the University of Virginia School of Medicine in 2005. He’s also on Twitter: @BretStetka

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Oviea Akpotaire and Jeffrey Okonye put in long days working with patients at the veterans’ hospital in south Dallas as fourth-year medical students at the University of Texas Southwestern.

They’re in a class of 237 people and they’re two of only five black men in their class.

“I knew the ones above us, below us,” Okonye says. “We all kind of know each other. It’s comforting to see another person that looks like you.”

While more black men graduated from college over the past few decades, the number of black men applying to medical school has dropped. In 1978, 1,410 black men applied to medical school and 542 ended up enrolling. In 2014, both those numbers were down — 1,337 applied and 515 enrolled.

Those figures come from a report from the Association of American Medical Colleges. Every other minority group — including Asians and Hispanics — saw growth in applicants. There was also an uptick in applications by black women.

Enrollment statistics for 2015 are just out and they show a modest gain of 8 percent more black men entering medical school over the year before.

“This is a positive sign,” says Marc Nivet, AAMC’s chief diversity officer, “but it does not change the fact that for 35 years the number has been trending poorly.”

“I was really surprised,” says Akpotaire, who is studying internal medicine. “I sent [the study] to my mom and dad immediately. You would think the conditions would be a lot different than they were in 1978.”

Diversity among doctors is important for patient health. People are more likely to follow doctors’ directions on things like medication or exercise if they can identify with them.

Dr. Dale Okorodudu, a third-year pulmonary and critical care fellow at UT Southwestern, says making cultural connections can make a big difference.

“If you can relate to [patients], it’s a lot easier for them to feel at home and comfortable with you,” he says.

Okorodudu wrote a blog post about an experience at Parkland Hospital that stuck with him. He was walking down the hallway on the 10th floor when a black man stopped him:

“It’s good to see you brother!” I had never met this man, but I knew exactly what he was talking about. With a large smile on his face and a look of pride, he extended his arm to give me a handshake. “There aren’t too many of us doing what you do. I’m glad we got some representation in here.”

For years, Okorodudu has been trying to figure out why so few black men go into medicine. His conclusion: the lack of role models.

“If you’re a black male, let’s say you’re growing up in an inner-city neighborhood,” he says. “There’s so many things directly in front of you that you have the option to go into.”

The options range from music and sports to small business and church, Okorodudu says those professions are visible and present in the lives of young African-American boys. “But when you talk about the medical workforce, none of us are directly there in front of them,” he says.

Okorodudu decided to become a doctor when he was 18. A year from now, when he’s done with his fellowship, he’ll be 32.

Med student Jeffrey Okonye points out that for students like him, who embraced math and science, there are much faster ways to “make it.”

“A lot of friends of mine, black males, are engineers,” Okonye says. “They go to school for four years. They have a job, great pay, even had internships in undergrad I was highly jealous of. Whereas my route, four years undergrad, then another four years of school, and then another X amount of training after that.”

So why did he take the longer route?

“It’s hard to describe the feeling you get when you make someone actually feel better,” Okonye says. “When you can see them go from one state to another and recognize that you were a part of literally changing this person’s life.”

A desire to care for others isn’t the only thing that Okonye, Akpotaire and Okorodudu have in common. All three have had doctors or nurses in their families. And all three are the children of immigrants from Nigeria. Okorodudu says that means the group of black men who are applying to medical school now is very different from the group in 1978.

“In 1978, those people we’re looking at, a lot of them were probably black American males” whose families had been in this country for generations, he says. Today’s black medical school students may be more recent immigrants from Nigeria or the Caribbean, he says. “So if we broke it down that way, that factoid is actually even more alarming.”

The AAMC report suggests how to restock the doctor pipeline. Among the ideas: create more mentoring programs, expand financial aid options, and persuade medical schools to put less emphasis on standardized tests scores like the MCATs.

Okorodudu is trying to help with an online service called DiverseMedicine. Users connect with mentors on chat or video.

Sometimes, he says, the key to getting kids interested is simply seeing a black man in a white coat.

This story is part of a reporting partnership that includes NPR, local member stations and Kaiser Health News.

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In 2010, Rodney Bock was arrested for carrying a loaded gun into a restaurant in Yuba City, Calif., north of Sacramento. Bock had severe mental illness and was later found incompetent to stand trial. He was released on bail, but was rearrested after he failed to appear at a court hearing.

Bock, 56, was placed in the Sutter County jail, awaiting transfer to a state hospital. While there, he began suffering hallucinations. After more than two weeks in jail, Bock hanged himself.

Mentally ill defendants like Bock, who are declared incompetent to stand trial, are supposed to be transferred to state mental hospitals for treatment within two or three months. But more than 300 of them throughout California are languishing in county jails because there’s simply no bed space.

Bock’s daughters are now plaintiffs in a lawsuit filed by the American Civil Liberties Union, charging two state agencies, including the Department of State Hospitals, with denying mentally ill inmates their right to due process — and the treatment they need.

“Jail is simply too dangerous a place for these most vulnerable defendants,” said Micaela Davis, lead attorney in the lawsuit. “We have inmates that are waiting eight, nine months and sometimes over a year before being transferred to a facility for treatment.”

California’s new state budget includes more than $17 million to add beds for defendants declared incompetent to stand trial. But not everyone agrees that’s the best approach.

Stephen Manley is a mental health court judge in Santa Clara County. His court helps defendants struggling with severe mental illnesses, including bipolar disorder or schizophrenia, find alternatives to incarceration.

Manley doesn’t want more psychiatric hospital beds; he wants to reserve state hospitals for the most violent defendants.

“We send far too many people to state hospitals who do not pose a risk to public safety,” he says, “because we don’t work with them to figure out if there isn’t a local alternative.”

Manley believes the psychiatric hospitals are already overcrowded — and understaffed. “As long as we keep overcrowding the hospitals, all we do is feed the fire,” he says, referring to violence within the hospitals.

Last year alone, there were more than 1,800 physical assaults at Napa State Hospital, a psychiatric institution in the heart of Northern California’s wine country. More than 80 percent of the patients there have been referred by the criminal justice system, and hospital officials say patients who are there to have their sanity restored for trial inflict the most serious injuries.

Ryan Navarre, with the organization representing Napa Hospital police, says that even officers are at risk. He recalls one patient specifically who put rocks into his socks and then spun them around “violently,” he says.

Throughout California, state psychiatric hospitals are working to find a balance between treatment and security for patients and staff.

Meanwhile, Manley thinks the best solution for nonviolent offenders is to create more community-based treatment facilities.

“If we add another 500 beds – and people — to a state hospital, all we do is make the problem worse,” he says.

But funding is already inadequate for mental health treatment. And creating more community-based programs raises new challenges — including resistance from neighbors who don’t really want to live near facilities whose clients are mentally ill criminal defendants.

This post was produced by KQED’s State of Health blog.

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A drug that’s already approved for treating leukemia appears to dramatically reduce symptoms in people who have Parkinson’s disease with dementia, or a related condition called Lewy body dementia.

A pilot study of 12 patients given small doses of nilotinib found that movement and mental function improved in all of the 11 people who completed the six-month trial, researchers reported Saturday at the Society for Neuroscience meeting in Chicago.

And for several patients the improvements were dramatic, says Fernando Pagan, an author of the study and director of the Movement Disorders Program at Georgetown University Medical Center. One woman regained the ability to feed herself, one man was able to stop using a walker, and three previously nonverbal patients began speaking again, Pagan says.

“After 25 years in Parkinson’s disease research, this is the most excited I’ve ever been,” Pagan says.

If the drug’s effectiveness is confirmed in larger, placebo-controlled studies, nilotinib could become the first treatment to interrupt a process that kills brain cells in Parkinson’s and other neurodegenerative diseases, including Alzheimer’s.

One of the patients in the pilot study was Alan Hoffman, 74, who lives with his wife, Nancy, in Northern Virginia.

Hoffman was diagnosed with Parkinson’s in 1997. At first, he had trouble moving his arms. Over time, walking became more difficult and his speech became slurred. And by 2007, the disease had begun to affect his thinking.

“I knew I’d dropped off in my ability to read,” Hoffman says. “People would keep giving me books and I’d have read the first chapter of about 10 of them. I had no ability to focus on it.”

“He had more and more difficulty making sense,” Nancy Hoffman says. He also became less active, less able to have conversations, and eventually stopped doing even household chores, she says.

But after a few weeks on nilotinib, Hoffman “improved in every way,” his wife says. “He began loading the dishwasher, loading the clothes in the dryer, things he had not done in a long time.”

Even more surprising, Hoffman’s scores on cognitive tests began to improve. At home, Nancy Hoffman says her husband was making sense again and regained his ability to focus. “He actually read the David McCullough book on the Wright Brothers and started reading the paper from beginning to end,” she says.

The idea of using nilotinib to treat people like Alan Hoffman came from Charbel Moussa, an assistant professor of neurology at Georgetown University and an author of the study.

Moussa knew that in people who have Parkinson’s disease with dementia or a related condition called Lewy body dementia, toxic proteins build up in certain brain cells, eventually killing them. Moussa thought nilotinib might be able to reverse this process.

His reasoning was that nilotinib activates a system in cells that works like a garbage disposal — it clears out unwanted proteins. Also, Moussa had shown that while cancer cells tend to die when exposed to nilotinib, brain cells actually become healthier.

So Moussa had his lab try the drug on brain cells in a Petri dish. “And we found that, surprisingly, with a very little amount of the drug we can clear all these proteins that are supposed to be neurotoxic,” he says.

Next, Moussa had his team give the drug to transgenic mice that were almost completely paralyzed from Parkinson’s disease. The treatment “rescued” the animals, he says, allowing them to move almost as well as healthy mice.

Moussa’s mice got the attention of Pagan from Georgetown’s Movement Disorders Program. “When Dr. Moussa showed them to me,” Pagan says, “it looked like, hey, this is type of drug that we’ve been looking for because it goes to the root of the problem.”

The pilot study was designed to determine whether nilotinib was safe for Parkinson’s patients and to determine how much drug from the capsules they were taking was reaching their brains. “But we also saw efficacy, which is really unheard of in a safety study,” Pagan says.

The study found that levels of toxic proteins in blood and spinal fluid decreased once patients began taking nilotinib. Also, tests showed that the symptoms of Parkinson’s including tremor and “freezing” decreased. And during the study patients were able to use lower doses of Parkinson’s drugs, suggesting that the brain cells that produce dopamine were working better.

But there are some caveats, Pagan says. For one thing, the study was small, not designed to measure effectiveness, and included no patients taking a placebo.

Also, nilotinib is very expensive. The cost of providing it to leukemia patients is thousands of dollars a month.

And finally, Parkinson’s and dementia patients would have to keep taking nilotinib indefinitely or their symptoms would continue to get worse.

Alan Hoffman was okay for about three weeks after the study ended and he stopped taking the drug. Since then, “There’s (been) a pretty big change,” his wife says. “He does have more problems with his speech, and he has more problems with cognition and more problems with mobility.”

The Hoffmans hope to get more nilotinib from the drug’s maker, Novartis, through a special program for people who improve during experiments like this one.

Meanwhile, the Georgetown team plans to try nilotinib in patients with another brain disease that involves toxic proteins: Alzheimer’s.

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Four companies running urgent care centers in New York have agreed to disclose more fully which insurance plans they accept, following an inquiry by the state’s attorney general that found unclear or incomplete information on their websites that could result in larger-than-expected bills for consumers.

The agreements mark the first enforcement action brought under New York’s new law that targets surprise medical bills, seen as one of the broadest in the nation. The law aims to reduce the number of consumers who get such bills when they unknowingly see providers who are not part of their insurance plan networks.

Although many consumers don’t realize it, visits to urgent care clinics can lead to such out-of-network bills.

In July, New York Attorney General Eric T. Schneiderman sent strongly worded letters to about 20 urgent care clinics, asking for more information. Some of their websites, the letters noted, could be improperly listing which health plans they were part of, potentially a deceptive business practice. Similar concerns have been raised by advocates in other states, who note that urgent care centers often say they “work with” or “accept” insurance, but don’t clearly say whether they are part of particular insurers’ networks.

Such statements “may lead consumers to believe that an out-of-network urgent care center is … ‘in network’ with their health plan,” the July 2 letters said.

That’s important because consumers who go to clinics that aren’t part of their plans’ networks might owe the balance between clinic charges and what their insurers pay toward out-of-network visits, sometimes resulting in large bills.

Those bills, also known as balance bills, are part of the complex way that health care is paid for in the U.S. They occur because insurers form networks of doctors, hospitals and other providers who have agreed to negotiated rates, which are generally lower than their usual fees.

Patients who go outside the network for care — because they want to, don’t know or are seen by an out-of-network provider while at an in-network facility — are subject to balance billing.

Although such bills have long led to consumer complaints, relatively few states have addressed balance billing except for emergency room care.

After reviewing the responses to its July letters, the attorney general’s office determined the information from the four companies, which have more than a half-dozen facilities altogether, was unclear, incomplete or not specific enough.

Under the agreement announced Friday, those owners will specifically list all the health plans they contract with as in-network providers and stop using the terms “works with” or “accepts.” They must also clearly explain that if they are out of network, the consumer could incur higher charges.

New York’s law covering surprise bills law went into effect in March, imposing new requirements on hospitals, doctors and other medical providers. Among other things, the law requires that most health groups and facilities disclose in writing or on their websites the names of the health plans with whom they participate.

The urgent centers that signed agreements are: 181st Street Urgent Care in Manhattan; Brookdale Urgent Care, affiliated with Brookdale Hospital; New York Doctor’s Urgent Care with two locations in Manhattan; and Cure Urgent Care, with three locations in Manhattan and Long Island.

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