Mental Health

There’s a fascinating take on schizophrenia in the Wilson Quarterly that upends the strictly genetic model. New thinking on severe mental illness contends it’s much more complex and the simple biomedical approach is a road that’s reached a dead end. Thankfully, earlier and more damaging theories have been thrust aside. For instance, the psychoanalytical theory that blamed the schizophrenogenic mother for her child’s mental illness, which left a lot of collateral damage in its wake, is now viewed as garbage. New thinking emerged in the 1990s that concluded it’s all in the genes. But researchers are finding it’s not that simple. The trauma that happens to an individual has a large impact on on the strength of the mind and its vulnerabilities. Mental health and mental illness are a combination of not only mind and body but social experience.

As author Tanya Marie Luhrmann, PhD, explains:

In his Second Discourse (1754), Jean Jacques Rousseau describes human beings as made up out of each other through their interactions, their shared language, their intense responsiveness. “The social man, always outside of himself, knows only how to live in the opinions of others; and it is, so to speak, from their judgment alone that he draws the sentiment of his own existence.” We are deeply social creatures. Our bodies constrain us, but our social interactions make us who we are. The new more socially complex approach to human suffering simply takes that fact seriously again.

The epidemiological data in the article on migrants is eye-opening:

Epidemiologists have now homed in on a series of factors that increase the risk of developing schizophrenia, including being migrant, being male, living in an urban environment, and being born poor. One of the more disconcerting findings is that if you have dark skin, your risk of falling victim to schizophrenia increases as your neighborhood whitens.

After reading this article, it feels as though we’re finally on to something big — fresh thinking, new treatments and hope:

All this—the disenchantment with the new-generation antipsychotics, the failure to find a clear genetic cause, the discovery of social causation in schizophrenia, the increasing dismay at the comparatively poor outcomes from treatment in our own health care system—has produced a backlash against the simple biomedical approach. Increasingly, treatment for schizophrenia presumes that something social is involved in its cause and ought to be involved in its cure.

In recognition of Prostate Cancer Awareness Month, Eila Skinner, MD, chair of the urology department at Stanford, took questions via the @SUMedicine Twitter feed and Scope on prostate cancer and the research advancements in the screening, diagnosis and treatment of the disease. Below she responds to a selection of the submissions, which ranged from the controversy over the PSA test to the ways the field of genetics is changing prostate-cancer research.

@Prach82 and @gaisison ask: Why is the PSA test not considered to be reliable? Is the PSA test still advisable as a basic screening tool for prostate cancer? Are there updates on the recommendations?

PSA (prostate specific antigen) is a protein that was originally discovered at Stanford and can be detected in the blood. Men with prostate cancer tend to have higher levels of this protein. There is no question that prostate cancer can be detected earlier using this test combined with a prostate examination compared with an exam alone. It is estimated that the cancer can be detected on an average of 5 to 10 years earlier. It is also clear that cancers detected with PSA screening are more likely to be caught before they spread and at a stage when they are more likely to be cured with current treatments. So why the controversy?

First, men with other common prostate problems, like non-cancerous prostate enlargement (called BPH) can have an elevated PSA. Because of this only about 20-30 percent of men with elevated PSA on screening actually have cancer. They often have to undergo invasive testing like prostate biopsy in order to know that there is no cancer there. These tests are expensive and can sometimes cause side effects like infection. We are always searching for a more accurate test to use for screening, and a number of potential alternatives are being developed. Some are already available, like the urine PCA3 test. This test is still very expensive and has not yet gained widespread use as a screening tool.

Secondly, prostate cancer is usually very slow growing. It might take 10 to 30 years for an early cancer to become one that is life threatening. The risk of cancer goes up with age, so many of the men diagnosed with cancer using PSA testing at age 70 or 80 are never going to live long enough for their cancer to cause problems. Many patients are undergoing treatment today, such as surgery or radiation therapy, for cancers that are not destined to threaten their life.

Finally, we still don’t have proof that if every man got tested, even at age 50 or 60, they would end up living longer than ones who didn’t get tested. Current studies trying to test this have been difficult to complete. They suggest that there may be some benefit, but 40 or more men may have to be treated to save one life. Because the treatment can cause significant side effects, it isn’t clear if this is worth it from a public health perspective.

Still, we shouldn’t give up on the PSA test. We need to be smarter about using the test and learning how to predict how a cancer is going to behave in an individual patient. In other words, use the test to find the cancer, but don’t treat everyone’s cancer the same way. Many cancers can be safely watched, thus avoiding the side effects of treatment. On the other hand, the patient with an aggressive cancer that is picked up earlier might be saved with treatment.

At this point, I’d recommend that you discuss the pros and cons of testing with your doctor.

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This may come as a surprise, but a growing body of scientific evidence suggests that having more power is associated with less stress and anxiety. Take the Whitehall studies of health in the British civil service that found a higher governmental rank was strongly correlated with lower mortality rates. Or, consider the work of Stanford biology professor Robert Sapolsky, PhD, on the influence of social hierarchy on primate health. His measurements of the stress hormone cortisol in baboons showed lower levels of the hormone in high-ranking troop members.

Now new research from Stanford psychologist James Gross, PhD, and a Harvard team offers more evidence that higher rank is associated with less anxiety and lower levels of cortisol. In the study, which was published today in the Proceedings of the National Academy of Sciences, researchers examined both cortisol measurements and self-reported anxiety levels within a group of high-ranking government and military officials who were enrolled in a Harvard executive leadership program. Study results showed the high-ranking leaders were less stressed according to both measures.

A Stanford news release explains how researchers teased out specifics from the findings to better understand the relationship between leadership roles and stress level:

The critical element seems to be a sense of control. The connection between power and tranquility was dependent on the total number of subordinates a leader had and on the degree of authority or autonomy a job conferred.

It’s possible, in other words, that the feeling of being in charge of one’s own life more than makes up for the greater amount of responsibility that accompanies higher rungs on the social ladder.

The present study is correlational, meaning it is unable to say whether leadership leads to low stress levels, or whether people who are predisposed to feel little stress are more likely to be leaders. But [researchers] view the study as an initial look at a topic that has relevance to anyone who lives in our inherently hierarchical modern society.

“By looking at real leaders, people who really have a lot of real-world responsibility, we can learn a lot about stress and health in general,” Gross said.

Previously: Anxiety shown to be important risk factor for workplace absence, Stanford health psychologist Kelly McGonigal discusses how stress shapes us and How work stress affects wellness, health-care costs
Photo by Bruce MacRae

Today on the Atlantic health channel, there’s an interesting post examining why a specialist-based system for psychiatric care is ineffective in India and how local mental-health advocates’ are working to forge a new model for delivering mental health services. Christie Thompson writes:

On paper, the Indian government has taken significant steps toward providing mental health care for its 1.2 billion citizens. The National Mental Health Programme, launched in 1982, mandating that basic psychiatric care be provided in every government-run primary health center. The government provides basic training for all primary health center doctors, and pays for psychiatric medication to be stocked and available to patients.

“At the central level, there seems to be good progress,” says David Nash, CEO of Indian mental health non-profit the Banyan. “At the implementation level, it’s a disaster.” Out of 626 districts across India, 125 have some mental health programming in place, Nash says.

…

The Indian Mental Health Policy Group hopes to redirect the psychiatric focus of the mental health movement toward more holistic healing. In late June, the group released a set of policy proposals for the District Mental Health Program. The Group advised a national “focus on improved quality of life of the client vs. mere symptom reduction… [including] the need for social protection and effective poverty reduction policies.”

“The whole country is moving toward this paradigm shift, where we’re looking at mental health from a well-being, development lens, and less from an illness sort of lens,” [Vandana Gopikumar, a member of the Indian Mental Health Policy Group] says. “As far as possible, have treatment available locally. And treatment doesn’t just mean popping pills.”

Previously: What I did this summer: Stanford medical student helps India nonprofit create community-health maps and Stanford researchers work to curb obesity, hunger in India
Photo by McKay Savage

Today is the last day of our Ask Stanford Med installment focused on prostate health. Questions about prostate cancer and the latest advancements in screening, diagnosing and treating the disease can be submitted to Eila Skinner, MD, chair of the urology department here, until 5 p.m.

Details about the prevalence of prostate cancer and Skinner’s credentials can be found in our earlier post:

Nearly two thirds are diagnosed in men aged 65 or older and one in six men in America will be diagnosed with the disease during his lifetime, according to statistics from the American Cancer Society.

One of the most highly respected urologic surgeons in the nation, Skinner served as the vice chair of the urology department at the University of Southern California prior to being named chair here in February. Her primary research interests are in the area of cancer prevention, bladder cancer and urinary tract reconstruction. As medical director of the “Real Men Cook” Foundation since 2003, she has coordinated education and screening for prostate cancer for more than 1,000 Los Angeles-area African-American and Latino men annually.

Questions can be submitted to Skinner by either sending a tweet that includes the hashtag #AskSUMed or posting your question in the comments section of the previous entry.

Previously: Ask Stanford Med: Urology chair taking questions on prostate cancer and the latest research, Study calls for increased awareness for minorities and gay men following prostate cancer treatment, Making difficult choices about prostate cancer and To screen or not to screen? When it comes to prostate and breast cancers, that’s still the question

In anticipation of the inaugural Stanford Medicine X conference this Sept. 28-30, I’ll be highlighting some of the research being presented during the three-day event.

Among the exciting range of speakers presenting in the research, practice and business tracks is CNN contributor Amanda Enayati. She will be exploring research showing how neurofeedback, biofeedback and virtual therapists may be able to relieve stress and, potentially, treat post-traumatic stress disorders. As she explains in her presentation abstract:

Stress often plays out on the frontiers of medicine, with its reach extending from neuropsychiatric disorders like depression, anxiety and addiction, to chronic and degenerative diseases like heart disease, diabetes and cancer.

We have grown accustomed to media stories about “technostress” the ways in which technology bedevils us. (I myself recently wrote a story about the potentially pernicious effects of social media on young people’s self and body image.) And yet the relationship between technology and stress is far more complex - and hopeful - than many might assume.

While fast-emerging technologies strike some as an indifferent and demanding slavemaster, they also have an equal - and perhaps greater - capacity to serve as savior by blazing innovative paths toward better health and well-being.

For more information on the conference or to register, visit the Medicine X conference website.

More news about the Medicine X conference is available in the Medicine X category.

Previous research has linked the gene monoamine oxidase A (MAOA) with risk taking and aggression. But findings recently published in Progress in Neuro-Psychopharmacology & Biological Psychiatry suggest that this so-called “warrior gene” is associated with higher self-reported happiness in women.

In the study (.pdf), scientists examined data from a population-based sample of 345 men and women who participated in the longitudinal mental health study Children in the Community. The DNA of study participants was also collected and analyzed for MAOA gene variation. Additionally, volunteers’ self-reported happiness was scored by a widely used and validated scale. Researchers’ findings are described in a University of South Florida release:

After controlling for various factors, ranging from age and education to income, the researchers found that women with the low-expression type of MAOA were significantly happier than others. Compared to women with no copies of the low-expression version of the MAOA gene, women with one copy scored higher on the happiness scale and those with two copies increased their score even more.

While a substantial number of men carried a copy of the “happy” version of the MAOA gene, they reported no more happiness than those without it.

So, why the genetic gender gap in feeling good?

The researchers suspect the difference may be explained in part by the hormone testosterone, found in much smaller amounts in women than in men. Chen and his co-authors suggest that testosterone may cancel out the positive effect of MAOA on happiness in men.

Researchers say future studies are needed to better understand which specific genes influence resilience and subjective well-being and how genetics, along with life experiences, shape individuals’ happiness.

Previously: New study links generational language problems to gene mutations, Patients’ genetics may play a role in determining side effects of commonly prescribed painkillers and Common genetic Alzheimer’s risk factor disrupts healthy older women’s brain function, but not men’s
Photo by Drew Mackie

Thank you for sharing your questions about the potential link between mental health disorders and Internet addiction. I hope these answers help increase your understanding of how excessive Internet use may be harmful to one’s health.

@myr00dle asks: Is it true that a leading cause of ADHD is excessive Internet use?

Studies have suggested a link between excessive Internet use and attention deficit and hyperactivity disorder. For example, a 2004 South Korean study of 535 elementary students found that 33 percent of those with attention deficit disorder were “addicted” to the Internet. Similarly, a 2008 Taiwanese study of 216 college students reported that 32 percent of “Internet addicts” had attention deficit disorder compared with only 8 percent of non-addicts. However, while such studies show a strong correlation, they do not establish cause-and-effect. It is possible that kids who are already attention-deficient are more likely to gravitate to the Internet. Still, it seems intuitive that it would be hard to go from spending 56 seconds, on average, on every web page we visit to reading Dostoevsky.

James asks: Is there any evidence that Internet addiction is dopaminergic? On a related note, which psychological disorders are associated with increased Internet addition?

Based on the studies conducted so far, depression appears to be the most common condition occurring in individuals with problematic Internet use. The studies, however, don’t tell us if the person sought to “self-medicate” a depression by going online or if the depression resulted from excessive time spent using the Internet, perhaps at the expense of more rewarding real-life interactions.

Problematic Internet use and problematic online video game use have been called “behavioral addictions.” The neurotransmitter dopamine has long been implicated in addiction to substances and some preliminary small studies suggest a link between a dysfunctional dopamine system and problematic Internet or online video game use as well. In one study, “Internet addicts” were found to have altered glucose metabolism in brain regions that include major dopamine projections. Another study linked a variant of the dopamine D2 receptor gene with excessive online video game use. A third study used positron emission tomography (PET) to show lower levels of D2 dopamine receptors in parts of the brain of individuals with “Internet addiction.” Finally, a recent study showed lower levels of the dopamine transporter in parts of the brain of problematic Internet users.

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Last week, I experienced my first Facebook-era death. It had been several years - long before the ubiquity of social media - that I had last lost a relative, and I quickly discovered that experiencing loss and grieving online comes with a unique set of pros and cons.

I learned of my uncle’s stroke the old-fashioned way: via phone. My parents and I kept in steady contact that way over the next 36 hours, but it was Facebook that filled me in on certain details about my uncle’s status and my relatives’ whereabouts. The social networking site also enabled me to quickly express support, both before and after he passed, for family members scattered across the country. (“My heart goes out to you,” I posted on the wall of one of my cousins.)

I was 1,840 miles away from the hospital where my uncle lay, but the keyboard brought us closer. Being on Facebook helped me feel less isolated and helpless; if nothing else I could “like” someone’s comment on the need for prayers and positive thoughts about my uncle. I could feel like I was doing something.

My uncle had a warm, wonderful smile, but seeing it at that moment felt like a punch in the gut – another reminder that he was gone. As long as I was on Facebook, avoidance wasn’t an option.

But there were definite down-sides to being so connected (and yet so far away). When one relative wrote several hours after the stroke, “Things don’t look good,” it filled me with additional angst and left me with only questions. Did something just happen that I didn’t know about? Had she just received new information from his doctors, or was she merely conveying a general concern? I had no way of knowing; it felt inappropriate to ask in the comments section.

And after my uncle passed, it became impossible when on Facebook to escape what had happened. I logged in the morning after to be greeted with his photo; my cousin had just changed his profile picture to one of his dad and it was the first thing I saw in my newsfeed. My uncle had a warm, wonderful smile, but seeing it at that moment felt like a punch in the gut – another reminder that he was gone. I felt the same way later that day, when a link to the obituary was posted. As long as I was on Facebook, avoidance wasn’t an option.

Well before my uncle’s stroke I had a conversation with Stanford psychiatrist Elias Aboujaoude, MD, about the potential pitfalls of using social media at times like these. “The challenge is to avoid the tendency, online, to speed up and dumb down whatever we are engaged in,” he told me. “Grieving is complex and difficult, and it takes time, and if it feels simple, easy or more efficient online, then maybe we are diminishing the process somehow.”

My grieving didn’t necessarily feel diminished, but I can’t help but feel that the connections I made last week were somewhat artificial: Though Facebook made me feel close with my far-away family, I was still technically (physically) alone with my grief. And as handy as Facebook is, it couldn’t deliver what I needed the most while mourning: a hug.

Previously: 9/11: Grieving in the age of social media

Who’d think that clogging up the garbage disposal would clean up the kitchen?

Yet, as a new study by molecular and cellular physiologist Tom Sudhof, MD, and his Stanford colleagues, just published online in Science Translational Medicine, suggests just that. As I wrote in my release about the study:

. . . blocking the activity of cells’ in-house garbage disposals — known in the biology business as proteasomes — . . . both delayed the onset of symptoms in laboratory mice that are highly prone to neurodegeneration and significantly increased their longevity.

Proteasomes are cell components that destroy banged-up proteins. Not just nerve cells but virtually all cells in creatures ranging from yeast to humans contain multitudes of these tiny tubular machines, which suck the defective proteins into their holes and chew them into smithereens.

You might expect that when proteins get so bent out of shape that they can no longer do their job, we’d be better off without them. So, a lot of scientific effort and corporate expense have been devoted to efforts to treat neurodegenerative disorders such as Alzheimer’s disease by ridding patients’ bodies (and therefore, it is hoped, their brains) of faulty proteins.

But Sudhof thinks this common-sense conclusion may need to be revisited. In a separate experiment described in the same study, his team also examined brain tissue from Alzheimer’s and Parkinson’s patients - two of a growing number of diseases for which the clumping together of misfolded proteins is believed to be at least partially culpable - and observed signs of the same deficits in healthy biochemical activity that inhbiting proteasomes had restored in the experimental mice.

Sudhof suspects that shoving the pharmacological equivalent of a spoon into a cell’s proteasomes, which causes the buildup of damaged proteins, results in a fair number of those proteins - either randomly or with the assistance of physical-therapist molecules called “chaperones” - reverting back to the correct shape, restoring key biochemical processes without which nerve cells die.

Photo by Suzie Tremmel