Can wearing tinted glasses that block “blue light” short-circuit a manic episode? Are allergies tied to seasonal mood patterns? Does a parent’s age influence whether his or her kids will develop bipolar?
Or to get more technical: What role does the ANK3 gene play in risk factors for bipolar? Do brain circuits fire differently in people with and without bipolar when they’re making quick decisions? Will sending electrical impulses through the scalp—a process known as transcranial magnetic stimulation—improve deficits in working memory and executive function?
Those are just a very, very few of the puzzles researchers are trying to solve these days. To get an idea of how many scientists are out there trying to pin down the whys and wherefores of bipolar, think about this: The journal Bipolar Disorders receives more than 300 articles seeking publication in a year, according to co-editor K.N. Roy Chengappa, MD, a psychiatry professor at the University of Pittsburgh School of Medicine.
And that’s not counting the papers that go to journals with a broader perspective, like Psychiatry Research, or publications like Molecular Psychiatry that are devoted to a specialized field, or overseas periodicals like Acta Psychiatrica Scandinavica.
Chronicling specific findings about bipolar over the past decade would take an encyclopedia. However, certain trends emerge. For one thing, Chengappa says clinical studies on complementary therapies like yoga and mindfulness were virtually non-existent 10 years ago. And he’s seen the number of submissions related to neuroscience and genetics roughly triple in that time.
As yet, there’s no definitive answer for what causes bipolar disorder to emerge, much less how to prevent that from happening. Science can’t explain why some people respond to standard treatments and some don’t. Over the past decade, however, insight into bipolar has grown exponentially—and several developments hold great promise for the future.
Not least is the snowballing emphasis on a “one brain” approach, which encourages collaboration in and across disciplines by recognizing that a range of brain-based disorders share common roots. Brain Canada, an umbrella organization for neuroscience research, explains it this way: “Looking at the brain as one system can lead to breakthroughs that will have impact on multiple conditions.”
Former U.S. Rep. Patrick Kennedy put a spotlight on this idea when he launched the One Mind coalition in 2011. He modeled the undertaking on the “race for space” that started when his uncle, President John F. Kennedy, called for America to put a man on the moon within a decade. The younger Kennedy’s “moon shot to the mind” has twin aims: first, to mobilize resources, and second, to streamline processes for sharing and building on the work that’s being done.
Governments, foundations and institutions around the world are moving in the same direction. The Human Brain Project, established in Europe in 2013, enlists 23 organizations in 13 countries in an effort to simulate the complete brain on a supercomputer within a decade. The BRAIN Initiative, also launched in 2013, puts the U.S. government’s muscle behind an ambitious attempt to map every single neuron in what’s been dubbed the Human Connectome.
The BRAIN Initiative—a clever acronym for Brain Research through Advancing Innovative Neurotechnologies—seeks to speed up development of better methods to “see” what goes on in our noggins.
“A lot of the action in the brain is electrochemical and moves very, very quickly, and very small electrochemical changes can be hard to detect,” explains Stephen M. Strakowski, MD, author of The Bipolar Brain: Integrating Neuroimaging and Genetics.
Strakowski founded the prestigious bipolar research program at the University of Cincinnati College of Medicine, where he holds professorships in biomedical engineering, psychology, and a third department that reflects crossover prospects for the future: psychiatry and behavioral neuroscience.
He says magnetic resonance imaging (MRI)—the workhorse of human neuroscience research—has become immensely faster and sophisticated, far more affordable, and also more comfortable for study participants over the past 10 years. But major technological leaps are needed “to identify certain types of neurotransmitters or certain types of brain structures that are beyond our capability to measure now.”
A lot of the action in the brain is electrochemical and moves very, very quickly, and very small electrochemical changes can be hard to detect.
Jeffrey Borenstein, MD, president and CEO of the Brain & Behavior Research Foundation and editor in chief of Psychiatric News, cites the shining example of optogenetics. That technology opened whole new areas of research after it was introduced in 2005 because it allows scientists to connect an animal’s behavior to the activity of selected neurons.
Optogenetics involves treating brain cells with a light-sensitive protein so that they respond to laser pulses. At present, it is only used in animal models (mice, tadpoles and the like). Its applications to bipolar research are in the early stages, but so far optogenetics has enabled neuroscientists to explore relationships between manic behavior and the body’s internal clock.
While an earlier body of neuroscience research zooms in on individual synapses, such as the action of serotonin receptors, the “one brain” approach encompasses a larger view of brain circuitry. The buzzword here is “connectivity”—as in the journal Brain Connectivity, which debuted in April 2011 to cover the burgeoning field.
“Structural connectivity” examines how the brain is wired. (Hence the Human Connectome Project to map our every neuron, just as the Human Genome Project mapped our DNA.) “Functional connectivity,” on the other hand, asks how networks in the brain work together to generate our thoughts, emotions and actions, whether or not they are directly attached.
“It’s a totally different way of looking at the brain,” says Amit Anand, MD, a pioneering researcher in connectivity and mood disorders who is now based at the Cleveland Clinic Lerner College of Medicine.
It’s known that in people who are depressed, blood flow decreases in the sophisticated prefrontal cortex, which handles planning and control, and increases in the relatively primitive limbic system, seat of emotion, motivation and memory. As understanding of brain processing advanced, Anand explains, “people started thinking it’s not so much the decreasing or increasing activation of one area of the brain, but the connectivity of the cortical and limbic areas that may be the problem.”
It may help to think of the brain as “a series of parallel processors that function in tandem,” Strakowski says, each handling an aspect of the job at hand. For example, reading taps into the brain’s circuits for processing sounds, recognizing shapes, and categorizing meaning, for starters—not to mention the complicated workings of our memory.
Strakowski says scientific understanding of relatively “simple” functions like vision is fairly advanced. “For more complex behaviors that are disrupted in bipolar disorder, such as emotional control, network science is still under development,” he says.
It may be that mood symptoms of bipolar arise when structural connections in the brain’s emotional networks aren’t properly wired, so the circuits misfire when the network is activated. Another area of interest is something called the default mode network.
For more complex behaviors that are disrupted in bipolar disorder, such as emotional control, [brain] network science is still under development.
It turns out the brain is actually incredibly busy when we’re not doing anything. Neural systems chatter away to each other all the time, busily organizing and processing and staying alert for demands from the outside world. This baseline activity that occurs when we zone out is the default mode network (DMN), also referred to as “resting state connectivity.” Studies have found disruptions in resting state connectivity in people with bipolar.
The question now is what to do with this information. Anand’s team has started a long-term study to see if scans mapping brain connectivity can be used to predict which young people with depressive symptoms will go on to develop bipolar. Other researchers are adapting the principles of biofeedback to see if people can influence their state of mind based on real-time information from rsfMRI (that’s resting state functional magnetic resonance imaging).
The intersection between technology and discovery can also be seen in genetics research focused on bipolar. For one thing, the “sample size” of study participants seems to be reaching critical mass, in part because the cost of mapping an individual’s DNA has become relatively cheap in the past 10 years—dropping from more than $1 billion for the first genomes to down below $1,000.
And like neuroscientists, genetics researchers around the world are collaborating to leverage the knowledge of individual labs.
The Psychiatric Genomics Consortium, founded in 2007, allows investigators from more than 80-plus institutions in 25 countries to share genetic data from more than 170,000 study participants. The U.S.-based Genomic Psychiatry Cohort (GPC), formed the following year, involves a dozen academic institutions, the National Institutes of Health, and almost 40,000 participants in the pursuit of answers specific to bipolar and schizophrenia.
That database also offers relatively unusual ethnic diversity, with some 6,000 African-Americans and 8,000 people of Latino ancestry in the mix with Caucasians tracing back to various parts of Europe.
“Understanding how risks play out in different populations is very, very important,” notes Carlos Pato, MD, PhD, one of the driving forces behind the GPC. “We don’t want to become focused on one group of people and not understand how to help every one of our patients.”
Before DNA sequencing became so accessible, genetics researchers focused on isolated and/or homogenous populations. That made it easier to identify gene variants that showed up only in families with high rates of bipolar or another psychiatric disorder. When Pato and his wife, Michele Pato, MD—both professors at the University of Southern California’s Keck School of Medicine—first partnered on an ongoing genetic study 25 years ago, they turned to self-contained communities of Portuguese islanders.
One thing researchers have learned as the data base grows is where not to look for answers to what causes bipolar.
“If there were one gene causing the disorder, we would have found it with the sample size right now,” says Melvin G. McInnis, MD, director of the Prechter Bipolar Research Programs at the University of Michigan. “There’s no magic bullet, no smoking gun. So we are looking for many genes, each with a very small effect in influencing susceptibility.”
So far, more than 20 genes are on the list of potential candidates—although exactly what role they play isn’t known. Furthermore, it’s looking like some of the genes “for bipolar” may be factors in other brain-based disorders like depression, schizophrenia, even autism. It’s possible there are genes associated with particular symptoms, so that “sleep disturbance in mania might be shared with sleep disturbance in other illnesses,” Carlos Pato says.
“The genes may not know that their job is to create a diagnosis that we poor doctors can use,” he adds with wry humor.
To make matters even more complicated, scientists have widened their scope of investigation to an additional layer of “controllers” or modulators that govern whether a particular gene is turned on or off.
As science painstakingly assembles the probable genetic actors in bipolar, researchers already have their eye on a larger prize: personalized medicine. Given that bipolar disorder runs in families, what’s the likelihood that you will develop the illness if you have close relatives with a diagnosis? And if you do have bipolar, which treatments will work best in your specific case?
“Genetics is not about destiny, it’s about risk,” says Michele Pato. “The better we understand your risk, the more we can do to help you and maybe even pre-empt some of the serious and long-term consequences of the illness because we diagnosed it early.”
Pato notes that although identical twins share more than 99 percent of their DNA, it’s not a given that both (or neither) will develop an illness like bipolar. Because their experiences in life and everything they’re exposed to will never be identical, “the expression of the genes ends up being different in the two twins,” she explains.
Psychiatric disorders typically emerge during late adolescence and young adulthood. Although risk varies from family to family, only 20 percent of children overall who have a parent with bipolar will develop a diagnosable mental illness later in life. Figuring out which teenagers will be affected, and why, and what would be most helpful to keep them well, has become a vital area in research and clinical practice.
Anne Duffy, MD, MSc, FRCPC, says those kinds of issues were “very much not on people’s radar” a decade ago.
“People are realizing, ‘You know what, we’re studying end-stage illness. If we want to be able to develop new treatment targets and prevent the fallout from illness, we really need to be looking at the early stages of illness development,’ ” she says.
Duffy first started following children of parents with bipolar disorder in the mid-1990s in Ottawa, home base for what she says is now the largest and longest-running high-risk cohort study in the world. She later expanded her work to the Maritime Bipolar Registry in Nova Scotia and more recently to Alberta, where she is on the faculty of the University of Calgary’s Cumming School of Medicine.
Genetics is not about destiny, it’s about risk. The better we understand your risk, the more we can do to help you …
“What we’re trying to do is better risk prediction, better early intervention, and to better understand the genetically sensitive pathways that lead young people into illness,” she explains. “We need to understand what protects those at familial risk and what factors determine illness.”
Thus the drive to create a risk index—a checklist of biological, neurological and psychological indicators that throw up red flags. High emotionality, a tendency to ruminate, childhood anxiety, and depressive episodes would all raise someone’s risk level, Duffy says.
On a personal level, having an individual risk indicator would allow people with a family history of bipolar to make more informed choices. Knowing that drug use is a proven trigger for psychiatric disorders might influence an adolescent to stay away from marijuana.
“What I tell the kids is, if I come from a family where multiple people have died of lung cancer, my friends might be smoking but I’m not going to,” Duffy explains.
From a clinical perspective, identifying leading risk factors would help distinguish teens who are experiencing what might be called “everyday” psychological challenges from those who should be directed into more intensive interventions.
“If I have a family history of breast cancer and I tell that history to my doctor, I’m going to get referred to a high-risk breast cancer clinic. In psychiatry, we don’t do that,” Duffy notes.
She sees hope in efforts like the Transformational Research in Adolescent Mental Health partnership in Quebec and the Orygen Youth Health Clinical Program in Australia, which are taking on the challenge “to translate the research into evidence-based clinical care pathways.”
Personalized medicine also aims to eliminate the trial-and-error process that so many people with bipolar go through to find effective medication. Instead of having to try one prescription after another and experiment with combinations, Michele Pato says, “wouldn’t it be good if … we could do a genetic test and say, ‘You’re going to do better on this’?“
The Holy Grail for researchers is finding biomarkers that would predict how your body will respond to this or that compound. The hunt represents a layer of genetic research that drills down to what genes are doing at the cellular level and “opens a window to the biology of the brain,” as the Prechter’s MicInnis puts it.
One prominent example is calcium, an ion that plays an important role in many cell functions. Groups around the world are poking and prodding at its role in bipolar and other mood disorders. McInnis and an interdisciplinary team from the University of Michigan have been exploring the activity of a “calcium gene” by taking skin cells from people with bipolar and coaxing those cells through a process that ultimately yields nerve cells. That enables the scientists to study how calcium ions influence the way nerve cells, specifically in neurons, communicate with each other.
The inflammatory mechanism has been implicated in cardiovascular disease, obesity, autoimmune diseases … people with bipolar have these at much higher rates than the general population.
Calcium is one of an “enormous number of molecules that are being looked at,” explains McInnis. He says studying proteins in the brain, as both structural and functional elements, has “a rich history and an exciting future.”
Serotonin, dopamine and a number of other neurotransmitters implicated in mood disorders fall into the class of proteins known as amines. Mood researchers have also become intrigued by molecules in the amino acid category, including glutamate and GABA (gamma-aminobutyric acid).
Then there are cytokines, proteins that regulate various inflammatory responses. Cytokines get busy as part of the body’s reaction to stress, and chronic stress over time produces wear and tear on tissues, cells, and nerves (including neurons in the brain).
In the past five years or so, scientists have begun paying closer attention to the inflammatory process as a factor in bipolar. In fact, researchers in Australia and elsewhere are starting to look at whether aspirin and other over-the-counter antioxidants would be useful as an add-on treatment for bipolar. As with so many areas in research, however, it will be some time before any findings translate into clinical care.
“Would I say right now that every bipolar patient should be on an anti-inflammatory?” asks Mark Frye, MD, chairman of the psychology and psychiatry department at the Mayo Clinic in Rochester, Minnesota. In a word, no—at least, not until it’s proven that benefits outweigh the potential for harm, since non-steroidal anti-inflammatory drugs like ibuprofen can have long-term side effects.
Frye is a co-author on a 2012 paper titled “Can bipolar disorder be viewed as a multi-system inflammatory disease?” The conclusion there: Pretty much.
In other words, bipolar mood symptoms may be merely one manifestation of an underlying inflammation process that also contributes to what are called “co-morbid” medical conditions. Call it a unified theory of illness.
“The inflammatory mechanism has been implicated in cardiovascular disease, obesity, autoimmune diseases such as diabetes,” says Frye. “We know people with bipolar have these at much higher rates than the general population.”
Figuring out the biological pathways common to both bipolar and heart disease, say, may turn up useful biomarkers that will speed up accurate diagnosis and improve individualized treatment.
From a researcher’s perspective, our current understanding of bipolar disorder parallels the state of infectious disease research 40 years ago or cancer science 20 years ago.
Discovering that bacteria cause fever and other symptoms of infection ultimately led to antibiotics. There are now blood tests that can identify which bacterium is causing a case of pneumonia. And Carlos Pato notes that science can now distinguish among cancers based on their genetic profile, “and that can tell us exactly what chemotherapy to give. That’s the kind of potential.”
Pato and others in the field of bipolar research use words like “optimistic” and “enthusiastic” when talking about advances. On the other hand, experts also emphasize that scientific discovery proceeds at a deliberate and incremental pace, so translating a discovery in the genetics lab to tests at the doctor’s office doesn’t happen overnight.
“Can we point to some amazing findings that we can take home and apply to treating patients today? No,” says Carlos Pato. “But are we feeling like we’re vastly closer to getting there? Yes.”
• • • • •
Advances in imaging technology allow researchers & physicians to delve deeper into the inner workings of the bipolar brain.
Once upon a time, scientists gleaned discoveries about which regions of the brain link to what functions based on people whose brains had stopped working properly because of head injuries or neurological diseases such as stroke.
Then came the ability to track oxygen flow through functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) to see what areas “lit up” when someone was asked to perform a specific task. PET scans also can track glucose molecules or specific neurotransmitters to detect patterns of energy use in the brain.
As imaging technology and computational science grow ever more powerful, scientists are deepening their understanding of the entire ecosystem of the organ. (One popular metaphor is being able to hear a whole symphony instead of listening to just the string section.) We now know there aren’t really specific areas in the brain controlling specific functions, but rather networks that cooperate in incredibly complex ways.
In order to understand current bipolar disorder research, you must first have an understanding of genes & DNA.
The first thing you need to know is that DNA, our biological blueprint, is made up of four nucleic acids known as bases. These bases link up along a connected pair of spiraling strands—the famous double helix. Each base pair is known as a nucleotide, and there are more than 3 billion nucleotides in human DNA.
The second thing you need to know is that a gene is essentially an address along your DNA—a subsection of nucleotides that operate either alone or with other genes to produce a certain trait, like eye color.
Generally speaking, genes work by encoding various proteins to perform all the various functions that are going on in our cells. This process of making and directing proteins is known as gene expression, and it’s happening at a furious rate every minute in every cell, including brain neurons.
Now imagine a gene as a pair of socks. Any sock you buy will have the same general shape and use, so you could mix and match socks of different patterns to make a pair. Similarly, genes come in variations known as alleles. An individual gene actually consists of paired alleles, one from each parent.
That’s why although we all have genes for eye color, we don’t all have the same color eyes. There are alleles for blue eyes, others for brown, and so on. The color of your eyes depends on your combination of alleles, including some that moderate the particular shade of that color.
Similarly, variations in alleles determine whether you are or aren’t carrying a susceptibility to bipolar disorder. But simply carrying a number of high-risk genes doesn’t mean your fate is sealed, because there are many influences—from stresses in your environment to what you ate for breakfast—governing whether and how a gene is expressed.
The presence of a biomarker within an individual indicates disease. Could this be a new frontier for diagnosing bipolar disorder?
By definition, a biomarker is a measurable substance whose presence indicates disease, infection, or environmental exposure. “A biomarker could be a gene, but it could also be a protein, or it could be a brain imaging marker,” explains Mark Frye, MD, a Mayo Clinic psychiatrist and member of the International Society for Bipolar Disorders’ biomarkers task force.
Finding reliable biomarkers for bipolar would make a huge difference in assessing risk for developing the illness, diagnosing it at an earlier stage, and predicting an individual’s response to various medications. Even as discoveries accumulate, however, it will be a good while before the science is ready for prime time.
“We have some early data that shows we do see different proteins in the blood for bipolar depression in comparison to major depressive disorder,” Frye notes. “Can that be used to make a diagnosis or guide treatment right now? No, but this is where future clinical research is going.”
Definitive answers on the mechanisms of bipolar still lie in the future. In the meantime, researchers have been finding useful answers to help you cope.
Erin Michalak, PhD, who heads a bipolar research program based at the University of British Columbia in Vancouver, has seen a “paradigm shift” in the field when it comes to recognizing the importance of factors and treatments beyond the biomedical.
“We know now from the science that a large degree of how people fare over time is dictated by psychological and social factors—how strong their social support network is, how well they deal with stigma, do they have a strong sense of identity or a healthy spiritual life,” she says.
Michalak is team leader of CREST.BD, an international network of scientists, clinicians and people with lived experience. (CREST.BD is shorthand for Collaborative RESearch Team to study psychosocial factors in Bipolar Disorder.) Established in 2007, the innovative project emphasizes finding and disseminating practical applications for improving the wellness of people with bipolar.
Study topics range from medication adherence and cognitive functioning to quality of life and self-management. One recent international study involved questioning individuals with bipolar about their strategies for preventing progression into hypomania or mania.
“Many of them talked about medications, but many of them also talked about things that would have been seen as peripheral research areas until quite recently,” Michalak says. For example, “Mindfulness practices might have been seen as a fringe area of science. Now mindfulness-based approaches have credence in bipolar science.”
Science has also been generating solid evidence about the benefits of cognitive behavioral therapy, dialectical behavior therapy, and other psychotherapies, both alongside and independent of medication. One of the most influential developments since bp Magazine began publishing is a treatment approach called interpersonal and social rhythm therapy (IPSRT).
In fact, the understanding that people with bipolar are especially susceptible to disruptions in daily routine, and therefore benefit greatly from establishing structure in their lives, has become gospel since the seminal study on IPSRT was published in 2005.
“When IPSRT was first developed, it was the only psychosocial therapy that really targeted social rhythms,” notes Holly A. Swartz, MD, a University of Pittsburgh psychiatry professor who has been involved in IPSRT research for more than a decade. “I would say at this point almost every psychosocial treatment for bipolar includes some component of monitoring daily rhythms.”
The intervention grew out of research into the biology of our circadian system, or how environmental cues such as sunlight affect recurring physiological processes like the sleep-wake cycle. Light travels via specialized nerves from the eyes to the part of the brain that serves as the “central pacemaker.” Researchers have found that sensors in other parts of the body, such as the skin and gastrointestinal tract, also feed information back to the central pacemaker to help regulate the circadian system.
“There has been a huge advance in identifying the cascade of genes and gene products that control your circadian biology,” says Swartz. Although that research is done primarily in animal models, she notes, “there’s growing evidence that circadian rhythm is implicated in bipolar disorder.”
Social rhythm therapy extends the definition of “environmental cues” to include daily activities like when you typically eat breakfast and regular routines like walking the dog. Interpersonal psychotherapy was originally developed as a time-limited method to treat depression. An offshoot of cognitive behavioral therapy, it focuses on the links between mood and social stressors such as conflict in a relationship, grief, and major life transitions.
Swartz says disturbances in social rhythms also have been linked to medical conditions like diabetes, migraines, and cancer. So interventions that aim to regularize daily and social rhythms—even something as simple as getting up at the same time every day—can have all-around benefits.
“I think it’s very empowering,” Swartz says. “These are principles that we can help people understand, strategies that we can help people learn. I think that they’re good, overall health-promoting approaches to living, too.”
Printed as ” Frontiers of Knowledge”, Winter 2015
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I understand people needed ‘to beg’ for help when wanting to increase research and treatments for many diseases. I hope our society has grown up enough to no longer require a group to beg. Those with mood disorders outnumber those with cancers.
Politicians need a vested interest. Patrick Kennedy has one. Where are the others?
Patrick Kennedy’s talks and ” moon shot to the moon ” are very inspiring as are his efforts. His comparison to his uncle JFK’s goal and commitment to putting a man on the moon to finding answers to diseases of the brain is illuminating. He points out that JFK did more than talk. He increase the budget for this project that year by more an amount larger than the previous eight years combined. While I find the reports on recent studies hopeful I would like to know how much money today would be an equivalent amount to the monies dedicated by our government the man on the moon project. I would like to know how to find answers to the question regarding mental illness research dollars and other programs. Person suffering with mental illness and their families are a relatively silent group. But a large one. But we do have the strength to pull a lever and vote. When and where is there an effort to show us which elected officials have ( as JFK did ) a support these efforts with more than just words. The lives of those suffering also matter. And I feel that we can do more than just beg for help
Hi, thank you for this article. The inflammatory process is also strongly affected through diet e.g. gluten sensitivity and histamine sensitivities. Asthma, arthritis, and gluten sensitivity are all over represented I believe in the bipolar population. (including myself!). I am more stable on a gluten free diet, with low histamine e.g. no berries or green tea. Low Vit D can be an issue as we get older and I also manage better with high Vit D supplementation – as well as high Fish Oil and a high level probiotic for my gut. Without being able to take any psychtrophic meds (CYP450 genetic liver problem), I use what I can and monitor the results very closely with my Psychiatrist.
I am 63 years old. I have been bipolar for over 40 years. I would like to leave my brain to a bipolar research team. I contacted Harvard but have never heard back from their bipolar research program. Is your program interested or can you point me to a research program that would accept it when i pass?
That’s a lot of good information. I have Bipolar 1 disorder and would like to have seen more information about addictions. In my experience there is a definite relationship between the two.