Our healthcare challenges are very complex and do not fit neatly into existing scientific disciplines; solving them requires the combined expertise and efforts of many scientific and technical disciplines. The NIH mHealth Training Institute (mHTI) was created to serve as an incubator for developing transdisciplinary scientists capable of co-creating mHealth solutions for “wicked” healthcare problems.
As one earlier example, Lisa Marsch — Changing Behavior
Lisa Marsch, Ph.D., speaks at the mHealth Training Institute 2015 (mHTI) on “Changing Behavior.” Dr. Marsch is Associate Professor of Psychiatry and Director, Center for Technology and Behavioral Health at Dartmouth College.
There is also a MD2K Webinar series that is part of the Training Core of the MD2K Center. These webinars are part of the curriculum that MD2K is providing to students in both data science and the biomedical disciplines to further the process of building the next generation of scientists capable of using these highly sophisticated biomedical applications.
There is a steadily growing literature on the role of the immune system in psychiatric disorders. So far, these advances have largely taken the form of correlations between specific aspects of inflammation (e.g. blood plasma levels of inflammatory markers, genetic mutations in immune pathways, viral or bacterial infection) with the development of neuropsychiatric conditions such as autism, bipolar disorder, schizophrenia and depression. A fundamental question remains open: why are psychiatric disorders and immune responses intertwined? To address this would require a step back from a historical mind–body dualism that has created such a dichotomy. We propose three contributions of active inference when addressing this question: translation, unification, and simulation.
To illustrate these contributions, we consider the following questions. Is there an immunological analogue of sensory attenuation? Is there a common generative model that the brain and immune system jointly optimise? Can the immune response and psychiatric illness both be explained in terms of self-organising systems responding to threatening stimuli in their external environment, whether those stimuli happen to be pathogens, predators, or people? Does false inference at an immunological level alter the message passing at a psychological level (or vice versa) through a principled exchange between the two systems?
The human brain is a complex, adaptive system comprised of billions of cells with trillions of connections. The interactions between the elements of the system oppose this seemingly limitless capacity by constraining the system’s dynamic repertoire, enforcing distributed neural states that balance integration and differentiation. How this trade-off is mediated by the brain, and how the emergent, distributed neural patterns give rise to cognition and awareness, remains poorly understood.
Here, I argue that the thalamus is well-placed to arbitrate the interactions between distributed neural assemblies in the cerebral cortex. Different classes of thalamocortical connections are hypothesized to promote either feed-forward or feedback processing modes in the cerebral
cortex. This activity can be conceptualized as emerging dynamically from an evolving attractor landscape, with the relative engagement of distinct distributed circuits providing differing constraints over the manner in which brain state trajectories change over time.
In addition, inputs to the distinct thalamic populations from the cerebellum and basal ganglia, respectively, are proposed to differentially shape the attractor landscape, and hence, the temporal evolution of cortical assemblies. The coordinated engagement of these neural macrosystems is then shown to share key characteristics with prominent models of cognition, attention and conscious awareness. In this way, the crucial role of the thalamus in mediating the distributed, multi-scale network organization of the central nervous system can be related to higher brain function.
This article proposes that biologically plausible theories of behavior can be constructed by following a method of “phylogenetic refinement,” whereby they are progressively elaborated from simple to complex according to phylogenetic data on the sequence of changes that occurred over the course of evolution. It is argued that sufficient data exist to make this approach possible, and that the result can more effectively delineate the true biological categories of neurophysiological mechanisms than do approaches based on definitions of putative functions inherited from psychological traditions.
As an example, the approach is used to sketch a theoretical framework of how basic feedback control of interaction with the world was elaborated during vertebrate evolution, to give rise to the functional architecture of the mammalian brain. The results provide a conceptual taxonomy of mechanisms that naturally map to neurophysiological and neuroanatomical data and that offer a context for defining putative functions that, it is argued, are better grounded in biology than are some of the traditional concepts of cognitive science.
The focus on the brain in mental health research today is understandable. A person with a broken leg probably won’t hesitate to see a doctor, but the median time from first psychosis to psychiatric care in the U.S. is 74 weeks. Perhaps, the logic goes, a broken-brain model will shift responsibility from the person to the organ.
But there is no evidence that reframing mental illnesses as brain disorders reduces the associated stigma. Wherever doctors describe someone with a mental illness as having a chemical imbalance or abnormal brain circuitry, they provide reasons to fear that person. A German survey showed that the more people learned about the biology of mental illnesses, the more they reported a desire for social distance from people with a psychiatric diagnosis. A U.S. study showed that from 1996 to 2006, the American public increasingly saw mental illnesses as neurobiological, but this did not “significantly lower odds of stigma.”
The view that substance addiction is a brain disease, although widely accepted in the neuroscience community, has become subject to acerbic criticism in recent years. These criticisms state that the brain disease view is deterministic, fails to account for heterogeneity in remission and recovery, places too much emphasis on a compulsive dimension of addiction, and that a specific neural signature of addiction has not been identified. We acknowledge that some of these criticisms have merit, but assert that the foundational premise that addiction has a neurobiological basis is fundamentally sound. We also emphasize that denying that addiction is a brain disease is a harmful standpoint since it contributes to reducing access to healthcare and treatment, the consequences of which are catastrophic.
Here, we therefore address these criticisms, and in doing so provide a contemporary update of the brain disease view of addiction. We provide arguments to support this view, discuss why apparently spontaneous remission does not negate it, and how seemingly compulsive behaviors can co-exist with the sensitivity to alternative reinforcement in addiction. Most importantly, we argue that the brain is the biological substrate from which both addiction and the capacity for behavior change arise, arguing for an intensified neuroscientific study of recovery. More broadly, we propose that these disagreements reveal the need for multidisciplinary research that integrates neuroscientific, behavioral, clinical, and sociocultural perspectives.
It would be particularly interesting if training autobiographical memory processes more broadly could positively affect the trauma memory or associated posttraumatic appraisals without the individual ever discussing the trauma or its meaning or deliberately retrieving the trauma memory itself. That is, we were interested in whether improving the ability to retrieve concrete, specific details of all memories would flow on to increases in the (typically poor) visual and sensory quality and temporal features of a trauma memory. Because poor quality of a trauma memory is associated with poorer prognosis (Ehlers & Clark, 2000), intervention-driven improvement in trauma memory quality may represent one potential mechanism through which autobiographical memory-based training programs help to improve PTSD (Hitchcock et al., 2017; Moradi et al., 2014).
Likewise, training someone to flexibly move between specific events and generalized representations of the past may help to constrain overly generalized, negative beliefs (as suggested by the results of Hitchcock et al., 2017). Because the extrapolation of meaning attributed to the trauma (e.g., other people cannot be trusted, there is something wrong with me as a person) to the self and world more broadly is another strong predictor of prognosis, any effect of intervention on generalized posttraumatic appraisals could represent an alternate mechanism through which autobiographical memory-based training programs help to improve PTSD.
Brain structural covariance norms capture the coordination of neurodevelopmental programs between different brain regions. We develop and apply anatomical imbalance mapping (AIM), a method to measure and model individual deviations from these norms, to provide a lifespan map of morphological integration in the human cortex. In cross-sectional and longitudinal data, analysis of whole-brain average anatomical imbalance reveals a reproducible tightening of structural covariance by age 25 y, which loosens after the seventh decade of life. Anatomical imbalance change in development and in aging is greatest in the association cortex and least in the sensorimotor cortex. Finally, we show that interindividual variation in whole-brain average anatomical imbalance is positively correlated with a marker of human prenatal stress (birthweight disparity between monozygotic twins) and negatively correlated with general cognitive ability. This work provides methods and empirical insights to advance our understanding of coordinated anatomical organization of the human brain and its interindividual variation.
The mice quickly learned which musical arrangement that, when played, caused a dopamine release and the feel-good sensation. Their brains then began to rewire themselves to play that song more often, thereby triggering the pleasure hit of dopamine.
“In essence, the mice learned to repeat the same pattern of brain activity that had been evoked previously by hearing those musical notes,” said Vivek Athalye, a doctoral candidate at UC Berkeley and the paper’s co-first author.
The researchers noted that these findings are a striking example of Thorndike’s Law — a long-held principle of psychology stating that actions that lead to positive reinforcement are repeated more frequently. However, these findings likely represent the first time that this principle has been directly observed in the brain.
“In some ways, these results are entirely expected,” said Dr. Costa. “It makes sense that the brain would mimic the feeling of reward it gets from an enjoyable experience by producing the corresponding pattern of neural activity. But it had never been tested.”
Participants, who were expecting to take part in a study of the effects of drugs on creativity, spent four hours together in a room that had been set up to resemble a psychedelic party, with paintings, coloured lights and a DJ. To make the context seem credible and hide the deception, the study also involved ten research assistants in white lab coats, psychiatrists, and a security guard.
The 33 participants had been told they were being given a drug which resembled the active ingredient in psychedelic mushrooms and that they would experience changes in consciousness over the 4-hour period. In reality, everyone consumed a placebo. Among the participants were several actors who had been trained to slowly act out the effects of the ostensible drug. The researchers thought that this would help convince the participants that everyone had consumed a psychedelic drug and might lead them to experience placebo effects.
Social interactions and relationships are often rewarding, but the neural mechanisms through which social interaction drives positive experience remain poorly understood. In this study, we developed an automated operant conditioning system to measure social reward in mice and found that adult mice of both sexes display robust reinforcement of social interaction. Through cell-type-specific manipulations, we identified a crucial role for GABAergic neurons in the medial amygdala (MeA) in promoting the positive reinforcement of social interaction. Moreover, MeA GABAergic neurons mediate social reinforcement behavior through their projections to the medial preoptic area (MPOA) and promote dopamine release in the nucleus accumbens. Finally, activation of this MeA-to-MPOA circuit can robustly overcome avoidance behavior. Together, these findings establish the MeA as a key node for regulating social reward in both sexes, providing new insights into the regulation of social reward beyond the classic mesolimbic reward system.
It might well be in the rallying of our own bodily resources that our greatest opportunities lie. When we reconsider all that we gain by being animals, we’re confronted by some powerful resources for positive change. Just think of the gobsmacking beauty of bonding. If you have a dog beside you as you read this, bend down, look into her eyes, and stroke her. Via the hypothalamus inside your body, oxytocin will get to work, and dopamine – organic chemicals implicated in animal bonding – and, before you know it, you’ll be feeling good, even in the dark times of a pandemic.
And, as it happens, so will your dog, who will experience a similar physical response to the bond between you both. Oxytocin is produced in the hypothalamus of all mammals. In other words, our bodies might well be our best and most effective tool in the effort to strike a new balance between humans and the rest of the living world. If we can tip ourselves more into a bonding frame of mind, we might find it easier to recognise the beauty and intelligence that we’re hellbent on destroying. By accepting that we’re animals too, we create the opportunity to think about how we might play to the strengths of our evolutionary legacies in ways that we all stand to gain from. If we can build a better relationship with our own reality and, indeed, a better relationship with other animals, we’ll be on the road to recovery.
Glynn taps on the control panel keyboard and calls up a scene from Inside Out where Joy and Sadness walk into the Realm of the Subconscious. Glynn hits Play; Joy and Sadness enter a dark room and see a forest of giant broccoli, lit from the side so it seems outlined in a bright green. They move to a red staircase headed down into infinity and then meet another character, the clownish imaginary friend Bing Bong, imprisoned in a cage of candy-colored balloons. “These are all basically as saturated a color as one can achieve in digital cinema today,” Glynn says.
Then he cues it up again, in super-high-end digital cinema fireworks, using everything the screen can give us. “They go through the doors, and you see the little long shot of them in the distance, then all of a sudden we kind of have everything.” The shot widens, and the camera heads toward the broccoli forest, but now the broccoli is laser-pointer green, glowing against the blackness.
The red archway around the staircase is the most vivid red I have ever seen, and when Joy and Sadness start walking down the stairs, the edges of the screen disappear. The room, the world, is nothing but black except for the stairs. The balloons of Bing Bong’s prison look unearthly, like a Jeff Koons dog with eldritch powers. “I want to say 60 percent of this frame is outside the gamut of traditional digital cinema,” Glynn says. “We have a version of this film that has been creatively approved and built for exhibition on televisions that don’t exist yet.”