Sunday, February 02, 2020

Netflix Neurology: Inside the Brain of Aaron Hernandez (for a few seconds)


from Dr. Ann McKee / Boston University


A recent addition to the Netflix “making a murderer” franchise is Killer Inside: The Mind of Aaron Hernandez. At the end of any such story, there is no single answer as to what “made” the murderer.

The story of Aaron Fernandez is still in the public eye because of his fame as a professional football player for the New England Patriots (2010-2012). He was so successful that he signed a 5 year, $40 million contract with the team in August 2012. His alleged involvement in a July 2012 double homicide came to light in 2014, after he had been charged with the June 2013 murder of his friend, Odin Lloyd. For the latter crime, he was found guilty and sentenced to life without parole. He was acquitted of the double homicide, but two days later he hanged himself with a bed sheet in his jail cell.

His brain was donated to the Boston University CTE Center. From extensive coverage in the New York Times and elsewhere, we already knew that the autopsy revealed extensive chronic traumatic encephalopathy (CTE).

If you hope to gain insight into repetitive head injury, brain pathology, and violent behavior from watching this documentary, you'll be disappointed. The 3-part series spent 5 minutes on CTE and 3 hours 15 minutes on everything else his childhood, violent father, hurtful mother, immense athletic talent, football career, ex-con friends, girlfriend and daughter, heavy drug use, street life, weapons collection, paranoia, alleged shootings, alleged same-sex relationships, arrests, murder trials, conviction, appeal, recorded jailhouse telephone conversations, outwardly professed homophobia, death by suicide, and numerous interviews with friends and former players.

Much of this material was pruient and unnecessary, especially the speculations about his hidden sexual orientation and how this might have fueled his anger.


Prosecution Considered a “Fear of Outing” Motive

This argument was preposterous and a rarity in the history of violence involving the LGBTQ community: Hernandez supposedly feared that his friend would reveal his secret life as a bisexual man, so he killed Lloyd to preserve his image as a hyper-masculine heterosexual man. This baffling obsession with sexuality is distracting and dangerous, as aptly explained by D. Watkins:
There's no evidence proving that Hernandez's sexuality made him a killer. So why is the newly resurfaced Hernandez conversation centered around his sex life? Probably because sex is juicy, forbidden and learning that Hernandez may have been gay provides the consumers with content for endless hours of gossip about what public figures do in their personal lives.
Fortunately, this argument was not allowed at trial.


The Potential Role of CTE Was an Afterthought

A Rolling Stone interview with director Geno McDermott revealed the project began as a 90 minute documentary initially presented at DOC NYC in 2018. Netflix was interested in expanding the doc into a multi-part series. The gay angle emerged when high school friend/lover Dennis SanSoucie agreed to an on-camera interview. Other additions included newly available recordings of prison phone calls, and a coda about CTE, the neurodegenerative disease that may be associated with repeated concussions in high-impact sports (in concert with other poorly delineated factors).

At the very end of Killer Inside, self-serving celebrity defense attorney Jose Baez spoke about the family's decision to donate Aaron's brain to the CTE Center at Boston University.



Dr. Ann McKee with the brain of Aaron Fernandez


Dr. McKee said Hernandez had very advanced disease for a 27 year old:
...and not only was it advanced microscopically, especially in the frontal lobes which are very important for decision-making, judgment and cognition, this would be the first case we've ever seen of that kind of damage in such a young individual.

I can say this is substantial damage that undoubtedly took years to develop. This is not something that is developed acutely or just in the last several years. I imagine these changes had been evolving over maybe even as long as a decade.



Then we see interviews with non-experts, who make causal connections between Aaron's CTE and his erratic, violent, tragic behavior. Worst of all is sleazy lawyer Jose Baez, who drummed up business for other players to sue the NFL under false pretenses (there is currently no way to accurately diagnose CTE in living persons).

Why didn't Aaron's brother, who grew up with the same abusive father and played football for many years, become a murderer? I'll let former NFL player Jermaine Wiggins have the last word:
My thoughts to people who think that CTE was somehow involved, I think that's an absolute cop out. There are thousands of former NFL players out there that might have dealt with concussions, I've dealt with them. So to use that as a cop out? I'm not... no, no. C'mon, we're smarter than that, people.”

Further Reading

Is CTE Detectable in Living NFL Players?
this 2013 post is still true today

Brief Guide to the CTE Brains in the News. Part 1: Aaron Hernandez

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Monday, January 27, 2020

People Neurology: Bennet versus Ann feud captured live!



In a People Neurology exclusive, contentious footage of Dr. Ann McKee and Dr. Bennet Omalu was captured at the 5th Annual Chronic Traumatic Encephalopathy Conference. Dr. Omalu was not invited due to their long-standing animosity, but he crashed the party anyway during Dr. McKee's highly anticipated Keynote. While she was presenting quantitative proteomic analysis of the postmortem brain tissue of Aaron Hernandez, Dr. Omalu stood up and admonished the entire audience: “Remember, I discovered CTE! [NOTE: this is false.1] You will all answer for this on judgment day.”

The crowd gasped...
 
“Don't believe the blonde white woman who claimed she discovered CTE!”

“Ha. I never claimed I discovered CTE,” Dr. McKee snorted.
 
“His criteria don’t make sense to me! I don’t know what he’s doing.”

“The final decision is still with the doctor who is examining. Not every CTE case will have all those [NINDS] guidelines,” Dr. Omalu retorted.

“His criteria for diagnosing CTE are all over the map,” McKee said.

“This is the problem. People lump me with him, and they lump my work with him, and my work is nothing like this.”




The acrimonious exchange, the conference, and the ridiculous magazine cover are all fictitious, but the quotes are faithful renditions reported by the Washington Post in a scathing critique:
From scientist to salesman
How Bennet Omalu, doctor of ‘Concussion’ fame, built a career on distorted science

. . .
Nearly 15 years [after his first paper], Omalu has withdrawn from the CTE research community and remade himself as an evangelist, traveling the world selling his frightening version of what scientists know about CTE and contact sports. In paid speaking engagements, expert witness testimony and in several books he has authored, Omalu portrays CTE as an epidemic and himself as a crusader, fighting against not just the NFL but also the medical science community, which he claims is too corrupted to acknowledge clear-cut evidence that contact sports destroy lives.

. . .
But across the brain science community, there is wide consensus on one thing: Omalu, the man considered by many the public face of CTE research, routinely exaggerates his accomplishments and dramatically overstates the known risks of CTE and contact sports, fueling misconceptions about the disease, according to interviews with more than 50 experts in neurodegenerative disease and brain injuries, and a review of more than 100 papers from peer-reviewed medical journals.

Much of the reporting isn't new: it was widely known four years ago that Omalu exaggerated his contributions to the field (including the “discovery” of CTE), and that he blasted his critics:

“There is a good deal of jealousy and envy in my field. For me to come out and discover the paradigm shift, it upset some people. I am well aware of that.”

What was new is that respected experts publicly questioned Omalu's past work and his widely disseminated claims.

The biggest revelation was that the histology images in one influential paper did not show CTE, and did not appear to be from the brain of the subject in question.
McKee and other experts confirmed, in interviews, something that long has been an open secret in the CTE research community: Omalu’s paper on Mike Webster — the former Pittsburgh Steelers great who was the first NFL player discovered to have CTE — does not depict or describe the disease as the medical science community defines it.

On the more technical side, the WaPo article provided a basic overview of the CTE pathology and what it does to the brain, along with helpful graphics.

Our sister station, Netflix Neurology, will review Killer Inside: The Mind of Aaron Hernandez (the former NFL player and convicted murderer who died by suicide while incarcerated).



Ann McKee with the brain of Aaron Hernandez,
which showed extensive CTE findings


Footnote

1 In 1928, Harrison S. Martland published PUNCH DRUNK, a paper about boxers with brain damage. And the CTE syndrome was first named by Macdonald Critchley in 1949: Punch-drunk syndromes: The chronic traumatic encephalopathy of boxers.

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Tuesday, December 31, 2019

Computational Psychiatry, Self-Care, and The Mind-Body Problem

Schematic example of how the “mind” (cerebral cortex) is connected to the “body” (adrenal gland) - modified from Fig. 1 (Dum et al., 2016):
“Modern medicine has generally viewed the concept of psychosomaticdisease with suspicion. This view arose partly because no neural networks were known for the mind, conceptually associated with the cerebral cortex, to influence autonomic and endocrine systems that control internal organs.”

Psychosomatic illnesses are typically seen in pejorative terms — it's all in your head so it must not be real! Would a known biological mechanism lessen the stigma? For over 40 years, Dr. Peter Strick and his colleagues have conducted careful neuroanatomical tracing studies of motor and subcortical systems in the primate brain. A crucial piece of this puzzle requires detailed maps of the anatomical connections, both direct and indirect. How do the frontal lobes, which direct our thoughts, emotions, and movements, influence the function of peripheral organs?

In their new paper, Dum, Levinthal, and Strick (2019) revisited their 2016 work. The adrenal medulla (within the adrenal gland) secretes the stress hormones adrenaline and noradrenaline. To trace the terminal projections back to their origins in the spinal cord and up to the brain, the rabies virus was injected in the target tissue. The virus is taken up at the injection site and travels backward (in the retrograde direction) to identify neurons that connect to the adrenal medulla with one synapse: sympathetic preganglionic neurons in the spinal cord. Longer survival times allow the virus to cross second-, third-, and fourth-order synapses. The experiments revealed that cortical influences on the adrenal originate from networks involved in movement, cognition, and affect.

Modified from Fig. 5 (Dum et al., 2016). Pathways for top-down cortical influence over the adrenal medulla. Motor areas are filled yellow, and medial prefrontal areas are filled blue. (A) lateral surface. (B) medial wall.

The mind–body problem: Circuits that link the cerebral cortex to the adrenal medulla

“The largest influence originates from a motor network that includes all seven motor areas in the frontal lobe. ... The motor areas provide a link between body movement and the modulation of stress. The cognitive and affective networks are located in regions of cingulate cortex. They provide a link between how we think and feel and the function of the adrenal medulla.”
Based on these anatomical results, the authors concluded with a series of speculative links to alternative medicine practices, including yoga and Pilates; smiling to make yourself feel better; and back massage for stress reduction.
Because of this arrangement, we speculate that there is a link between the cortical control of 'core' muscles and the regulation of sympathetic output. This association could provide a neural explanation for the use of core exercises, such as yoga and Pilates, to ameliorate stress.
  • The orofacial representation of M1 provides a small focus of output to the adrenal medulla.
This output may provide a link between the activation of facial muscles, as in a 'standard' or 'genuine' smile, and a reduction in the response to stress.
  • Another large motor output region is in postcentral cortex, corresponding to the sensory representation of the trunk and viscera in primary somatosensory cortex.
This output may provide a neural substrate for the reduction of anxiety and stress that follows passive stimulation of back muscles during a massage.
I was a bit surprised to see these suggestions in a high-impact journal. Which leads us to the next topic.




Self-Care and Its Discontents

What can be bad about trying to reduce daily stress and improve your own health?

A recent paper by Jonathan Kaplan (Self-Care as Self-Blame Redux: Stress as Personal and Political)1 is critical of the way the self-care movement shifts the burden of alleviating stress-related maladies from society to the individual. Economic disadvantage is disproportionately associated with poor health outcomes, to state the obvious. Kaplan argues that focusing on individual self-care blames the victim for their response to a chronically stressful environment, rather than focusing on ways to effect structural changes to improve living conditions. In his efforts to highlight social inequities as a cause of stress-related illnesses, Kaplan goes too far (in my view) to discount all self-help practices that aim to preserve health.

It can be empowering for patients to be active participants in their health care, whether at the doctor's office, in the hospital, or at home. One great example is CREST.BD: A Collaborative Research and Knowledge Exchange Network at the University of British Columbia. They've established the Bipolar Wellness Centre (online resource to support evidence-based bipolar disorder self-management) and developed a Quality of Life Tool (free web-based tool to help people with bipolar disorder and healthcare providers use CREST.BD’s bipolar-specific quality of life scale).2

Then we have the wellness industry. Depending on what pop health source you read, there are 5, 45, 25, 12, 10, 10, 20 (etc.) essential self-care practices that you can incorporate into your daily routine (if you have the time and money). Wellness lifestyle insta-brands of the rich and famous hold up an impossible standard for upper-middle class white women [mostly]3 to attain. Perhaps our friendly neuroanatomists want to work on their core strength — they can follow @sianmarshallpilates for Pilates inspiration!


Back to Kaplan's point about blame...




It's easy to urge your followers to “stay happy!” and “move on!” if you have a net worth of $250 million, and if you don't have a psychiatric diagnosis. These 'Six Things' occupy a place in the pantheon of victim-blaming. People with mental illnesses are not effortlessly able to “stay happy!” or “move on!” or stop repetitive hand-washing (OCD) or avoid reckless spending (manic episode). And this is NOT their fault. And it doesn't make them mentally weak.

Most psychiatric disorders, in essence, involve thoughts, emotions, and/or behaviors that spin out of control. Here, I'm using control in a colloquial (but not absolute) sense, meaning: it's frequently difficult to stop a downward spiral once it gets started. Although overly simplistic...
  • Major depression involves thoughts (ruminations) and feelings of worthlessness and utter bleakness that spin out of control.
  • Generalized anxiety disorder involves thoughts (worry) about an imagined awful future that spin out of control.
  • Panic disorder involves a thwarted escape or safety response to perceived danger that has spun out of control.
  • Mania involves elevated mood and intense motivation for reward that spin out of control.
  • Obsessive-compulsive disorder involves maladaptive repetitive behaviors (that spin out of control) meant to quell maladaptive worrisome thoughts that have spun out of control.
  • Borderline personality disorder involves overly intense negative emotions that spin out of control and lead to self-destructive behaviors.
If people were able to control all this (without external intervention), the condition wouldn't reach the level of “disorder” — causing functional impairment and (usually) significant distress (but not always; e.g., people in the midst of a full-blown manic episode lack insight). I know this cartoonish level of description can raise the specter of free will and responsibility, especially in the context of criminal behavior. Are people with antisocial personality disorder not accountable for their horrible deeds? This timeless debate is beyond the scope of this post.


Computational Psychiatry

Or you can get mathematically fancy and formalize every single mental illness as a result of “faulty Bayesian priors”. Meaning, the brain's own “prediction machine” has incorporated inaccurate assumptions about the self or others or how the world works. A disordered Bayesian brain also ignores empirical evidence that contradicts these assumptions. The process of active inference — the brain's way of minimizing “surprise” when reconciling a top-down internal model and bottom-up external input  — has gone awry (Prossner et al., 2018; Linson & Friston, 2019). Although a sense of agency (or control) is a critical part of the active inference framework, I don't think an impairment in active inference is a choice. Or that one has control over this impairment. In fact, there's a Bayesian formulation of behavioral control (or lack thereof) that considers depression in terms of pessimistic, overly generalized priors, i.e. the depressed person assumes a lack of control over their circumstances.

Learned Helplessness (Huys & Dayan, 2009).


Using this mathematical model, you can confound the “stay happy!” crowd when you use all 24 equations to explain the concept of learned helplessness and its relevance to human depression.

Maybe one day, Bayesians will have a stable of Instagram influencers. Get to work on your branding ideas!


Footnotes

1 Thanks to Neuroskeptic for tweeting about this paper, along with the quote that individuals may "end up being seen (and seeing themselves) as responsible for their own failures to adequately ameliorate the stresses that they suffer."

2 Full Disclosure: my late wife was a Peer Researcher with CREST.BD.

3 While searching for health and wellness Instagram influencers, I was pleasantly surprised to find @hellolaurenash (a Chicago-based blogger, editor, and yoga and meditation teacher who founded a holistic wellness platform for marginalized communities) and @mynameisjessamyn (a body-positive yoga expert who wants to change the largely white and thin face of yoga and make the practice more accessible to all). I know absolutely nothing about the prevalence of diversity among health and wellness Instagram influencers, just like I know absolutely nothing about Computational Psychiatry.


References

Dum RP, Levinthal DJ, Strick PL. (2016). Motor, cognitive, and affective areas of the cerebral cortex influence the adrenal medulla. Proceedings of the National Academy of Sciences 113(35): 9922-9927.

Dum RP, Levinthal DJ, Strick PL. (2019). The mind–body problem: Circuits that link the cerebral cortex to the adrenal medulla. Proceedings of the National Academy of Sciences 116(52): 26321-26328.

Friston K, Schwartenbeck P, FitzGerald T, Moutoussis M, Behrens T, Dolan RJ. (2013). The anatomy of choice: active inference and agency. Frontiers in Human Neuroscience 7:598.

Huys QJ, Dayan P. (2009). A Bayesian formulation of behavioral control. Cognition 113(3):314-328.

Kaplan J. (2019). Self-Care as Self-Blame Redux: Stress as Personal and Political. Kennedy Inst Ethics J. 29(2):97-123.  PDF.

Linson A, Friston K. (2019). Reframing PTSD for computational psychiatry with the active inference framework. Cognitive Neuropsychiatry 24(5):347-368.

Prosser A, Friston KJ, Bakker N, Parr T. (2018). A Bayesian Account of Psychopathy: A Model of Lacks Remorse and Self-Aggrandizing. Computational Psychiatry 2:92-114.

Smash the wellness industry

... Wellness is a largely white, privileged enterprise catering to largely white, privileged, already thin and able-bodied women, promoting exercise only they have the time to do and Tuscan kale only they have the resources to buy.

Finally, wellness also contributes to the insulting cultural subtext that women cannot be trusted to make decisions when it comes to our own bodies, even when it comes to nourishing them. We must adhere to some sort of “program” or we will go off the rails.

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Friday, November 29, 2019

Pheromone Friday



Pheromones, emitted chemicals that elicit a social response in members of the same species, have been most widely studied in insects as a mode of communication. In the insect world, pheromones can signal alarm, mark trails, control worker bee behavior, and elicit sexual behavior.

Sex pheromones are the chemicals that come to mind in popular lore. Do human beings secrete substances that are likely to attract potential mates? Unscrupulous players in the fragrance industry would like you to believe that's the case. Unable to attract women (or men)? There's a difference between marketing an intoxicating and sensual fragrance that's pleasing to the nose and snake oil such as:




Amazon even cautions prospective customers about SexyLife.





{BTW, humans lack a functional vomeronasal organ, the part of the accessory olfactory system that detects pheromones / chemosignals / non-volatile molecules (Petrulis, 2013).}


Don't we already know that human pheromones are a crock?

It depends on how you define pheromone, some would say.1 “In mammals [rodents], few definitive cases have been identified in which single pheromone compounds evoke robust sexual behaviours, which might reflect an important contribution of signature mixtures in sexual communication” (Gomez-Diaz & Benton 2013, The joy of sex pheromones). In rodents, reproductive responses to “odor blends” or chemosignals are heavily modulated by experience, as opposed to the instinctive and fixed behaviors elicited by pheromones in insects. The evidence supporting the existence of mammalian pheromones is so weak that Richard Doty has called it The Great Pheromone Myth.

If rats don't have “pheromones” per se, why look for them in humans? Tristram Wyatt, who believes that human pheromones probably exist, wrote a paper called The search for human pheromones: the lost decades. He criticized the literature on four androgen-related steroids (androstenone, androstenol, androstadienone and estratetraenol), saying it suffers from publication bias, small sample sizes, lack of replication, and commercial conflicts of interest. There is no bioassay-based evidence that these molecules are human pheromones, yet “the attraction of studies on androstadienone (AND) and/or estratetraenol (EST) seems unstoppable” (Wyatt, 2015).

{Curiously, the SexyLife ad accurately lists the putative male pheromones, although their depicted functions are pure fantasy.}

Unstoppable it is. Supporters of human pheromones have recently published positive results on male sexual cognition, male dominance perception, cross-cultural chemosignaling of emotions, and sex differences in the main olfactory system.2


Olfactory Attraction

On the other hand, a null finding from 2017 drew a lot of attention from popular media outlets and Science magazine, where the senior author stated: “I’ve convinced myself that AND and EST are not worth pursuing.” In that study, AND & EST had no effect on the participants' attractiveness ratings for photographs of opposite-sex faces (Hare et al., 2017).

The evolutionary basis of Smell Dating was given a cold shower by studies showing that the fresh (and odorless) armpit sweat of men and women, when incubated in vitro with bacteria that produce body odor, were rated identically on pleasantness and intensity (reviewed in Doty, 2014). Meanwhile, the day-old smelly armpit sweat of men was rated as equally unpleasant by men and women.3 Likewise, pleasantness and intensity ratings for female armpit sweat did not differ between men and women. This doesn't bode well for heterosexual dating...

Odors and fragrances are an important part of attraction, of course, but don't call them pheromones.


Footnotes

1 There is an accepted definition for "pheromone".

2 Since humans don't have an accessory olfactory system with its fun vomeronasal organ, the main olfactory system would have to do the pheromone-detecting work.

3 This could be due to larger apocrine glands, hairy armpits, and more carnivorous diets in men (Doty, 2014).


Further Reading

Scientific post in favor of human pheromones:
“Whether one chooses to believe in the existence of human pheromones or not, steroids clearly serve an essential olfactory signaling function that impacts broadly ranging aspects of the human condition from gender perception to social behavior to dietary choices.”

PET studies on AND, EST, and sexual orientation:

References

Doty RL. (2014). Human Pheromones: Do They Exist? In: Mucignat-Caretta C, editor. Neurobiology of Chemical Communication. Boca Raton (FL): CRC Press/Taylor & Francis; Chapter 19.

Gomez-Diaz C, Benton R. (2013). The joy of sex pheromones. EMBO Rep. 14(10): 874-83.

Hare RM, Schlatter S, Rhodes G, Simmons LW. (2017). Putative sex-specific humanpheromones do not affect gender perception, attractiveness ratings orunfaithfulness judgements of opposite sex faces. R Soc Open Sci. 4(3):160831.

Petrulis A. (2013). Chemosignals, hormones and mammalian reproduction. Horm Behav. 63(5): 723-41.

Wyatt TD. (2015). The search for human pheromones: the lost decades and the necessity of returning to first principles. Proc Biol Sci. 282(1804):20142994.


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Monday, November 11, 2019

Olfactory Attraction and Smell Dating


Smell Dating, an interactive exhibit by Tega Brain and Sam Lavigne


A conceptual art installation, an extended olfactory performance piece, an elaborate participatory project, or an actual smell-based dating service? Smell Dating is all of these and more!




How it works
  1. We send you a t-shirt
  2. You wear the shirt for three days and three nights without deodorant.
  3. You return the shirt to us in a prepaid envelope.
  4. We send you swatches of t-shirts worn by a selection of other individuals.
  5. You smell the samples and tell us who you like.
  6. If someone whose smell you like likes the smell of you too, we'll facilitate an exchange of contact information.
  7. The rest is up to you.

My initial view of the project was based a recent showing of the interactive exhibit, where the participants could sniff small swatches of cloth, rate the unknown wearer's attractiveness (UNATTRACTIVE — NEUTRAL — ATTRACTIVE), learn how others voted, and see basic background information about the wearer (e.g., 30 year old female bisexual pescatarian). The first two I sniffed were odorless, but then there was #8...

The art installation is part of Useless Press, “a publishing collective that creates eclectic Internet things.” I assumed it was an elaborate joke, not an actual matchmaking service, but the artists must have had a grant to implement the idea in real life.





In Shanghai, people signed up over a two week period and paid ¥100 to become a “member.”
Smell Dating @ Shanghai [culminated] in the Sweat Lab, a participatory installation event... Visitors are invited to volunteer in the Smell Dating Sweat Lab and intimately experience the smells of strangers. During this event we will prepare the smell samples from our members t-shirts. Shirts will be meticulously cut up and batched to be sent back to Smell Dating members.

Smell Dating premiered in New York in March 2016 and received extensive press coverage, most of which took it seriously. Young female writers at The Guardian, Business Insider, Time, Racked, and a gay man at HuffPo tried out the service. The Buzzfeed reporter realized, “Yes, this is mostly a stunt-y gag” but also touched on the science behind smell and attraction. The health reporter at Time wrote about the underlying science in detail (e.g., major histocompatibility complex) and interviewed smell scientists, including Dr. Noam Sobel (founder of SmellSpace.com), Dr. Richard Doty (author of The Great Pheromone Myth), and Dr. Gary Beauchamp (Emeritus Director of the Monell Chemical Senses Center).

The creators of Smell Dating (Tega Brain and Sam Levine) consulted with olfactory scientists and provided an extensive reading list on the web site.

Most everyone agrees that odors evoke emotion, and the sense of smell has a unique relationship to autobiographical memory. But, as Richard Doty asks, do human pheromones exist?
While it is apparent that, like music and lighting, odors and fragrances can alter mood states and physiological arousal, is there evidence that unique agents exist, namely pheromones, which specifically alter such states?

It turns out that scientific opinion on this matter is decidedly mixed, even polarizing, as I'll discuss in the next post.


Reference

Doty RL. (2014). Human Pheromones: Do They Exist? In: Mucignat-Caretta C, editor. Neurobiology of Chemical Communication. Boca Raton (FL): CRC Press/Taylor & Francis; Chapter 19.




Smell Dating from Tega Brain.

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Saturday, November 02, 2019

The Neural Correlates of Channeling the Dead



November 2nd is the Day of the Dead, a Mexican holiday to honor the memory of lost loved ones. If you subscribe to certain paranormal belief systems, the ability to communicate with the dearly departed is possible via séance, which is conducted by a Medium who channels the spirit of the dead.

Since I do not subscribe to a paranormal belief system, I do not think it's possible to communicate with my dead wife. Nor am I especially knowledgeable about the differences between mediumship vs. channeling:
Mediumship is mostly about receiving and interpreting messages from other worlds.

Mediums often deliver messages from loved ones and spirit guides during readings.
. . .

...channeling is often about receiving messages from other types of entities, such as nature spirits, spirit guides, or even angels.

In short, Channels can communicate with a broader class of non-corporeal entities, for instance Mahatma Ghandi or Cleopatra (not only the dead relatives of paying clients).

What seems to be uncontroversial, however, is that Channels who enter into a trance state to convey the wisdom of Gandhi may experience an altered or “expanded” state of consciousness (regardless of the veracity of their communications). This permuted state of arousal should be manifest in the electroencephalogram (EEG) as an alteration in spectral power across the range of frequency bands (e.g., theta, alpha, beta etc.) that have been associated with different states of consciousness.

A group of researchers at the Institute of Noetic Sciences adopted this view in a study of persons who claimed the ability to channel (Wahbeh et al., 2019). The participants (n=13; 11 ♀, 2 ) were on average 57 year old white women of upper middle class socioeconomic status, representative of the study site in Marin County, California. The authors screened 155 individuals to arrive at their final sample size.1 Among the stringent inclusion criteria was the designation of being a Channel who directly and actively conveys the communications of a discarnate entity or spirit (rather than being a passive relay).2 The participants were free of major psychiatric disorders, including psychosis and dissociation (according to self-report). Oh, and they had the ability to remain still during the channeling episodes, which was advantageous for the physiological measurements.

The participants alternated between channeling and no-channeling in 5 minute blocks while EEG and peripheral physiological signals (skin conductance, heart rate, respiration, temperature) were recorded. At the end of each counterbalanced session (run on separate days), voice recordings were obtained while the participants read stories.




Contrary to the authors' predictions, they found no significant differences between the channeling and no-channeling conditions for any of the physiological measures, nor for the EEG analyzed in standard frequency bands (theta 3–7 Hz; alpha 8–12 Hz; beta 13–20 Hz and low gamma 21–40 Hz) across 64 electrodes. I'll note here that the data acquisition and analysis methods were top-notch. The senior author (Arnaud Delorme) developed the widely used EEGLAB toolbox for data analysis, which was described in one of the most highly cited articles in neuroscience.3

Modest differences in voice parameters were observed: the channeled readings were softer in volume and slower in pace. The authors acknowledged that the participants could have impersonated an alternate voice during the channeling segments, whether consciously or unconsciously.

So does this mean that channeling is a sham? The authors don't think so. Instead, they recommended further investigation: “future studies should include other measures such as EEG connectivity analyses, fMRI and biomarkers.”


Footnotes

1 This is a rather esoteric population, so I won't fault the researchers for having a small sample size.

2 “The channeler goes into a trance state at will (the depth of the trance may vary) and the disincarnate entity/spirit uses the channeler’s body with permission to communicate directly through the channeler's voice, body movements, etc. (rather than the channeler receiving information mentally or otherwise and then relaying what is being received).”

3 I was rather critical of a previous study by this research group, which was ultimately retracted from Frontiers in Neuroscience. See Scientific Study Shows Mediums Are Wrong 46.2% of the Time.


Reference

Wahbeh H, Cannard C, Okonsky J, Delorme A. (2019). A physiological examination of perceived incorporation during trance. F1000Research 8:67.



Bev Tull, the fake medium on Bad Girls.

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Sunday, October 06, 2019

Is Mourning Rewarding? (revisited)



Can we reduce the persistent, unbearable pain of losing a loved one to 15-20 voxels of brain activity in the nucleus accumbens (O'Connor et al., 2008)? No? Then what if I told you that unrelenting grief — and associated feelings of sheer panic, fear, terminal aloneness, and existential crisis — isn't “suffering”. It's actually rewarding!

Well I'm here to tell you that it isn't.

Looking back on a post from 2011, you never realize it's going to be you.1


The top figure shows that activity in the nucleus accumbens was greater in response to grief-related words vs. neutral words in a group of 11 women with “Complicated” Grief (who lost a mother or sister to breast cancer in the last 5 years), compared to a group of 10 women with garden-variety Non-complicated Grief (O'Connor et al., 2008). Since the paper was published in 2008, and the standards for conducting fMRI studies have changed (larger sample sizes are necessary, no more “voodoo correlations”), I won't go on about that here.


When Grief Gets Complicated?

Grief is never simple, it's always complicated. The death of a cherished loved one can create a situation that seems totally intolerable. Almost everyone agrees that navigating such loss doesn't rely on one acceptable road map. Yet here it is. Normal people are supposed to move through a one year mourning period of “sorrow, numbness, and even guilt and anger. Gradually these feelings ease, and it's possible to accept loss and move forward.” If you don't, well then it's Complicated. This is a stigmatizing and limiting view of what it means to grieve the loss of a loved one.2

But is there really such there a thing as Complicated Grief? Simply put, it's “a chronic impairing form of grief brought about by interference with the healing process.” There are “maladaptive thoughts and dysfunctional behaviors” according to The Center for Complicated Grief. However, it's not named as an actual disorder in either of the major psychiatric manuals. In ICD-11, preoccupation with and longing for the deceased, accompanied by significant emotional distress and functional impairment beyond six months, is called Prolonged Grief Disorder. In DSM-5, Complicated Grief has morphed into Persistent Complex Bereavement Disorder, a not-exactly-reified condition subject to further study.


Dopamine Reward

Dopamine and its putative reward circuitry are way more complex than a simple one-to-one mapping. Studies in rodents have demonstrated that the nucleus accumbens (NA) can code for negative states, as well as positive ones, as shown by the existence of “hedonic coldspots” that generate aversive reactions, in addition to the usual hotspots (Berridge & Kringelbach, 2015). These studies involved microinjections of opioids into tiny regions of the NA.




If a chronically anguished state is portrayed as rewarding, it's time to recalibrate these terms. As I said in 2011:

If tremendous psychological suffering and loss are associated with activity in brain regions such as the ventral tegmental area and nucleus accumbens, isn't it time to abandon the simplistic notion of dopamine as the feel-good neurotransmitter? To quote the authors of Mesolimbic Dopamine in Desire and Dread (Faure et al., 2008):
It is important to understand how mesocorticolimbic mechanisms generate positive versus negative motivations. Dopamine (DA) in the nucleus accumbens is well known as a mechanism of appetitive motivation for reward. However, aversive motivations such as pain, stress, and fear also may involve dopamine in nucleus accumbens (at least tonic dopamine signals).

Grief-Related Words Are Rewarding

So what happens when you take a disputed diagnostic label and combine it with reverse inference in a neuroimaging study? (when you operate under the assumption that activity in a particular brain region must mean that a specific cognitive process or psychological state was present).

The NA activity was observed while the participants viewed grief words vs. neutral words that were superimposed over a photograph: a photo of the participant's deceased mother or a photo of someone else's mother. And it didn't matter whose mother was pictured, the difference was due to the words, not the images.3



Sample stimulus provides an [unintentional?] example of the emotional Stroop effect.


That's pretty hard to explain by saying that “the pangs of grief would continue to occur with NA activity, with reward activity in response to the cues motivating reunion with the deceased” if the effect is not specific to an image of the deceased.


Yearning and the Subgenual Cingulate

Why beat a dead horse, you ask? Because a recent study (McConnell et al., 2018) did not heed the advice above (sample size should be increased, beware reverse inference). The participants were 9 women with Complicated Grief (CG), 7 women with Non-complicated Grief (NG), and 9 Non-Bereaved (NB). The NA finding did not replicate, nor were there any differences between CG and NG and NB (over the entire brain). A post-hoc analysis then extracted a single question from a 19-item inventory and found that yearning for the dead spouse in all 16 Bereaved participants was correlated with activity in the subgenual cingulate (“depression-land” or perhaps “rumination-land”), for the comparison of an anticipation period vs. presentation of spouse photo. There were 5 spouse photos and 5 photos of strangers (note that it was not possible to predict which would be presented). The authors recognized the limitations of the study, yet pathologized yearning in Complicated and Non-complicated Grief alike.

I realize that the general motivation behind these experiments might be admirable, but you really can't come to any conclusions about how grief — a highly complex emotional response unique to each individual — might be represented in the brain.


Footnotes

1 See There Is a Giant Hole Where My Heart Used To Be from October 2, 2018.

The posts on illness and death that I never wrote:
(yes, I was really serious about these)

2 I was skeptical when someone sent me this book, It's OK That You're Not OK: Meeting Grief and Loss in a Culture That Doesn't Understand (by Megan Devine). I thought it was going to be overly 'self-helpy'. But it's actually been immensely helpful.

3 The idea of creating a self-relevant stimulus set was utterly horrifying to me.


References

Berridge KC, Kringelbach ML. (2015). Pleasure systems in the brain. Neuron 86(3):646-64.

Faure A, Reynolds SM, Richard JM, Berridge KC. (2008). Mesolimbic dopamine in desire and dread: enabling motivation to be generated by localized glutamate disruptions in nucleus accumbens. J Neurosci. 28:7184-92.

McConnell MH, Killgore WD, O'Connor MF. (2018). Yearning predicts subgenual anterior cingulate activity in bereaved individuals. Heliyon 4(10):e00852.

O'Connor MF, Wellisch DK, Stanton AL, Eisenberger NI, Irwin MR, Lieberman MD. (2008). Craving love? Enduring grief activates brain's reward center. Neuroimage 42:969-72.


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