“Design fiction” skirts reality to provoke discussion and debate

I want to suggest that readers have a look at David Adams Science and Culture essay in the June 16 issues of PNAS. Here is its beginning:

In October 2015, researchers presented an unusual paper at a computer science conference in London. The paper described the promising results of a pilot project in which a local community used surveillance drones to enforce car parking restrictions and to identify dog owners who failed to clean up after their pets. Controlled by four elderly retirees, the drones buzzed around the city and directed council officials on the ground.

The paper and its accompanying video generated lively discussion about the ethics and regulation of drone use among delegates at the CHI PLAY conference. But there was a catch: The paper, the video, and the pilot scheme were fictional, as the researchers admitted at the end of both the paper and the presentation.

The researchers had invented the scenario as a way to focus attention on how drone technology—a topic of study for some of the people in the room—could shape and change society. The team thought that presenting the idea as if it were real—for example, showing familiar street signs in the video warning drivers about a drone-controlled zone—would provoke discussion about a future in which such use of technology was considered mundane.

The practice is called design fiction. Originally used in product design, the approach is finding increasing use in scientific and medical fields as a way to explore the possible consequences of technological development. These projects are not so much experiments designed to test a hypothesis as they are orchestrated scenarios designed to provoke forward-thinking discussion and debate. From climate science and artificial intelligence to wearable technologies and healthcare, researchers are creating and sharing often dystopian tales about the near future. And they’re tracking people’s reactions to these scenarios to help reshape the way researchers conceive the technology they are developing.

Dynamic Views of MindBlog

In my review of old blog posts I've come across mention of a link I placed at the top right corner os this page...Dynamic Views of MindBlog, which disappeared at some point without my noticing it (was Blogger/Google trying to shut it down?, I dunno.), I've put it back in. If you click on the link you have the options of view Deric's MindBlo in Classic, Flipcard, Magazine, Mosaic, Sidebar, Snapshot, or Timeslide formats. Give it a try!

Followup on MindBlog's Istanbul lecture on our subjective "I"

Forgive me for inflicting my nostalgia trip on you as I do the following re-post from Oct. 18, 2010. 78 year old Deric is struck by the more grandiose professory gravitas of the 68 year old Deric.

A previous post has pointed to a web text version of the piano recital and lecture I gave at "Cognitive VII", an international cognitive neuroscience meeting held in Istanbul May 18-20 of this year. The organizers indicated they would send a video of the piano performance and lecture, and after a number of tries, I have finally received, and now posted,  a video. It is missing a short bit of audio just after the beginning, and unfortunately deletes the last part of the talk on emotions and the evolution of music.  Still, it gives you a taste of the setting.

Training internal resilience

I want to point to an interesting article by Eva Holland on relieving trauma, which is very relevant to the potential mental0health fallout from living through our current pandemic. Some clips describing a therapy called E.M.D.R., eye movement desensitization and reprocessing:

E.M.D.R. was developed in the late 1980s and greeted with much skepticism at first. “It sounded like yet another of the crazes that have always plagued psychiatry,” Bessel van der Kolk, a trauma expert, wrote in “The Body Keeps The Score.” But clinical trials and peer-reviewed studies that spoke to its efficacy piled up over the three decades since its invention, and Dr. van der Kolk and many others eventually adopted it as part of their therapeutic practice.

It works like this: A therapist prompts the patient to move their eyes back and forth, rhythmically, behind their eyelids. (Devices that beep or buzz help to encourage and regulate the eye movements.) At the same time, the therapist talks the patient through the traumatic event or events at issue, leading them through a series of questions about how their body is reacting to the discussion. It is a strange, and strangely physical, experience. The precise mechanisms at play are not fully understood, but the theory is that something about the eye motion, combined with the focused discussion, can lay the intrusive memories to rest.

E.M.D.R. taught me an important lesson: that internal resilience can be deliberately cultivated...I had never before thought of resilience as a muscle I could train and strengthen. The idea felt empowering.

In a reversal of this therapy, the therapist asks the client to recall four resources from their memories: a places where they have left safest and happiest, a nurturing figure, a protector, and a source of wisdom. The author reports:

As I held a vibrating pod in each hand, and as my eyes rolled back and forth behind my eyelids in time to their pulsing, following the vibrations from left to right and back again, I thought about my grandmother — my nurturing figure, who had died when I was 18. I pictured her at the open kitchen window of her suburban bungalow....The pods pulsed. My eyes moved from side to side. I felt loved and safe. To my surprise, I felt stronger, too. In the time since, I have sometimes called up those sensory memories of my grandmother when I’m upset, or when I feel in need of support. It always helps.

The article proceeds to discuss further techniques for cultivating resilience that do not involve paying a therapist.

How we get stronger.

Gretchen Reynolds points to studies on weight lifting monkeys that show weight training initially prompts increases in muscle strength by increasing neural input to muscles via the reticulospinal tract. Only later do the muscles actually start to grow.

Significance Statement

We provide the first report of a strength training intervention in non-human primates. Our results indicate that strength training is associated with neural adaptations in intracortical and reticulospinal circuits, whilst corticospinal and motoneuronal adaptations are not dominant factors.

Abstract

Following a program of resistance training, there are neural and muscular contributions to the gain in strength. Here, we measured changes in important central motor pathways during strength training in two female macaque monkeys. Animals were trained to pull a handle with one arm; weights could be added to increase load. On each day, motor evoked potentials in upper limb muscles were first measured after stimulation of the primary motor cortex (M1), corticospinal tract (CST) and reticulospinal tract (RST). Monkeys then completed 50 trials with weights progressively increased over 8-9 weeks (final weight ∼6kg, close to the animal’s body weight). Muscle responses to M1 and RST stimulation increased during strength training; there were no increases in CST responses. Changes persisted during a two-week washout period without weights. After a further three months of strength training, an experiment under anesthesia mapped potential responses to CST and RST stimulation in the cervical enlargement of the spinal cord. We distinguished the early axonal volley and later spinal synaptic field potentials, and used the slope of the relationship between these at different stimulus intensities as a measure of spinal input-output gain. Spinal gain was increased on the trained compared to the untrained side of the cord within the intermediate zone and motor nuclei for RST, but not CST, stimulation. We conclude that neural adaptations to strength training involve adaptations in the RST, as well as intracortical circuits within M1. By contrast, there appears to be little contribution from the CST.

Mindblog does another anti-aging experiment.

This is a repeat of a MindBlog post done Oct. 10, 2010, encountered during an on-and-off review I'm doing of old blog posts. Five comments on the post can be seen by clicking the link to the original post. I'm halfway tempted, it now being roughly 10 years later, to repeat the experiment.

I find myself both spooked and sparked by my second foray into anti-aging chemistry (the first being the unsuccessful resveratrol dalliance described in a previous post.) A colleague pointed me to work of Bruce Ames and collaborators (also here) which has led to the marketing by Juvenon of a dietary supplement containing Acetyl L-carnitine, alpha-lipoic acid, and the B-vitamin biotin. Experiments on rats show that these compounds reverse the age related decay in energy metabolism in mitochondria and also inhibit oxidative damage to mitochondrial lipids. So... the idea is that these supplements might energize and juice you up a bit.  The Juvenon supplement contains (per day) 600 mcg biotin, 2000 mg of acetyl-L-carnitine, and 800 mg of alpha lipoic acid.  I though $40 was a bit steep for a 30 day supply, and so I bought the equivalent supplements from Swanson Health Products for significantly less money.  I decided to take 600 mg of the carnitine/day, 1000 mg/day of the alpha lipoic acid,  and 1000 mcg/day of biotin,  half at breakfast, half at lunch (by the way, this is slightly less than 1% of the levels used in the rat experiments.) From the homework I have done so far, the levels of these supplements being taken have no documented adverse side effects.

The results?  Well.... sufficiently dramatic that I really can't credit that it is all a placebo effect,  because I go into any such experiment as an unbeliever... The first several days I felt a phase change, a  step up in energy level and kinetic energy that made me like a 20-something again, a bit incredulous, as in "whoa.. where did this come from."  With both brain and body feeling like an automobile engine running at 2,000 r.p.m. even when it was not in gear,  I cut the levels of the supplements by a half after three days.   After another three days of energy I didn't know what to do with,  generating what felt like excess brain and body "noise,"  I stopped the supplement,  deciding that my normal fairly robust daily routines (including daily gym work or swimming, running, or weights) apparently had all the energy they needed.

Any experiences or references from blog readers would be appreciated.

Our brain's chemistry of love neutralizes its chemistry of fear.

Arthur Brooks, in his biweekly Atlantic Column, offers some very sane comments on the underlying fear that virtually all of us experience, especially in this time of COVID-19. He notes several surveys that show an increase of 10-20% in fear, anxiety, and stress over the past 10-20 years. There will always be threats to face and things to fear, and his stance is that...

The way to combat fear within ourselves is with its opposite emotion—which is not calmness, or even courage. It’s love...The Chinese philosopher Lao Tzu wrote in the Tao Te Ching, “Through Love, one has no fear.” More than 500 years later, Saint John the Apostle said the same thing: “There is no fear in love. But perfect love drives out fear, because fear has to do with punishment. The one who fears is not made perfect in love.”

Love neutralizes fear. It took about 2,000 years, but contemporary neurobiological evidence has revealed that Lao Tzu and Saint John were absolutely on the money...Fear is a primary emotion processed in the amygdala, a part of the brain that detects threats and signals to the body to produce the stress hormones that make us ready for fight or flight. This is largely involuntary, and, while necessary for survival, is unpleasant..The fear response is also maladapted to modern life. For example, a friend of mine with a large Twitter following once told me that he felt his chest tighten every day as he clicked on the social media app on his phone. His amygdala was alerting him that dangerous threats lay ahead, and he was getting a dose of adrenaline and cortisol in response—even though nothing was likely going to harm him.

However, we have a natural modulator of the hyperactive amygdala: the neuropeptide oxytocin, sometimes called the “love molecule.” Oxytocin is often produced in the brain in response to eye contact and touch, especially between loved ones. The feeling it creates is intensely pleasurable; indeed, life would be unbearable without it. There is evidence that an oxytocin deficit is one reason for the increase in depression during the coronavirus pandemic, with its lockdowns and social distancing.

Oxytocin has also been found to reduce anxiety and stress by inhibiting the response of the amygdala to outside stimuli. If you have loving contact with others, the outside world will seem less scary and threatening to you. What Saint John asserted is literally true: Perfect love drives out fear.

Brooks continues by noting many trends that over the past 20-30 years have decreased the amount of love in our lives, leading to an epidemic of loneliness.He then suggests concrete steps to bring more love into our lives by first sharing our fears with someone we trust, and by expressing you appreciation, affection or love for a friend or family member whom you would not normally address in this way.

A calming Brahms Romance for Monday afternoon.

Yet another item I've stumbled upon in my review of old MindBlog posts:

Urgent care for our brains.

I gave a Zoom lecture to the Austin Prime Timers group on May 17 titled "Urgent care for our brains" and thought I might as well point to the lecture text and graphics here on MindBlog. The text is informal, casual, and directed to our current situation with COVID-19.

Mindblog's back office has expanded

I want to introduce two new young MindBlog editorial assistants, Markus and Martin, three month old Abbysinian kittens who are in training to be the next generation after Marvin and Melvin, now 12 years old, who have been noted in numerous posts since their employment in summer of 2008.

Benefits of exercise on aging brain obtained without exercise - by plasma transfer.

There is a large literature on beneficial effects of exercise on brain health in agings adults such as improving memory and cognition. Mouse experiments by Horowitz et al. raise the possibility that affluent human couch potatoes might be able to obtain these benefits by receiving injections of plasma (blood without its cellular components) from people who have exercised. They transferred plasma from regularly exercising adult or aged mice to aged sedentary mice. This increased the formation of new hippocampal neurons, increased the concentrations of neurotrophic factors, and improved cognition in behavioral tests of the sedentary mice. Their abstract:

Reversing brain aging may be possible through systemic interventions such as exercise. We found that administration of circulating blood factors in plasma from exercised aged mice transferred the effects of exercise on adult neurogenesis and cognition to sedentary aged mice. Plasma concentrations of glycosylphosphatidylinositol (GPI)–specific phospholipase D1 (Gpld1), a GPI-degrading enzyme derived from liver, were found to increase after exercise and to correlate with improved cognitive function in aged mice, and concentrations of Gpld1 in blood were increased in active, healthy elderly humans. Increasing systemic concentrations of Gpld1 in aged mice ameliorated age-related regenerative and cognitive impairments by altering signaling cascades downstream of GPI-anchored substrate cleavage. We thus identify a liver-to-brain axis by which blood factors can transfer the benefits of exercise in old age.

We navigate with stereo smell

From Wu et al.:

Significance

The human brain exploits subtle differences between the inputs to the paired eyes and ears to construct three-dimensional experiences and navigate the environment. Whether and how it does so for olfaction is unclear, although humans also have two separate nasal passages that simultaneously sample from nonoverlapping regions in space. Here, we demonstrate that a moderate internostril difference in odor intensity consistently biases recipients’ perceived direction of self-motion toward the higher-concentration side, despite that they cannot report which nostril smells a stronger odor. The findings indicate that humans have a stereo sense of smell that subconsciously guides navigation.

Abstract

Human navigation relies on inputs to our paired eyes and ears. Although we also have two nasal passages, there has been little empirical indication that internostril differences yield directionality in human olfaction without involving the trigeminal system. By using optic flow that captures the pattern of apparent motion of surface elements in a visual scene, we demonstrate through formal psychophysical testing that a moderate binaral concentration disparity of a nontrigeminal odorant consistently biases recipients’ perceived direction of self-motion toward the higher-concentration side, despite that they cannot verbalize which nostril smells a stronger odor. We further show that the effect depends on the internostril ratio of odor concentrations and not the numeric difference in concentration between the two nostrils. Taken together, our findings provide behavioral evidence that humans smell in stereo and subconsciously utilize stereo olfactory cues in spatial navigation.

(By the way, a previous MindBlog post points to work showing binaral rivalry between the nostrils, analogous to the binocular rivalry that has been studied for over a century.)

The enlightenment returns.

 OhMyGawd..... I just came across the following MindBlog post from March 31, 2009, celebrating Obama's statement on restoring government guided by rationality and scientific integrity.  I pray that I can do do a similar post next March with Biden's name replacing Obama's.....

I have been almost reduced to tears of gratitude by Obama's statements on restoring an American government that is guided by rationality and scientific integrity rather than a conservative religious faith that distorts both. Kurt Gottfried and Harold Varmus (see below) write an editorial in Science Magazine that salutes this (Here is the President's memorandum):

The authors of the Declaration of Independence and the Constitution of the United States were children of the Enlightenment. They understood the power that flows from combining human reason with empirical knowledge, and they assumed that the political system they were creating would thrive only in a culture that upheld the values of the Enlightenment. And thrive it did, in large part because our people and government upheld those values throughout most of U.S. history. Recently, however, the precepts of the Enlightenment were ignored and even disdained with respect to the manner in which science was used in the nation's governance. Dogma took precedence over evidence, and opinion over facts. Happily, as was made clear by two policy announcements by President Barack Obama on 9 March 2009, the break in the traditionally harmonious relationship between science and government is now ending

As the president put it, "promoting science isn't just about providing resources--it is also about protecting free and open inquiry … free from manipulation or coercion, and listening to what [scientists] tell us, even when it's inconvenient--especially when it's inconvenient." In using the words "manipulation" and "coercion," the president was not speaking purely in the abstract; he was alluding to recent breaches of a code to which government must adhere if science is to play its proper role in advising the government on such complex issues as public health, climate change, or environmental protection. When the government systematically disregards this code, it undermines the historic role of science as a bulwark of an enlightened democracy.

In the president's Memorandum on Scientific Integrity last week, addressed to the heads of all executive departments and agencies, he directed those officials to neither suppress nor alter scientific and technological findings solicited in the process of policy formulation. He also asked that scientific information developed or used by the government be made readily available to the public. To put these directives in place, the president requested the director of the Office of Science and Technology Policy to develop, within 120 days, recommendations "designed to guarantee scientific integrity throughout the executive branch" and to ensure "that scientific data is never distorted or concealed to serve a political agenda."

(Kurt Gottfried is a cofounder of the Union of Concerned Scientists and chair of its board of directors. He is professor of physics emeritus at Cornell University. Harold Varmus is president of the Memorial Sloan-Kettering Cancer Center, a cochair of the President's Council of Advisors on Science and Technology, and a former director of the National Institutes of Health.)

How stress triggers inflammation

Acute stress seems to amplify inflammatory disease despite the fact many stress hormones such as cortisol actually suppress the immune system. Qing et al. show that this is because the rise in adrenaline (epinephrine) and norepinephrine levels during acute stress triggers the release of the pro-inflammatory cytokine interleukin-6 (IL-6) by brown fat cells. IL-6 is the signal for liver release of the glucose needed for the fight or flight response, but this comes at the cost of enhancing mortality to a subsequent inflammatory challenge. Here is their abstract:

Highlights

• IL-6 is the dominant endocrine cytokine induced by acute stress in mice

• Stress-inducible IL-6 is produced in brown adipocytes via ADRB3 signaling

• IL-6 is required for stress hyperglycemia and adaptive “fight or flight” responses

• Stress-induced IL-6 decreases tolerance to a subsequent inflammatory challenge

Summary

Acute psychological stress has long been known to decrease host fitness to inflammation in a wide variety of diseases, but how this occurs is incompletely understood. Using mouse models, we show that interleukin-6 (IL-6) is the dominant cytokine inducible upon acute stress alone. Stress-inducible IL-6 is produced from brown adipocytes in a beta-3-adrenergic-receptor-dependent fashion. During stress, endocrine IL-6 is the required instructive signal for mediating hyperglycemia through hepatic gluconeogenesis, which is necessary for anticipating and fueling “fight or flight” responses. This adaptation comes at the cost of enhancing mortality to a subsequent inflammatory challenge. These findings provide a mechanistic understanding of the ontogeny and adaptive purpose of IL-6 as a bona fide stress hormone coordinating systemic immunometabolic reprogramming. This brain-brown fat-liver axis might provide new insights into brown adipose tissue as a stress-responsive endocrine organ and mechanistic insight into targeting this axis in the treatment of inflammatory and neuropsychiatric diseases.

Gay scientists isolate christian gene.

 Another of my old posts, from March 18, 2009:

My thanks to friend Mark Weber for bringing this satire to my attention.

Nearest neighbors shape educational attainment regardless of class origin.

From Hedefalk and Dribe:

Significance

Much neighborhood research has focused on contemporary and segregated cities in the United States, but less on small and more homogenous cities. Additionally, neighborhood conditions are often estimated using administrative borders, which bias results. We adopt a long-term perspective on the importance of childhood neighbors, using more realistic methods of neighborhood conditions. We estimate individual neighborhoods at the address level, using geocoded longitudinal microdata (1939 to 2015) for a medium-sized Swedish town. We show that even when growing up in an economically relatively equal population, when higher education expanded greatly, the social class of the nearest childhood neighbors was important for educational achievements, regardless of social class and schools. Associations are strongest for boys, but with similar patterns across genders.

Abstract

We study the association between sociospatial neighborhood conditions throughout childhood and educational attainment in adulthood. Using unique longitudinal microdata for a medium-sized Swedish town, we geocode its population at the address level, 1939 to 1967, and link individuals to national registers, 1968 to 2015. Thus, we adopt a long-term perspective on the importance of nearby neighbors during a period when higher education expanded. Applying a method for estimating individual neighborhoods at the address level, we analyze the association between the geographically weighted social class of the nearest 6 to 100 childhood neighbors (ages 2 to 17), and the likelihood of obtaining a university degree by age 40, controlling for both family social class and school districts. We show that even when growing up in a town with relatively low economic inequality, the social class of the nearest same-age neighbors in childhood was associated with educational attainment, and that the associations were similar regardless of class origin. Growing up in low-class neighborhoods lowered educational attainment; growing up in high-class neighborhoods increased attainment. Social class and neighborhoods reinforced each other, implying that high-class children clustered with each other had much higher odds of obtaining a university degree than low-class children from low-class neighborhoods. Thus, even if all groups benefited from the great expansion of free higher education in Sweden (1960s to 1970s), the large inequalities between the classes and neighborhoods remained unchanged throughout the period. These findings show the importance of an advantageous background, both regarding the immediate family and the networks of nearby people of the same age.

An interlude of Grieg's Lyric Pieces

Almost every afternoon around 4 p.m. I open up my Steinway B and read some piano scores stored on my iPad. It takes very little effort to do a video of the playing using my iPhone with a small condenser microphone plugged into its usb port. Here are a few of the starting pieces in Grieg's Lyric Pieces series.

Lower socioeconomic status and the acceleration of aging.

An analysis from Steptoe and Zaninotto, who show that lower wealth correlates with accelerated aging independently of the presence of health conditions:

Significance

Lower socioeconomic status (SES) is a determinant of many of the health problems that emerge at older ages. The extent to which lower SES is associated with faster decline in age-related functions and phenotypes independently of health conditions is less clear. This study demonstrates that lower SES (defined by wealth) is related to accelerated decline over 6 to 8 y in 16 outcomes from physical, sensory, physiological, cognitive, emotional, and social domains, independently of diagnosed health conditions, self-rated health, education, and other factors. It provides evidence for the pervasive role of social circumstances on core aging processes and suggests that less affluent sectors of society age more rapidly than more privileged groups.

Abstract

Aging involves decline in a range of functional abilities and phenotypes, many of which are also associated with socioeconomic status (SES). Here we assessed whether lower SES is a determinant of the rate of decline over 8 y in six domains—physical capability, sensory function, physiological function, cognitive performance, emotional well-being, and social function—in a sample of 5,018 men and women aged 64.44 (SD 8.49) y on average at baseline. Wealth was used as the marker of SES, and all analyses controlled for age, gender, ethnicity, educational attainment, and long-term health conditions. Lower SES was associated with greater adverse changes in physical capability (grip strength, gait speed, and physical activity), sensory function (sight impairment), physiological function (plasma fibrinogen concentration and lung function), cognitive performance (memory, executive function, and processing speed), emotional well-being (enjoyment of life and depressive symptoms), and social function (organizational membership, number of close friends, volunteering, and cultural engagement). Effects were maintained when controlling statistically for other factors such as smoking, marital/partnership status, and self-rated health and were also present when analyses were limited to participants aged ≤75 y. We conclude that lower SES is related to accelerated aging across a broad range of functional abilities and phenotypes independently of the presence of health conditions and that social circumstances impinge on multiple aspects of aging.

Exaggerated meta-perceptions predict intergroup hostility between American political partisans

An interesting study from Moore-Berg et al. showing that Democrats think (have the meta-perception) that Republicans view them more negatively than they actually do, and vice versa. The bottom line is that "partisan meta-perceptions are subject to a strong negativity bias with Democrats and Republicans agreeing that the shadow of partisanship is much larger than it actually is, which fosters mutual intergroup hostility."

Significance

Although much current research highlights differences between political partisans, our research provides evidence that strong partisan biases in meta-perceptions are largely symmetrical for Democrats and Republicans. This suggests that biased meta-perceptions are a consequence of shared psychology rather than merely a consequence of divergent ideological convictions. Meta-perceptions represent evaluations that are distinct from perceptions at a core psychological level: While negative perceptions, such as dehumanization, can be thought of as offensive or reprehensible, meta-perceptions are inferences about what others think and can, therefore, be false. The theoretical distinctions between perceptions and meta-perceptions suggest that practical approaches to reducing negative meta-perceptions may be distinct from those that aim to reduce negative perceptions.

Abstract

People’s actions toward a competitive outgroup can be motivated not only by their perceptions of the outgroup, but also by how they think the outgroup perceives the ingroup (i.e., meta-perceptions). Here, we examine the prevalence, accuracy, and consequences of meta-perceptions among American political partisans. Using a representative sample (n = 1,056) and a longitudinal convenience sample (n = 2,707), we find that Democrats and Republicans equally dislike and dehumanize each other but think that the levels of prejudice and dehumanization held by the outgroup party are approximately twice as strong as actually reported by a representative sample of Democrats and Republicans. Overestimations of negative meta-perceptions were consistent across samples over time and between demographic subgroups but were modulated by political ideology: More strongly liberal Democrats and more strongly conservative Republicans were particularly prone to exaggerate meta-perceptions. Finally, we show that meta-prejudice and meta-dehumanization are independently associated with the desire for social distance from members of the outgroup party and support for policies that harm the country and flout democratic norms to favor the ingroup political party. This research demonstrates that partisan meta-perceptions are subject to a strong negativity bias with Democrats and Republicans agreeing that the shadow of partisanship is much larger than it actually is, which fosters mutual intergroup hostility.

Brain correlates of the muting of our emotions as we age.

 (This is a re-post of the MindBlog post of Oct. 1, 2008, as relevant today as then.)

My boyfriend in the early 19980’s was a pharmacy graduate student whose t-shirt read “Drugs are my life.” If I were to wear such a t-shirt now it would read “Hormones and neurotransmitters are my life.” I increasingly feel that all this verbal stuff we do - chattering in person or in the electronic ether, writing blogs, etc. - is a superficial veneer, noise on top of what is really running the show, which is the waxing and waning of hormones and neurotransmitters directed by an “it”, a martian inside us utterly running its own show. These compounds regulate our assertiveness versus passivity , our trust versus mistrust, our anxiety versus calm, our pleasure during antipication and reward. (They function, respectively, in neural systems that use testosterone, oxytocin, adrenaline, and dopamine.). The swings in these systems become less dramatic as we 'mellow' with aging.

Dreher et al. have published an interesting bit of work that deals specifically with the muting of the intensity of the pleasures we feel during anticipation and reward, in their article on “Age-related changes in midbrain dopaminergic regulation of the human reward system.” Their data show what is going on as we experience less excitement at opening a present when we are 60 than when we are 10 years old. There are changes in the brain's production of dopamine, which plays a central role in our reward system, as well as in which parts of the brain respond to it, and by how much they respond. (a recent brief article on dopamine and the reward system of the brain is here.) Here is their abstract, followed by a figure from the paper.

The dopamine system, which plays a crucial role in reward processing, is particularly vulnerable to aging. Significant losses over a normal lifespan have been reported for dopamine receptors and transporters, but very little is known about the neurofunctional consequences of this age-related dopaminergic decline. In animals, a substantial body of data indicates that dopamine activity in the midbrain is tightly associated with reward processing. In humans, although indirect evidence from pharmacological and clinical studies also supports such an association, there has been no direct demonstration of a link between midbrain dopamine and reward-related neural response. Moreover, there are no in vivo data for alterations in this relationship in older humans. Here, by using 6-[18F]FluoroDOPA (FDOPA) positron emission tomography (PET) and event-related 3T functional magnetic resonance imaging (fMRI) in the same subjects, we directly demonstrate a link between midbrain dopamine synthesis and reward-related prefrontal activity in humans, show that healthy aging induces functional alterations in the reward system, and identify an age-related change in the direction of the relationship (from a positive to a negative correlation) between midbrain dopamine synthesis and prefrontal activity. These results indicate an age-dependent dopaminergic tuning mechanism for cortical reward processing and provide system-level information about alteration of a key neural circuit in healthy aging. Taken together, our findings provide an important characterization of the interactions between midbrain dopamine function and the reward system in healthy young humans and older subjects, and identify the changes in this regulatory circuit that accompany aging.


Legend (click on figure to enlarge). Statistical t maps of the within-groups effects in the different phases of the reward paradigm. (A) (Left) Main effect of anticipating reward in young subjects during the delay period, showing activation in the left intraparietal cortex, ventral striatum, caudate nucleus, and anterior cingulate cortex. (Right) Main effect of anticipating reward in older subjects during the delay period, showing activation in the left intraparietal cortex only. The glass brain and the coronal slice indicate that no ventral striatum activity was observed in older subjects. (B) (Left) Main effect of reward receipt in young subjects at the time of the rewarded outcome showing activation in a large bilateral prefronto-parietal network. (Right) Main effect of reward receipt in older subjects at the time of the rewarded outcome showing bilateral prefronto-parietal activation.