Thursday, October 12, 2017

Does Tourette's Syndrome Have Adaptive or Evolutionary Benefits?

A number of different mental "disorders" are hypothesized to have been adaptive under certain conditions during prehistoric times. What about Tourette's? An article that I wrote recently on the topic came to the following conclusions:

Possible Benefits Associated with Tourette's:

  • Reduced inhibitory pressure on reflexes and motor pathways
  • Heightened efficiency in the use of force
  • Reduced reaction time and refined rhythmic activity
  • Increased innate and instinctual behaviors
  • Advanced ability for improvisation or extemporization
  • Increased defensiveness, withdrawal, avoidance, vigilance, and opportunism
  • Stimulus hunger, adaptive restlessness and unhesitating reactivity

Click here to read the entire article for free:

Tourette Syndrome in the Context of Evolution and Behavioral Ecology


Tourette syndrome, and the closely related spectrum of tic disorders, are inherited neuropsychiatric conditions characterized by the presence of repetitive and stereotyped movements. Tics are elicited by either environmental experiences or internal signals that instruct the basal ganglia to initiate automatic or procedural movements. In most vertebrates the basal ganglia encode instructions for habitually used sequences of motor movements that are essential to survival. Tic disorders may represent evolved phenotypes with a lower threshold for basal ganglia-directed actions. This may have produced a susceptibility to extraneous tics, but also produced fast-acting tactical solutions to immediate physical problems. During periods of nonstop movement, continual foraging, and sustained vigilance, it may have been advantageous to allow subcortical motor commands to intrude into ongoing motor activities. It is clear that the engrams for individual motor responses held in the basal ganglia are selected by converging cortical and subcortical inputs. This form of convergent action selection results in the selection of the most contextually reinforced actions. Today people with Tourette’s have tics that seem arbitrary and inappropriate; however, this may be due to the vast discrepancies in reinforcement between the ancestral environment and the modern one. In prehistoric environments, the motor behaviors of individuals with tic disorders may have been appropriate in environmental context, and had ecological relevance in survival and self-promotion.

Keywords: basal ganglia, evolution, executive control, neuroecology, procedural memory, tics, Tourette’s disorder


Tourette syndrome (TS) is an inherited neuropsychiatric disorder characterized by multiple sudden, repetitive, nonrhythmic motor movements called tics. Motor tics include unplanned, stereotyped movements such as eye blinking, facial twitching, and head, arm, hand or shoulder movements. Phonic tics include noises, syllables, words and phrases. Some tics are highly conspicuous, whereas other can be very subtle and masked. Tourette’s is defined as part of a spectrum of tic disorders, which includes both transient and chronic tics, most with prepubertal onset. Although individuals with TS have been described since antiquity, the systematic study of individuals with tic disorders began in the nineteenth century [1]. Only a few decades ago Tourette syndrome was considered a rare and bizarre syndrome, most often associated with the exclamation of obscene words (coprolalia), socially inappropriate remarks, mimicking, and derogatory gestures [2]. However, none of these behaviors are universal. In fact, the most well-known symptom, coprolalia, only occurs in about 10% of cases [3].

The DSM-5 recognizes three types of tic disorders: Tourette’s disorder, persistent motor or vocal tic disorder and provisional tic disorder. The diagnostic criteria for Tourette’s in the DSM-5 are: A. Both multiple motor and one or more vocal tics have been present at some time during the illness, although not necessarily concurrently. B. The tics may wax and wane in frequency but have persisted for more than 1 year since first tic onset. C. Onset is before age 18 years. D. The disturbance is not attributable to the physiological effects of a substance or another medical condition.

Merely a few decades ago, TS symptoms were thought to be caused by pent up, or “repressed” anger, and psychoanalysis was thought to be a productive form of treatment. Today many Tourette’s researchers instead think that Tourette’s represents some kind of malfunction in the neurological systems that ensure that necessary urges are properly attended to [4]. It is now known that the disorder is neurological in etiology, rather than psychological, and symptom reduction can be achieved by modifying dopaminergic transmission. Medications and behavioral therapy are the most common forms of treatment [5]. Although Tourette’s is the most severe of the tic spectrum disorders [1], most cases are relatively mild [5], and many cases probably go undiagnosed [6]. The severity of tics decreases during adolescence and pronounced Tourette’s is relatively rare in adulthood [7]. Furthermore, Tourette’s is thought by some to be continuous with normal human variation and all people are thought to be capable of movements that qualify for the “tic” label [6].

Between 1 and 10 children per 1,000 have TS and additionally, as many as 10 per 1,000 have a tic disorder [4]. This incidence exceeds a mere chance effect due to high mutation rates (1 in 1,000) and thus may be suggestive of past positive selection [8]. Because TS has high prevalence and a very strong genetic component [4], the persistence of the polymorphisms involved suggests an origin in natural history. It presents with similar prevalence rates, worldwide [9] indicating that it was an established nosological entity before the first humans left Africa. Because it presents during the period of fertility we can assume that natural selection had the opportunity to select against these alleles. Yet, TS exists today as a relatively prevalent disorder. This amounts to an evolutionary enigma commensurate to the one identified for schizophrenia [10]. The present opinion article will explore the possibility that the clinical manifestations of tic disorders may be associated, perhaps in low levels, with certain adaptive advantages in specific environments. It is certainly possible that natural selection may have only favored subclinical traits or been advantageous in low genetic penetrance in clinically unaffected relatives.

Seizure activity, chorea, dystonia and myoclonus are other movement disorders that probably were not adaptive nor selected by evolution on the basis of their ability to adaptively alter behavior. Unlike tic disorders these movement disorders can be medical signs or symptoms, and are often precipitated by injury, drugs, or relatively rare medical disease states. Tic behavior is more complex, and may fit the adaptationist program as it has aspects of contextual responsivity and intentionality.

Tourette Syndrome and Evolutionary Medicine

The costs of TS are well known and include constrained mobility, occupational disability and psychological stress and suffering [11]. The defensive value; however, may be hidden due to discrepancies between our modern and ancestral environments. Many traits that are known to have been adaptive in our ancestral environment are now seen as maladaptive in our present society, and this has been termed an “environmental mismatch” [12]. The growing field of evolutionary medicine attempts to identify and explicate such mismatches. Researchers have shown that a large number of “pathological” conditions have compensating benefits and over time the literature has come to accept many of these as adaptive responses [13]. Clinical states associated with adaptive properties include diabetes mellitus, diarrhea, fever, inflammation, obesity, sneezing, sickle cell anemia and vomiting [14]. The literature emphasizes that disorders with evolutionary components work within physical constraints, and often involve functional compromises and tradeoffs.

Following the pioneering work of Panksepp [15] there has been a movement to understand psychiatric disturbances in terms of the underlying evolutionary mechanisms. Many articles have analyzed various forms of psychopathology in terms of evolutionary medicine [16], and this area of research has been referred to as “evolutionary psychopathology.” Researchers in this field have concluded that there were probably multiple, alternative, cognitive strategies to deal with the problems and obstacles that recurred in our evolutionary past. Furthermore, they emphasize that individual differences in developmental patterns may not always represent disease, but in fact represent biological, naturally selected responses to pressing environmental concerns [17, 18]. Many articles in the last two decades have espoused this view and reconceptualized various forms of psychopathology as adaptive, cognitive syndromes that have ecological utility [19]. These articles have given thoughtful treatments to disorders such as: anxiety, hypothesized to represent a careful, cautious strategy [20]; depression, a socially submissive strategy [21]; schizophrenia, a defensive, vigilant and impulsive strategy [22]; psychopathy, a socially selfish and opportunistic strategy [23]; and PTSD, a threat-avoidant strategy [24]. Similarly, many “behavioral syndromes” have been discovered in mammalian species and are thought to represent adaptive responses to particular scenarios, despite the fact that they appear maladaptive when taken out of their ecological context [25].

Williams and Nesse [25] suggest that in order to determine that a disorder or disease has adaptive qualities which were positively selected in the past, it is important to be able to show that the trait is relatively prevalent, heritable, and that susceptibility varies within a population. These are all true of TS. However, it is also necessary to show how the trait’s purported benefits may have outweighed the costs [13]. It does not appear that individuals with TS would have suffered great hardships or had barriers to reproduction in the ancestral environment. Furthermore, Tourette’s does not adversely affect intelligence or life expectancy [26]. Both children and adults with TS have been shown to be very psychologically hardy, and despite the frustrations associated with their symptoms, are surprisingly well-functioning in social, emotional and behavioral measures [3]. In fact, they are remarkably similar to control children without TS on most psychosocial measures. This suggests that despite the accompanying physical limitations, TS may not necessarily have unduly hampered reproductive success due to psychological or motivational factors.

Possible Compensatory Benefits of Tourette Syndrome

Compensating benefits associated with Tourette syndrome have been reported in studies comparing individuals with TS to controls [6]. Georgiou and researchers [27] found that patients with TS when tested in terms of kinematics were in certain respects more force efficient, compared to controls, and made fewer inefficient cycles of motoric acceleration and deceleration on complicated motor tasks. On average, individuals with TS perform behavioral tests of cognitive motor control more quickly and accurately than their typical developing peers do [28]. Children with TS have exhibited a significant processing advantage in judging time intervals [29]. Individuals with TS also exhibit enhanced levels of cognitive control over their oculomotor responses and increased performance is associated with tic severity [30]. The study authors speculate [31] that the enhanced cognitive control of motor activity seen in TS patients may stem from the constant requirement to suppress tics; however, the enhancements may actually be inherent to TS.

Individuals with TS have been reported to excel in certain types of competitive sports [5; 32]. Furthermore, it has been claimed that tics can allow improvisation and extemporization with musical instruments. Patients report that they are physically slower, less coordinated and have a diminished knack for repartee when they are on medicines that reduce ticcing [33] (although people without Tourette’s taking neuroleptics report this as well). There have not yet been any systematic research efforts aimed at delineating the motor advantages and deficits in individuals with TS, but further research may be illuminative.

When an individual with TS stops making a conscious effort to suppress their symptoms, or if they become emotionally aroused, tics are more likely to emerge [36]. Tics have been shown to decrease in frequency during concentration on an absorbing activity [6]. Another aspect of tics is that even though they are often described as irresistible, they are typically consciously suppressible or at least able to be delayed. Touretters describe these “premonitory urges” as having properties akin to an itching sensation. Like the impulse to scratch an itch, tics can be inhibited but only with the expenditure of some degree of mental effort and restraint [3]. Given the fact that they can be deliberately suppressed it seems clear that tics would not have compromised reproductive success and survival by bursting forth during extremely inopportune times.

Neurologist and author Oliver Sacks has written about the compensatory advantages of TS. He states that clinical observers of Tourette’s routinely note a peculiar quickness of movement. Sacks [33] also wrote a story about a pilot and surgeon with severe Tourette syndrome whose tics have been documented to go into almost complete abeyance during his operations. In fact, a dozen or so M.D.s with Tourette syndrome work quite safely as surgeons [34]. Sacks describes the musician [35], “Witty Ticcy Ray,” in the following way:

“…a weekend jazz drummer of real virtuosity, famous for his sudden and wild extemporizations, which would instantly arise from a tic or a compulsive hitting of a drum, and would instantly be made the nucleus of a wild and wonderful improvisation, so that the ‘sudden intruder’ would be turned into a brilliant advantage (p. 94).”

Many probands lose all noticeable manifestations of their Tourette’s when singing, dancing or acting and can remain tic free when moving rhythmically or continuously [33; 32]. Leckman and Cohen [6] ask, from the Darwinian viewpoint, whether there might be an advantage in having vulnerability to develop TS. They claim to have made clinical observations that TS patients have a “thinner barrier to stimulation,” and may have been more “aware of dangers” in the ancestral past. The present article will take another perspective and argue that a propensity for tics may have amounted to a form of restlessness that ensured that the individual remained physically and motorically integrated with their immediate environment. During periods of nonstop movement, and repetitive foraging motions it may have been advantageous to allow subcortical motor commands to intrude into ongoing motor activities.

TS symptomatology may therefore exist on a continuum with two ends: one extreme involving simple, isolated motor tics and vocalizations which are largely irrelevant, seemingly arbitrary and a have the potential to be a nuisance. The other extreme perhaps involves rapid inventiveness, disinhibition of basal impulses, and unhesitating reactivity. Perhaps the isolated and inappropriate tics are a natural tradeoff that occurs when the threshold for activity of the basal ganglia is adaptively lowered. Ticcing disorders may descend from an environment when social propriety mattered far less than speedy reactions. Furthermore, in the ancestral past there may have been less social stigma on wild, loose behavior. Tics often appear as risqué, irreverent or even antisocial, but this may simply be because they are not filtered by the frontal lobe. Thus tics may merely be the striatum’s most appropriate associations untempered by forethought, tolerance, empathy or compassion.

The Neuroscience of Tourette Syndrome

The mental instructions for discrete movements usually pass through a complex network of cognitive filters in the frontal cortex. The PFC normally either potentiates or inhibits the impulses originating from the dorsal striatum, permitting some and curtailing others. The putamen (which controls automatic movements previously learned by repetition) sends its instructions on to the premotor cortex which passes its activity on to the adjoining motor cortex. Normally inputs from prefrontal and premotor areas are combined and integrated with inputs from the dorsal striatum in this way, and are then sent to the motor cortex. The motor cortex delivers these motor programs to the muscles by way of the spine or cranial nerves. During tics, the frontal cortex fails to inhibit the caudate nucleus and putamen, structures which lie directly beneath it. In Tourette’s the putamen has been shown to be overactive. Furthermore, TS has been associated with lack of activity in three areas: 1) the dorsolateral prefrontal cortex (concerned with generating appropriate actions); 2) the left basal ganglia (concerned with the control of automatic movements; and 3) the anterior cingulated cortex (an area concerned with focusing attention on actions [37].

The determinants of the selection of a motor plan come from either: 1) external environmental stimuli, or 2) internal stimuli. Engrams for specific motor plans are triggered in the striatum when they are converged upon by a set of inputs from cortical and subcortical areas, and activated above a certain threshold. The cooccurrence of a specific set of stimuli in the environment, or in internally generated thinking, will initiate a complex search function, characterized by spreading activation, to select the corresponding motor outputs [38]. Thus, despite the fact that they may seem arbitrary, tics are actually chosen with high specificity.

Today individuals with Tourette’s report feeling a sense of reward accompanying their ticcing actions. Reward is associated with high levels of dopamine release which is known to promote habit formation in the basal ganglia, increasing the frequency of the action. Thus dopamine serves to capture and reinforce striatal behaviors engraining these patterns as habitual tics [39]. This process may leave individuals, especially those that are genetically predisposed to Tourette’s, to be vulnerable to maladaptive motor tics when contextually unnecessary responses are captured. In the prehistoric past humans were responsible for activities such as finding or making physical shelter, protecting their bodies from predators, and foraging for food. These activities determined their reinforcement schedule. Today we rarely do any of these things. What the basal ganglia found motivating in ancestral times, was probably very different from what it finds motivating today. In the ancestral past the motor plans that were converged upon may have been more likely to be advantageous movements rather than extraneous, idiosyncratic ones.

In his book, The Triune Brain in Evolution [40], the late Paul MacLean describes the basal ganglia as the reptilian brain (also referred to as the archipallium or R complex). He describes how it can be taken to represent the dominant mediator of adaptive behavior in reptiles, amphibians and fish. He describes the basal ganglia, limbic system and neocortex as three different biological computers linked together, different in structure and chemistry, tens of millions of years apart in provenance, and each with its own representations of time, space, motor repertoire and subjectivity. He describes their functionality as intermeshing; independent but not autonomous. Much of his life’s work was dedicated to explicating how the basal ganglia is responsible for the largest proportion of behavior in nonmammalian vertebrates, their learned behaviors, tropistic behaviors, repetitive behaviors, social displays, species-specific master routines and individual-specific, idiosyncratic subroutines. The large size and vast integration of the basal ganglia in humans is clear evidence of its importance in human behavior. Perhaps it should not be surprising that the human gene pool produces phenotypes where this system is granted increased autonomy.   

Tourette Syndrome, Stress and Phenotypic Plasticity

The phenotypic characteristics of organisms ranging from plants to mammals have been shown to make various plastic responses to environmental stressors [41]. Phenotypic plasticity is accomplished when environmental cues signal dormant genes to be expressed, or expressed genes to become silent in a process known as epigenetics. Stress has been shown to demand variant body types, behaviors, reproductive tactics, and life-history strategies. Epigenetic responses to chronic stress cause the mammalian brain to respond with a number of adaptive adjustments that increase vigilance, threat awareness, and physical responsivity [22,42]. Stressful environments probably put more pressure on animals to react quickly and efficiently [43]. Most vertebrates, under times of severe or chronic stress, must use their muscles vigorously, and for sustained periods [44]. It is known that after extended exposure to stress, higher-order cognitive brain areas are toned down relative to the areas responsible for reflexes, and the execution of coordinated, sequenced, or procedural movements [44]. The documented association between stress and TS may suggest that stress causes the expression of genes that lead to increased ticcing behaviors, because tic-like behaviors may have been particularly adaptive in a stressful, or adverse environment.

Psychogenic stress is known to exacerbate TS symptoms on the order of days, weeks and months. Psychological stress has been tied closely to early onset, and has been shown to precede flare-ups. Stress reliably accelerates TS disease progression and worsens symptoms [3]. Tics have been known to increase in frequency as a result of stress, fatigue, and anxiety [39]. Also ticcing disorders can be triggered during childhood by a traumatic event. Tic severity [45] and TS diagnosis [46] has been associated with maternal psychosocial stress during pregnancy. This strong association between TS and stress may suggest that an adverse or hostile environment may have favored tics. If TS constitutes a “predictive adaptive response” to stress then it should be informative for researchers to focus heavily on the molecular pathways that tie stress to TS exacerbation.

Stress is strongly associated with basal ganglia upregulation in mammals from rats to humans. Memory is multifaceted and different facets are mediated by different brain areas. Explicit memory for movement supports consciously accessible knowledge, such as memory of what one just did or what one did yesterday, and this is mediated by the medial temporal lobe, in particular, by the hippocampus [47]. Procedural or habit memory for movement, on the other hand, is responsible for simple stimulus-response associations such as the memory to stop a car when the light is red, and this is mediated by the caudate nucleus [48]. Hippocampus and caudate-based memory systems work in parallel and have been described as cooperative by some and competitive by others [49]. Studies have found that chronic stress significantly increases activity in the caudate nucleus [50] and improves performance on simpler, habitual and/or well-rehearsed tasks [51; 52]. In both humans and rodents, chronic stress has been associated with a substantial decrease in the use of hippocampal dependent learning strategies and a dramatic increase in the use of caudate-based learning strategies [53]. Combat veterans with PTSD, especially those that were using the caudate heavily in life-threatening situations (such as riflemen), exhibit hypertrophic caudate nuclei and atrophic hippocampi [54].  It seems that a consequence of chronic stress is to shift away from explicit processing (PFC and hippocampus dependent) and toward rigid, stimulus-response, implicit processing (caudate and amygdala dependent) [55; 56].

Humans under intense chronic stress have been shown to exhibit improved simple reaction time [57], potentiated reflexes and increased speed for habitual movements [58]. In fact, Vasterling and collaborators [57] suggest that this heightened behavioral reactivity may represent an evolutionarily-mediated neurobiological response to stress “in preparation for life-preserving action.” A similar type of behavioral disinhibition may have permitted TS individuals to react without deliberately reflecting on their decisions, helping them to escape harm and attain resources quickly and without hesitation. It seems possible that TS is an evolved phenotype, intended to adopt a different life-history strategy that allowed affected individuals to react quickly without the normal inhibitory pressures on their reflexes and natural instincts.


The present article concludes that it is plausible that the genes that predispose people to Tourette syndrome, and the spectrum of tic disorders, may have been naturally selected for their role in rapid physical responding. Tics have been conceptualized here as automatic selections from lower brain centers about appropriate tactical movements. This may be associated with the compensating benefits enumerated in Figure 1.

Figure 1

Hypothesized Benefits of Tic Disorders

  • Reduced inhibitory pressure on reflexes and motor pathways
  • Heightened efficiency in the use of force
  • Reduced reaction time and refined rhythmic activity
  • Increased innate and instinctual behaviors
  • Advanced ability for improvisation or extemporization
  • Increased defensiveness, withdrawal, avoidance, vigilance, and opportunism
  • Stimulus hunger, adaptive restlessness and unhesitating reactivity

Tic and tic-like behaviors were probably only adaptive in certain contexts. The intrusion of tics may have been most adaptive when they were incorporated into an ongoing series of movements. Tics that emerged as isolated and discrete movements, when no other behaviors were being performed, or that were not applied to physical objects in the environment may have been less likely to be adaptive. In other words, tics may have been useful, during more active times, as integrated adjustments to ongoing motor behavior.

The statistical age of highest tic severity is typically between eight and twelve, with most individuals experiencing declining tic severity as they reach adolescence. [59]. In many cases, a complete remission of tic symptoms occurs after adolescence [60, 61]. Why would this epidemiological pattern be so widespread? Is it possible that tic-like behavior is part of a learning arc, benefiting children by helping them to refine movement, coordination, and motor praxis?

It will be difficult to determine irrefutably if what we know as TS was in fact an adaptive condition in the ancestral past. The hypothesis presented here is largely exploratory, and underspecified, in part due to the paucity of related research. The present article has made untested assumptions about stress-ecology and the nature of striatal cognition in the wild. It can perhaps be argued that TS and other tic disorders in general have no adaptive qualities. Most common tics observed in modern populations would probably amount to handicaps in an ancestral environment. They might make an individual unattractive to potential mates, betray one’s location to a predator. and waste valuable energy. Common tics like toe crunching, throat clearing, and abdominal tensing would probably have been useless for prehistoric foragers that exhibited them. Moreover, the present hypothesis offers no explanation for chronic tics. However, this type of exploratory writing is generally thought to be progressive as it is well known that analyzing disease states from an evolutionary perspective can integrate seemingly unrelated findings, elucidate pathophysiology, and ultimately refocus clinical research and treatment strategy.

Comparative behavior and neurophysiology could provide insight. Perhaps other species have an equally low but consistent prevalence of ticcing phenotypes as well. It would be interesting to see if there are analogues, or possibly homologues of TS in other species. If there were homologues of TS in species closely related to humans, it would be relatively easy to use molecular techniques to show this given that the genes responsible could be identified. Looking at the evolutionary signatures in the behavioral genetics of TS, might tell us more about its possible role as an adaptation. Further kinematic and biomechanic studies comparing individuals with TS to controls on measures of fluidity, efficiency and speed could help to determine what kinesiological advantages TS individuals have if any. 

It is possible that today tics are often not contextually relevant because of the artificial nature of the modern environment. Caudate hyperactivity in the ancestral past may have led to the potentiation of important procedural and habitual movements, increasing reliance on action patterns that had proven effective. In modern society it may simply lead to the intrusion of eccentric responses. The existence of TS may represent natural human variation and may demonstrate that sometimes it was adaptive to allow the basal ganglia and its procedural memories to dominate behavior uninhibited.


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Lose Weight By Teaching Your Stress System to Better Tolerate Hunger

Our bodies were designed to go for days without eating. Our prehistoric ancestors would not experience undue stress the way we do from missing just one meal. However, we have spoiled our bodies. Every time we get hungry, we start to breathe very shallowly. This is because we haven’t learned to retain our calm while hungry. The best way to overcome this is to spend several minutes pairing fasting with diaphragmatic breathing.

Skip a meal, or at least delay a meal for 2 to 4 hours. When you do so focus on the sensation of hunger and the way it affects your breathing. Don’t skip a meal in the middle of a hectic day, this will further traumatize your relationship with hunger. Rather you want to pair the fast with pure calm. Fasting for more than a single meal can be stressful as well. When I skip a meal, I do nothing and just relax for the 3 or 4 hours when I am at my hungriest. A few hours after your normal mealtime, you will notice recurring pangs of hunger. The hunger pangs are driven by shallow breathing, but diaphragmatic breathing will make them disappear.

All your life until now you have paired hunger with shallow breathing. Dissociate these by using paced breathing to override hunger’s ability to highjack your stress system. I have found that by pairing diaphragmatic breathing with hunger, I have dramatically soothed my hunger drive and I eat less now because of it.

The best way to ensure that you are breathing diaphragmatically is by using the breath pacer app Breathe 2 Relax. This is sometimes called a breath metronome. It will help you ensure that you are taking longer deeper breaths. Breathing in the range of 1-2 seconds per breath during hunger will make your hunger more neurotic. Breathing in the range of 4 to 12 seconds per breath will help you bring peace to hunger. Breathing on longer intervals recruits the diaphragm, which in turn recruits the relaxation response. You want to flood your hunger pains with the relaxation response. For my full description of how to achieve diaphragmatic breathing click here.

Diaphragmatic Fasting Activity

Plan to skip dinner or lunch and spend 2 to 4 hours quelling your hunger pangs using diaphragmatic breathing. Concentrate on the sensations of hunger and how they make your breathing shallow. It is best to breath along with a breath metronome somewhere in the range of 4-10 seconds for each inhalation and 6 to 12 seconds for each exhalation. Pair paced breathing with hunger for at least an hour during this fast. You should start to see results within the first two sessions.

Here are some books that I found really helpful in thinking about weight loss:

Wednesday, October 11, 2017

Practice Breathing Diaphragmaticaly While Speaking to Improve Your Vocal Composure

We all breathe shallowly and fail to use the diaphragm, especially while we are speaking to other people. The exercise below will help you to incorporate an easy, natural, diaphragmatic breathing pattern into your speech pattern. This will make you feel less anxious when speaking, will loosen the tension in your throat, and will improve the quality of your voice.

Without the exercises below it is very difficult to teach yourself to breathe with long, deep breaths while speaking. It is hard to focus on what you want to say while monitoring each breath. The best way to train this is to read out loud while breathing diaphragmatically. You will be accustomed to speaking within a very narrow tidal range (shallow breaths).  The trick to calming down your speech is to prolong the speaking time and ensure that it is not punctuated by anxious gasps. Speaking is exhalation, so you want to speak for as long as you can until you run out of air. I think that the activity below is a fantastic breathing retraining exercise.

Activity Diaphragmatic Speaking: Sit down with a good book and begin reading out loud. As you do so take a very deep, slow breath in and read aloud until you have no breath left to exhale. Do this repeatedly for five minutes or as long as you would like. To do this you have to stop reading for several seconds during each inhalation – do so patiently. You should find that you inhale for somewhere between 5 and 10 seconds and that you speak/exhale for between 6 and 12 seconds. Try to keep your voice at the same volume even when you have almost reached the end of your exhalation. It helps to speak in a calm, friendly voice. If you speak loudly and deeply while doing this activity your voice will become louder and deeper with time.

This method also works very well with singing. You can employ the tactic above when singing along to a song. The only problem is that as you inhale deeply you will be unable to sing several words in the song. Embrace this because deep inhalations permit deep exhalations and will improve your singing voice.

Activity Diaphragmatic Singing: Sing along to a song without breathing shallowly. Take a slow, deep inhalation until you cannot breathe in any more. Then sing until you have no more air left to exhale. Stop singing and inhale completely even if the vocalist in the song you are listening to continues to sing. Once you have taken a full breath in sing until you have no more air left to exhale. Repeat for five minutes, or as long as you would like.   

I have been practicing diaphragmatic breathing for three years now but I just recently realized that as soon as I begin speaking to someone I completely stop breathing diaphragmatically. It became natural for me to breathe deeply on long intervals when I am alone. But as soon as someone started talking to me, I would breathe very shallowly. Because of this I would try to take breaks from conversation to try to regain my composure. At some point I had to force myself to continue to breathe deeply and diaphragmatically in social situations. It was very difficult at first because I was afraid that others would think I looked too calm.

Most people have a tendency to breathe shallowly when they are around others. A part of us is afraid that breathing calmly around others is the ultimate insult. We are almost afraid that the other person will become angry if they see us breathing too deeply. We breathe the most shallowly around people that we respect or fear. This is partly because when we breathe deeply, our emotional reactivity decreases, and our facial response time is delayed. Basically our faces become calmer and appear less attentive. Notice that when you breathe on long intervals during a conversation, your face goes blank and nonexpressive. We need to get over this fear that someone will see us and think that we look too calm. The best way to train this is to try to retain diaphragmatic breath during social encounters. It becomes more and more natural with practice.

Wednesday, September 28, 2016

Peer Reviewed Article Explains How the Brain Creates Consciousness

I have been writing and fine-tuning this manuscript for more than ten years now and it is finally published. It outlines my model of working memory and my theory of how the brain and the mind are linked. They are linked by a very specific pattern of neural activity that creates the continuity of consciousness.

The open access article is titled:

Incremental Change in the Set of Coactive Cortical Assemblies Enables Mental Continuity

and can be read here for free:


This opinion article explores how sustained neural firing in association areas allows high-order mental representations to be coactivated over multiple perception-action cycles, permitting sequential mental states to share overlapping content and thus be recursively interrelated. The term “state-spanning coactivity” (SSC) is introduced to refer to neural nodes that remain coactive as a group over a given period of time. SSC ensures that contextual groupings of goal or motor-relevant representations will demonstrate continuous activity over a delay period. It also allows potentially related representations to accumulate and coactivate despite delays between their initial appearances. The nodes that demonstrate SSC are a subset of the active representations from the previous state, and can act as referents to which newly introduced representations of succeeding states relate. Coactive nodes pool their spreading activity, converging on and activating new nodes, adding these to the remaining nodes from the previous state. Thus, the overall distribution of coactive nodes in cortical networks evolves gradually during contextual updating. The term “incremental change in state-spanning coactivity” (icSSC) is introduced to refer to this gradual evolution. Because a number of associated representations can be sustained continuously, each brain state is embedded recursively in the previous state, amounting to an iterative process that can implement learned algorithms to progress toward a complex result. The longer representations are sustained, the more successive mental states can share related content, exhibit progressive qualities, implement complex algorithms, and carry thematic or narrative continuity. Included is a discussion of the implications that SSC and icSSC may have for understanding working memory, defining consciousness, and constructing AI architectures.

    1. Introduction

    The present article will delineate a simplistic but previously overlooked nonlinear dynamic pattern of brain activity. Two hypothetical constructs are introduced to describe this pattern. The first construct is state-spanning coactivity (SSC), which occurs when cortical nodes exhibit sustained coactivity during the span of short-term memory. The gradual evolution of SSC exhibits a distinctive spatiotemporal pattern of turnover as it plays out in real time. The second construct introduced here, incremental change in state-spanning coactivity (icSSC), refers to this pattern of turnover. icSSC conveys that the set of nodes that are simultaneously coactive changes incrementally as newly activated nodes are added and others are deactivated while a distinct subset remains in SSC. Spreading activity from the nodes in SSC select: 1) inactive neural nodes for activation, 2) active nodes for deactivation, and 3) active nodes for sustained activation. Because a distinct subset of nodes is always conserved from one brain state to the next, each state is embedded recursively in the previous state, amounting to an iterative process that has the potential to progress algorithmically toward a complex result. The general intention of the present article is to propose a qualitative model delineating the theoretical functions of SSC and icSSC from the perspective of cognitive neuroscience.
    The term SSC can be used either to denote a property or to designate a set of neurons. icSSC denotes a property or process. Both are related to the construct of working memory, which is defined as a system responsible for the transient holding and processing of attended information. The fundamental assumption made by this article is that the content of working memory can be said to be in SSC; and as working memory progresses over time, the content can be said to exhibit icSSC. This assumption is applied not only to working memory as the same could be said of attention, consciousness or short-term memory. icSSC can be taken to be the underlying neural substrate of mental continuity. As proposed here, mental continuity is a process where a gradually changing collection of mental representations held in attention/working memory emerges from the icSSC of neural nodes. The thematic and narrative quality created by this continuity during internally generated thought may be largely congruent with key facets of conscious experience. In the course of exploring how neural continuity creates mental continuity, this article will attempt to integrate current theoretical approaches while remaining consistent with prevailing knowledge.
    Table 1: Definition of Key Terms
    Instantaneous Coactivity
    The coactivity of a set of cortical nodes in a single instant or state.
    State-spanning Coactivity (SSC)
    Sustained coactivity exhibited by a set of two or more cortical nodes that spans two or more consecutive brain states
    Incremental Change in State-spanning Coactivity (icSSC)
    The process in which a set of three or more neural nodes exhibiting SSC undergoes a shift in group membership, where at least two nodes remain in SSC and at least one is deactivated and replaced by a new node
    Mental Continuity
    The recursive interrelatedness of consecutive mental states made possible by icSSC

    Animals are information-processing agents. They receive unprocessed data through sensory receptors, expose it to a massively parallel network of nodes and channels, and allow the interaction between the activity and the existing network to determine behavior. Even small invertebrates with elementary nervous systems exhibit ongoing, internally generated neural activity that temporarily biases the network weights. Because it involves mechanisms that include sustained firing, this continuous endogenous processing constitutes a fleeting form of SSC, even in animals like the nematode and fruit fly. In vertebrates, however, SSC involves the coactivation of high-level representations from long-term memory within a single, massively interconnected representational network (telencephalon). Each such representation is a record of the distribution of past neural activity corresponding to a recognizable stimulus or motor pattern. An instantaneous attentional state is composed of a novel combination of these template-like representations which together create contextual, cognitive content. The mammalian neocortex can hold a number of such mnemonic representations coactive for hundreds of milliseconds, using them to make predictions by allowing them to spread their activation energy together, throughout the thalamocortical network. This activation energy converges on the inactive representations in long-term memory that are the most closely connected with the current group of active representations, making them active and pulling them into SSC. Thus, new representations join the representations that recruited them, are incorporated into the set of coactive parameters in SSC and used in subsequent searches.
    When the activity of certain nodes can be sustained for several seconds at a time, as in primate association cortex, the complexity of search in such a system increases. Highly sustained activity allows prioritized representations to act as search parameters for multiple perception-action cycles. This permits more dynamic icSSC, whereby goal-relevant representations can be held constant as others are allowed to change. The icSSC taking place in association areas allows task-pertinent representations to be maintained over multiple cycles, in order to direct complex sequences of interrelated mental states. The individual states in a sequence of such states can be considered interrelated because they share representational content. The associations linking these sequences are saved to memory, impacting future searches and ultimately permitting semantic knowledge, planning, and systemizing. 

    2. Sustained firing, attentional updating, and memory decay

    Mammals regularly encounter scenarios involving sets of stimuli that may remain present (or relevant) throughout the experience. In order to systemize such a scenario, it may be necessary to maintain mental representations of the pertinent contextual stimuli during the experience, and even afterward. Mammalian brains are well-equipped to do exactly this. The glutamatergic pyramidal neurons in the prefrontal cortex (PFC), parietal cortex, and other association cortices, are specialized for sustained firing, allowing them to generate action potentials at elevated rates for several seconds at a time (Fuster, 2009). In contrast, neurons in other brain areas, including cortical sensory areas, often remain persistently active for periods of mere milliseconds unless sustained input from either the environment or association areas makes their continued activity possible (Fuster, 2009). A neuron may exhibit tonic sustained firing due to temporary changes in the strength of certain synapses (short-term synaptic modification (Stokes, 2015)), its intrinsic biophysical properties, extrinsic circuit properties (reverberatory circuits), or dopaminergic innervation (Durstewitz & Seamans, 2002). Prolonged activity of neurons in association areas is largely thought to allow the maintenance of specific features, patterns and goals (Baddeley, 2007).
    Goldman-Rakic (1987; 1990) first suggested that the phenomenon of sustained firing in the PFC is responsible for the information maintenance capabilities of the temporary storage buffers of working memory. Goldman-Rakic (1995) also proposed that the PFC is parceled into several specialized regions, each of which is responsible for detecting, representing and sustaining a different extraction of multimodal information. Since then, the PFC, along with a number of association areas, has been divided into increasingly smaller modules, each with unique receptive/projective fields and functional properties including faculties such as short-term spatial memory, short-term semantic memory, response switching, error detection, reward anticipation, impulse suppression, and many others. Working memory, executive processing and cognitive control are now widely thought to stem from the active maintenance of patterns of activity in the PFC, especially the dorsolateral PFC, that correspond to goal-relevant features  and patterns (Fuster, 2002). The temporary persistence of these patterns ensures that they continue to transmit their effects on network weights as long as they remain active, biasing ongoing processing, and affecting the interpretation of stimuli that occur during their episode of continual firing (Miller & Cohen, 2001). This persistence ensures that context from the recent past is taken into account during action selection.
    During any experience, some neural nodes exhibit more prolonged sustained firing than others. I will assume that in general the most enduringly active nodes correspond to what attention is most focused on, or the underlying theme that remains most constant as other contextual features change. From subjective introspection we know that when we envision a scenario in our mind’s eye, we often notice it transform into a related but distinctly different scenario (James, 1978). These two scenarios are related because our brain is capable of icSSC. In other words, the distribution of active neurons in the brain transfigures incrementally from one configuration to another, instead of changing all at once. If it were not for the phenomenon of icSSC, instantaneous information processing states would be time-locked and isolated (as in most serial and parallel computing architectures), rather than continuous with the states before and after them.
    These observations point to the notion that every cortical state is composed of a subset of elements from the previous state, and also composed of increasingly smaller subsets of elements of states directly before that. In fact, when comparing successive cortical states, the shorter the time difference between two states (on the order of seconds to fractions of milliseconds), the more similar in composition the two states will be. For instance, over the span of 10 milliseconds, a relatively large proportion of nodes will exhibit uninterrupted coactivity; however, over 10 seconds, this proportion will be much smaller. Here, we will be concerned with neural nodes exhibiting SSC at two distinct levels: A) short-term memory/priming, i.e., elements of long-term memory activated above baseline (for seconds to minutes); and B) the focus of attention/immediate memory, i.e., a small, perhaps more active subset of A (for milliseconds to a few seconds). Items in SSC within the focus of attention likely demonstrate active neural binding whereas items in SSC within short-term memory may not.
    Mental continuity and icSSC require a densely interconnected representational system such as a neural network that is capable of holding two or more representations (each specifying discrete and separate informational content) active over the course of two or more points in time (Fig. 1). The sustained activity of a single representation over time does not provide any context or associative/relational content, and so should not be taken to be sufficient for mental continuity. More than one representation is needed. Although its limits are presently being debated, the human neocortex is clearly capable of holding numerous representations active over numerous points in time.