Autism: The [NEW] Hypothesis

FORGET EVERYTHING YOU'VE BEEN TOLD ABOUT AUTISM! Here I present the latest empirical evidence from the past 10 years in Neuroscience, and show how it can all be 'weaponized' for everyday use, by ordinary 'folks'.

FORGET EVERYTHING YOU’VE BEEN TOLD ABOUT AUTISM! Here I present the latest empirical evidence from the past 10 years in Neuroscience, and show how it can all be ‘weaponized’ for everyday use, by ordinary ‘folks’.

The Bayesian Brain Hypothesis

Download the full-text (168 pages of empirical evidence) below, if plugin is failing (it’s a 23 MB PDF)

ABSTRACT

The Hypothesis (Peter Vang, 2023)

Conclusion

The hypothesis which I herein propose is …

(1) that due to maturational delay during the fetal developmental phase in utero, the fetus’ SCN is not fully developed on time, which thereby causes lifelong ‘time-perception mismatch’ between the internal Circadian Clock and the universal space-time and that the fetal developmental delay of Circadian Rhythmicity is likely due to Maternal Circadian Disruption during gestation. The fetal SCN is interconnected with the Maternal SCN, as during gestation, it is the maternal SCN that manages both her own and the fetus’ Circadian Rhythmicity. This is done via Melatonin being passed from the maternal Pineal Gland via the umbilical cord to the fetus’ SCN, which then is entrained for future self- governance of Circadian Rhythmicity. Numerous studies of mammalian Circadian interactions between mother and offspring have provided evidence for the life-long detrimental effects of fetal Circadian Rhythmicity, due to maternal Circadian Disruption during gestation.

(2) that the pervasive maturational delay of 30-40% (compared to typical developing controls) in cortical development gives rise to delayed development of crucial fundamental cognitive functions, especially in regard to Inhibitory control over the Motor System, which in turn explains the impulsive, hyperactive, and inattentive symptoms of ADHD. However, I would herein extend the Unified Theory of ADHD (Barkley, 1997) with The Bayesian Brain Hypothesis, as the maturational delay in Inhibitory control do not only impair current behavior, but also and even more detrimentally future behavioral action, due to the ‘non-effectiveness’ of the Internal Model’s Active (Interoceptive) Inference on Goal-Directed Behaviors, since the efferent copies do not reach their intended targets in time to prevent instinctive, impulsive reflexive behavior based solely on arousal and valence, without forethought.

(3) that the Autistic symptomatology can be explained using the HIPPEA (van de Cruys et al. 2014) and IMAC (Fermin et al. 2022) models, by adding the proposed Subjectively Experienced Embodied Selfhood model as I herein have presented. Combined, these three can lay the empirical foundation for future experimental studies, as well as revision of current therapeutic ‘standards’ so as to move away from ABA, since it has now been substantiated, that the causality is not behavioral, but neurobiological, rendering current beliefs on ABA effectiveness as based on a fallacy.

(4) that Neurodiversity as an explanatory concept must be abolished, as the empirical evidence provided herein, emphatically proves, that Autistic or ADHD behavior ‘is [NOT] just a different way that ones brain works’ and toward a truthful, empirical acceptance of the neurobiological defects that are the cause of the ‘altered cognitive style’. It is detrimental and self-stigmatizing to be labeled as ‘different’ from societal norms, based on societal beliefs of a person with ASD/ADHD and there subjective needs, by evaluating (and demanding) the individual to ‘learn’ and ‘exhibit’ acceptable societal norms for Quality of Life, when these individuals have a different valuation of Quality of Life, than that which is being forced upon them, by societal pressures.

Additional information

Ad 1) The cause of this maturational delay is yet not fully understood, but is widely accepted as fact in the literature on ADHD, which have been shown by neuroimaging studies to result in a 30-40% maturational delay in specific areas of the brain. These areas are crucial for Inhibition of Motor Commands. As the well-known symptoms of ADHD is impulsivity, hyperactivity, and inattention are all related to Inhibition, and as described above, the Internal Model has to be able to either ‘explain away’ or ‘move away’ from the automatic enactment of incoming sensory signals (both interoceptive, exteroceptive, and proprioceptive),a delayed maturation of Inhibition can account for all these symptoms. The ADHD brain is simply not able to ‘resist’ temptations, and acts purely on impulse, without forethought or conscious deliberation of Expected Value, Energy Expenditure, or long-term survival needs present in mind. Furthermore, post-natal entrainment of infant Circadian Rhythmicity is done via Melatonin in breast-milk, and through Zeitgeber (time-giver) entrainment via the ‘structured-across-the- day’ feeding, sleeping, nursing, and playing, which strengthens the accuracy of the infants internal clock and rhythmicity. It is a known fact, that 80% of persons with ASD/ADHD suffers from sleep disturbances, that 30-40% suffers from Restless Legs Syndrome, Obesity, Diabetes Type II, Anxiety, Depression, and a long host of somatic comorbidities, which all can be explained by the correlation to Circadian Disruption.

Ad 2) For the longest time, these behaviors have been attributed to the persons ‘free will’, and was in earlier times described as a ‘moral failing’, until Dr. Russell A. Barkley, PhD, published his book ‘ADHD and the Nature of Self-Control’ in 1997, wherein he provided the empirical evidence for his Unified Theory of ADHD. His theory is based on the maturational delay as the root cause of the lack of inhibitory control by the higher-order Executive Functions to manage the lower-order somatomotor actions (e.g., excessive motor movement, resulting in physical restlessness as well a verbal (non-willed) outburst, attentional agitation by task-irrelevant stimuli etc.). Executive Functions are based on the ability to Self- Speech (covert talking to oneself, Mind’s Voice, Inner Voice etc.), as Self-Speech is needed to alter or inhibit impulsive actions. Self-Play (‘seeing for oneself’ Mind’s Eye, Mentalization) requires that inhibitory control is activated and fully functional, so as to suppress instinctive Reflex Arcs or Automatic Responses, by way of reappraisal of the ‘Object of Excitation’s (the Trigger Event’s stimulus) affective quality, in service of Emotional Regulation via Self-Emoting (feeling for oneself) as part of Goal-Directed Behavior based on conscious, cognitive decision-making processes. Without Self-Speech being fully developed, no other Executive Function will have any effect on motor commands. A child of age 3-5 can be sitting in the sandbox while hitting another child in the head with his plastic shovel, while overtly uttering ‘STOP, STOP, STOP!!!’, yet it having no actual effect on his motoric actions. This is due to the fact, that the Self- Speech Executive Function is delayed in its maturation, and therefore do not have the neuronal connectivity in place yet, to restrict motor movements, regardless of cognitive intentions. I hypothesize, that this maturational delay is causal for the symptoms of Bayesian Brain Dysfunction as neither Bayesian Belief updating of the Internal Model, nor Empirical Priors will be able to exert any actual control over the Motor Control System, and nor will Posterior Beliefs being Precision Weighted and updated into the Internal Model, and that any future action-plans will therefore not have any effect on behavior. This has long been stated by Dr. Barkley as; ADHD is not a disorder of Knowledge, it is however, a disorder of Performance!. Further proof of this being the case can be found in the pharmacological evidence which shows, that 80-90% of the ‘disinhibited behaviors’ are temporarily managed as the medication creates neuronal connectivity and neuromodulatory regulation of e.g., Dopamine and Norepinephrine, which in turn is efficacious on ‘Top-down’ control of behavior, which I hypothesize to be related to Bayesian Brain and Active (interoceptive) Inference being able to function as designed, temporarily while the medication is effective in the brain.

Ad 3) Future work needs to be done to provide detailed explanatory evidence for the combined effect of these 3 models, but I hypothesize that it will result in novel CBT (I have already performed test-cases with late-diagnosed adults with ADHD/ASD, where ‘reprogramming’ of Prior Beliefs have been successful in not only updating or altering Empirical Priors (cf. traumas, anxieties, self-efficacy, self-esteem etc.), but actually discontinuing their future influence on the Internal Model, by reprogramming cognitive beliefs and values of past experiences thus altering the memories of past events, so that the Precision Weighting of incoming sensory signals (e.g., trauma triggering stimuli) can be ‘explained away’ by cognitive therapy that alters the Agents’ Perceptual Inference by ‘installing’ a redirect mechanism (NLP programmed belief updating), that tells the conscious awareness, that ‘although this may feel as the same as back then, look around and realize, that you are not there anymore, right!?”. This protocol have been tested on more than 50 willing participants within the ADDspeaker Community, who I have personally had therapeutic sessions with, while we (the community) worked on refining the protocols, so as to optimize efficacy and longevity.

Ad 4) I have written extensively on the harmful effects of this Sugar-Coating Concept, and I refer the reader to my articles on my blog (link in footer).

I wish to thank the reader for the time and effort afforded me, and conclude this essay with a hope that it will prove informational for most, enlightening for some, and inspirational for yet others.

Peter Vang

January 22, 2023

AUTISM: The Hypothesis

Reference

Allen, M., Levy, A., Parr, T., & Friston, K. J. (2022). In the Body’s Eye: The computational anatomy of interoceptive inference. PLoS Computational Biology, 18(9). https://doi.org/10.1371/JOURNAL.PCBI.1010490

Barkley, R. A. (2012). Executive Functioning and Self-Regulation: Extended Phenotype, Synthesis, and Clinical Implications. In Executive Functioning and Self-Regulation: Extended Phenotype, Synthesis, and Clinical Implications. http://www.russellbarkley.org/content/ADHD_EF_and_SR.pdf

Barrett, L. F. (2017). The theory of constructed emotion: an active inference account of interoception and categorization. Social Cognitive and Affective Neuroscience, 12(1), 1–23. https://doi.org/10.1093/scan/nsw154

Barrett, L. F., & Quigley, K. S. (2021). Interoception: The Secret Ingredient. Cerebrum: The Dana Forum on Brain Science, 2021. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8493823/

Barrett, L. F., & Simmons, W. K. (2015). Interoceptive predictions in the brain. Nature Reviews Neuroscience, 16(7), 419–429. https://doi.org/10.1038/nrn3950

Clark, A. (2013). Whatever next? Predictive brains, situated agents, and the future of cognitive science. Behavioral and Brain Sciences, 36(3), 181–204. https://doi.org/10.1017/S0140525X12000477

Fermin, A. S. R., Friston, K., & Yamawaki, S. (2022). An insula hierarchical network architecture for active interoceptive inference. Royal Society Open Science, 9(6), 220226. https://doi.org/10.1098/rsos.220226

Friston, K. (2010). The free-energy principle: a unified brain theory? Nature Reviews. Neuroscience, 11(2), 127–138. https://doi.org/10.1038/nrn2787

Garcés, M., & Finkel, L. (2019). Emotional Theory of Rationality. Frontiers in Integrative Neuroscience, 13. https://doi.org/10.3389/FNINT.2019.00011

Garfinkel, S. N., Tiley, C., O’Keeffe, S., Harrison, N. A., Seth, A. K., & Critchley, H. D. (2016). Discrepancies between dimensions of interoception in autism: Implications for emotion and anxiety. Biological Psychology, 114, 117–126. https://doi.org/10.1016/j.biopsycho.2015.12.003

Haker, H., Schneebeli, M., & Stephan, K. E. (2016). Can Bayesian theories of autism spectrum disorder help improve clinical practice? Frontiers in Psychiatry, 7(JUN). https://doi.org/10.3389/fpsyt.2016.00107

Hutchinson, J. B., & Barrett, L. F. (2019). The power of predictions: An emerging paradigm for psychological research. Current Directions in Psychological Science, 28(3), 280. https://doi.org/10.1177/0963721419831992

James, William. (1890). The Principles of Psychology. The Principles of Psychology, 1+2 https://www.gutenberg.org/ebooks/57628

Lawson, R. P., Rees, G., & Friston, K. J. (2014). An aberrant precision account of autism. Frontiers in Human Neuroscience, 8(MAY). https://doi.org/10.3389/fnhum.2014.00302

McKinley, M. J., Yao, S. T., Uschakov, A., McAllen, R. M., Rundgren, M., & Martelli, D. (2015). The median preoptic nucleus: front and centre for the regulation of body fluid, sodium, temperature, sleep and cardiovascular homeostasis. Acta Physiologica (Oxford, England), 214(1), 8–32. https://doi.org/10.1111/apha.12487

Palmer, C. J., Seth, A. K., & Hohwy, J. (2015). The felt presence of other minds: Predictive processing, counterfactual predictions, and mentalising in autism. Consciousness and Cognition, 36, 376–389. https://doi.org/10.1016/J.CONCOG.2015.04.007

Pellicano, E., & Burr, D. (2012). When the world becomes ‘too real’: a Bayesian explanation of autistic perception. Trends in Cognitive Sciences, 16(10), 504–510. https://doi.org/10.1016/j.tics.2012.08.009

Peters, A., McEwen, B. S., & Friston, K. (2017). Uncertainty and stress: Why it causes diseases and how it is mastered by the brain. Progress in Neurobiology, 156, 164–188. https://doi.org/10.1016/j.pneurobio.2017.05.004

Quattrocki, E., & Friston, K. (2014). Autism, oxytocin and interoception. Neuroscience and Biobehavioral Reviews, 47, 410–430. https://doi.org/10.1016/j.neubiorev.2014.09.012

Russell, J. A. (2003). Core Affect and the Psychological Construction of Emotion. Psychological Review, 110(1), 145–172. https://doi.org/10.1037/0033-295X.110.1.145

Sennesh, E., Theriault, J., Brooks, D., van de Meent, J. W., Barrett, L. F., & Quigley, K. S. (2022). Interoception as modeling, allostasis as control. Biological Psychology, 167, 108242. https://doi.org/10.1016/J.BIOPSYCHO.2021.108242

van de Cruys, S., Evers, K., van der Hallen, R., van Eylen, L., Boets, B., de-Wit, L., & Wagemans, J. (2014). Precise minds in uncertain worlds: predictive coding in autism. Psychological Review, 121(4), 649– 675. https://doi.org/10.1037/A0037665

van de Cruys, S., Vanmarcke, S., van de Put, I., & Wagemans, J. (2018). The Use of Prior Knowledge for Perceptual Inference Is Preserved in ASD. Clinical Psychological Science, 6(3), 382–393. https://doi.org/10.1177/2167702617740955

Tilføj din kommentar her - Feedback er altid velkomment!