Original Paper: Autism, Stress and The Creative Brain

April 2009

Note: This was my original hypothesis paper (thought process). I started this journey with my own realization of my own autism. I knew that my own brain wasn’t broken and seemed to be working in overdrive and I asked the question: What if these brains already had a unique way of processing information and that was amplified? What would the consequences be and how could it happen. Since that time epigenetics (stress mechanisms, or gene-environment interaction) became mainstream and some of the percentages of the population have shifted. I have a very busy brain, so grabbing quotes (or speaking in script) is often how I communicate, as writing (communication of my multilayered and multidirection thinking) has always been my biggest struggle. I know this isn’t how typical papers are written, nor the correct way… but it was a way that worked for me.

Autism, Stress and The Creative Brain

The evidence collected in this theory suggest that the minds of a subpopulation within the Autism Spectrum inherently process information differently than the norm, or those within the average or majority population. These subgroups of individuals may have evolved or adapted neurophysiologically atypical in order to receive more or uniquely process information from their sensory systems.

“This means creative individuals remain in contact with the extra information constantly streaming in from the environment” says Peterson…”The normal person classifies an object, and then forgets about it, even though that object is much more complex and interesting than he or she thinks. The creative person, by contrast, is always open to new possibilities.” (Peterson 2000)

Just like certain individuals are born athletically unique, typically with more or less fast or slow twitch muscle fibers, it could be similar in the brain. Most, or the average population (60-80%) would have a general combination of brain processing potentials, but the creative individual (15-20%) would have more specific processing potentials for a unique sensory experience of the world (Casanova 2008, Courchesne 2005), usually receiving more information to process or processing the information from the senses in an atypical fashion (sometimes called lateral thinking).

“They’re not random (genes for Autism & Schizophrenia),” says Thomas Insel, Director of the National Institute on Mental Health. “They tend to cluster around genes that are important for brain development.”


Throughout our history, we have always had communities and villages with a core (majority) group of stabilizing, social, community-oriented individuals, and we have always the periphery minds; the innovators, the scientists, the geeks, the artists and the creative.

Leo Kanner published his first paper identifying autistic children in 1943. Kanner didn’t know why the children, all born in the 1930s, acted that way, but noticed the parents were college-educated and career-oriented: lawyers, psychiatrists, scientists. He wrote, “In the whole group, there are very few really warmhearted fathers and mothers. For the most part, the parents, grandparents, and collaterals are persons strongly preoccupied with abstractions of a scientific, literary, or artistic nature, and limited genuine interest in people.”

“People divide roughly, it seems to me, into two kinds, or rather a continuum is stretched between two extremes. There are people people and things people.” —W. D. Hamilton, recognised as one of the most significant evolutionary theorists of the 20th century (2005, p. 205)

From his book “Avoid Boring People” James Watson states:

“It may be that (Mr. X) is not entirely to blame for his social ineptitude. His repeated failures to comprehend the emotional states of those he presided over might be indicative of the genetic hand he was dealt as a mathematical economist—the very cards that endowed him with great quantitative intelligence may also have disable the normal faculties for reading human faces and voices. The social incapacity of mathematicians is no mere stereotype; many of most brilliant are mild to full-blown cases of Asperger’s syndrome (the high-intelligence form of autism), perhaps the most genetically determined of known human behavioral “disabilities.” (Watson 2007)

In a simplistic understanding this population could be more susceptible because of additional information received by the sensory systems through abnormal, “not a reflection of the majority”, differences in the brain. And the extra energy and resource demand this puts on the body, its systems and organs. This sensitivity is also reflected in allergies, sensory dysfunction and emotional dysregulation. This is inclusive of over 50 disorders, most prominently are Autism spectrum, Personality Disorders, Alzheimer’s, Bipolar, and Schizophrenia and all of the organ dysfunctions that are typical in this group including Thyroid Dysfunction, Asthma, Kidney infections, GI dysfunctions, Immune dysfunction.

Neuroatypical, more readily affected by Neurotoxins, creating predictable patterns of Neurological and Neuropsychiatric Dysfunction

Spectrum disorders as Deterministic Chaos Patterns

1. An Initial Condition

2. Multiple and varied influences

3. A predictable pattern of outcomes

An initial condition: Lowered Latent Inhibition or unique brain mechanisms for sensory and information processing. Biochemical, neurophysiological, genetic and adaptive uniqueness of an internally varied group of individuals (approximately 20% of population); increased nutritional needs (precursor resources) and sensitivity in relation to the increased dendritic growth and information processing required.

Small but significant environmental influences: Lack of proper nutritional resources, exposures to toxins that affect mineral balances (heavy metals), fat-balances, neuro-inhibitors, neurotoxins, inflammation and endocrine influencers (chemicals/pesticides/hormones) on a more susceptible population; Negative social imprinting, primal need of acceptance unfulfilled, average personality (instead of individual health) being assumed the ideal. Sensory timelines ignored, the need for additional input neglected/or blocked for foundational learning.

Predictable Outcomes: The co-morbity and spectrum disorders of emotional, behavioral, developmental, personality, neurological and sensory dysfunction as a result from individuals with the capacity to perceive more or uniquely process incoming stimuli from environment; Autism, ADHD, Personality Disorders (BPD), Bipolar, Alzheimer’s, Schizophrenia and ensuing physical complaints, from pain disorders, endocrine/organ issues to bowel and sensory dysfunctions.

Oscillation or Periodic Cycles (required in Chaotic Systems): As demonstrated by Circadian and Ultradian rhythms suggesting a rebuilding or oscillating pattern for restorative neurochemical/energy needs of the brain/body.

Science might be giving us all the clues we need to solve this puzzle but science (old rules of science) could be preventing us from seeing it….

Stuck in the wrong box: Conventional medicine has typically seen diseases as having a single organic cause, and each disease was a separate individual entity. Diseases were from a dysfunction or mutation, something inherently wrong. Modern science has proven this to be an incorrect analogy.


With a new framework for delineating these disorders, it could be hypothesized that children develop the more distressing symptoms of Autism FROM ANY STRESSOR in the environment (as well as many other neurological and behavioral disorders, depending on the individuals’ initial “starting point” and the combination and timing of environmental factors involved). This stress would impede the ability to build neural pathways and the brain would then attempt to protect itself from excessive stimulation, more than what it can handle at the time, due to lack of and combination of resources needed. What the evidence seems to be suggesting is that our genetic or neurophysiological make-up, our responses to and our influences coming from the environment, the increases in our exposures to toxins that affect mineral balances (heavy metals), neurotoxins, inflammation (autoimmunity) and endocrine influencers (pesticides/hormones) could be creating a greater stress on the systems within a particular population. And quite possibly these populations, in evolutionary terms, could be ones that filter less of their sensory information, allowing them to be what some consider more “creative”, but the trade-off could be an increased susceptibility to dysfunction when the environment is not conducive to neural growth.

Children having a genetic predisposition could make them more prone to environmental damage. A neuro-atypical individual, plus neurotoxic exposure could create neurophysiological dysfunction.


It might not be the lack of evidence; it might be a lack of framework to make sense of the evidence.

Initial Condition: Creativity and Mental Illness—Genetic Connections—Comorbidity— BrainGut —Sensory-related Behavior — Percentage of Population—Environmental Factors: Nutrition and the Mind– Plasticity—Toxicity—Autoimmunity—Oxidative Stress—Importance of Acceptance—The Role of Emotion—Rhythms & Restoration

Creativity and Mental Illness

Creativity could be seen as a unique capacity of an individual to receive more sensory information than the normal from their environment. While Mental disorders are often associated with an overabundance of sensory information.

The list of famous, successful and influential individuals who have made tremendous impact to our lives and culture that have/had these disorders, are in the tens of thousands…please go tohttp://www.disabled-world.com/artman/publish/article_0060.shtml for detailed examples.

Andreasen, NC (1987). Creativity and mental illness: Prevalence rates in writers and their first-degree relatives. American Journal of Psychiatry, 144, 1288-129222.

“She (Andreasen) found that 80% of the writers said they had experienced either manic-depressive illness or major depression, while only 30% of the people in noncreative jobs said they had.”

Burch, G.S., Pavelis, C., Hemsley, D.R. and Corr, P.J. (2006). Schizotypy and creativity in visual artists. British Journal of Psychology, 97, 177-90. These findings lend support to other studies reporting higher schizotypy scores in artistic and creative cohorts, although provide some of the first evidence of higher unusual experiences and impulsive nonconformity…in visual artists.

Csikszentmihalyi, M. Creativity: The Work and Lives of 91 Eminent People. HarperCollins 1996. Psychology Today, Jul/Aug 96. If I had to express in one word what makes their personalities different from others, its complexity. They show tendencies of thought and action that in most people are segregated. They contain contradictory extremes; instead of being an “individual,” each of them is a “multitude.”

Dawson M, Soulières I, Gernsbacher MA, Mottron L (2007) The level and nature of autistic intelligence. Psychological Science 18:657-62 Their scores were, on average, 30 percentile points, and in some cases more than 70 percentile points, higher than their scores on the Wechsler scales of intelligence. Typically developing control children showed no such discrepancy, and a similar contrast was observed when a sample of autistic adults was compared with a sample of nonautistic adults. We conclude that intelligence has been underestimated in autistics.

Eysenck, H. J. (1994). Creativity and personality: Word association, origence, and Psychoticism. Creativity Research Journal, 7, 209-216. http://dx.doi.org/10.1016/S0191-8869(96)00162-6. The results are consistent with the idea that different forms of creative behaviour are related to distinct characteristics of personality.

Frosch WA: Moods, madness and music; Major affective disease and musical creativity. Comprehensive Psychiatry, 1987; 28: 315-322.

Goertzel, M. G., Goertzel, V. & Goertzel, T. G. (1978). 300 eminent personalities: A Psychosocial analysis of the famous. San Francisco: Jossey-Bass. The three forms of data converge on the conclusions that (a) exceptional creativity is often linked with certain symptoms of psychopathology and (b) this linkage has some degree of genetic foundation. Nevertheless, this relationship is not equivalent to the claim that creative individuals necessarily suffer from psychopathology. A theoretical interpretation is offered in terms of the cluster of cognitive abilities and dispositional traits required for creative behavior and the impact of genetic and environmental factors in the emergence of this cluster.

Hayashi M, Kato M, Igarashi K, Kashima H (2008) Superior fluid intelligence in children with Asperger’s disorder. Brain and Cognition 66:306-10. http://dx.doi.org/10.1016/j.bandc.2007.09.008. The results showed that children with Asperger’s disorder outperformed on the test of fluid reasoning than typically developing children. We suggest that individuals with Asperger’s disorder have higher fluid reasoning ability than normal individuals, highlighting superior fluid intelligence.

Jamison, K. R. (1989). Mood disorders and patterns of creativity in British writers and artists. Psychiatry, 52, 125-134. The association between extreme states of emotion and mind and creativity not only is fascinating but also has significant theoretical, clinical, literary and societal-ethical implications. These issues…include the understanding of cognitive, perceptual, mood and behavioral changes common to manic, depressive and creative states; the potential ability to lessen the stigma of mental illness; effects of psychiatric treatment (for example, lithium) on creativity; and concerns raised about genetic research on mood disorders

Jamison, K. R. (1993). Touched with fire: Manic-depressive illness and the artistic temperament. New York: Free Press. Psychiatry, 125-134.

Kaufman, J.C. (2001). The Sylvia Plath effect: Mental illness in eminent creative writers. The Journal of Creative Behavior, 35(1).

Ludwig, AM. (1992). Creative achievement and psychopathology: Comparison among professions. American Journal of Psychotherapy, 46, 330-356. The results, in their entirety, suggest (a) that different patterns of psychopathology, if any, tend to be associated with different professions and at different periods in individuals’ lives, (b) that different professions are associated with different levels of creative achievement, and (c) that certain types of psychopathology are associated with creative achievement across all professions.

Ludwig, A. M. (1995). The price of greatness: Resolving the creativity and madness controversy. New York: Guilford Press.

Ludwig AM: Reflections on creativity and madness. Am J Psychotherapy, 1989; 43: 4-14

“As adults, between 59% and 77% of artists, writers and musicians suffered mental illness, while only 18% to 29% of the other professionals did.” ~ Arnold M. Ludwig

Heaton P, Wallace GL (2004) Annotation: the savant syndrome. Journal of Child Psychology and Psychiatry 2004 45:899-911. Results: It has long been observed that savant skills are more prevalent in individuals with autism than in those with other disorders. Therefore, in this annotation we seek to explore the parameters of the savant syndrome by considering these skills within the context of neuropsychological accounts of autism. A striking finding amongst those with savant skills, but without the diagnosis of autism, is the presence of cognitive features and behavioural traits associated with the disorder. Conclusions: We thus conclude that autism (or autistic traits) and savant skills are inextricably linked and we should therefore look to autism in our quest to solve the puzzle of the savant syndrome.

Myerson, A., & Boyle, R. D. (1941). The incidence of manic-depression psychosis in certain socially important families: Preliminary report. American Journal of Psychiatry, 98, 11-21.

Nikanorova, M, Temin P. Epilepsy and Genius of Dostoevsky. Russian Neurology and Psychiatry: Abstracts from the 22nd International Epilepsy Congress, Dublin, Ireland. Epilepsia, 38 S.3, 273, 1997.

Peterson, JB, & Carson, S. (2000). Latent inhibition and openness to experience in a high-achieving student population. Personality and Individual Differences, 28, 323-332.

“Scientists have wondered for a long time why madness and creativity seem linked,” says Carson. “It appears likely that low levels of latent inhibition and exceptional flexibility in thought might predispose to mental illness under some conditions and to creative accomplishment under others.”

Post, F. (1996). Verbal creativity, depression and alcoholism: An investigation of one hundred American and British writers. British Journal of Psychiatry, 168, 545-555. A hypothesis is developed, which links the greater frequency of affective illnesses and alcoholism in playwrights and prose writers, in comparison with poets, to differences in the nature and intensity of their emotional imagination

Sass, L.A., & Sculdberg, D. (Eds.). (2000-2001). Creativity and the schizophrenia spectrum [Special issue]. Creativity Research Journal, 13(1).

Simonton, D. K. (2004). Creativity in science: Chance, logic, genius, and zeitgeist.
Cambridge, England: Cambridge University Press.

University Of Toronto (2003, October 1). Biological Basis For Creativity Linked To Mental Illness. ScienceDaily. Retrieved September 8, 2008, from http://www.sciencedaily.com /releases/2003/10/031001061055.htm

Wellcome Trust (2008, October 15). People With Autism Make More Rational Decisions, Study Shows. ScienceDaily. Retrieved December 7, 2008, from http://www.sciencedaily.com /releases/2008/10/081015110228.htm

People with autism-related disorders are less likely to make irrational decisions, and are less influenced by gut instincts, according to research funded by the Wellcome Trust. The study adds to the growing body of research implicating altered emotional processing in autism. Decision-making is a complex process, involving both intuition and analysis: analysis involves computation and more “rational” thought, but is slower; intuition, by contrast, is much faster, but less accurate, relying on heuristics, or “gut instincts”.

Bad Boys Really do get More Girls. From issue 2661 of New Scientist magazine, 18 June 2008, page 12 http://www.newscientist.com/article/mg19826614.100 The traits are the self-obsession of narcissism; the impulsive, thrill-seeking and callous behaviour of psychopaths; and the deceitful and exploitative nature of Machiavellianism. At their extreme, these traits would be highly detrimental for life in traditional human societies. People with these personalities risk being shunned by others and shut out of relationships, leaving them without a mate, hungry and vulnerable to predators. But being just slightly evil could have an upside: a prolific sex life, says Peter Jonason at New Mexico State University in Las Cruces. “We have some evidence that the three traits are really the same thing and may represent a successful evolutionary strategy.”

Silberman S (2001) The Geek Syndrome. Wired.com 9.12 http://www.wired.com/wired/archive/9.12/aspergers.html

“Autism – and its milder cousin Asperger’s syndrome – is surging among the children of Silicon Valley. Are math-and-tech genes to blame?”

Nugent, B (2008) Field Guide to the Nerd. Psychology Today.7/8 http://psychologytoday.com/articles/pto-20080717-000009.html

Besides, nerds can learn social skills if they approach them with the same intellectual rigor they bring to calculus, says Lawrence Welkowitz, a psychologist at Keene State College. He’s found that nerds can often master the subtleties of social interaction, compensating for disinclination with focus and practice. He runs a peer-mentoring program in which popular kids take nerds under their wing and give them tips on how to be cool. The exposure to the popular kids’ world gives nerds a taste of social acceptance, which inspires them to keep working at it. But the socialization process isn’t easy: At first, nerds tend to get more depressed as they get more social. “They realize it’s hard, and they’ve been missing out on a lot,” he says. “But eventually, they get more skilled.”

Quote from neurodiversity.com/bio_grandin.html

Q: What would happen if the autism gene was eliminated from the gene pool?

A: You would have a bunch of people standing around in a cave, chatting and socializing and not getting anything done.

Temple Grandin


Neurotransmitters & Hormones related to Personality & Dysfunctions


Normal Dopamine: (From NewScientist Feb. 2009: How to control a Herd by David Robson):

Interest in the idea of a herd mentality has been renewed by work into mirror neurons – cells that fire when we perform an action or watch someone perform a similar action. It suggests that our brains are geared to mimic our peers. “We are set up for ‘auto-copy’,” says Haidt.

Neurological evidence seems to back this idea. Vasily Klucharev, at the Donders Centre for Cognitive Neuroimaging in Nijmegen, the Netherlands, found that the brain releases more of the reward chemical dopamine when we fall in line with the group consensus (Neuron, vol 61, p 140). His team asked 24 women to rate more than 200 women for attractiveness. If a participant discovered their ratings did not tally with that of the others, they tended to readjust their scores. When a woman realized her differing opinion, fMRI scans revealed that her brain generated what the team dubbed an “error signal”. This has a conditioning effect, says Klucharev: it’s how we learn to follow the crowd.

(Those with altered dopamine receptors…could be those who don’t follow the crowd, or at least are not chemically conditioned or rewarded to do so….they are novelty, sensory, new experience seekers or depend more on rational thought than on peer pressure)

Abnormal Dopamine: (from Helen Fisher PhD, Chemistry.com)

Explorers have a very active dopamine system, a brain chemical associated with the tendency to seek novelty, among other qualities. …Explorers have more energy than most people; they tend to be restless, sometimes fast-paced. And they are highly curious—”For always roaming with a hungry heart,” as Tennyson put it. Constantly generating new ideas or creative insights, they easily shift their attention from one thing to another.

Our research suggests that in high novelty-seeking individuals,

the brain is less able to regulate dopamine.“

Dr David Zald
Vanderbilt University

From TIME online:

Why We Take Risks — It’s the Dopamine By Alice Park. Tuesday, Dec. 30, 2008

Earlier studies in rats had shown that animals that tend to explore and take more risks in new environments also tend to have fewer of these inhibitory receptors (for Dopamine), and Zald wanted to find out if the same was true in people. “This is one of those situations where the data came out essentially perfectly,” he says. “The results were exactly as we predicted they would be, based on the animal data.” That is, like the rats, humans who were more spontaneous and eager to take risks had fewer dopamine-regulating receptors than those who were more cautious. (Zald 2004)

Zald DH, Boileau I, El-Dearedy W. Dopamine Transmission in the Human Striatum during Monetary Reward Tasks. J. Neurosci. 24: 4105-4112; doi:10.1523/JNEUROSCI.4643-03.2004

Zald DH, Cowan RL, Riccardi P. Midbrain dopamine receptor availability is inversely associated with novelty-seeking traits in humans. J Neurosci. 2008 Dec 31;28(53):14372-8. PMID: 19118170

DeYoung CG, Peterson JB, Higgins DM. Higher-order factors of the Big Five predict conformity: Are there neuroses of health? (2002) Personality and Individual Differences, 33 (4), pp. 533-552. We present a biologically predicated model of these two personality factors, relating them to serotonergic and dopaminergic function, and we label them Stability (Emotional Stability, Agreeableness, and Conscientiousness) and Plasticity (Extraversion and Openness). Based on this model, we hypothesize that Stability will positively predict conformity (as indicated by socially desirable responding) and that Plasticity will negatively predict conformity. A structural equation model indicates that conformity is indeed positively related to Stability (university sample: β=0.98; community sample: β=0.69; P<0.01 for both) and negatively related to Plasticity (university sample: β=−0.48, P<0.07; community sample: β=−0.42, P<0.05). These findings suggest that there are pros and cons of conformity, such that the most thorough conformists will tend to be stable but also rigid, less able to adjust to novelty or change.

BPD: Dopamine Dysfunction in Borderline Personality Disorder: A Hypothesis: europsychopharmacology (2004) 29, 1029–1039, advance online publication, 24 March 2004; doi:10.1038/sj.npp.1300424

Some researchers believe that dopamine dysfunction may be also involved in the development of borderline personality disorder (BPD) because of evidence that dopamine is involved in cognitive and emotional processing and the regulation of impulsive behaviors (which are related to BPD symptoms). In addition, antipsychotic medications that target dopamine receptors in the brain seem to reduce BPD symptoms

SCHIZOPHRENIA: Gupta M, Chauhan C, Bhatnagar P, et al. Genetic susceptibility to schizophrenia: role of dopaminergic pathway gene polymorphisms. Pharmacogenomics. 2009 Feb;10(2):277-91.

The dopamine (DA) hypothesis is the oldest and most established of the schizophrenia hypotheses. It has evolved from clinical observations, and received empirical validation from antipsychotic treatment and more direct testing from imaging studies. Although clearly not sufficient to explain the complexity of this disorder, it offers a direct relationship to symptoms and to their treatment.

High levels of the neurotransmitter dopamine (or its agonists) in the brain are thought to lower latent inhibition (Swerdlow 2003). Certain dysfunctions of the neurotransmitter glutamate have also been implicated, and the glutamate hypothesis of schizophrenia is increasingly being seen as an alternative to the dopamine hypothesis of schizophrenia. (Bills 2004)

Swerdlow NR, Stephany N, Wasserman LC, Talledo J, Sharp R, Auerbach PP. Dopamine agonists disrupt visual latent inhibition in normal males using a within-subject paradigm. Psychopharmacology. 2003 Sep;169(3-4):314-20. PMID 12610717

Bills C, Schachtman TR, Serfozo P, et al. (2005) Effects of metabotropic glutamate receptor 5 on latent inhibition in conditioned taste aversion. Behavioural Brain Research. 157 (1), pp. 71-78.


Gadow KD, Roohi J, DeVincent CJ, Hatchwell E. Association of ADHD, tics, and anxiety with dopamine transporter (DAT1) genotype in autism spectrum disorder. J Child Psychol Psychiatry. 2008 Dec;49(12):1331-8.


British Association For The Advancement Of Science (2007, September 13). Testosterone In Womb Linked To Autism. ScienceDaily. Retrieved January 8, 2009, from http://www.sciencedaily.com /releases/2007/09/070912160304.htm

Brosnan MJ. Digit ratio and faculty membership: implications for the relationship between prenatal testosterone and academia. Br J Psychol. 2006 Nov; 97(Pt 4):455-66

Dr Brosnan said that men having levels of testosterone very much higher than normal for males would also create the right hemisphere dominated brain which could help in science. The extremes of low testosterone and high testosterone for men would create the scientific brain, and the normal range in the middle would create the ‘social science’ brain.

“This right brain development is at the expense of language abilities and people skills that men with a more usual level of testosterone develop and which can help them in social science subjects like psychology or education.”

Brosnan MJ. Digit ratio as an indicator of numeracy relative to literacy in 7-year-old British schoolchildren Br J Psychol. 2008 Feb; 99(Pt 1):75-85

The researchers then looked at boys’ and girls’ test performances separately and compared them to finger-length ratio measurements. They found a clear link between high prenatal testosterone exposure, indicated by the longer ring finger compared to the index finger, and higher scores on the math SAT.

Similarly, they found higher literacy SAT scores for the girls among those who had lower prenatal testosterone exposure, as indicated by a shorter ring finger compared with the index finger.

The researchers also compared the finger-lengths ratios to all the children’s SAT scores and found that a relatively longer ring finger—indicating greater prenatal exposure to testosterone—meant a wider gap in scores for math versus literacy (writing and critical reading).

“Finger ratio provides us with an interesting insight into our innate abilities in key cognitive areas,” Brosnan said, in a prepared statement. The results will be detailed in an upcoming issue of the British Journal of Psychology. LiveScience Staff (2007) Finger Length Predicts SAT Performance. posted: 5/22 Retrieved from livescience.com


Harris CL, Dinn WM, Marcinkiewicz JM. Partial seizure-like symptoms in borderline personality disorder. Epilepsy & Behavior, Volume 3, Issue 5, October 2002, Pages 433-438

Mendez MF, Catanzaro P, Doss RC, et al. Seizures in Alzheimer’s disease: clinicopathologic study. J Geriatr Psychiatry Neurol. 1994 Oct-Dec;7(4):230-3

Melvin CL, Carey TS, Goodman F, et al. Effectiveness of antiepileptic drugs for the treatment of bipolar disorder: findings from a systematic review. J Psychiatr Pract. 2008 Mar;14 Suppl 1:9-14

Hyde TM, Weinberger DR. Seizures and schizophrenia. Schizophr Bull. 1997;23(4):611-22

“The shower curtain of inhibition was a term introduced by a Hungarian neuroanatomist by the name of Szentagothai. Otherwise it was also called a strong vertical flow of inhibition by Vernon Mountcastle. Having a lot of wires together without insulating them from adjacent modules may promote what is called ephaptic conduction, amplification, and therefore seizures.” ~Dr. Manuel Casanova

We know that epilepsy involves temporary bursts of excessive electrical activity in different locations in the brain, locations which house our bodily sensations and functions as well as our memories and emotions. Psychiatrist Dr. David Bear states that the abnormal brain activity found in temporal lobe epilepsy can play a role in creative thinking and the making of art by uniting sensitivity, insight and sustained, critical attention. According to Dr. Bear:

“A temporal lobe focus in the superior individual may spark an extraordinary search for that entity we alternately call truth or beauty.”

What is also clear in the discussion of genius and epilepsy is that some of the most famous people in history had seizures. People with epilepsy have excelled in every area. A list of people who are responsible for changing civilization as we know it, all of whom are strongly suspected or known to have had epilepsy. It’s an impressive group.

~Retrieved from epilepsy.com, Topic Editor: Steven C. Schachter, M.D. 12/15/06 http://www.epilepsy.com/epilepsy/famous

The anticonvulsants are a diverse group of pharmaceuticals used in the treatment of epileptic seizures. Anticonvulsants are also increasingly being used the treatment of bipolar disorder, since many seem to act as mood stabilizers. The goal of an anticonvulsant is to suppress the rapid and excessive firing of neurons that start a seizure. Failing this, a good anticonvulsant would prevent the spread of the seizure within the brain and offer protection against possible excitotoxic effects that may result in brain damage. However, anticonvulsants themselves have been linked to lowered IQ in children. (from Wikipedia 1/2009)

(reduce GABA, reduce dendritic growth and neuronal firing in the brain, these brains have more information than normal-they need more resources, when the resources are blocked/neglected…the stimulation grows unchecked and un-insulated…the anticonvulsants could theoretically stops them from having too much information…more information is a higher IQ, stop the communication, you stop seizures, but could we just stop the inflammation and toxicity and any other issues that would create the seizures?)

Re-examining Classical Physics guidance of “ridding the diets” of fat b/c of calories:

Taha AY, Huot PS, Reza-López S, et al. Seizure resistance in fat-1 transgenic mice endogenously synthesizing high levels of omega-3 polyunsaturated fatty acids. J Neurochem. 2008 Apr;105(2):380-8.

The major molecular targets of marketed anticonvulsant drugs are 1) voltage-gated sodium channels; 2) components of the GABA system, including GABAA receptors, the GAT-1 GABA transporter, and GABA transaminase; and 3) voltage-gated calcium channels.

Börjesson SI, Hammarström S, Elinder F. Lipoelectric modification of ion channel voltage gating by polyunsaturated fatty acids. Biophys J. 2008 Sep;95(5):2242-53. Epub 2008 May 23

Recall GABA/AUTISM connection from studies such as:

Ma DQ, Whitehead PL, Menold MM, …PERICAK-VANCE MA. Identification of significant association and gene-gene interaction on GABA receptor subunit genes in autism. Am J Hum Genet 2005 Sep;77(3):377-88.


CHARACTER TYPES by Dr. Michael Lesser

Orthomolecular Psychiatry

What is wholly unique about Dr. Lesser theory is that he believes ALL individuals have these in-balance and out-of-balance personas. That the mental illnesses we see are reflections of a particular personality simply gone awry, out-of-balance, or maladaptive.

Dr. Lesser determined his character typing using first the “Five Factor Model (FFM)”of personality and then the biochemical markers of histamine, cortisol, serotonin and copper/zinc/magnesium; he noticed there were certain patterns within each “character-type”.

Dr. Lesser, suggests that the “Stoic” personality is the most common of all character types, estimating over 50% of his patients’ exhibit these traits. Why would this be significant? Because over 50% makes the Stoic Personality “normal” or the “average” personality. And if there is a majority personality and our current medical model assumes a static state initial condition, when there are actually variable initial conditions corresponding to unique physiological and neurophysiological aspects that reflect personality….then we have been making many incorrect assumptions about timelines, expectations and the measurement of “ideal”….

(percentages estimated)

the Stoic:

Dependable, Selfless, Organized, Uncomplaining, Considerate, Calm, Friendly, Even-keeled, Capable, Giving

the Guardian:
Steady, Reliable, Other-directed, Safety-conscious, Attentive to detail, Vigilant, Conscientious, Efficient, Serious, Fastidious

the Warrior:
Dedicated, Fun-loving, Charming, Persuasive, Passionate, Spontaneous, Decisive, Leader, Calculating, Inhibited


the Star:
Energetic (and energizing), Loving, Intense, Passionate, Intuitive, Creative, Exuberant, Charismatic, Dominant, Dramatic

the Lover:
Outgoing, Attractive, Empathic, Loving, Sexual, Flirtatious, Warm, Emotionally expressive, Sensitive, Seductive

the Dreamer:
Visionary, Humble, Spiritual, Sensitive, Gentle, Introspective, Solitary, Cerebral, Shy, Eccentric

-Lesser M, Kapklein CJ. (2003) The Brain Chemistry Plan. Perigee Trade.

Michael Lesser, M.D., has published more than 50 peer-reviewed journal articles on orthomolecular psychiatry, including the premier academic review in the field. He is the founder of the Orthomolecular Medical Society and Nutritional Medicine, a communications company that sponsors world conferences on nutrition and vitamin therapy. He has been in private practice for over 20 years and has testified before the U.S. Senate on nutrition and mental health.

Personality types from DR. HELEN FISHER, PhD.

Helen E. Fisher, PhD biological anthropologist is a Research Professor in the Department of Anthropology at Rutgers University. She has written five books on the evolution and future of human sexuality, monogamy, adultery and divorce, gender differences in the brain, the chemistry of romantic love.

Interview from TIME magazine:

You basically break people down into four broad temperaments, each associated with certain brain chemicals.

There was a great deal of data that people vary in terms of their expression of dopamine and norepinephrine, serotonin, estrogen and oxytocin and testosterone. I culled from the academic literature all of those data points that show that these particular brain-chemical systems are related to certain aspects of personality. And I saw constellations of temperament traits that seemed to be associated with these chemicals.

What are the four types?
People who express dopamine — I call them Explorers — tend to be risk-taking, curious, creative, impulsive, optimistic and energetic. The traits associated with the serotonin system express themselves in what I call Builders. They’re cautious but not fearful, calm, traditional, community-oriented, persistent and loyal. Directors have traits associated with activity in the testosterone system. These people tend to be very analytical, decisive, tough-minded; they like to debate and can be aggressive. The fourth type is the Negotiator. Men or women who express activity in the estrogen system tend to be broadminded imaginative, compassionate, intuitive, verbal, nurturing, altruistic and idealistic.

How did you choose the four types and ascertain who they like?
They emerged out of the genetic literature. I didn’t impose them. I read the literature, and I found them. And then I developed the questionnaire to make sure these people did express these four [types of temperament] and expressed them in these ways. That study was done on 40,000 people. And then on the dating site Chemistry.com.

BELINDA LUSCOMBE (2009). The Biology of Dating: Why Him, Why Her. 1/31.TIME Magazine. http://www.time.com/time/health/article/0,8599,1876113,00.html

An Evolutionary Advantage

Why might a socially balanced, effective filtering Personality be more common?
From an evolutionary standpoint they represent stability, community & socializing personalities. Linear thinking, salt of the earth, socially-oriented, core characteristics for a stable community.

And the more creative, less socially inclined, less filtering Peripheral Minds?
Might represent the possibilities of human experience, passion, innovation, change-makers, reality-truth seekers. The periphery of human existence, the forces of change, exuberance, understanding and the seekers of knowledge and fundamental understanding.






There could easily be an evolutionary advantage to stability plus possibility in social structures and communities.

The mistakes of the measuring stick

(Everyone is unique in their own way…but there are patterns of similarities)

We all have different potentials and different inborn skills. We are all equal and needed and special and important to our community, our families, and the advancement of the human race. And there could be an evolutionary benefit to having a minority with variable neurophysiological experiences of the world…

How did this happen?

The Bell Curve gone wrong: Measure the average.

Unfortunately the Average Acumen might fall to the average personality. Or the Stoic. So all standards, testing, developmental expectations would be for the traits of the average Stoic who has very effective filtering systems and social-based skills. So they develop and learn very differently than less-filtering character types: the Star, the the Lover and the Dreamer. These character types need more information to learn the same concepts, because they learn them fundamentally and with more information.

Their learning curve appears to be different. They may need more information, more possibilities, more challenges, and different angles to fully identify with the concept at hand (including sensory information). Or learn different skills at different times in their development (See “Brain Matures a Few Years Later but at normal Pace for ADHD” Shaw 2007).These differences will seem un-normal, slow or scattered, but they must build the same foundations as all children must.

My thoughts:

Genius: someone who sees reality differently or more clearly than others; one who receives or comprehends more information from their environment than the norm.

Madness: someone who sees reality differently or more clouded than others; one who receives but cannot comprehend the excessive information coming in from their environment.

Further prominent examples of genius and madness: Einstein’s son, Eduardo and James Watson’s son with schizophrenia. John Nash. …. Many great scientists in our past or present could be associated with either a personality disorder or within the Autistic-Asperger’s spectrum. Asperger’s is also known as the “Geek-Syndrome”…

This is the fine line. And there could be any number of stressors that could cause the circuitry in the brain to not fully process information and lead to sensory dysfunction. It is possible that this “excess” of information could lead an individual to require learning information differently than the norm, sometimes more quickly and sometimes it could take much longer, either because of distractions (or longer ways around), or because they learn things much more intimately and fundamentally than their peers and this takes more precise information and sometimes more information than what is offered or available at that time (but the thought still got started, the dendrites were put into action and want to finish their circuitry). And ultimately this increased information, with its subsequent dendrites, neural responses, and neurotransmitters are not produced in a vacuum, they are not just available in a static manner, they need to be manufactured and regulated by a multitude of organs, systems, raw material and energy, we could make an assumption from the evidence that if any of these pathways are inhibited in any way the information would not be processed properly or the pathways would have difficulty being built…and these necessary components would naturally and under normal conditions work differently than those who filter their environments more efficiently (don’t receive as much information) and these individuals, who have more information to process (creative), would require more nutritional or raw materials from their systems and their outside environment than the average, a person receiving less sensory input.


Genes, Inherited traits, Expression, Patterns and Clues

A genetic disease is very different than an inheritable genetic susceptibility, especially when we know that we can no longer look for that “magic bullet” answer from genetic research…

Scientists have spent years looking for a “schizophrenia gene” and an “autism gene,” but the search has been frustrating. They have ID’d genes that make people susceptible to the disorders, but none of those genes are shared by enough people … “They’re not random,” says Thomas Insel, director of the NIMH “They tend to cluster around genes that are important for brain development.” (Shute 2008)

Baron-Cohen S, Auyeung B, Ashwin E, Knickmeyer R. Fetal testosterone and autistic traits: A response to three fascinating commentaries. Br J Psychol. 2009 Feb; 100(Pt 1):39-47

Baron-Cohen S, Ring HA, Bullmore ET. The amygdala theory of autism

Neuroscience & Biobehavioral Reviews. Volume 24, Issue 3, May 2000, Pages 355-364. doi:10.1016/S0149-7634(00)00011-7

Bailey A, Palferman S, Heavey L, et al. Autism: the phenotype in relatives. J Autism Dev Disord. 1998 Oct;28(5):369-92. There is broad agreement that genetic influences are central in the development of idiopathic autism. Whether relatives manifest genetically related milder phenotypes, and if so how these relate to autism proper, has proved a more contentious issue. A review of the relevant studies indicates that relatives aresometimes affected by difficulties that appear conceptually related to autistic behaviors. These range in severity from pervasive developmental disorders to abnormalities in only one area of functioning, and possibly extend to related personality traits. Issues involved in clarifying the components of milder phenotypes and their relationship to autism are outlined

Brain Differences Identified In Adolescents With Mental Illness. ScienceDaily. American College of Neuropsychopharmacology (2007), December 10. Retrieved September 9, 2008, from http://www.sciencedaily.com /releases/2007/12/071208081554.htm

Brosnan MJ. Digit ratio and faculty membership: implications for the relationship between prenatal testosterone and academia. Br J Psychol. 2006 Nov;97(Pt 4):455-66

Burmeister M, McInnis MG, Zöllner S. Psychiatric genetics: progress amid controversy. Nat Rev Genet. 2008 Jul;9(7):527-40. Several psychiatric disorders — such as bipolar disorder, schizophrenia and autism — are highly heritable, yet identifying their genetic basis has been challenging, with most discoveries failing to be replicated. However, inroads have been made by the incorporation of intermediate traits (endophenotypes) and of environmental factors into genetic analyses.

Carter CS, Macdonald A, Botvinick M, et al. Parsing executive processes: strategic vs. evaluative functions of the anterior cingulate cortex. Proc Natl Acad Sci U S A 2000; 97:1944–1948

Casanova MF. The significance of minicolumnar size variability in autism: a perspective from comparative anatomy. In: Zimmerman AW, ed. Autism: Current theories and evidence. Totowa, N.J.: Humana Press; 2008 Oct 15, in press

Chiu PH, Kayali MA, Kishida KT. Self responses along cingulate cortex reveal quantitative neural phenotype for high-functioning autism. Neuron. 2008 Feb 7;57(3):463-73

Courchesne E, Carper R, Akshoomoff N. Evidence of brain overgrowth in the first year of life in autism. JAMA. 2003;290:337–344.

“Judith Rapoport, chief of the child psychology branch at the National Institute of Mental Health and one of the researchers, sees a similarity. She’s spent the past three decades studying how children’s brain development is affected by disorders like schizophrenia. The brains of children with early-onset schizophrenia are much larger than normal in the first few years of life, for instance. Children with autism also have an unusual amount of brain growth before age 3. In this new work, she and her colleagues found that two places where variations in genes tended to cluster in people with schizophrenia were also more common in people with autism.” (Shute 2008)

Courchesne E, Pierce K. Why the frontal cortex in autism might be talking only to itself: local over-connectivity but long-distance disconnection. Curr Opin Neurobiol 2005;15(2):225-230. Increased local but reduced long-distance cortical-cortical reciprocal activity and coupling would impair the fundamental frontal function of integrating information from widespread and diverse systems and providing complex context-rich feedback, guidance and control to lower-level systems.

Crespi, BJ. (2008) Genomic imprinting in the development and evolution of psychotic spectrum conditions. Biological Reviews 83:441-493.

Crespi, BJ., Summers, K. and Dorus, S. (2007). Adaptive evolution of genes underlying schizophrenia. Proceedings of the Royal Society of London Series B, Biological Sciences, 274, 2801-10. Recent theory has proposed a resolution: that genetic liability to schizophrenia has evolved as a secondary consequence of selection for human cognitive traits. This hypothesis predicts that genes increasing the risk of this disorder have been subject to positive selection in the evolutionary history of humans and other primates

Cloninger C, Gottesman I. Genetic and environmental factors in antisocial behavior disorders. In: Mednick S, Moffitt T, Stack S, editors. The causes of crime. New biological approaches. New York7 Cambridge University Press; 1987. p. 92– 109. Our findings support the importance of both genetic and environmental factors in antisocial behavior among women as well as the possibility that the relative importance of each set of influences differs by sex in both childhood and adulthood.

Duke University Medical Center (2005, August 3). Complex Gene Interactions Account For Autism Risk. ScienceDaily. Retrieved December 30, 2008, from http://www.sciencedaily.com /releases/2005/08/050803063300.htm

Filtering Systems: Receptors in the Brain

Excitatory and Inhibitory Pathways for Information Management


GLUTAMATE: A genome scan was previously performed and pointed to chromosome 6q21 as a candidate region for autism. This region contains the glutamate receptor 6 (GluR6 or GRIK2) gene, a functional candidate for the syndrome. Glutamate is the principal excitatory neurotransmitter in the brain and is directly involved in cognitive functions such as memory and learning. (Jamain, 2008). Among the new clues is stronger evidence for an association between autism and sites of genes for neurexins, molecules that build glutamate synapses; the connection machinery by which brain cells communicate.

GABA: Since one of the primary functions of GABA is to inhibit nerve cells from firing, it plays a key role in telling the body to “slow down.” The GABA system therefore acts as a sort of information filter, preventing the brain from becoming over-stimulated, the researchers explained. “Impairing the GABA system could overwhelm the brain with sensory information, leading to both the behavior and the pattern of cell damage that emerges in autism,” said John Hussman, Ph.D., a study co-author and president of The Hussman Foundation, one of the groups that funded the study. The researchers examined 14 genes that encode portions of the GABA receptor in 470 Caucasian families. Of those families, 266 included more than one person with autism and 204 included one autistic individual. The team tested for associations between particular gene variants and the disease. They also applied sophisticated statistical methods designed to zero in on the effects of particular gene combinations. The researchers found that one of the GABA receptor genes, GABRA4, is involved in the origin of autism. Moreover, they report, GABRA4 appears to increase autism risk through its interaction with a second GABA gene, GABRB1. (Pericak-Vance, M. American Journal of Human Genetics, September 2005; vol 77)

Frith CD, Frith U. The self and its reputation in autism. Neuron. 2008 Feb 7;57(3):331-2. The findings reveal an unusual lack of brain activity in mid cingulate cortex when they make their investments. We speculate that this may arise because autistic individuals are unaware that they will also gain or lose reputation in their partner’s eyes

Gogtay N, Sporn A, Clasen LS. Et al. Structural Brain MRI Abnormalities in Healthy Siblings of Patients With Childhood-Onset Schizophrenia. Am J Psychiatry 2003 160: 569-571. Healthy siblings of patients with childhood-onset schizophrenia share brain MRI abnormalities with the patients that may follow a similar pattern of progression. Developmental brain abnormalities in childhood-onset schizophrenia may thus be genetic trait markers.

Herguner S, Mukaddes NM. Autism and Williams syndrome: a case report. World J Biol Psychiatry. 2006;7(3):186-8

Molecular genetic studies have shown that deletion at the elastin gene (Chromosome 7) may account for the cardiovascular abnormalities seen in WS, but autistic features are likely caused by other genes flanking elastin. Charactristics: loose joints in childhood, stiff joints as adults, love of music-often perfect pitch, friendly/cheerful demeanor, elfin-like facial features.

Herpertz, S. Evidence of abnormal amygdala functioning in borderline personality disorder: a functional MRI study.Biological Psychiatry , Volume 50 , Issue 4 , Pages 292 – 298

Hilleke E, Pol H, Schnack HG, et al. Genetic Contributions to Human Brain Morphology and Intelligence. J. Neurosci. 26: 10235-10242; doi:10.1523/JNEUROSCI.1312-06.2006

Jamain S, Betancur C, Quach H. Linkage and association of the glutamate receptor 6 gene with autism. 2002, Volume 7, Number 3, Pages 302-310

Kendler KS, Aggen SH, Czajkowski N, The Structure of Genetic and Environmental Risk Factors for DSM-IV Personality Disorders. A Multivariate Twin Study Arch Gen Psychiatry. 2008;65(12):1438-1446.

Lin Y, Bloodgood BL, Hauser JL. Activity-dependent regulation of inhibitory synapse development by Npas4. Nature 455, 1198-1204 (30 October 2008) | doi:10.1038/nature07319; Received 5 May 2008; Accepted 25 July 2008; Published online 24 September 2008

Liu XQ, Paterson AD, Szatmari P. Genome-wide Linkage Analyses of Quantitative and Categorical Autism Subphenotypes.The Autism Genome Project Consortium.
Biological Psychiatry 2008 Jul 15

Livesley J. Toward a genetically-informed model of borderline personality disorder. Department of Psychiatry, The University of British Columbia, Vancouver, Canada. J Personal Disord. 2008 Feb;22(1):42-71

Livesley WJ, Jang KL. The Behavioral Genetics of Personality Disorder. Annual Review of Clinical Psychology 4:247-274 (2008)

Ludwig-Maximilians-Universität München (2008, August 1). Advances In The Field Of Schizophrenia Research: New Genetic Factors Identified. ScienceDaily. Retrieved September 9, 2008, from http://www.sciencedaily.com /releases/2008/07/080730155350.htm

According to estimates, approximately one in every hundred persons experiences a schizophrenic episode at least once in their lives.. in addition to environmental factors, genetic components are crucial—approximately 80 percent according to estimations. Thus, close relatives of a schizophrenic patient are more susceptible to fall ill themselves.

Meador-Woodruff JH, Healy DJ. Glutamate receptor expression in schizophrenic brain. Brain Res Rev 2000; 31: 288-294

Momoi T, Fujita E, Senoo H, Momoi M. Genetic factors and epigenetic factors for autism: endoplasmic reticulum stress and impaired synaptic function. Cell Biol Int.;34(1):13-9.
The molecular pathogenesis of ASD (autism spectrum disorder), one of the heritable neurodevelopmental disorders, is not well understood, although over 15 autistic-susceptible gene loci have been extensively studied. A major issue is whether the proteins that these candidate genes encode are involved in general function and signal transduction. Several mutations in genes encoding synaptic adhesion molecules such as neuroligin, neurexin, CNTNAP (contactin-associated protein) and CADM1 (cell-adhesion molecule 1) found in ASD suggest that impaired synaptic function is the underlying pathogenesis. However, knockout mouse models of these mutations do not show all of the autism-related symptoms, suggesting that gain-of-function in addition to loss-of-function arising from these mutations may be associated with ASD pathogenesis. Another finding is that family members with a given mutation frequently do not manifest autistic symptoms, which possibly may be because of gender effects, dominance theory and environmental factors, including hormones and stress. Thus epigenetic factors complicate our understanding of the relationship between these mutated genes and ASD pathogenesis. We focus in the present review on findings that ER (endoplasmic reticulum) stress arising from these mutations causes a trafficking disorder of synaptic receptors, such as GABA (gamma-aminobutyric acid) B-receptors, and leads to their impaired synaptic function and signal transduction. In the present review we propose a hypothesis that ASD pathogenesis is linked not only to loss-of-function but also to gain-of-function, with an ER stress response to unfolded proteins under the influence of epigenetic factors.

Moalem S, Percy ME. (2004). The quandary of reductionism: relevance to Alzheimer disease research. Journal of Alzheimers Disease, 4(6): 531-7

Modern science has embraced reductionism, seeking ever-smaller parts to explain the whole. Although reductionistic approaches are successful in very simple biological modeling, they are not necessarily appropriate for systems of increasing complexity. Drawing on famous historical examples of how non-reductionist thinking has benefited mankind, and of how reductionism has sometimes led to erroneous conclusions, we call attention to the need to move away from purely linear reasoning in order to succeed in addressing many of the problems we face with the predicted demographic increase in seniors, and the increase in numbers of those afflicted with Alzheimer disease. The time has come to reconsider and seriously question our most basic assumptions and beliefs surrounding what we believe Alzheimer disease to be, without which we run the risk of missed opportunities and failure. (Moalem, 2004)

Nichols CP, Sheldon KM, Sheldon MS. Evolution and Personality: What Should a Comprehensive Theory Address and How? Social and Personality Psychology Compass. 2(2):968-984 (2008)

NIH/National Institute of Mental Health (2007, February 19). Largest-ever Search For Autism Genes Reveals New Clues. ScienceDaily. Retrieved December 30, 2008, from http://www.sciencedaily.com /releases/2007/02/070218183245.htm. Clues emerged adding to evidence that implicates components of the brain’s glutamate neurotransmitter system in autism. Glutamate increases neuronal activity and plays an important role in wiring up the brain during early development.

The Autism Genome Project (AGP) Consortium. Mapping autism risk loci using genetic linkage and chromosomal rearrangements. Nature Genetics. Published online: 18 February 2007, doi:10.1038/ng1985) Linkage and copy number variation analyses implicate chromosome 11p12-p13 and neurexins, respectively, among other candidate loci. Neurexins team with previously implicated neuroligins for glutamatergic synaptogenesis, highlighting glutamate-related genes as promising candidates for contributing to ASDs.

Shaw P, Eckstrand K, Sharp W, et al. Attention-deficit/hyperactivity disorder is characterized by a delay in cortical maturation. PNAS, 2007 104:19649-19654. doi:10.1073/pnas.0707741104

Brain Matures a Few Years Later but at normal Pace for ADHD

Thakkar KN, Polli FE, Joseph RM. Response monitoring, repetitive behaviour and anterior cingulate abnormalities in autism spectrum disorders (ASD). Brain. 2008 Sep;131(Pt 9):2464-78. Epub 2008 Jun 11. These findings suggest that in ASD, structural and functional abnormalities of the ACC compromise response monitoring and thereby contribute to behaviour that is rigid and repetitive rather than flexible and responsive to contingencies. Illuminating the mechanisms and clinical significance of abnormal response monitoring in ASD represents a fruitful avenue for further research.

Thompson PM, Cannon TD, Narr KL, et al. Genetic influences on brain structure Nature Neuroscience 4, 1253 – 1258 (2001) Published online: 5 November 2001; | doi:10.1038/nn758

Spectacular images of the brain’s wiring reveal that more aspects of intelligence are inherited than previously known http://www.newscientist.com/article&#8230;

“It is clear that intelligence is at least partly genetically determined. This was supported by the discovery in 2001 that the volume of the brain’s grey matter, made up of “processor” cells, is heritable and correlates with certain elements of IQ (Nature Neuroscience, DOI: 10.1038/nn758). The amount of white matter, which provides the connections between these processors, has since been shown to be heritable too (Journal of Neuroscience, vol 26, p 10235). Now it seems that the quality of these connections, which is governed by the integrity of the protective myelin sheath that encases them, is also largely genetic, and correlates with IQ

Trottier G, Srivastava, Walker CD. Etiology of infantile autism: a review of recent advances and neurobiological research. J Psychiatry neurosci. 1999Mar;24(2):103-115. In summary, the prevailing view is that autism is caused by a pathophysiologic process arising from the interaction of an early environmental insult and a genetic predisposition.

Judson MC, Bergman MY, Campbell DB, Dynamic gene and protein expression patterns of the autism-associated Met receptor tyrosine kinase in the developing mouse forebrain. J Comp Neurol. 2009 Apr 10;513(5):511-31.

The establishment of appropriate neural circuitry depends on the coordination of multiple developmental events across space and time. These events include proliferation, migration, differentiation, and survival-all of which can be mediated by hepatocyte growth factor (HGF) signaling through the Met receptor tyrosine kinase. We previously found a functional promoter variant of the MET gene to be associated with autism spectrum disorder, suggesting that forebrain circuits governing social and emotional function may be especially vulnerable to developmental disruptions in HGF/Met signaling. …Temporally, peak expression of transcript and protein occurs during the second postnatal week. This period is characterized by extensive neurite outgrowth and synaptogenesis, supporting a role for the receptor in these processes. Collectively, these data suggest that Met signaling may be necessary for the appropriate wiring of forebrain circuits, with particular relevance to the social and emotional dimensions of behavior. (c) 2009 Wiley-Liss, Inc.

Zhang K, Zheng Z, Gao X. Possible Relationship between the COMT Gene Vel158 Met Polymorphism and Psychometric IQ in Girls of the Qinba Region in China. Neuropsychobiology 2007;56:98-103 (DOI: 10.1159/000112950)

Objective: Catechol-O-methyltransferase (COMT) gene was hypothesized to have a relationship with human prefrontal cortex (PFC) function and individual cognitive abilities. The object of this study was to investigate the possible impact of genotypes of COMT Val158Met polymorphism on cognitive ability among children living in the Qinba region in China. Conclusion: Our results indicate that COMT gene Val158Met polymorphism may be related to the intelligence of Chinese girls, although the results cannot withstand multiple testing. Consequently, further studies with larger samples and perfect design still need place more emphasis on the gender difference and compensation effect of dopamine activity in PFC.

ADDICTION: Ming D. Li & Margit Burmeister. New insights into the genetics of addiction. Nature Reviews Genetics, 2009; DOI: 10.1038/nrg2536 “The comparison of peaks for addictions to multiple substances on certain chromosomal locations confirms that genetic vulnerability to different substances overlaps, in part,” Li says. He further points out that variants in several genes, including aldehyde dehydrogenases, GABRA2, ANKK1, and neurexins 1 and 3, have already been associated with addictions to multiple drugs. In recommending a future direction for research into the genetics of addiction, Li suggests focusing on CHRNA5, CHRNA3 and CHRNB4 clusters, among other variants. University of Virginia Health System (2009, March 16). Common Genes Tied To Alcohol, Nicotine, Cocaine Addictions. ScienceDaily. Retrieved March 16, 2009, from http://www.sciencedaily.com /releases/2009/03/090310142912.htm

(Are addictions self-medicating because of lack of proper resources to begin with? Are those genes related to neurodev/psych genes?)


(Information comes in from ALL the sensory organs, but filter through common pathways of the cerebellum)

It could be hypothesized that the varied progressive symptoms/dysfunctions of these disorders stem from aspects of sensory processing: Too much information and/or not enough resources to process information.

The success of mainstream treatments (like ABA/OT), which give the children additional, focused, repetitive information, may be a clue that these minds did not or cannot process or receive this information for neurophysiological programming. These therapies may work by completing the pathways for learned behavior/knowledge which had been previously or continues to be clouded by excessive “noise” (similar to information bottlenecks) or the lack of resources and raw materials needed to build these pathways from the incoming sensory information (myelination).

Could these therapies at times be similar to pulling a truck through the mud? Yes, you can get results (the truck moves), but might it be easier if we first got rid of the mud?

Critical learning periods during childhood, the peripheral mind and the lack of resources complicated by too much information could create information “bottlenecks”; either not learning when they need to, the information is not able to get through (or myelinated appropriately, see Bartzokis 2004) or not having enough information for complete processing.

THOUGHT: (Sensory information is also learned and myelinated) And retraining seemingly unrelated aspects of the senses, such as Behavioral Optometry, Cerebellar “exercises” that re-stimulate or retrain vision, hearing or balance, will reportedly make vast improvements in behavior, emotions, memory and in some cases increase IQ (IQ may also be related GABA, hence the lowered IQ with GABA-inhibiting drugs of anti-epileptics). (thought: could this type of retraining be either finishing or rewiring or improving the brain’s sensory “learning” to work more efficiently and this eliminates confusing or unfinished “business” as a drain on resources, less confusing, less bottlenecks, more info can get through, get myelinated, get recalled, get neurotransmitted.)

Allen G, Muller RA, Courchesne E. Cerebellar function in autism: functional magnetic resonance image activation during a simple motor task. Biol Psychiatry 2004;56(4):269-278.

Armando B, Laurent M, Patricia J. Enhanced and diminished visuo-spatial information processing in autism depends on stimulus complexity. Brain 2005 128(10):2430-2441; doi:10.1093/brain/awh561

Ashwin E, Ashwin C, Rhydderch D, et al. Eagle-eyed visual acuity: an experimental investigation of enhanced perception in autism. Biol Psychiatry. 2009 Jan 1;65(1):17-21. Epub 2008 Jul 23.

Belmonte MK, Cook EH, Jr., Anderson GM, et al. Autism as a disorder of neural information processing: directions for research and targets for therapy. Mol Psychiatry 2004;9(7):646-663. The broad variation in phenotypes and severities within autism spectrum disorders suggests the involvement of multiple predisposing factors, interacting in complex ways with normal developmental courses and gradients

Birnbaum MH. Behavioral optometry: a historical perspective. J Am Optom Assoc. 1994 Apr;65(4):255-64. PMID 8014367. The past 50 years has brought substantial growth in the scope of behavioral optometric care, with consideration of the role of vision in relation to school achievement, VDT use, sports, spatial and motor organization, and information-processing. Models of care emphasize prevention, remediation, rehabilitation, and enhancement. Behavioral optometry is an integral component of optometric education and practice.

Blakemore SJ, Tavassoli T, Calò S, Thomas RM, Catmur C, Frith U, Haggard P (2006) Tactile sensitivity in Asperger syndrome. Brain and Cognition 2006 61:5-13

Bogdashina, O. (2003). Sensory perceptual issues in autism and Asperger Syndrome: different sensory experiences – different perceptual worlds. Jessica Kingsley, London.

Crespi B. J :

Figure from Ashwin et al. 2008 (Biological Psychiatry)

(Crespi cont.) Might this be an isolated finding, a quirk of neurodevelopmental nature? Previous work has revealed enhanced auditory pitch discrimination in autism (Bonnel et al. 2003; O’Riordan and Passetti 2006), as well as increased sensitivity to vibration and thermal pain (Cascio et al. 2008), increased tactile sensitivity (Blakemore et al. 2006), olfactory sensitivities comparable to those of canines (Bogdashina 2003, p. 54), superior abilities in visual search tasks (O’Riordan et al. 2001), generally enhanced perception of relatively simple, static stimuli (Mottron et al. 2006), and evidence for ‘enhanced functioning and role of the primary visual cortex’ (Caron et al. 2006). More generally, autistics have recently been shown to exhibit higher ‘fluid intelligence’ – a form of problem-solving intelligence independent of acquired knowledge, higher than that of non-autistic controls (Dawson et al. 2007; Hayashi et al. 2008), also lending support to the idea that the previously-perceived association of autism with mental retardation is due to biases in ascertainment and diagnosis (Skuse 2007).

The implications of these findings for our understanding of the autistic and so-called normal brains, the evolutionary bases of autism, and societal perception of autistics, are difficult to overstate. The simplest, albeit preliminary, neurological explanation for perceptual and analytic enhancements in autistics is that their brains are ‘tuned’ to higher frequencies (Blakemore et al. 2006) due to differences in neuronal micro-architecture (Casanova et al. 2003) and greater emphasis on left-hemispheric, local-processing, high-frequency abilities (Ivry and Robertson 1998; Cook 2002; Han et al. 2002; Wang et al. 2007). At an evolutionary level, Grandin and Johnson (2005) have likened autistic savant talents to the enhanced sensory and memory skills of animals, and strong signals of positive Darwinian selection along the human lineage have consistently been reported for genes underlying sensory perception (e. g., Nielsen et al. 2005).

Whatever the proximate and ultimate explanations for eagle-eyed autism, Ashwin et al. (2008) have opened new doors to our understanding of perception, and the many meanings of what it means to be human and autistic.

Lowered Latent Inhibition: UNDER STRESS

…Note from the text of the full paper that stress causes the release of the hormone corticosterone which lowers latent inhibition. In a nutshell, when an organism runs into problems that cause stress the resulting release of stress hormones causes the mind to shift into a state where it will examine factors in the environment that it normally ignores. This allows the organism to look for solutions to the stress-causing problem that would be ignored in normal and less stressed circumstances.

From Future Pundit:

So perhaps we could hypothesize something like this under stressful conditions, or in personality conjurations characterized by increased novelty-sensitivity, approach behavior, and DA activity, decreased LI is associated with increased permeability and flexibility of functional cognitive and perceptual category [see Barsalou (1983)for a discussion of such categories ].Imagine a situation where current plans are not producing desired outcomes —a situation where current categories of perception and cognition are in error, from the pragmatic perspective. Something anomalous or novel emerges as a consequence (Peterson, 1999), and drives exploratory behavior. Stress or trait-dependent decreased LI, under such circumstances, could produce increased signal (as well as noise), with regards to the erroneous pattern of behavior and the anomaly that it produced. This might offer the organism, currently enmeshed in the consequences of mistaken presuppositions, the possibility of gathering new information, where nothing but categorical certainty once existed. Decreased LI might therefore be regarded as advantageous, in that it allows for the perception of more unlikely, radical and numerous options for reconsideration, but disadvantageous in that the stressed or approach-oriented person risks ‘‘drowning in possibility,’’ to use Kierkegaard ’s phrase.

Low Latent Inhibition Plus High Intelligence Leads To High Creativity? By Randall Parker. 2003 October 05 04:54 PM http://www.futurepundit.com/archives/001684.html. retrieved 10/27/08

Bonnel A, Mottron L, Peretz I, et al. (2003) Enhanced pitch sensitivity in individuals with autism: a signal detection analysis. Journal of Cognitive Neuroscience 2003 15:226-35.

Caron MJ, Mottron L, Berthiaume C, Dawson M (2006) Cognitive mechanisms, specificity and neural underpinnings of visuospatial peaks in autism. Brain 129:1789-802.

Casanova MF, Buxhoeveden D, Gomez J (2003) Disruption in the inhibitory architecture of the cell minicolumn: implications for autisim. Neuroscientist 9:496-507. The modular arrangement of the neocortex is based on the cell minicolumn: a self-contained ecosystem of neurons and their afferent, efferent, and interneuronal connections. The authors’ preliminary studies indicate that minicolumns in the brains of autistic patients are narrower, with an altered internal organization. More specifically, their minicolumns reveal less peripheral neuropil space and increased spacing among their constituent cells. The peripheral neuropil space of the minicolumn is the conduit, among other things, for inhibitory local circuit projections. A defect in these GABAergic fibers may correlate with the increased prevalence of seizures among autistic patients. This article expands on our initial findings by arguing for the specificity of GABAergic inhibition in the neocortex as being focused around its mini- and macrocolumnar organization. The authors conclude that GABAergic interneurons are vital to proper minicolumnar differentiation and signal processing (e.g., filtering capacity of the neocortex), thus providing a putative correlate to autistic symptomatology.
Brain Anatomical Network and Intelligence

by: Yonghui Li, Yong Liu, Jun Li, Wen Qin, Kuncheng Li, Chunshui Yu, Tianzi Jiang

PLoS Comput Biol, Vol. 5, No. 5. (29 May 2009), e1000395.

Author Summary: Networks of interconnected brain regions coordinate brain activities. Information is processed in the grey matter (cortex and subcortical structures) and passed along the network via whitish, fatty-coated fiber bundles, the white matter. Using maps of these white matter tracks, we provided evidence that higher intelligence may result from more efficient information transfer. Specifically, we hypothesized that higher IQ derives from higher global efficiency of the brain anatomical network. Seventy-nine healthy young adults were divided into general and high IQ groups. We used diffusion tensor tractography, which maps brain white matter fibers, to construct anatomical brain networks for each subject and calculated the network properties using both binary and weighted networks. We consistently found that the high intelligence group’s brain network was significantly more efficient than was the general intelligence group’s. Moreover, IQ scores were significantly correlated with network properties, such as shorter path lengths and higher overall efficiency, indicating that the information transfer in the brain was more efficient. These converging evidences support the hypothesis that the efficiency of the organization of the brain structure may be an important biological basis for intelligence.

Cascio C, McGlone F, Folger S, Tannan V, Baranek G, Pelphrey KA, Essick G (2008) Tactile perception in adults with autism: a multidimensional psychophysical study. Journal of Autism and Developmental Disorders 2008 38:127-37.

Han S, Weaver JA, Murray SO, Kang X, Yund EW, Woods DL (2002) Hemispheric asymmetry in global/local processing: effects of stimulus position and spatial frequency. Neuroimage 17:1290-9.

THOUGHT: Wouldn’t more information equal more work equal more fuel?

Ivry, RB and Robertson LC (1998) The Two Sides of Perception. MIT Press.

Mottron L, Dawson M, Soulières I, Hubert B, Burack J (2006) Enhanced perceptual functioning in autism: an update, and eight principles of autistic perception. Journal of Autism and Developmental Disorders 36:27-43.

O’Riordan MA, Plaisted KC, Driver J, Baron-Cohen S (2001) Superior visual search in autism. Journal of Experimental Psychology 27:719-30

O’Riordan M, Passetti F (2006) Discrimination in autism within different sensory modalities. Journal of Autism and Developmental Disorders 2006 36:665-75. It is possible that the enhanced discrimination ability in vision in autism might extend to other modalities and further that they may underlie many reports of unusual touch and audition. The present study investigated the performance of children with and without autism on auditory and tactile discrimination tasks and revealed superior auditory but comparable tactile discrimination in autism relative to controls. These results extend previous findings of perceptual discrimination in autism and may be relevant for a neuro-developmental hypothesis of the disorder.

Wang L, Mottron L, Peng D, Berthiaume C, Dawson M (2007) Local bias and local-to-global interference without global deficit: a robust finding in autism under various conditions of attention, exposure time, and visual angle. Cognitive Neuropsychology 24:550-74.

Clark DL, Arnold LE, Crowl L, Bozzolo H. Vestibular Stimulation for ADHD: randomized controlled trial of Comprehensive Motion Apparatus, J Atten Disord, 2008 Mar;11(5):599-611. Epub 2008 Jan 14.

Dotigny F, Ben Amor AY, Burke M Vaucher E Neuromodulatory role of acetylcholine in visually-induced cortical activation: Behavioral and neuroanatomical correlates. Neuroscience, 2008 Jul 17;154(4):1607-18.

Lugo E, Doti R, Faubert J (2008) Ubiquitous Crossmodal Stochastic Resonance in Humans: Auditory Noise Facilitates Tactile, Visual and Proprioceptive Sensations. PLoS ONE 3(8): e2860. doi:10.1371/journal.pone.0002860

Gao J, Parsons LM, James M. Bower. Cerebellum Implicated in Sensory Acquisition and Discrimination Rather Than Motor Control. Science 26 April 1996: Vol. 272. no. 5261, pp. 545 – 547. DOI: 10.1126/science.272.5261.545. Recent evidence that the cerebellum is involved in perception and cognition challenges the prevailing view that its primary function is fine motor control. A new alternative hypothesis is that the lateral cerebellum is not activated by the control of movement per se, but is strongly engaged during the acquisition and discrimination of sensory information. Magnetic resonance imaging of the lateral cerebellar output (dentate) nucleus during passive and active sensory tasks confirmed this hypothesis. These findings suggest that the lateral cerebellum may be active during motor, perceptual, and cognitive performances specifically because of the requirement to process sensory data.

Gutschalk A, Micheyl C, Oxenham AJ Neural Correlates of Auditory Perceptual Awareness under Informational Masking PLoS Biology Vol. 6, No. 6, e138 doi: 10.1371/journal.pbio.0060138. Our ability to detect target sounds in complex acoustic backgrounds is often limited not by the ear’s resolution, but by the brain’s information-processing capacity

Nagai M, Kishi K, Kato S. Insular cortex and neuropsychiatric disorders: a review of recent literature. Eur Psychiatry. 2007 Sep;22(6):387-94. Epub 2007 Apr 9. Recent neuroimaging data, including voxel based morphometry, PET and fMRI, revealed that the insular cortex was involved in various neuropsychiatric diseases such as mood disorders, panic disorders, PTSD, obsessive-compulsive disorders, eating disorders, and schizophrenia. Investigations of functions and connections of the insular cortex suggest that sensory information including gustatory, olfactory, visual, auditory, and tactile inputs converge on the insular cortex, and that these multimodal sensory information may be integrated there.

Rice, S. Barone, D.Jr. Critical periods of vulnerability for the developing nervous system: evidence from humans and animal models. Environ Health Perspect. 2000 June; 108(Suppl 3): 511–533. Vulnerable periods during the development of the nervous system are sensitive to environmental insults because they are dependent on the temporal and regional emergence of critical developmental processes (i.e., proliferation, migration, differentiation, synaptogenesis, myelination, and apoptosis) …Furthermore, various clinical disorders in humans (e.g., schizophrenia, dyslexia, epilepsy, and autism) may also be the result of interference with normal ontogeny of developmental processes in the nervous system. Of critical concern is the possibility that developmental exposure to neurotoxicants may result in an acceleration of age-related decline in function. This concern is compounded by the fact that developmental neurotoxicity that results in small effects can have a profound societal impact when amortized across the entire population and across the life span of humans

J.E. Lugo et al. Multisensory Integration: Central Processing Modifies Peripheral Systems. Psychological Science, October 2008. These results demonstrate that during multisensory integration, the brain not only continuously binds information obtained from the senses, but also acts directly on that information by modulating activity at peripheral levels

Bower JM, Parsons LM. Rethinking the “lesser brain”. Sci Am. 2003 Aug;289(2):50-7. Other findings indicate that the cerebellum may play important roles in shortterm memory, attention, impulse control, emotion, higher cognition, the ability to schedule and plan tasks, and possibly even in conditions such as schizophrenia and autism. Additional neurobiological experiments-both on the pattern of sensory inputs to the cerebellum and on the ways in which the cerebellum processes that information-also suggest a need to substantially revise current thinking about the function of this organ

Association for Psychological Science (2008, November 14). How Our Senses Combine To Give Us A Better View Of The World. ScienceDaily. Retrieved December 7, 2008, from http://www.sciencedaily.com /releases/2008/11/081112194925.htm

BMC Neuroscience (2008, August 12). Sound Adds Speed To Visual Perception. ScienceDaily. Retrieved December 7, 2008, from http://www.sciencedaily.com /releases/2008/08/080811200557.htm

Wake Forest University Baptist Medical Center (2004, February 20). Study Provides New Insights About Brain Organization. ScienceDaily. Retrieved December 7, 2008, from http://www.sciencedaily.com /releases/2004/02/040220074652.htm

Wake Forest University Baptist Medical Center (2003, November 10). Dyslexia May Involve Both Vision And Hearing. ScienceDaily. Retrieved December 7, 2008, from http://www.sciencedaily.com /releases/2003/11/031110054404.htm

Thought: Interconnections of the sensory systems AND the unique qualities within this community suggest not only a need for unique resources, but a need for unique stimulation, and unique potential.

Physicist David Bohm (1982) asserts that the root cause of this crisis of perception lies in our habit of seeing and experiencing ourselves and our world as constituted of separately existent fragments. “The notion that all these fragments are separately existent is evidently an illusion, and this illusion cannot do other then lead to endless conflict and confusion.”


Unique starting points or processing potentials create unique but predictable outcomes from distinct environmental influences.


“Could autism and schizophrenia be cousins? New research shows that people with schizophrenia have rare variations in genes that control brain development and that each person has a unique pattern of mutations. The finding is startlingly similar to new research on autism…. Thomas Insel, a psychiatrist who heads the National Institute of Mental Health, calls the new understanding that disorders like schizophrenia and autism have unique origins in each person a “Tolstoy moment”(Happy families are all alike; every unhappy family is unhappy in its own way) in mental health. ~ (Shute 2008).

findings such as the frequency of comorbidity among the major diagnostic entities have led to systematic studies of their boundaries and renewed questions about categorical vs dimensional approaches to classification. (Insel 2008: Psychiatric Epidemiology)

Anckarsater, H, Stahlberg, O, et al. The Impact of ADHD and Autism Spectrum Disorders on Temperament, Character, and Personality Development. Am J Psychiatry, 2006 163: 1239-1244. RESULTS: Patients with ADHD reported high novelty seeking and high harm avoidance. Patients with autism spectrum disorders reported low novelty seeking, low reward dependence, and high harm avoidance. Character scores (self-directedness and cooperativeness) were extremely low among subjects with neuropsychiatric disorders, indicating a high overall prevalence of personality disorders, which was confirmed with the SCID-II. Cluster B personality disorders were more common in subjects with ADHD, while cluster A and C disorders were more common in those with autism spectrum disorders. The overlap between DSM-IV personality disorder categories was high, and they seem less clinically useful in this context. CONCLUSIONS: ADHD and autism spectrum disorders are associated with specific temperament configurations and an increased risk of personality disorders and deficits in character maturation.

Bartzokis G, Lu PH, Mintz J. Quantifying age-related myelin breakdown with MRI: novel therapeutic targets for preventing cognitive decline and Alzheimer’s disease. J Alzheimers Dis. 2004;6(6 suppl):S53-S59.

The development, maintenance, and repair of myelin is the single most important factor affecting cognition and behavior, according to a UCLA neurology professor who has collected extensive data on the nerve insulator. In an article to be published in an upcoming issue of Biological Psychiatry, George Bartzokis, MD, asserts that myelin may be the universal cause or contributor to a wide range of neuropsychological brain disorders, from autism to Alzheimer’s disease. http://www.neuropsychiatryreviews.com/07jan/myelin.html

Blalock JE, Harbour-McMenamin D, Smith EM. Peptide hormones shared by the neuroendocrine and immunologic systems. J. Immunol., Aug 1985; 135: 858S – 861S

Craddock N, O’Donovan MC, Owen MJ. Psychosis Genetics: Modeling the Relationship Between Schizophrenia, Bipolar Disorder, and Mixed (or “Schizoaffective”) Psychoses. Schizophr Bull. 2009 May;35(3):482-90. Epub 2009 Mar 27

Stanford University Medical Center (2005, November 9). Children Of Bipolar Parents Score Higher On Creativity Test, Stanford Study Finds. ScienceDaily. Retrieved March 27, 2009, from http://www.sciencedaily.com /releases/2005/11/051109092005.htm

Researchers at the Stanford University School of Medicine have shown … that a sample of children who either have or are at high risk for bipolar disorder score higher on a creativity index than healthy children. The findings add to existing evidence that a link exists between mood disorders and creativity……The researchers had hypothesized that the scores of children with ADHD would differ significantly from the scores of bipolar children so they were surprised when the scores did not. Chang said this indicates that mania is not what is fueling the creativity. “The kids with ADHD who hadn’t been manic yet still had very high levels of creativity”

Crespi B. J. and C. Badcock (2008) Psychosis and autism as diametrical disorders of the social brain. Behavioral and Brain Sciences 31: 284-320

Abstract: Autistic-spectrum conditions and psychotic-spectrum conditions (mainly schizophrenia, bipolar disorder, and major depression) represent two major suites of disorders of human cognition, affect, and behavior that involve altered development and function of the social brain. We describe evidence that a large set of phenotypic traits exhibit diametrically opposite phenotypes in autistic-spectrum versus psychotic-spectrum conditions, with a focus on schizophrenia. This suite of traits is inter-correlated, in that autism involves a general pattern of constrained overgrowth, whereas schizophrenia involves undergrowth. These disorders also exhibit diametric patterns for traits related to social brain development, including aspects of gaze, agency, social cognition, local versus global processing, language, and behavior. Social cognition is thus underdeveloped in autistic-spectrum conditions and hyper-developed on the psychotic spectrum. We propose and evaluate a novel hypothesis that may help to explain these diametric phenotypes: that the development of these two sets of conditions is mediated in part by alterations of genomic imprinting. Evidence regarding the genetic, physiological, neurological, and psychological underpinnings of psychotic-spectrum conditions supports the hypothesis that the etiologies of these conditions involve biases towards increased relative effects from imprinted genes with maternal expression, which engender a general pattern of undergrowth. By contrast, autistic-spectrum conditions appear to involve increased relative bias towards effects of paternally expressed genes, which mediate overgrowth. This hypothesis provides a simple yet comprehensive theory, grounded in evolutionary biology and genetics, for understanding the causes and phenotypes of autistic-spectrum and psychotic-spectrum conditions.

Insel, T.R., Fenton, W.S. (2005). Psychiatric Epidemiology: It’s Not Just About Counting Anymore. Archives of General Psychiatry, 62(6), 590-592.

King-Casas, B, Sharp, C, Lomax, L, et al. (2008) The rupture and repair of cooperation in borderline personality disorder. Science. 321:806-810. Neurally, activity in the anterior insula, a region known to respond to norm violations across affective, interoceptive, economic, and social dimensions, strongly differentiated healthy participants from individuals with BPD. These neural and behavioral data suggest that norms used in perception of social gestures are pathologically perturbed or missing altogether among individuals with BPD

Murali KS, Ramanathan G. A new spectrum of personality disorders?
The British Journal of Psychiatry (2008) 192: 233. doi: 10.1192/bjp.192.3.233

A basic structural abnormality in the frontal cortex might cause these individuals to have higher psychiatric comorbidity (not only of ASPD and SSPD) and the abnormal characteristics identified might not be entirely explained by the co-occurrence of these two disorders. The authors have rightly identified that the results could not merely be due to the additive effects of both disorders, but that the increased prevalence of personality disorder in the study population might be due to a common confounder that does not lie on the causal pathway between ASPD/SSPD and abnormality in characteristics.

Newcorn, J, Sprich, S. Comorbidity of attention deficit hyperactivity disorder with conduct, depressive, anxiety, and other disorders. Am J Psychiatry, 1991 148: 564-577 FINDINGS: The literature supports considerable comorbidity of attention deficit hyperactivity disorder with conduct disorder, oppositional defiant disorder, mood disorders, anxiety disorders, learning disabilities, and other disorders, such as mental retardation, Tourette’s syndrome, and borderline personality disorder. CONCLUSIONS: Subgroups of children with attention deficit hyperactivity disorder might be delineated on the basis of the disorder’s comorbidity with other disorders. These subgroups may have differing risk factors, clinical courses, and pharmacological responses. Thus, their proper identification may lead to refinements in preventive and treatment strategies. Investigation of these issues should help to clarify the etiology, course, and outcome of attention deficit hyperactivity disorder.

Pauc, R. Comorbidity of dyslexia, dyspraxia, attention deficit disorder (ADD), attention deficit hyperactive disorder (ADHD), obsessive compulsive disorder (OCD) and Tourette’s syndrome in children: A prospective epidemiological study. Clinical Chiropractic, Vol. 8, No. 4. (December 2005), pp. 189-198. doi:10.1016/j.clch.2005.09.007 Results A clear pattern of comorbidity was demonstrated. Whilst not always quantifiable, no patient was found to have one condition in isolation and comorbidity rates were found at incidences of up to 95%, representing an increase on the expected prevalence in a general population of 160-2300%.Conclusion The patterns of comorbidity occurred with such frequency that it would suggest that there could be an argument for the downgrading of these conditions from disorders per se to symptoms and that further investigation might suggest that the patterns of comorbidity may fit the criteria for a developmental delay syndrome.

Phelps, J. Bipolar Disorder: Particle or Wave? DSM Categories or Spectrum Dimensions? Psychological Times. July 2006, Vol. XXIII, No. 8. Psychiatric diagnosis is currently based on a system of categories, much like the Linnaean classification in biology. However, a seemingly opposite diagnostic system is emerging, usually dubbed the “dimensional view,” in which related psychiatric conditions such as major depressive disorder (MDD) and bipolar disorder (BD) are seen as end points of a spectrum.

Shute, N. (2008). Autism and Schizophrenia Linked. UsNews.com, 3/31, On-Parenting Blog. http://www.usnews.com/blogs/on-parenting/2008/3/31/autism-and-schizophrenia-linked.html

Soderstrom H, Nilsson T, Sjodin AK, et al. The childhood-onset neuropsychiatric background to adulthood psychopathic traits and personality disorders. Compr Psychiatry, 2005 Mar-Apr;46(2):111-6. http://dx.doi.org/10.1016/j.comppsych.2004.07.030. we compared total and factor PCL-R scores to Axis I disorders, including childhood-onset neuropsychiatric disorders, and to Axis II personality disorders, to establish the convergence of psychopathic traits with other psychiatric diagnoses, and to identify possible unique features. Psychopathic traits were positively correlated with bipolar mood disorder and negatively with unipolar depression. The total PCL-R scores as well as the Factor 2 (unemotionality) and Factor 3 (behavioral dyscontrol) scores were significantly correlated with attention-deficit/hyperactivity disorder, Asperger’s syndrome/high-functioning autistic traits, CD, substance abuse, and the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition Cluster B personality disorders.

Stahlberg O, Soderstrom H, Rastam M, Gillberg C. Bipolar disorder, schizophrenia, and other psychotic disorders in adults with childhood onset AD/HD and/or autism spectrum disorders. J Neural Transm, 2004 Jul;111(7):891-902. Conclusion: Current diagnostic criteria have to be revised to acknowledge the comorbidity of bipolar and/or psychotic disorders in AD/HD and ASD.

Xue Ming, Brimacombe M, Chaaban J. Autism spectrum disorders: concurrent clinical disorders. J Child Neurol. 2008 Jan;23(1):6-13. Medical and psychiatric co-occurrences included sleep disorders, epilepsy, food intolerance, gastrointestinal dysfunction, mood disorder, and aggressive and self-injurious behaviors. These results showed a high prevalence of multiple medical and psychiatric co-occurrences. There may be common pathophysiologic mechanisms resulting in clinical subgroups of autism spectrum disorders

Walker J, Curtis V, Shaw P, Murray RM. Schizophrenia and bipolar disorder are distinguished mainly by differences in neurodevelopment. Neurotox Res. 2002 Aug-Sep;4(5-6):427-436

Thought: When we begin to see these entities as connected patterns, we can begin to see the patterns of development and the research delineating what we once that were “separate” disorders can now be seen as interconnected…and the evidence begins making a more coherent picture of the whole. Just like climates, similarities and variability…and not distinguished entities.

BRAINGUT: Enteric Nervous System

Recently a study in ScienceDaily from Dr. Pat Levitt stated that the Met Gene was implicated in both Autism and Gut disorders. “Met Gene is expressed in the brain during development and is important for a number of different processes, including cell migration, development of excitatory and inhibitory neurons, synapse formation, and myelination”. (Levitt 2009) So if the “second brain” also needs these same pathways built during critical “learning” periods for sensory organs, such as digestive system and immune system (both have sensory aspects, both need to respond readily to environmental conditions and become programmed to respond), could this genetic relation to these processes be another affirmation that these individuals are not getting the necessary resources to build neurological pathways?
“The Second Brain”: The enteric nervous system also makes use of more than 30 neurotransmitters, most of which are identical to the ones found in CNS, such as acetylcholine, dopamine, and serotonin. The enteric nervous system has the capacity to alter its response depending on such factors as bulk and nutrient composition. In addition, ENS contains support cells which are similar to astroglia of the brain and a diffusion barrier around the capillaries surrounding ganglia which is similar to the blood-brain barrier of cerebral blood vessels. (Gershon 1999, Wikipedia 2009)

Aszalós Z. Neurological and psychiatric aspects of some gastrointestinal diseases. Orv Hetil. 2008 Nov 2;149(44):2079-86

Costedio MM, Hyman N, and Mawe GM. (2007) Serotonin and its role in colonic function and in gastrointestinal disorders. Diseases of the Colon and Rectum 50: 376-388

Delvaux M. Alterations of sensori-motor functions of the digestive tract in the pathophysiology of irritable bowel syndrome. Best Pract Res Clin Gastroenterol. 2004 Aug;18(4):747-71

Levy SE, Souders MC, Ittenbach RF. Relationship of dietary intake to gastrointestinal symptoms in children with autistic spectrum disorders. Biol Psychiatry. 2007 Feb 15;61(4):492-7. In this sample, there was a high rate of reported gastrointestinal symptoms, despite lack of medical causes

Gershon MD (July 1999). The enteric nervous system: a second brain. Hosp Pract (Minneap) 34 (7): 31–2, 35–8, 41–2 passim.

Grundy D. 5-HT system in the gut: roles in the regulation of visceral sensitivity and motor functions. Eur Rev Med Pharmacol Sci. 2008 Aug;12 Suppl 1:63-7. the perception of functional gastrointestinal disorders such as irritable bowel syndrome (IBS) has shifted fundamentally. Such disorders are now thought of as serious diseases characterized by perturbations in the neuronal regulation of gastrointestinal function. The concept of visceral hypersensitivity, the characterization of neuronal networks in the ‘brain–gut axis’ and the identification of several novel 5-HT-mediated mechanisms have contributed to this shift

Mulak A, Bonaz B. Irritable bowel syndrome: a model of the brain-gut interactions Med Sci Monit. 2004 Apr;10(4):RA55-62. Disturbances at every level of neural control of the gastrointestinal tract can affect modulation of gastrointestinal motility, secretion, immune functions as well as perception and emotional response to visceral events

Nikolov RN, Bearss KE, Lettinga J. Gastrointestinal Symptoms in a Sample of Children with Pervasive Developmental Disorders. J Autism Dev Disord. 2008 Sep 13. Compared to children without GI problems, those with GI problems showed greater symptom severity on measures of irritability, anxiety, and social withdrawal

Taulant B, Maya T, Yun L, Shai . Glia Are Essential for Sensory Organ Function in C. elegans. Science, October 31, 2008, Vol. 322. no. 5902, pp. 744 – 747 DOI: 10.1126/science.1163074. Sensory organs are composed of neurons, which convert environmental stimuli to electrical signals, and glia-like cells, whose functions are not well understood… Our results suggest that glia are required for multiple aspects of sensory organ function.

Vandvik PO, Wilhelmsen I, Ihlebaek C, Farup PG. Comorbidity of irritable bowel syndrome in general practice: a striking feature with clinical implications. Aliment Pharmacol Ther, 2004 Nov 15;20(10):1195-203. Results: Patients with irritable bowel syndrome (67% females, mean age 50, s.d. 16) reported 20 of 22 comorbid symptoms significantly more frequent than controls (odds ratios = 2-7, P < 0.001). The somatic comorbidity score correlated with psychological distress (R = 0.46, P < 0.001). Patients with high somatic comorbidity reported higher levels of mood disorder, health anxiety, neuroticism, adverse life events and reduced quality of life and increased health care seeking when compared to those with low and intermediate somatic comorbidity (P-values < 0.05). Conclusions: Our findings support the hypothesis that structured assessment of comorbid somatic symptoms might identify subgroups with different aetiology and needs of treatment.

Brown, H. (2005) A brain in the head, and one in the gut: Scientists study connection between digestive and psychiatric problems. Aug.5: International Herald Tribune.

But 95 percent of the body’s serotonin is housed in the gut, where it acts as a neurotransmitter and a signaling mechanism. Serotonin also acts as a go-between, keeping the brain in the skull up to date with what is happening in the brain below. Such communication is mostly one way, with 90 percent traveling from the gut to the head.”You can run any test you want on people with IBS, and their GI tracts look essentially normal,” Mawe said. The default assumption has been that the syndrome is a psychosomatic disease. ~Gary M. Mawe, professor of anatomy and neurobiology at the University of Vermont (Brown, 2005)

Percentage of Population estimate (15-20%)

“12-month prevalence of 26.2%, with half of all cases reporting onset by age 14 and three quarters by age 24. What should we make of these numbers? If one quarter of the population has a mental disorder each year…?”

~Dr. Thomas Insel

Director NIMH

Chabrol, H , Montovany, A, Chouicha, K, et al. Frequency of Borderline Personality Disorder in a Sample of French High School Students. Can J Psychiatry, 2001;46:847–849.

Davydow DS, et al. Posttraumatic stress disorder in general intensive care unit survivors: a systematic review. Gen Hosp Psychiatry 30(5), 2008.

From 15 separate studies: “clinically significant” PTSD symptoms was 22% (n=1,104), and the median point prevalence of clinician-diagnosed PTSD was 19% (n=93).

Thoughts on PTSD & BPD:

(Could PTSD have a direct relationship with the increased memory/emotional response to sensory experience in this “peripheral” population?)

The consistency around the 20% mark for the population is an extremely important clue. This mathematical representation is a uniqueness of experience in a minority, 20%, of the population. The research on PTSD, that after a traumatic event it is not a “random” number of individuals that develop this syndrome. It appears to affect those that are more susceptible…to memory, emotions, and experience of their surroundings. The same is true for those that express “emotional dysregulation” in the study of French students, not exactly a disorder, but what seems to be a precursor to “borderline personality”, borderline personality is characterized by emotional dysregulation, fear of abandonment (aka not fitting in/not being normal), they are also many times highly personable, flexible in thought and action, successful, creative, dynamic individuals…

U.S. Census Bureau Population Estimates by Demographic Characteristics. Table 2: Annual Estimates of the Population by Selected Age Groups and Sex for the United States: April 1, 2000 to July 1, 2004 (NC-EST2004-02) Source: Population Division, U.S. Census Bureau Release Date: June 9, 2005. http://www.census.gov/popest/national/asrh/

New Freedom Commission on Mental Health. (2003). Achieving the promise: Transforming mental health care in America. Final report (DHHS Pub. No. SMA-03-3832). Rockville, MD: U.S. Department of Health and Human Services, Substance Abuse and Mental Health Services Administration. http://www.nimh.nih.gov/health/publications/the-numbers-count-mental-disorders-in-america.shtml

“One out of five children, one in four adults diagnosable

with a mental health disorder in any given year.”

Environmental Factors & Metabolic Pathways


Perception & Sensory

  1. A wider view of reality would take longer and a more fundamental learning skill-set in order to file info into long-term memory. And when learning every aspect of a particular problem is required in order to resolve a condition, it’s easy to understand that in some cases it never happens, so the foundation of said subject never gets laid and built upon, or the child/adult lives their lives unresolved and in constant conflict/crisis mode.

It could be hypothesized that the brain was set-up this way to finish thoughts started, to inspire or even demand for human to “figure things out” and all of these pathways serve a purpose, anger, frustration, obsession, compulsion, single-mindedness…starting a multitude of “branches”, more than the normal individual, gives their brains much more to do, more directions to follow, more information to take in…which could serve a purpose.

Nutrition & Resources

  1. Intense mental needs (equivalent to running mini-mental marathons on a daily basis) lead to intensely delicate balance of chemicals, requirements, recovery and restoration. Just as physical demands require additional provisions, so does mental demands, they actually require MORE energy and resources. The brain uses 20% of total calorie needs (75% during infancy) daily for “normal” functioning, the brain represent 2-3% of body weight, it also receives it’s energy from primarily glucose, unlike the body which can use either glucose or fat for energy. So living in the mind and especially when the mind is in overdrive, can be a drain on the systems, resources and organs of the body.

Social & Acceptance

  1. So what would happen to any child if they felt or knew they were fundamentally different and that being different would mean that they would not be understood or accepted, socially rejected or shunned? And the alternative, what would happen to any child if they spent their lives trying to fit in by being something they are not? Because this competition to be the best “normal” as possible, when that normal is defined by personality characteristics as opposed to value characteristics, causes emotional unrest in these individuals, when our values are on a personality preferences that they simply can never become. You cannot wish or train yourself into physiological personality characteristic & traits.

People evolve for a multitude of purposes, our bodies are created to adapt and change. If the “geeks/artists/scientists” of the world are lacking filters or have other chemical uniqueness that allows them to live with more possibilities, then the biochemically individuality of these individuals may also set them up to be more environmentally sensitive or have compensatory actions, such as emotional sensitivity (different than norm) as a way to balance the influx of information.

Nutrition and the Mind

Drugs show an effect. Drugs can demonstrate a particular mechanism of action. Drugs have linear, singular, straight-line observable, cause and effect action. Drugs work beautifully once something is broken or depleted. This shows a direct effect and it is this type of disease that is in the realm of Classical Physics. Classical Physics in medicine also assume a static starting point.

But research has shown that our physiological minds are in constant ebb and flow; a reflection and response to our environment. Evolutionary Biology is demonstrating this fact. And changing the nutritional components of food in order to “kill germs”, preserve and make food more economically viable, created a multitude of subtle changes in the availability, combination and interaction of nutrition of those foods and their inherent properties. And this in turn could reflect and impact the ability of our minds to process information (especially frontal lobes) and for the interactive systems of the body to function optimally.

Bartzokis G. Acetylcholinesterase inhibitors may improve myelin integrity. Biol Psychiatry. 2006 Oct 26

Bartzokis G. Brain myelination in prevalent neuropsychiatric developmental disorders: primary and comorbid addiction. Adolesc Psychiatry. 2005;29:55-96.PMID: 18668184

The role of nutrition may be particularly important. In order to build membranes – “and myelin is the ultimate membrane” – the body requires sufficient supplies of essential fatty acids found in fish oils, flaxseed, grains and nuts. But the diets of young people are notoriously poor, he says, and likely to be deficient in key nutrients.

(LaFee 2006) http://www.signonsandiego.com/news/science/20060208-9999-lz1c08myelin.html

Dr. Bartzokis and his team described the younger brain undergoing myelination and what can happen if those connections don’t develop normally.

Dr. Bartzokis believes that humans brains myelinate different circuits at varying points throughout life, which may explain why the brain diseases of young people are frequently very different than those of older people.

An example is if myelin is disrupted early in life, basic circuits that govern language and social communication might not develop normally, hence autism.

If the problems develop in school-age children, the inability to process information fast and effectively might result in the development of attention deficits. Later in adolescence, problems with myelin can impair a person’s ability to think clearly, a common feature of schizophrenia. http://www.schizophrenia.com/sznews/archives/002685.html

Benton D, et al. Vitamin supplementation for one year improves mood. Neuropsychobiology 1995;32(2):98 –105. this improvement in mood was associated in particular with improved riboflavin and pyridoxine status. In females baseline thiamin status was associated with poor mood and an improvement in thiamin status after 3 months was associated with improved mood.

Bennett P, Brostoff J. The health of criminals related to behavior, food, allergy and nutrition. J Nutr Environ Med 1997;7:359 – 66. From this study, the proportion of the persistent young offender population with maladaptive behaviours linked to food allergy, food intolerance and nutritional problems is cautiously estimated to be 75% whereas 18% of the young non-offender population is similarly affected

Bilici M, Yildirim F, Kandil S, et al. Double-blind, placebo-controlled study of zinc sulfate in the treatment of attention deficit hyperactivity disorder. Prog Neuropsychopharmacol Biol Psychiatry. 2004 Jan;28(1):181-90. CONCLUSIONS: Zinc monotherapy was significantly superior to placebo in reducing symptoms of hyperactivity, impulsivity and impaired socialization in patients with ADHD. Although by themselves, these findings may not be sufficient, it may well be considered that zinc treatment appears to be an efficacious treatment for ADHD patients having older age and high BMI score with low zinc and FFA levels.

Black M. Zinc deficiency and child development. Am J Clin Nutr 1998;68:464S– 9S [Suppl.]. Zinc is a trace metal that is present in the brain and contributes to its structure and function. Limited evidence from both animal and human studies suggests that zinc deficiency may lead to delays in cognitive development. Although the mechanisms linking zinc deficiency with cognitive development are unclear, it appears that zinc deficiency may lead to deficits in children’s neuropsychologic functioning, activity, or motor development, and thus interfere with cognitive performance.

Breakey J. The role of diet and behavior in childhood. J Paediatr Child Health 1997;33:190– 4.

Chen L, Wing-Ho Y. Zinc modulates GABAergic neurotransmission in rat globus pallidus

Neuroscience Letters, Volume 409, Issue 3, 6 December 2006, Pages 163-167

Chiang P, Gordon R, et al. S-adenosylmethionine and methylation. FASEB J 1996;10:471–80.

Cohen JH, et al. Psychological distress is associated with unhealthful dietary practices. J Am Diet Assoc, 102(5):699-703, 2002.

Collipp, P.J., et al. Zinc deficiency: Improvement in growth and growth hormone levels with oral zinc therapy. Ann. Nutr. Metab., 26: 287 (1982).

Cunningham-Rundles, C., et al. Zinc deficiency, depressed thymic hormones and T-lymphocyte dysfunction in patients with hypogammaglobulinemia. Clin. Immunol. Immunopathol., 21: 387 (1981).

Ebaldi M, Murrin LC, Pfeiffer RF. Hippocampal zinc thionein and pyridoxal phosphate modulated synaptic function. Vitamin B-6. Annals of the New York Acad of Sci 1980. p. 189– 201. The hippocampus, a component of the limbic system, is a prominent subcortical structure, which not only contains high concentrations of zinc, but also exhibits regional variations in this essential element, with concentrations being highest in the hilar region and lowest in the fimbria. For example, the concentration of zinc in the mossy fiber axons has been estimated to approach 300-350 microM. Both zinc and pyridoxal phosphate (PLP) deficiency and excess have been reported to produce epileptic form seizures, which are blocked by gamma-aminobutyric acid (GABA). The proposed mechanism is that at physiological concentrations zinc stimulates the activity of the hippocampal pyridoxal kinase (50% stimulation at 1.7 x 10(-7) M), enhancing the formation of PLP, whereas in pharmacological doses zinc inhibits the activity of glutamate decarboxylase (GAD) directly (50% inhibition at 6.5 X 10(-4) M) by preventing the binding of PLP to HoloGAD

Franco JL, Posser T, Brocardo PS. Involvement of glutathione, ERK1/2 phosphorylation and BDNF expression in the antidepressant-like effect of zinc in rats. Behav Brain Res. 2008 Apr 9;188(2):316-23. Epub 2007 Nov 22.

Frangou. Omega-3 fatty acid EPA improves depression in people with bipolar alongside their existing medication. Br J Psychiatry. 188:46-50, 2006

Galland L.. Magnesium, stress and neuropsychiatric disorders. Magnes Trace Elem. 1991-1992;10(2-4):287-301

Gariballa, S. Forster, S. Multivitamin and mineral supplement improves mood in hospitalised elderly., Clin Nutr. 2007 Jul 25

Gesch C, Hammond S, Hampsom S, Eves A, Crowder M. Influence of supplementary vitamins, minerals, and essential fatty acids on the antisocial behaviour of young adult prisoners: randomized, placebocontrolled trial. Br J Psychol 2002;181:22– 8.

Gómez-Pinilla, F. Brain foods: the effects of nutrients on brain function. Nature Reviews Neuroscience 9, 568-578 (2008).

It has long been suspected that the relative abundance of specific nutrients can affect cognitive processes and emotions. Newly described influences of dietary factors on neuronal function and synaptic plasticity have revealed some of the vital mechanisms that are responsible for the action of diet on brain health and mental function. Several gut hormones that can enter the brain, or that are produced in the brain itself, influence cognitive ability. In addition, well-established regulators of synaptic plasticity, such as brain-derived neurotrophic factor, can function as metabolic modulators, responding to peripheral signals such as food intake. Understanding the molecular basis of the effects of food on cognition will help us to determine how best to manipulate diet in order to increase the resistance of neurons to insults and promote mental fitness.

Gray G. Diet, crime and delinquency: a critique. Nutr Rev 1986;44:89–94 [Suppl].

Hoffer A: Chronic schizophrenic patients treated ten years or more. J. Orthomolecular Medicine, 9:7-37, 1994. MASKS OF MADNESS

Improved mood and behavior during treatment with a mineral-vitamin supplement: an open-label case series of children. Journal of Child and Adolescent Psychopharmacology. Spring 2004; 14(1):115-22.

James SJ, Melnyk S, Fuchs G, et al. Efficacy of methylcobalamin and folinic acid treatment on glutathione redox status in children with autism. Am J Clin Nutr. 2009 Jan;89(1):425-30. Epub 2008 Dec 3. The significant improvements observed in transmethylation metabolites and glutathione redox status after treatment suggest that targeted nutritional intervention with methylcobalamin and folinic acid may be of clinical benefit in some children who have autism.

Kagi JHR, Schaffer A. Biochemistry of metallothionein. Biochemistry 1988;27:8509– 15.

Kanarek R. Nutrition and violent behavior. In: Reiss A, Miczek K, Roth J, editors. Understanding and preventing violence. Biobehavioral influences, vol. 2. Washington (DC)7 National Academy Press; 1994. p. 515– 39.

Circular Reasoning:

Thought: Prove to me that something is influential and interactive…but only by using the rules used to define effects in a singular, direct manner.

When you are faced with the problem of having to show a singular effect in order to prove it takes multiple influences to have an effect, this is called circular reasoning. It simply can’t be done. You can’t show truth by beginning with a false premise. In mathematics we create formulas based on observable facts in order to then test for the truth under new conditions. If the original formula for testing is based on an incomplete assumption it might just be the reason for the rifts in understandings and no clear picture for any of these disorders.

This exclusive reliance on a simplistic model of disease has limited and misled our understanding of human health from such factors as nutrition. Nutrition may not have a direct, singular or linear effect on health, not as we see the effects of germs or drugs….but nutrition has a much more over-reaching effect on things like gene expression, adaptive processes and the manifestation of complex disorders that resemble weather patterns in particular climates. (signaling pathways)

Kirov GK, Tsachev KN.. Magnesium, schizophrenia and manic-depressive disease. Neuropsychobiology. 1990;23(2):79-81

Kleimola, V., et al. (1983) The zinc, copper, and iron status in children with chronic diseases. Trace Element Analytical Chemistry in Medicine and Biology, Walter de Gruyter: New York

Krystal JH, D’Souza DC, Petrakis IL et al. (1999), NMDA agonists and antagonists as probes of glutamatergic dysfunction and pharmacotherapies in neuropsychiatric disorders. Harv Rev Psychiatry 7:125–143

Lien, L. Breakfast, Academic Performance and Mental Distress. Public Health Nutrition, 10(4), 422-428, 2006 July

Lin PY and Su KP. J. Omega 3 fish oil good for depression and bipolar. Clin Psychiatry, 2007 Jul;68(7):1056-61

London, EA. The environment as an etiologic factor in autism: a new direction for research, Environ. Health Perspect, 108 (2000) 401–404.

Liu J, Raine, A. The effect of childhood malnutrition on externalizing behavior. 2006 Oct;18(5):565-70.

RECENT FINDINGS: Externalizing behavior is associated with both macromalnutrition (e.g. protein) and micromalnutrition (e.g. iron and zinc). Both prenatal and postnatal malnutrition is implicated. The long-term effects of malnutrition on behavior could be reversible. The effects of docosahexaenoic acid/omega-3 long-chain essential fatty acid on externalizing behavior are more mixed. From animal and human findings, it is hypothesized that malnutrition impairs neurocognitive functioning by reducing neurons, alternating neurotransmitter functioning, and increasing neurotoxicity, and that such neurocognitive impairments predispose to externalizing behavior.

Markus, C. R. Panhuysen, G. Jonkman, L. M. Carbohydrate intake improves cognitive performance of stress-prone individuals under controllable laboratory stress. British Journal of Nutrition (1999), 82, 457–467


Mcleary, L. (2007) The Brain Trust Program. A Perigree Book; Penguin Group.

Taken from sharpbrains.com


In addition to being a thinking machine, the brain is also a flesh and blood organ that must comply with the laws of metabolism and physiology. Insight into both its ‘mental’ and ‘physical’ properties is vital for comprehending key aspects of brain health and function. … For it to participate in such mentally demanding endeavors, the brain would have relied on the prior existence of sophisticated neuronal circuitry. I suggest a nutritional basis for the dramatic cerebral expansion, with enhanced functionality (such as development of tool use and hunting strategy) being the natural responses of a larger, more plastic organ to novelty and environmental challenges. The common link between the evolutionary cerebral expansion and modern brain health/function resides in the massive wiring demands inherent in both processes. This marked amplification in neuronal connectivity is made possible by the enhanced production of synaptic membranes (nerve cell membranes in the regions of points of nerve cell contact).

How was it possible to fuel the production of major increases in neuronal number and synaptic density? This required the concordant expression of genetic potential (likely driven, in part, by the provision of an uninterrupted energy supply) and proper nutritional content – meaning high, sustained caloric and nutrient density. … persistent supply of nutrient dense calories is essential for brain expansion. To fully appreciate how energetically expensive brains are, consider that modern brains comprise about 2.3% of the body mass, yet consume almost one quarter of the available energy. Newborn brains utilize fully 75% of the body’s energy!

~Larry McCleary, M.D. Dr. McCleary is a former acting Chief of Pediatric Neurosurgery at Denver Children’s Hospital. He is trained and has practiced as a pediatric neurosurgeon and has completed post-graduate training in theoretical physics. His scientific publications span the fields of metabolic medicine, tumor immunology, biotechnology and neurological disease. http://www.sharpbrains.com/blog/2007/12/27/brain-evolution-and-why-it-is-meaningful-today-to-improve-our-brain-health/

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Muntjewerff JW, Van der Put N, Eskes T, et al. Homocysteine metabolism and B-vitamins in schizophrenic patients: low plasma folate as a possible independent risk factor for schizophrenia. Psychiatry Res 2003; 121:1–9.

Mustak MS, Rao TS, Shanmugavelu P, et al. Assessment of serum macro and trace element homeostasis and the complexity of inter-element relations in bipolar mood disorders. lin Chim Acta. 2008 Aug; 394(1-2):47-53. Epub 2008 Apr 8.

Peet, Stokes. A review of the current evidence (2005) suggests that essential fatty acids, particularly EPA and DHA may benefit a variety of mental health conditions. Drugs, 65(8):1051-9, 2005

Pinilla FG. The impact of diet and exercise on brain plasticity and disease. Nutr Health. 2006;18(3):277-84.

“Food is like a pharmaceutical compound that affects the brain,” said Fernando Pinilla, a UCLA professor of neurosurgery and physiological science who has spent years studying the effects of food, exercise and sleep on the brain. “Diet, exercise and sleep have the potential to alter our brain health and mental function.” http://www.news-medical.net/?id=39890

Pfeiffer C, Iliev V. A study of zinc deficiency and copper excess in the schizophrenias. Int Rev Neurobiol, 1972;72:141

Pfeiffer C, Braverman E. Folic acid and vitamin B-12 therapy for the low histamine, high copper biotype of schizophrenia. In: Botez M, Reynolds E, editors. Folic acid in neurology, psychiatry, and internal medicine. New York7 Raven Press; 1979. p. 483– 7.

Prasad AS, Mantzoros CS Beck FW. Zinc status and serum testosterone levels of healthy adults. Nutrition. 1996 May;12(5):344-8. :

Concluded that zinc may play an important role in modulating serum testosterone levels in normal men.

Nemets, H. et al., Omega-3 helps depressed children, A Controlled, Double-Blind Pilot Study. Am J Psychiatry 2006; 163:1098–1100

Richardson, M. Supplements of omega-3 and omega-6 improve reading, spelling and behaviour in children ages 5-12 years with Developmental Coordination Disorder. Pediatrics, 115(5):1360-6, 2005.

Thought: Why did we get rid of FAT from the diet anyway? My answer: Because the confines of Classical Physics and the 2nd Law of Thermodynamics dictates that the “only” direct linear effect of food on health (aka weight gain/obesity)was calories (calories in calories out).So…get rid of the highest caloric food group, aka FAT calories and you’d get rid of obesity….we’ve been travelling down the wrong path (singular blame) to health for a very long time because of our adherence to the wrong framework and ‘system’ of scientific thinking concerning human body and health…this is, in my opinion, the ‘crisis of perception’.

Rimland B. High dose vitamin B6 and magnesium in treating autism: response to study by Findling et al. J Autism Dev Disord 1998;28:581–2.

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Small GW, Silverman DH, Siddarth P, et al. Effects of a 14-day healthy longevity lifestyle program on cognition and brain function. Am J Geriatr Psychiatry. 2006 Jun;14(6):538-45.

Sowa-Kucma M, Legutko B, Szewczyk B, et al. Antidepressant-like activity of zinc: further behavioral and molecular evidence. Smetna 12, 31-343, Kraków, Poland.J Neural Transm. 2008 Sep 3

Schoenthaller S, Bier I. The effect of vitamin–mineral supplementation on juvenile delinquency among American schoolchildren. J Altern Complement Med 2000;6(1):7– 17.

Starobrat-Hermelin B. Szczecinie.. The effect of deficiency of selected bioelements on hyperactivity in children with certain specified mental disorders. Ann Acad Med Stetin. 1998;44:297-314

Stevens L, et al. Omega-3 fatty acids in boys with behavior, learning, and health problems. Physiol Behav 1996;59(4–5):915–20.

Stoll AL, et al. Omega-3 fatty acids and bipolar disorders: a review. Prostaglandins Leukot Essent Fatty Acids, 60:329-337, 1999

Treatment of Mood Lability and Explosive Rage with Minerals and Vitamins: Two case Studies in Children. Journal of Child and Adolescent Psychopharmacology. 2002 Fall;12(3):205-19

Wenstrup, D., Ehmann, W.D., and Markesbery W.R., Trace Element Imbalances in Isolated Subcellular Fractions of Alzheimer’s Disease Brains. Brain Research (1990) 533. 125-131.

Yasuhiro Y, Hideki F, Masayoshi I. Suppressive Effect of Zinc on the Toxicity of Mercury Chemical & pharmaceutical bulletinVol.25, No.7(19770725) pp. 1509-1518

Thought: A sub-hypothesis: Could peripheral minds retain more minerals and therefore more metals than the general population?

One aspect of these minds having unique processing and more sensory information than the average is that they might also require more nutritional building blocks (neurotransmitters) for this information to be processed correctly and timely.

As we evolved, these individuals could have adapted to retain more nutritional resources from the foods they ate, and therefore became unique vessels for retaining minerals (such as Zinc, Selenium, Iron, Magnesium, Copper).

It could be hypothesized that if they retain these minerals at a higher rate, they would also retain METALS and mineral substrates at a higher rate than in the average population. These minerals might cause more damage by their own inherent toxicity and by blocking the essentially needed minerals for sensory processing. (Blocking and toxic agents such as Mercury, Fluoride, Aluminum, MSG, Cadnium, Lead).

(This is very over-simplified, but I think a good question to ask and a place to start, I think ultimately it will be much more complicated, such as different minerals may make individuals more susceptible to different metals at different times, ie, youth is a time for neural growth and as we age these needs shift to maintenance. This might require a different combination of resources, so in youth we may need more zinc, which would make us more susceptible to mercury, as we age we may need more selenium, which might make us more susceptible to aluminum…if there is shown to be a relation and interaction.)

Zanarini MC, Frankenburg FR. Omega-3 fatty acid treatment of women with borderline personality disorder: a double blind, placebo-controlled pilot study. Am J Psychiatry, 160(1):167-169, 2003

University of California – Los Angeles (2006, May 22). Simple Lifestyle Changes May Improve Cognitive Function And Brain Efficiency. ScienceDaily. Retrieved January 23, 2009, from http://www.sciencedaily.com/releases/2006/05/060522150621.htm

“The debate has been more polarizing than it is in reality…Hopefully there is common ground in recognizing that autism is more complex. It’s not going to be solely explained by biology or genetics or a single environmental cause.

“It could be anything from the exposures in our physical surroundings — chemicals around us in homes, clothes, products, medications we take and food we eat…” (Allen 2009)

~Catherine Rice,

director of the Center for Disease Control

and Prevention’s national center for

birth defects and developmental disabilities

Allen, M. (2009) Another autism mystery: The rise in cases. Las Vegas Sun. Feb 20, 2009

“It’s a combination of being genetically vulnerable, and then having some kind of social or toxic exposure that tips you over,” Goldstein says. Dr. Gary Goldstein, president of Kennedy Krieger Institute, one of the leading U.S. facilities for autism research and treatment.


The brain has the ability to change and morph with experience, “damaged” or lesser functioning areas can change with stimulation. (mainstream has always thought the brain was “set” in stone to more or less once through childhood)

EPIGENETICS (Wikipedia 2009)

In biology, the term epigenetics refers to changes in phenotype (appearance) or gene expression caused by mechanisms other than changes in the underlying DNA sequence (hence the name epi – “in addition to” – genetics). These changes may remain through cell divisions for the remainder of the cell’s life and may also last for multiple generations. However, there is no change in the underlying DNA sequence of the organism; instead, non-genetic factors cause the organism’s genes to behave (or “express themselves”) differently. The best example of epigenetic changes in eukaryotic biology is the process of cellular differentiation. During morphogenesis, totipotent stem cells become the various pluripotent cell lines of the embryo which in turn become fully differentiated cells. In other words, a single fertilized egg cell – the zygote – changes into the many cell types including neurons, muscle cells, epithelium, blood vessels et cetera as it continues to divide. It does so by activating some genes while inhibiting others.

  • Oskar Hertwig, 1849-1922. Biological problem of today: preformation or epigenesis? The basis of a theory of organic development. W. Heinemann: London, 1896.
  • Deep Nutrition: Why Your Genes Need Traditional Food by Catherine Shanahan MD, and Luke Shanahan. Big Box Books, 2008.
  • Rudolf Jaenisch and A. Bird (2003) Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals. Nat. Genet. 33 (Suppl) 245-254.
  • Joshua Lederberg,The Meaning of Epigenetics, The Scientist 15(18):6, Sep. 17, 2001.
  • R. J. Sims III, K. Nishioka and D. Reinberg (2003) Histone lysine methylation: a signature for chromatin function. Trends Genet. 19, 629-637

Dr. Pat Levitt: “…developmental neurobiologists spent an enormous amount of time trashing each others’ work because one was either in the “nature school” or the “nurture school” regarding brain development. Of course, that was silly because we know that the brain is built through a genetic blueprint that takes information from the outside world and utilizes it to direct the developmental course to wire up circuits. This gene–environment interaction is one of the unique properties of the brain. So, of course, regarding ASD, it is not genetic versus environmental, irrespective of whether you think there is a principal cause that is genetic or environmental. Because ASDs have at their core disrupted brain development, in terms of etiology, both genetic and environmental influences must play roles because this is in the basis for brain development.” ~Dr. Pat Levitt. Annette Schaffer Eskind Chair and Professor of Pharmacology at the Vanderbilt Kennedy Center

Thought: (There has been a strong and heated debate between Neurodiversity (ND) and Environmental-Damage (ED) advocacy groups. “Genes or Environment.”

I think in many ways they have been pitted against each other when in reality they have a common enemy: An out-dated mode of scientific thinking. ND is fighting the sociological confines and ED is fighting physiological confines of a disease model (GTD) and Classical Physics. ND is up against the Central Limit Theorem and ED is up against Koch’s Postulate. When creating this new framework it’s much easier to see that they may actually be on the same team, neuroatypical more readily damaged by neurotoxins resulting in neurological burdens or dysfunction.)

Davidson RJ, Jackson DC, Kalin NH. Emotion, plasticity, context and regulation: perspectives from affective neuroscience. Psychological Bulletin, 2000; 126(6): 873-89.

Ecole Polytechnique Fédérale de Lausanne (2006, August 15). Rewiring The Mammalian Brain: Neurons Make Fickle Friends. ScienceDaily. Retrieved December 7, 2008, from http://www.sciencedaily.com /releases/2006/08/060814133621.htm. Scientists know that the strength of the connections between neurons changes to shape memories. They also know that the developing brain has a high level of plasticity as neurons forge connections with other neurons… “This continual rewiring of the microcircuitry of the brain is like a Darwinian evolutionary process,” notes Markram, “where a new experience triggers a burst of new connections between neurons, and only the fittest connections survive.”

Ornish D. Magbanua MJM, Weidner G, et al. Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. PNAS 2008 105:8369

In a small study, the researchers tracked 30 men with low-risk prostate cancer who decided against conventional medical treatment such as surgery and radiation or hormone therapy. The men underwent three months of major lifestyle changes, including eating a diet rich in fruits, vegetables, whole grains, legumes and soy products, moderate exercise such as walking for half an hour a day, and an hour of daily stress management methods such as meditation.

After the three months, the men had changes in activity in about 500 genes — including 48 that were turned on and 453 genes that were turned off. The activity of disease-preventing genes increased while a number of disease-promoting genes, including those involved in prostate cancer and breast cancer, shut down, according to the study published in the journal Proceedings of the National Academy of Sciences

Massachusetts Institute of Technology (2008, November 27). Adult Brain Neurons Can Remodel Connections. ScienceDaily. Retrieved December 7, 2008, from http://www.sciencedaily.com/releases/2008/11/081124174909.htm.

Overturning a century of prevailing thought, scientists are finding that neurons in the adult brain can remodel their connections. …sheds new light on the potential flexibility of cerebral cortex circuitry and architecture in higher-level brain regions that contribute to perception and cognition… extract clues regarding the contribution of structural remodeling to long-term adult brain plasticity — the brain’s ability to change in response to input from the environment — and what allows or limits this plasticity.”

Wall JT, Xu J, Wang X. Human brain plasticity: an emerging view of the multiple substrates and mechanisms that cause cortical changes and related sensory dysfunctions after injuries of sensory inputs from the body. Brain Res Brain Res Rev. 2002 Sep;39(2-3):181-215.

“We were taught at one time that it couldn’t happen – people who were mentally retarded couldn’t become average,” Mulick said. “But we found it can happen among at least some with autism.”

James Mulick PhD.

Pediatrics: Columbus Children’s Hospital

Toxicities and Environmental Components

Ashford N.A., Miller C. (1998) Chemical Exposures: Low Levels and High Stakes, John Wiley and Sons, Inc., New York.

Blaylock RL. The central role of excitotoxicity in autism spectrum disorders. JANA. 2003;6:7-19.

Blaylock RL. A possible central mechanism in autism spectrum disorders, part 2: immunoexcitotoxicity. Altern Ther Health Med. 2009 Jan-Feb;15(1):60-7.

Both androgens and glutamate alter neuronal and glial calcium oscillations, which are known to regulate cell migration, maturation, and final brain cytoarchitectural structure. Studies have also shown high levels of DHEA and low levels of DHEA-S in ASD, which can result from both mercury toxicity and chronic inflammation. Chronic microglial activation appears to be a hallmark of ASD. Peripheral immune stimulation, mercury, and elevated levels of androgens can all stimulate microglial activation. Linked to both transsulfuration problems and chronic mercury toxicity are elevations in homocysteine levels in ASD patients. Homocysteine and especially its metabolic products are powerful excitotoxins. Intimately linked to elevations in DHEA, excitotoxicity and mercury toxicity are abnormalities in mitochondrial function. A number of studies have shown that reduced energy production by mitochondria greatly enhances excitotoxicity. Finally, I discuss the effects of chronic inflammation and elevated mercury levels on glutathione and metallothionein.

Brown JS, Jr. Effects of Bisphenol-A and Other Endocrine Disruptors Compared With Abnormalities of Schizophrenia: An Endocrine-Disruption Theory of Schizophrenia. DOI 10.1093/schbul/sbm147. Schizophr Bull 35: 256-278. The pathologic and behavioral abnormalities attributed to exposure to endocrine disruptors like bisphenol-A (BPA) have been studied in animals. Mental conditions ranging from cognitive impairment to autism have been linked to BPA exposure by more than one investigation. Concurrent with these developments in BPA research, schizophrenia research has continued to find evidence of possible endocrine or neuroendocrine involvement in the disease. Sufficient information now exists for a comparison of the neurotoxicological and behavioral pathology associated with exposure to BPA and other endocrine disruptors to the abnormalities observed in schizophrenia. …These similarities can be observed in 11 broad categories of abnormality: physical development, brain anatomy, cellular anatomy, hormone function, neurotransmitters and receptors, proteins and factors, processes and substances, immunology, sexual development, social behaviors or physiological responses, and other behaviors

Chen, CW. Assessment of endocrine disruptors: approaches, issues, and uncertainties. Folia Histochem Cytobiol. 2001;39 Suppl 2:20–23. This paper focuses on the quantitative risk assessment of environmental endocrine-disrupting chemicals (EDCs) to human health. An EDC can be defined as an exogenous agent that interferes with the normal endocrine signaling and communication mechanisms. The normal feedback control system of natural hormones is responsible for regulatory mechanisms that maintain homeostasis. Hormones deliver their message to target cells by interacting with receptors, initiating signal transduction, gene transcription, and mRNA translation, and ultimately leading to cellular response. Because effects of EDCs include diverse disease endpoints such as cancer, reproductive toxicity, developmental toxicity, immune system effects, acute toxicity, and neurotoxicity, risk assessment of EDCs is necessarily endpoint-specific. From the quantitative viewpoint, it is best to model the normal endocrinology and then extend the model to include impacts attributable to a particular exogenous agent

Colborn T, Dumanoski D, Peterson Myers J. (1996) Our stolen future: Are we threatening our fertility, intelligence, and survival? A scientific detective story. New York: Dutton.

Durkin MS, Maenner MJ, Newschaffer CJ. Advanced Parental Age and the Risk of Autism Spectrum Disorder. American Journal of Epidemiology Advance Access published on December 1, 2008, DOI 10.1093/aje/kwn250. Am. J. Epidemiol. 168: 1268-1276. The autism study, led by University of Wisconsin-Madison epidemiologist Maureen Durkin, looked at more than 1,200 cases of autism, or 50 percent more than any previous study. The research team looked at more than 300,000 U.S. births. For instance, she said, factors that might influence the disorder in the children of older parents include age-related genetic and chromosomal damage, environmental toxins and the effects of infertility treatment. Susanne Rust(2009) Researcher finds link between age, birth order and autism Milwaukee Journal Sentinel. Wednesday, January 07, 2009

Kern, JK, Jones, AM. Evidence of Toxicity, oxidative stress and neuronal Insult. Autism Pathophysiology, 13 (2006) 171–181. According to the Autism Society of America, autism is now considered to be an epidemic. The increase in the rate of autism revealed by epidemiological studies and government reports implicates the importance of external or environmental factors that may be changing. This article discusses the evidence for the case that some children with autism may become autistic from neuronal cell death or brain damage sometime after birth as result of insult; and addresses the hypotheses that toxicity and oxidative stress may be a cause of neuronal insult in autism

Geier DA, Kern JK, Garver CR, et al. Biomarkers of environmental toxicity and susceptibility in autism. J Neurol Sci. 2008 Sep 24

Grandjean P, Landrigan PJ Developmental Neurotoxicity of Industrial Chemicals. The Lancet, November 8, 2006- Vol. 368. Grandjean and co-author Philip J. Landrigan, Professor at Mount Sinai School of Medicine, compiled a list of 202 environmental chemicals known to be toxic to the human brain using the Hazardous Substances Data Bank of the National Library of Medicine and other data sources. (The authors note that the list should not be regarded as comprehensive; for example, the number of chemicals that can cause neurotoxicity in laboratory animal tests exceeds 1,000.) The authors then examined the published literature on the only five substances on the list—lead, methylmercury, arsenic, PCBs and toluene—that had sufficient documentation of toxicity to the developing human brain in order to analyze how that toxicity had been first recognized and how it led to control of exposure. They found a similar pattern in how the risks of each substance were documented: first, a recognition of adult toxicity and episodes of poisoning among children, followed by a growing body of epidemiological evidence that exposure to lower levels of the substances caused neurobehavioral deficits in children. “Even if substantial documentation on their toxicity is available, most chemicals are not regulated to protect the developing brain,” says Grandjean. “Only a few substances, such as lead and mercury, are controlled with the purpose of protecting children. The 200 other chemicals that are known to be toxic to the human brain are not regulated to prevent adverse effects on the fetus or a small child.”

Han, R. Yang, Y.M., Dietrich, J., Luebke, A., Mayer-Pröschel, M. and Noble, M. (2008) Systemic 5-fluorouracil treatment causes a syndrome of delayed myelin destruction in the CNS. J. Biol. 7:12 link

Dr. Mark Noble: I think that if one wants to test the hypothesis that mercury is the primary causative agent in autism, that that is the wrong hypothesis. If one wants to test the hypothesis that mercury is one of many environmental factors that may contribute to this outcome that looks like the right hypothesis.

So if we look at what we can look at now, there is a limited number of agents where the sensitivity of analyses are sufficient to enable us to do reasonable studies, the organic materials, PCBs, a few other effects. That data may turn out to be extraordinarily compelling, particularly because of what we are hearing about the heavy metals and the chelation therapy. At least heavy metals are something that can be analyzed pretty well.

What I am specifically concerned with is that—with all respect and admiration and concern for the parents’ groups and everyone who has been trying to pursue the idea of a specific environment toxicant or a specific vaccination, just from a biological point of view, it doesn’t sound like a great hypothesis. It sounds like these may be pieces, that they happened at a particular time, but they are not going to apply to all the kids.

From the cell’s point of view, I don’t think it matters. Am I oxidized because of an inflammation? Am I oxidized because I got mercury? I don’t care, I’m oxidized, I am in electron deficit. The data that I am hearing just keeps agreeing with that. Even this idea of astrogliosis and the white-matter tracks, when we take these oligodendrocyte progenitors and expose them to oxidative stress, they turn into astrocytes. So even that is a really intriguing outcome. We have to look at specific astrocyte populations there.

So that is what I mean, that these all could be players. It doesn’t sound likely at this stage that any one of them is a player of central importance.

Autism and the Environment: Challenges and Opportunities for Research, Workshop Proceedings (2008) http://books.nap.edu/openbook.php?record_id=11946&page=R1

Larsson M, Weiss B, Janson S, et al. Associations between indoor environmental factors and parental-reported autistic spectrum disorders in children 6–8 years of age. NeuroToxicology, In Press, Corrected Proof, Available online 10 February 2009. doi:10.1016/j.neuro.2009.01.011

Potential contributions of environmental chemicals and conditions to the etiology of Autism Spectrum Disorders are the subject of considerable current research and speculation. The present paper describes the results of a study undertaken as part of a larger project devoted to the connection between properties of the indoor environment and asthma and allergy in young Swedish children. Results from the second phase of the DBH-study (DBH-II) indicate PVC flooring to be one important source of airborne phthalates indoors, and that asthma and allergy prevalence are associated with phthalate concentrations in settled dust in the children’s bedroom. Because these associations are among the few linking ASD with environmental variables, they warrant further and more extensive exploration….(Cone 2009) Vinyl flooring is commonplace in Sweden, where only about 1 percent of homes have carpeted floors. But it is uncommon in U.S. bedrooms, so it may not be related to autism among American children. However, carpeting contains other contaminants, including pesticides and brominated flame retardants, which have been found to harm brain development in animal tests. The scientists said their new finding “suggests that studies of other chemical contaminants with endocrine disruptor properties might yield useful insights into the genesis of autism. http://www.environmentalhealthnews.org/ehs/news/autism-and-vinyl-flooring

Lathe R. Environmental Factors and Limbic Vulnerability in Childhood Autism. American Journal of Biochemistry and Biotechnology 4 (2): 183-197, 2008. ISSN 1553-3468

Nataf, R,. Skorupka, C, Amet, L. Porphyrinuria in Childhood Autistic Disorder: Implications for Environmental Toxicity. Toxicology and Applied Pharmacology, 214 (2006) 99–108.

Nunez AA, Kannan K, Giesy JP, Et al. Effects of Bisphenol A on energy balance and accumulation in brown adipose tissue in rats.Chemosphere, Volume 42, Issue 8, 15 March 2001, Pages 917-922

Pall M. L. (2002) NMDA sensitization and stimulation by peroxynitrite, nitric oxide and organic solvents as the mechanism of chemical sensitivity in multiple chemical sensitivity. FASEB J, 16,1407-1417. Multiple chemical sensitivity (MCS) is a condition where previous exposure to hydrophobic organic solvents or pesticides appears to render people hypersensitive to a wide range of chemicals, including organic solvents. The hypersensitivity is often exquisite, with MCS individuals showing sensitivity that appears to be at least two orders of magnitude greater than that of normal individuals. This paper presents a plausible set of interacting mechanisms to explain such heightened sensitivity. It is based on two earlier theories of MCS: the elevated nitric oxide/peroxynitrite theory and the neural sensitization theory. It is also based on evidence implicating excessive NMDA activity in MCS. Four sensitization mechanisms are proposed to act synergistically, each based on known physiological mechanisms: Nitric oxide-mediated stimulation of neurotransmitter (glutamate) release; peroxynitrite-mediated ATP depletion and consequent hypersensitivity of NMDA receptors; peroxynitrite-mediated increased permeability of the blood–brain barrier, producing increased accessibility of organic chemicals to the central nervous system; and nitric oxide inhibition of cytochrome P450 metabolism. Evidence for each of these mechanisms, which may also be involved in Parkinson’s disease, is reviewed. These interacting mechanisms provide explanations for diverse aspects of MCS and a framework for hypothesis-driven MCS research

Palmer, R.F. Environmental mercury release, special education rates, and autism disorder: an ecological study of Texas. Health & Place, 2006, vol. 12, 2, pp. 203-209.

Shultz SR, Macfabe DF, Martin S, Intracerebroventricular injections of the enteric bacterial metabolic product propionic acid impair cognition and sensorimotor ability in the Long-Evans rat: further development of a rodent model of autism. Behav Brain Res. 2009 Jun 8;200(1):33-41. Epub 2008 Dec 30.

Walsh WJ, Rehman F. Methylation syndromes in mental illness. Abstract, Neuroscience Society. New Orleans; Nov. 1997.

Methylation: Rich van Konynenburg’s idea is that ineffective methylation is a major cause of fatigue. There are many possible reasons but those that he’s identified for which methylation is essential to are:

  1. To produce vital molecules such as Co Q-10 and carnitine.
  2. To switch on DNA and switch off DNA. This is achieved by activating and deactivating genes by methylation. This is essential for gene expression and protein synthesis. Proteins of course make up the hormones, neurotransmitters, enzymes, immune factors and are fundamental to good health. When viruses attack our bodies, they take over our own DNA in order to replicate themselves. If we can’t switch DNA/RNA replication off then we will become more susceptible to viral infection.
  3. To produce myelin for the brain and nervous system.
  4. To determine the rate of synthesis of glutathione which is essential for detoxification.
  5. To determine the rate of synthesis of glutathione which is an essential anti-oxidant as glutathione-peroxidase. Furthermore oxidative stress blocks glutathione synthesis – yet another vicious cycle!
  6. To control sulphur metabolism of the body, not just glutathione but also cysteine, taurine and sulphate. This is an important process for detoxification.
  7. As part of folic acid metabolism. This also switches on synthesis of new DNA and RNA.
  8. For normal immune function. The methylation cycle is essential for cell mediated immune function and blockages here will mean that infections will not be adequately dealt with. I know this clinically because many patients tell me that once they get on to their B12 injections (an essential co-factor for methylation) this seems to protect them from getting infections.

The overall effect here is that if the methylation cycle doesn’t work, the immune system mal-functions, the detoxification system mal-functions, our ability to heal and repair is reduced and the anti-oxidant system mal-functions. ~ (Dr. Sarah Myhill www.drmyhill.co.uk)

Walsh, WJ, Usman, A, Tarpey, J. Disordered Metal Metabolism In a Large Autism Population. Proceedings of the Amer. Psych. Assn.; New Research: Abstract NR109, New Orleans, May, 2001. http://www.hriptc.org/metal_autism.html

Welshons, WV, KA Thayer, BM Judy, JA Taylor, EM Curran and FS vom Saal. 2003. Large effects from small exposures. I. Mechanisms for endocrine disrupting chemicals with estrogenic activity. Environmental Health Perspectives 111:994-1006.

“if the mechanistic information concerning hormone action that we review here had been considered, the currently accepted practice of only testing very high doses to predict effects of doses thousands or even millions of times lower would have been recognized to be inappropriate. The result would have been that doses of EDCs, such as methoxychlor and bisphenol A, far below those currently being described as “safe” would, in fact, have been predicted to produce biological responses, and much lower doses would have been tested.”

In a non-monotonic dose response curve (NMDRC) , the shape of the dose response curve reverses as the level of contamination goes up. Some NMDRC are shaped like U’s, with high responses at low and at high levels of contamination. Others are shaped like inverted U’s with the greatest response in intermediate ranges. The puzzling but observable fact is that low doses may actually cause greater impact than high doses for a specific response.

Welshons et al. interprete this in the following way: At high doses, the contaminant is overtly toxic, poisioning the system and hence (in the example below), causing shrinkage of the prostate. At an intermediate dose (but very low dose… in the example below 0.2 parts per billion), DES turns on genes that stimulate prostate growth.

Retrieved from: OurStolenFuture.org. Colborn, T. (1996) Our stolen future: Are we threatening our fertility, intelligence, and survival?: a scientific detective story. New York: Dutton.


Arehart-Treichel, J. Immune-System Gene Linked to Schizophrenia Development. Psychiatry News 2007 42: 33-49

Jyonouchi H, Sun S, Le H. Proinflammatory and regulatory cytokine production associated with innate and adaptive immune responses in children with autism spectrum disorders

and developmental regression. J Neuroimmun.2001;20(1-2):170-179

Kronfol Z, Remick DG. Cytokines and the Brain: Implications for Clinical Psychiatry. Am J Psychiatry. 2000 May 1;157(5):683-694. Growing evidence suggests that, in addition to providing communication between immune cells, specific cytokines play a role in signaling the brain to produce neurochemical, neuroendocrine, neuroimmune, and behavioral changes. This signaling may be part of a generalized, comprehensive mechanism to mobilize resources in the face of physical and/or psychological stress and to maintain homeostasis

McGeer Pl, McGeer EG. Local neuroinflammation and the progression of Alzheimer’s disease. J Neurovirology 2002;8;529-538.

Singh VK, Jensen RL. Elevated levels of measles antibodies in children with autism
Pediatric Neurology, Volume 28, Issue 4, Page 292 (2002)

The essence of my (Dr. Vijendra Singh) “Autoimmune Hypothesis” is that a virus-induced autoimmune response to developing brain myelin may impair anatomical development of neural pathways in autistic children. This line of thinking relies on the fact that the speed of nerve-impulse transmission depends essentially on structural properties of the insulating myelin sheath, connecting nerve fibers, and axon diameter. The anatomical changes could ultimately lead to life-long disturbances of higher mental functions such as learning, memory, communication, social interaction, etc.

Singh, V.K., Immunotherapy for brain diseases and mental illnesses. Progress in Drug Research 48: 129-146 (1997)

Singh VK, et al. Antibodies to myelin basic protein in children with autistic disorder. Brain Behavior and Immunity 7: 97-103 (1997).

Singh VK. Neuro-immunopathogenesis in autism. In: NeuroImmune Biology: New Foundation of Biology, Vol. 1: 443-454 (2001)

Singh V.K., Immune-activation model in Alzheimer’s disease. Molecular and Chemical Neuropathology 28 (1996) 105-111.

To conclude, since everything changes with time, I firmly believe that it is time to re-evaluate the safety of vaccines and the manner in which we practice immunizations. Vaccines are well known to cause numerous adverse reactions in humans and no matter how rare they might be it is time to pay a closer attention to them. I don’t think the epidemiological studies will suffice the purpose but the laboratory-based experimental research is urgently needed. We need new policies simply because the existing policies are not in line with our modern knowledge of human immunology, virology, and genomics. This is clearly exemplified by our experimental approach involving laboratory techniques that did not exist 30-40 years ago when the vaccines were originally developed. Indeed, there is persuasive evidence to suggest that the MMR vaccine could potentially cause autism or a regressive form thereof in a significant number of children. At this juncture, I would also like to recommend a new policy of “Testing immunity before vaccination or immunization” that should help identify immunocompromised children who otherwise might react adversely to vaccines. The cost should not deter us from implementing this policy especially when the lives of hundreds and thousands of children and their families are concerned.

Research Associate Professor of Neuroimmunology

Could we also be asking the question: Is it vaccines or has the deterioration of our environment and nutrition created a situation where these individuals no longer have the capability or resources to recover from the stress of vaccines? Or is it a combination of both? Is it that vaccines now cause too much of a “distraction” of resources from myelination and brain processing development and adequate neuro-functioning? (*note: thinking in terms of variability, cumulative, ecosystem impairment….vaccines might merely be the most effective way to cause impairment within particular systems already under heavy burdens and predisposed neurophysiology that would directly and indirectly lead to the manifestation of symptoms)

And is this analogous to idea of sun damage…did we become “allergic” to the sun is the source of life on earth? Or is our inability to repair from the sun’s natural ‘damage’. A result of our depleted resources, such as antioxidants and Omega-3 fats? Is this a combination of the ozone(additional stress) and our lack of proper nutrition to repair? Wouldn’t the solutions come full circle, back to addressing our environment and the nutritional quality of our food/resources?

Black HS, Rhodes LE. The potential of omega-3 fatty acids in the prevention of non-melanoma skin cancer. Cancer Detect Prev. 2006;30(3):224-32. Epub 2006 Jul 26

In toto, there is strong circumstantial evidence from both experimental and clinical studies to support a role for omega-3 FA in the prevention of non-melanoma skin cancer (NMSC). In experimental animal studies there is direct evidence that dietary omega-3 FA inhibits ultraviolet radiation (UVR) carcinogenic expression, with regard to both increased tumor latent period and reduced tumor multiplicity. Equivalent levels of omega-6 FA increase UVR carcinogenic expression. Dietary omega-3 FA dramatically reduces the plasma and cutaneous pro-inflammatory and immunosuppressive PGE(2) levels in mice. Dietary omega-6 FA increases prostaglandin E synthase type 2 (PGE(2)) level. Dietary omega-3 FA significantly reduces the inflammatory response and sustains, or enhances, the delayed type hypersensitivity immune response in mice when compared to an equivalent dietary level of omega-6 FA. Supplementary omega-3 FA significantly increases the UVR-mediated erythema threshold in humans. Supplementary omega-3 FA significantly reduces the level of pro-inflammatory and immunosuppressive PGE(2) levels in Ultraviolet B-irradiated human skin.

Otsuka H, Harada M, Mori K, Hisaoka S, Nishitani H. Brain metabolites in the hippocampus-amygdala region and cerebellum in autism: an 1H-MR spectroscopy study. Neuroradiol.1999;41:517-519

Rockefeller University (2008, May 20). First Evidence Of Native Dendritic Cells In Brain Surprises Scientists. ScienceDaily. Retrieved October 9, 2008, from http://www.sciencedaily.com /releases/2008/05/080519103818.htm

Warren RP, Singh VK, Averett RE, et al. Immunologenetic studies in autism and related disorders. Mol Chem Neuropath.1996;28:77-81

Weissman JR, Kelley RI, Bauman ML, Cohen BH, Murray KF, et al. 2008 Mitochondrial Disease in Autism Spectrum Disorder Patients: A Cohort Analysis. PLoS ONE 3(11): e3815 doi:10.1371/journal.pone.0003815

OBJECTIVE: This article reviews recent developments in cytokine biology that are relevant to clinical psychiatry. METHOD: The authors reviewed English-language literature of the last 15 years that pertains to the biology of cytokines with emphasis on central nervous system effects in general and psychiatric disorders in particular. RESULTS: Growing evidence suggests that, in addition to providing communication between immune cells, specific cytokines play a role in signaling the brain to produce neurochemical, neuroendocrine, neuroimmune, and behavioral changes. This signaling may be part of a generalized, comprehensive mechanism to mobilize resources in the face of physical and/or psychological stress and to maintain homeostasis. The clinical implications of these findings are far-reaching and include a possible role for cytokines in the pathophysiology of specific psychiatric disorders such as major depression, schizophrenia, and Alzheimer’s disease. The effects of cytokines in the central nervous system may provide a possible mechanism for the “sickness behavior” of patients with severe infection or cancer, as well as for the neuropsychiatric adverse effects of treatment with interferons and interleukins.CONCLUSIONS: A better understanding of the role of cytokines in various brain activities will enhance knowledge of specific psychobiological mechanisms in health and disease and provide opportunities for novel treatment interventions. Kronfol Z, Remick DG. Cytokines and the Brain: Implications for Clinical Psychiatry. Am J Psychiatry. 2000 May 1;157(5):683-694

Oxidative Stress

James, JS, Cutler, P, Melnyk, S. Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism. Am J Clin Nutr 2004 80: 1611-1617

Conclusions: An increased vulnerability to oxidative stress and a decreased capacity for methylation may contribute to the development and clinical manifestation of autism.

James SJ, Melnyk S, Jernigan S, Metabolic endophenotype and related genotypes are associated with oxidative stress in children with autism. Am J Med Genet B Neuropsychiatr Genet. 2006 Dec 5;141B(8):947-56

We propose that an increased vulnerability to oxidative stress (endogenous or environmental) may contribute to the development and clinical manifestations of autism.

James SJ, Rose S, Melnyk S, et al. Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism. FASEB J. 2009 Mar 23. These results suggest that the autism LCLs exhibit a reduced glutathione reserve capacity in both cytosol and mitochondria that may compromise antioxidant defense and detoxification capacity under prooxidant conditions.-James, S. J., Rose, S., Melnyk, S., Jernigan, S., Blossom, S., Pavliv, O., Gaylor, D.W. Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism.

Eigsti IM, Shapiro T. A systems neuroscience approach to autism: biological,cognitive, and clinical perspectives. Ment Retard Dev Disabil. Res Rev 2003;9:205–15.

Serra JA, Dominguez RO, de Lustig ES, et al. Parkinson’s disease is associated with oxidative stress: comparison of peripheral antioxidant profiles in living Parkinson’s, Alzheimer’s and vascular dementia patients. J Neural Transm 2001;108:1135– 48.

Schulz JB, Lindenau J, Seyfried J, Dichgans J. Glutathione, oxidative stress and neurodegeneration. Eur J Biochem 2000;267:4904 –11.

In the past, Ohio State University (osu.edu 2009) researchers have discovered that:

  • Chronic stress can weaken the immune status of caregivers to the extent that they are more susceptible to the onset of some diseases;

  • High levels of psychological stress can slow the process of wound healing to such an extent as to increase the risks of recovery in procedures ranging from minor dental procedures to major surgery;

  • Vaccines given to protect against both bacterial and viral diseases may be impaired if the inoculations are given when a person is highly stressed;

  • Even in people who are normally considered to be “happy”, the effects of minor psychological stress can have health impacts.

Stanford University Medical Center (2009, February 16). New Test For Mysterious Metabolic Diseases. ScienceDaily. Retrieved March 1, 2009, from http://www.sciencedaily.com /releases/2009/02/090211094040.htm

Even when these patients are coming into the clinic looking pretty healthy, they have evidence of extra metabolic stress,” Enns said, noting the findings were surprising because none of the patients were in the midst of a health crisis such as organ failure when blood samples were taken. It is the first time such signs have been uniformly shown in the blood of patients across a wide range of mitochondrial disorders, he added.

The team saw that levels of glutathione, the body’s primary antioxidant, were significantly reduced in white blood cells from the 20 mitochondrial disease patients in the study. The observation means patients’ antioxidant defenses were indeed depleted.

Importance of Acceptance

Emotional Pain and Physical pain run on the same neural pathways.

Eisenberger NI and Lieberman MD. Why rejection hurts: A common neural alarm system for physical and social pain. Trends in Cognitive Sciences, 8, 294-300, 2004. Mounting evidence from the animal lesion and human neuroimaging literatures suggests that physical and social pain overlap in their underlying neural circuitry and computational processes. We review evidence suggesting that the anterior cingulate cortex plays a key role in the physical-social pain overlap. We also suggest that the physical-social pain circuitry might share components of a broader neural alarm system.

Eisenberger NI, Lieberman MD, and Satpute AB. Personality from a controlled processing perspective: An fMRI study of neuroticism, extraversion, and self-consciousness. Cognitive, Affective, and Behavioral Neuroscience, 5, 169-181, 2005. In response to an oddball task, neuroticism was associated with increased dorsal anterior cingulate cortex (dACC) reactivity, typically associated with discrepancy detection, whereas extraversion and self-consciousness were associated with lateral and medial frontoparietal networks, respectively, typically associated with task-focused (lateral) or self-focused (medial) controlled processes

Goldstein M, Brendel G, Tuescher O, et al. Neural substrates of the interaction of emotional stimulus processing and motor inhibitory control: an emotional linguistic go/no-go fMRI study. Neuroimage 2007; 36:1026–1040

Kronfol Z, Remick DG. Cytokines and the Brain: Implications for Clinical Psychiatry. Am J Psychiatry. 2000 May 1;157(5):683-694

Growing evidence suggests that, in addition to providing communication between immune cells, specific cytokines play a role in signaling the brain to produce neurochemical, neuroendocrine, neuroimmune, and behavioral changes. This signaling may be part of a generalized, comprehensive mechanism to mobilize resources in the face of physical and/or psychological stress and to maintain homeostasis. The clinical implications of these findings are far-reaching and include a possible role for cytokines in the pathophysiology of specific psychiatric disorders such as major depression, schizophrenia, and Alzheimer’s disease. The effects of cytokines in the central nervous system may provide a possible mechanism for the “sickness behavior” of patients with severe infection or cancer, as well as for the neuropsychiatric adverse effects of treatment with interferons and interleukins

Singh, V.K., Cytokine Regulation in autism. In: Cytokines and Mental Health (edited by Ziad Kronfol (2003), pp. 369-383, Kluwer Academic Publishers, Boston, MA, USA

University of Chicago (2007, February 20). Highly Accomplished People More Prone To Failure Than Others When Under Stress. ScienceDaily. Retrieved October 28, 2008, from http://www.sciencedaily.com /releases/2007/02/070218130822.htm. “These findings suggest that performance pressure harms higher working memory individuals by consuming the cognitive resources that they rely on for their superior performance — and as a result, higher working memory individuals respond by switching to the less accurate problem solving strategies normally used by lower working memory students,” Beilock said.

The Role of Emotion
I think we too often dismiss emotions as irrelevant, inconvenient “noise”, or even just a character flaw, when these emotions serve a purpose; as protection, guidance, and inspiration.

Take a look at dendrites, the computer programming of the brain. Dependent upon energy (ATP), neurochemicals, and electricity to create this wondrous and beautiful network of connecting branches. Every time we start a memory, learn a skill, build a neural pathway, this is what our brain kicks into gear. It builds a neuronet for every occasion, every moment…all day, every day. And it tries to finish and connect each and every one (remaining consistent and complete). This is how, as infants, we learn coordination, learn our environment, what to do, what not to do, it’s how we get “programmed”. We get constant feedback and each neuronet builds upon the previous forest built by our experience. (could be an indication for an increased susceptibility to PTSD?)

Seeing the mind as energy expenditure, information management and resource depletion.

Filtering: Emotion and Memory

Davidson RJ, Jackson DC, Kalin NH. Emotion, plasticity, context and regulation: perspectives from affective neuroscience. Psychological Bulletin, 2000; 126(6): 873-89.

Vodanovich, S. J. (2003). On the potential benefits of boredom: A neglected area in personality research. Psychology and Education, 40, 28-33.

Fisher HE, Aron A, Mashek D, Li H, Brown LL. Defining the brain systems of lust, romantic attraction, and attachment. Arch Sex Behav. 2002 Oct;31(5):413-9. Mammals and birds have evolved three primary, discrete, interrelated emotion-motivation systems in the brain for mating, reproduction, and parenting: lust, attraction, and male-female attachment. Each emotion-motivation system is associated with a specific constellation of neural correlates and a distinct behavioral repertoire. Lust evolved to initiate the mating process with any appropriate partner; attraction evolved to enable individuals to choose among and prefer specific mating partners, thereby conserving their mating time and energy; male-female attachment evolved to enable individuals to cooperate with a reproductive mate until species-specific parental duties have been completed.

Stanford University Medical Center (2005, November 9). Children Of Bipolar Parents Score Higher On Creativity Test, Stanford Study Finds. ScienceDaily. Retrieved October 28, 2008, from http://www.sciencedaily.com/releases/2005/11/051109092005.htm. Terence Ketter, MD, professor of psychiatry and behavioral sciences and a study co-author, said he became interested in the link between mental illness and creativity after noticing that patients who came through the bipolar clinic, despite having problems, were extraordinarily bright, motivated people who “tended to lead interesting lives.” He began a scholarly pursuit of this link and in 2002 published a study that showed healthy artists were more similar in personality to individuals with bipolar disorder (the majority of whom were on medication) than to healthy people in the general population. Some researchers believe that bipolar disorder or mania, a defining symptom of the disease, causes creative activity. Ketter said he believes that bipolar patients’ creativity stems from their mobilizing energy that result from negative emotion to initiate some sort of solution to their problems. “In this case, discontent is the mother of invention,” he said.

University of Arizona (2007, November 16). ‘Speed Of Thought’ Guides Brain’s Memory Consolidation. ScienceDaily. Retrieved October 28, 2008, from http://www.sciencedaily.com/releases/2007/11/071115164450.htm

Weissman, D. H., Roberts, K. C., Visscher, K. M. & Woldorff, M. G. (2006). The neural bases of momentary lapses in attention. Nature Neuroscience, 9, 971-978. Momentary lapses in attention frequently impair goal-directed behavior, sometimes with serious consequences. Nevertheless, we lack an integrated view of the brain mechanisms underlying such lapses. By investigating trial-by-trial relationships between brain activity and response time in humans, we determined that attentional lapses begin with reduced prestimulus activity in anterior cingulate and right prefrontal regions involved in controlling attention. Less efficient stimulus processing during attentional lapses was also characterized by less deactivation of a ‘default-mode’ network, reduced stimulus-evoked sensory activity, and increased activity in widespread regions of frontal and parietal cortex. Finally, consistent with a mechanism for recovering from attentional lapses, increased stimulus-evoked activity in the right inferior frontal gyrus and the right temporal-parietal junction predicted better performance on the next trial. Our findings provide a new, system-wide understanding of the patterns of brain activity that are associated with brief attentional lapses, which informs both theoretical and clinical models of goal-directed behavior.

Emotions Make the Memory Last: More Detail, Easier Recollection With Emotional Memories. Dolcos, F. Proceedings of the National Academy of Sciences. Feb. 4, 2005. News release, Proceedings of the National Academy of Sciences.http://www.webmd.com/balance/news/20050131/emotions-make-memory-last

Holzapfel W. Historical summary of Emotions and Memory Intertwined.. ISSN 0211-0040, Vol. 22, Nº 3-4, 2001, pages 383-388 http://dialnet.unirioja.es/servlet/articulo?codigo=208691

Amygdala (Wikipedia 2009)

Rhythms & Restoration Cycles

Marshall L, Born J (2007) The contribution to sleep to hippocampus-dependent memory consolidation. Trends Cogn Sci. 11:442-450.

Study confirms sleep essential for creativity. CNN (2004) Wagner U, Gais S, Haider H, Verleger R & Born J (2004) Sleep inspires insight. Nature. 427(6972):352-355. http://www.cnn.com/2004/HEALTH/01/21/sleep.creativity.ap/index.html

University of Wisconsin-Madison (2009, April 11). Sleep: Spring Cleaning For The Brain?. ScienceDaily. Retrieved April 15, 2009, from http://www.sciencedaily.com /releases/2009/04/090402143455.htm …more evidence for their theory of “synaptic homeostasis.” This is the idea that synapses grow stronger when we’re awake as we learn and adapt to an ever-changing the environment, that sleep refreshes the brain by bringing synapses back to a lower level of strength. This is important because larger synapses consume a lot of energy, occupy more space and require more supplies, including the proteins examined in this study. Sleep — by allowing synaptic downscaling — saves energy, space and material, and clears away unnecessary “noise” from the previous day, the researchers believe. The fresh brain is then ready to learn again in the morning.

Rossi, E (1982). Hypnosis and Ultradian Cycles: A New State(s) Theory of Hypnosis? The American Journal of Clinical Hypnosis, 25, 21-32.

Ernest Rossi with his ground-breaking work with what he calls Ultradian Rhythms.

His research in these rhythms discusses how the brain depletes essential neurochemicals and needs “restoration breaks” on particular rhythms during the course of the day. This gives us the understanding that these resources can be depleted and need constant attention to function at an optimal rate as to not engage “stress modes” of the mind and body.

Systems/Chaos Thinking

Western medical scientists are world class experts, exceedingly precise and astonishingly accurate with their work and knowledge. To borrow a phrase, Not Even Wrong, because they are not wrong. In fact, in their unrelenting adherence to the principals of those methods (of Classical Physics and modern medicine) that we can say and believe with utmost certainty that Autism and related disorders have nothing inherently wrong (or single cause). Which is why there are still experts who will contend, that within their scientific framework, Autism, Fibromyalgia, Personality disorders, etc. “don’t really exist”(as diseases) because existing in that scientific model means “a single organic cause” or something wrong to begin with (genetic disease). The acceptance that these disorders exist at all, is because we cannot deny the presence of such profound symptoms and sometimes, sometimes only because individuals and parents have not and would not allow them to be ignored.

Sterman JD. (2002) All models are wrong: reflections on becoming a systems scientist. System Dynamics Review. Volume 18, Issue 4, Pages 501 – 531.

“Thoughtful leaders increasingly recognize that we are not only failing to solve the persistent problems we face, but are in fact causing them. System dynamics is designed to help avoid such policy resistance and identify high-leverage policies for sustained improvement. What does it take to be an effective systems thinker, and to teach system dynamics fruitfully? Understanding complex systems requires mastery of concepts such as feedback, stocks and flows, time delays, and nonlinearity. Research shows that these concepts are highly counterintuitive and poorly understood. It also shows how they can be taught and learned. Doing so requires the use of formal models and simulations to test our mental models and develop our intuition about complex systems. Yet, though essential, these concepts and tools are not sufficient. Becoming an effective systems thinker also requires the rigorous and disciplined use of scientific inquiry skills so that we can uncover our hidden assumptions and biases. It requires respect and empathy for others and other viewpoints. Most important, and most difficult to learn, systems thinking requires understanding that all models are wrong and humility about the limitations of our knowledge. Such humility is essential in creating an environment in which we can learn about the complex systems in which we are embedded and work effectively to create the world we truly desire.”

Taken from “On becoming a Systems Scientist” (2002) by John D. Sterman: Jay W. Forrester Professor of Management at the MIT Sloan School of Management and Director of MIT’s System Dynamics Group.

Gleik, James. (2008) CHAOS: The making of a new science. Penguin.

Capra, Fritjof. (1984) The Turning Point: Science, Society and the Rising Culture. Bantam.

Greene, Brian. (2003). The Elegant Universe: Superstrings, Hidden Dimensions and the Quest for the Ultimate Theory. W.W. Norton & Company

Boccaletti S, Latora V, Moreno Y. Complex networks : Structure and dynamics. Physics reports. 2006, vol. 424, no4-5, pp. 175-308. Coupled biological and chemical systems, neural networks, social interacting species, the Internet and the World Wide Web, are only a few examples of systems composed by a large number of highly interconnected dynamical units.

Meadows, Donella H. (2008) Thinking in Systems: A Primer. Ed Diana Wright Sustainability Institute. Chelsea Green Publishing. (from p.2)

So, what is a system? A system is a set of things—people, cells, molecules, or whatever—interconnected in such a sway that they produce their own pattern of behavior over time. The system maybe buffeted, constricted, triggered, or driven by outside forces. But the system’s response to these forces is characteristic of itself, and that response is seldom simple in the real world….The system, to a large extent, causes its own behavior! An outside event may unleash that behavior, but the same outside event applied to a different system is likely to produce a different result. (p.34)…You’ll be thinking not in terms of a static world, but a dynamic one. You’ll stop looking for who’s to blame; instead you’ll start asking “What’s the system?”


It is the conclusion of this theory that our science, our environment, our mistaken interpretations, and our well intentioned but misguidance of nutrition information, environmental influences (chemicals), our educational standardization (assumptions of normal) and our communities (competiveness and comparisons) have created these unbalanced and unhealthy outcomes. Changing our understanding of the human body to an ecosystem scientific framework that interacts, is challenged and intimately influenced by our environment, nutrition, attitudes, economic motivations, community, and educational expectations will guide our future endeavors and begin to correct our mistakes of the past.

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