On This Day … 06 June [2022]

People (Births)

  • 1900 – Manfred Sakel, Ukrainian-American psychiatrist and physician (d. 1957).

People (Deaths)

  • 1961 – Carl Gustav Jung, Swiss psychiatrist and psychotherapist (b. 1875).
  • 2014 – Lorna Wing, English psychiatrist and physician; pioneered studies of autism (b. 1928).

Manfred Sakel

Manfred Joshua Sakel (06 June 1900 to 02 December 1957) was an Austrian-Jewish (later Austrian-American) neurophysiologist and psychiatrist, credited with developing insulin shock therapy in 1927.

Sakel was born on 06 June 1900, in Nadvirna (Nadwórna), in the former Austria-Hungary Empire (now Ukraine), which was part of Poland between the world wars. Sakel studied Medicine at the University of Vienna from 1919 to 1925, specialising in neurology and neuropsychiatry. From 1927 until 1933 Sakel worked in hospitals in Berlin. In 1933 he became a researcher at the University of Vienna’s Neuropsychiatric Clinic. In 1936, after receiving an invitation from Frederick Parsons, the state commissioner of mental hygiene, he chose to emigrate from Austria to the United States of America. In the US, he became an attending physician and researcher at the Harlem Valley State Hospital.

Dr. Sakel was the developer of insulin shock therapy from 1927 while a young doctor in Vienna, starting to practice it in 1933. It would become widely used on individuals with schizophrenia and other mental patients. He noted that insulin-induced coma and convulsions, due to the low level of glucose attained in the blood (hypoglycaemic crisis), had a short-term appearance of changing the mental state of drug addicts and psychotics, sometimes dramatically so. He reported that up to 88% of his patients improved with insulin shock therapy, but most other people reported more mixed results and it was eventually shown that patient selection had been biased and that it didn’t really have any specific benefits and had many risks, adverse effects and fatalities. However, his method became widely applied for many years in mental institutions worldwide. In the US and other countries it was gradually dropped after the introduction of the electroconvulsive therapy in the 1940s and the first neuroleptics in the 1950s.

Dr. Sakel died from a heart attack on 02 December 1957, in New York City, NY, US.

Carl Jung

Carl Gustav Jung (26 July 1875 to 06 June 1961) was a Swiss psychiatrist and psychoanalyst who founded analytical psychology. Jung’s work has been influential in the fields of psychiatry, anthropology, archaeology, literature, philosophy, psychology, and religious studies. Jung worked as a research scientist at the famous Burghölzli hospital, under Eugen Bleuler. During this time, he came to the attention of Sigmund Freud, the founder of psychoanalysis. The two men conducted a lengthy correspondence and collaborated, for a while, on a joint vision of human psychology.

Freud saw the younger Jung as the heir he had been seeking to take forward his “new science” of psychoanalysis and to this end secured his appointment as president of his newly founded International Psychoanalytical Association. Jung’s research and personal vision, however, made it impossible for him to follow his older colleague’s doctrine and a schism became inevitable. This division was personally painful for Jung and resulted in the establishment of Jung’s analytical psychology as a comprehensive system separate from psychoanalysis.

Among the central concepts of analytical psychology is individuation – the lifelong psychological process of differentiation of the self out of each individual’s conscious and unconscious elements. Jung considered it to be the main task of human development. He created some of the best known psychological concepts, including synchronicity, archetypal phenomena, the collective unconscious, the psychological complex and extraversion and introversion.

Jung was also an artist, craftsman, builder and a prolific writer. Many of his works were not published until after his death and some are still awaiting publication.

Lorna Wing

Lorna Gladys Wing OBE FRCPsych (07 October 1928 to 06 June 2014) was an English psychiatrist. She was a pioneer in the field of childhood developmental disorders, who advanced understanding of autism worldwide, introduced the term Asperger syndrome in 1976 and was involved in founding the National Autistic Society (NAS) in the UK.

Although Wing trained as a medical doctor, specialising in psychiatry, her focus narrowed to childhood developmental disorders in 1959. At that time autism was thought to affect around 5 in 10,000 children, but its prevalence in the 2010s was considered to be around 1 in 100 following the awareness raised by Wing and her followers. Her research, particularly with her collaborator Judith Gould, now underpins thinking in the field of autism. They initiated the Camberwell Case Register to record all patients using psychiatric services in this area of London. The data accumulated by this innovative approach gave Wing the basis for her influential insight that autism formed a spectrum, rather than clearly differentiated disorders. They also set up the Centre for Social and Communication Disorders, the first integrated diagnostic and advice service for these conditions in the UK.

Wing was the author of many books and academic papers, including Asperger Syndrome: a Clinical Account, a February 1981 academic paper that popularised the research of Hans Asperger. Although ground-breaking and influential, Wing herself cautioned in her 1981 paper that “It must be pointed out that the people described by the present author all had problems of adjustment or superimposed psychiatric illnesses severe enough to necessitate referral to a psychiatric clinic … (and) the series described here is probably biased towards those with more severe handicaps.”

Along with some parents of autistic children, she founded the organisation now known as the National Autistic Society in the UK in 1962. She was a consultant to NAS Lorna Wing Centre for Autism until she died. She was also President of Autism Sussex.

In the 1995 New Year Honours list Wing was appointed Officer of the Order of the British Empire for ‘services to the National Autistic Society’.

What is Alogia?

Introduction

In psychology, alogia (from Greek ἀ-, “without”, and λόγος, “speech” + New Latin -ia) is poor thinking inferred from speech and language usage.

There may be a general lack of additional, unprompted content seen in normal speech, so replies to questions may be brief and concrete, with less spontaneous speech. This is termed poverty of speech or laconic speech. The amount of speech may be normal but conveys little information because it is vague, empty, stereotyped, overconcrete, overabstract, or repetitive. This is termed poverty of content or poverty of content of speech. Under Scale for the Assessment of Negative Symptoms (SANS) used in clinical research, thought blocking is considered a part of alogia, and so is increased latency in response.

This condition is associated with schizophrenia, dementia, severe depression, and autism. As a symptom, it is commonly seen in patients suffering from schizophrenia and schizotypal personality disorder, and is traditionally considered a negative symptom. It can complicate psychotherapy severely because of the considerable difficulty in holding a fluent conversation.

The alternative meaning of alogia is inability to speak because of dysfunction in the central nervous system, found in mental deficiency and dementia. In this sense, the word is synonymous with aphasia, and in less severe form, it is sometimes called dyslogia.

Characteristics

Alogia may be on a continuum with normal behaviours. People without mental illness may have it occasionally including when fatigued or disinhibited, when writers use language creatively, when people in certain disciplines – such as politicians, administrators, philosophers, ministers, and scientists – use language pedantically, or in people with intelligence or little education. Hence, deciding if an individual has alogia depends on contextual clues. Is the person in control? Can the person moderate the effect if asked to be specific or concise? Is it better with another topic? Are there other significant symptoms?

Alogia is characterised by a lack of speech, often caused by a disruption in the thought process. Usually, an injury to the left side of the brain may cause alogia to appear in an individual. While in conversation, alogic patients will reply very sparsely and their answers to questions will lack spontaneous content; sometimes, they will even fail to answer at all. Their responses will be brief, generally only appearing as a response to a question or prompt.

Apart from the lack of content in a reply, the manner in which the person delivers the reply is affected as well. Patients affected by alogia will often slur their responses, and not pronounce the consonants as clearly as usual. The few words spoken usually trail off into a whisper, or are just ended by the second syllable. Studies have shown a correlation between alogic ratings in individuals and the amount and duration of pauses in their speech when responding to a series of questions posed by the researcher. The inability to speak stems from a deeper mental inability that causes alogic patients to have difficulty grasping the right words mentally, as well as formulating their thoughts. A study investigating alogiacs and their results on the category fluency task showed that people with schizophrenia who exhibit alogia display a more disorganised semantic memory than controls. While both groups produced the same number of words, the words produced by people with schizophrenia were much more disorderly and the results of cluster analysis revealed bizarre coherence in the alogiac group.

If the condition is assessed using a language other than the individual’s primary language, the medical professional needs to make sure that the problem is not from language barriers.

This condition is associated with schizophrenia, dementia, and severe depression.

Example

The following table shows an example of “poverty of speech” which shows replies to questions that are brief and concrete, with a reduction in spontaneous speech:

Poverty of SpeechNormal Speech
Q: Do you have any children?
A: Yes.
Q: Do you have any children?
A: Yes, a boy and a girl.
Q: How many?
A: Two.
Q: How old are they?
A: Edmond is sixteen and Alice is six.
Q: How old are they?
A: Six and sixteen.
Q: Are they boys or girls?
A: One of each.
Q: Who is the sixteen-year-old?
A: The boy.
Q: What is his name?
A: Edmond.
Q: And the girl’s?
A: Alice.

The following example of “poverty of content of speech” is a response from a patient when asked why he was in a hospital. Speech is vague, conveys little information, but is not grossly incoherent and the amount of speech is not reduced. “I often contemplate—it is a general stance of the world—it is a tendency which varies from time to time—it defines things more than others—it is in the nature of habit—this is what I would like to say to explain everything.”

Causes

Alogia can be brought on by frontostriatal dysfunction which causes degradation of the semantic store, the centre located in the temporal lobe that processes meaning in language. A subgroup of chronic schizophrenia patients in a word generation experiment generated fewer words than the unaffected subjects and had limited lexicons, evidence of the weakening of the semantic store. Another study found that when given the task of naming items in a category, schizophrenia patients displayed a great struggle but improved significantly when experimenters employed a second stimulus to guide behaviour unconsciously. This conclusion was similar to results produced from patients with Huntington’s and Parkinson’s disease, ailments which also involve frontostriatal dysfunction.

Treatment

Medical studies conclude that certain adjunctive drugs effectively palliate the negative symptoms of schizophrenia, mainly alogia. In one study, Maprotiline produced the greatest reduction in alogia symptoms with severity reduction in 50% of patients (out of 10). Of the negative symptoms of schizophrenia, alogia had the second best responsiveness to the drugs, surpassed only by attention deficiency. D-amphetamine is another drug that has been tested on people with schizophrenia and found success in alleviating negative symptoms. This treatment, however, has not been developed greatly as it seems to have adverse effects on other aspects of schizophrenia such as increasing the severity of positive symptoms.

Relation to Schizophrenia

Although alogia is found as a symptom in a variety of health disorders, it is most commonly found as a negative symptom of schizophrenia.

Previous studies and analyses conclude that at least three factors are needed to cover both the positive and negative symptoms of schizophrenia; the three are: psychotic, disorganization, and negative symptom factors. Studies suggest that an inappropriate affect is strongly associated with bizarre behaviour and positive formal thought disorder on a disorganisation factor; attention impairment correlates significantly with psychotic, disorganization, and negative symptom factors. Alogia contains both positive and negative symptoms, with the poverty of content of speech as the disorganization factor, and poverty of speech, response latency, and thought blocking as the negative symptom factors.

Alogia is a major diagnostic sign of schizophrenia, when organic mental disorders have been excluded.

In schizophrenia, negative symptoms including flattening of affect, avolition, and alogia are responsible for the considerable morbidity of the disease compared with other psychotic disorders. Negative symptoms are common in the prodromal and residual phases of the disease and can be severe. During the first year, negative symptoms can progress, especially alogia, which may start off from a relatively low rate. Within 2 years, up to 25% of patients will have significant negative symptoms. Psychotic symptoms tend to diminish as the individuals age, but negative symptoms tend to persist. Prominent negative symptoms at disease onset, including alogia, are good predictors of worse outcomes.

Negative symptoms can arise in the presence of other psychiatric symptoms. Positive symptoms are a common cause of apathy, social withdrawal, and alogia. Secondary causes of negative symptoms, such as depression and demoralisation, often remit within a year, which helps distinguishing them from primary negative symptoms. Symptoms that don’t diminish over a year with medications should be reconsidered as possible primary negative symptoms.

P.O.V. Neurotypical (2013)

Introduction

P.O.V. Neurotypical is a 2013 documentary film directed by Adam Larsen.

The film shows perspectives on life from the viewpoint of individuals on the autism spectrum. Neurotypical was shot mostly in North Carolina and Virginia.

Edited from Neurotypical in 2011.

Outline

Neurotypical is an unprecedented exploration of autism from the point of view of autistic people themselves. Four-year-old Violet, teenaged Nicholas and adult Paula occupy different positions on the autism spectrum, but they are all at pivotal moments in their lives. How they and the people around them work out their perceptual and behavioural differences becomes a remarkable reflection of the “neurotypical” world – the world of the non-autistic – revealing inventive adaptations on each side and an emerging critique of both what it means to be normal and what it means to be human.

Cast

  • Wolf Dunaway as himself.
  • Violet as herself.
  • Nicholas as himself.
  • Paula as herself.
  • Maddi as herself.
  • John as himself.

Production & Filming Details

  • Director(s):
    • Adam Larsen.
  • Producer(s):
  • Writer(s):
  • Music:
    • Darren Morze.
    • Michael Wall.
  • Cinematography:
    • Adam Larsen.
  • Editor(s):
    • Adam Larsen.
  • Production:
  • Distributor(s):
    • Janson Media (2013) (USA) (video).
    • Janson Media (2015) (USA) (video).
  • Release Date: 29 July 2013.
  • Running Time: 52 or 57 minutes.
  • Rating: Unknown.
  • Country: US.
  • Language: English.

Neurotypical (2011)

Introduction

Neurotypical is a 2011 documentary film directed by Adam Larsen.

The film shows perspectives on life from the viewpoint of individuals on the autism spectrum. Neurotypical was shot mostly in North Carolina and Virginia.

Edited into P.O.V. Neurotypical in 2013.

Outline

Neurotypical is an unprecedented exploration of autism from the point of view of autistic people themselves. Four-year-old Violet, teenaged Nicholas and adult Paula occupy different positions on the autism spectrum, but they are all at pivotal moments in their lives. How they and the people around them work out their perceptual and behavioural differences becomes a remarkable reflection of the “neurotypical” world – the world of the non-autistic – revealing inventive adaptations on each side and an emerging critique of both what it means to be normal and what it means to be human.

Cast

  • Wolf Dunaway as himself.
  • Violet as herself.
  • Nicholas as himself.
  • Paula as herself.
  • Maddi as herself.
  • John as himself.

Production & Filming Details

  • Director(s):
    • Adam Larsen.
  • Producer(s):
  • Writer(s):
  • Music:
    • Darren Morze.
    • Michael Wall.
  • Cinematography:
    • Adam Larsen.
  • Editor(s):
    • Adam Larsen.
  • Production:
  • Distributor(s):
    • Janson Media (2013) (USA) (video).
    • Janson Media (2015) (USA) (video).
  • Release Date: March 2011 (Thessaloniki Documentary Festival).
  • Running Time: 52 minutes.
  • Rating: Unknown.
  • Country: US.
  • Language: English.

Book: CBT Toolbox for Children and Adolescents

Book Title:

CBT Toolbox for Children and Adolescents: Over 220 Worksheets & Exercises for Trauma, ADHD, Autism, Anxiety, Depression & Conduct Disorders.

Author(s): Lisa Phifer.

Year: 2017.

Edition: First (1st).

Publisher: PESI Publishing & Media.

Type(s): Spiral-bound, Paperback and Kindle.

Synopsis:

The CBT Toolbox for Children and Adolescents gives you the resources to help the children in your life handle their daily obstacles with ease. Inside this workbook you’ll find hundreds of worksheets, exercises, and activities to help treat:

  • Trauma.
  • ADHD.
  • Autism.
  • Anxiety.
  • Depression.
  • Conduct Disorders.

Written by clinicians and teachers with decades of experience working with kids, these practical and easy-to-use therapy tools are vital to teaching children how to cope with and overcome their deepest struggles. Step-by-step, you’ll see how the best strategies from cognitive behavioural therapy are adapted for children.

Book: Camouflage: The Hidden Lives of Autistic Women

Book Title:

Camouflage: The Hidden Lives of Autistic Women.

Author(s): Dr Sarah Bargiela.

Year: 2019.

Edition: First (1st), Illustrated Edition.

Publisher: Jessica Kingsley Publishers.

Type(s): Hardcover and Kindle.

Synopsis:

Autism in women and girls is still not widely understood, and is often misrepresented or even overlooked. This graphic novel offers an engaging and accessible insight into the lives and minds of autistic women, using real-life case studies.

The charming illustrations lead readers on a visual journey of how women on the spectrum experience everyday life, from metaphors and masking in social situations, to friendships and relationships and the role of special interests.

Fun, sensitive and informative, this is a fantastic resource for anyone who wishes to understand how gender affects autism, and how to create safer supportive and more accessible environments for women on the spectrum.

What is the Gut-Brain Axis?

Introduction

The gut-brain axis is the biochemical signalling that takes place between the gastrointestinal tract (GI tract) and the central nervous system (CNS).

The term “gut-brain axis” is occasionally used to refer to the role of the gut flora in the interplay as well, whereas the term “microbiota–gut–brain (MGB or BGM) axis” explicitly includes the role of gut flora in the biochemical signalling events that take place between the GI tract and CNS.

Broadly defined, the gut-brain axis includes the central nervous system, neuroendocrine and neuroimmune systems, including the hypothalamic-pituitary-adrenal axis (HPA axis), sympathetic and parasympathetic arms of the autonomic nervous system, including the enteric nervous system and the vagus nerve, and the gut microbiota. The first of the brain-gut interactions shown, was the cephalic phase of digestion, in the release of gastric and pancreatic secretions in response to sensory signals, such as the smell and sight of food. This was first demonstrated by Pavlov.

Interest in the field was sparked by a 2004 study showing that germ-free (GF) mice showed an exaggerated HPA axis response to stress compared to non-GF laboratory mice.

As of October 2016, most of the work done on the role of gut flora in the gut-brain axis had been conducted in animals, or on characterising the various neuroactive compounds that gut flora can produce. Studies with humans – measuring variations in gut flora between people with various psychiatric and neurological conditions or when stressed, or measuring effects of various probiotics (dubbed “psychobiotics” in this context) – had generally been small and were just beginning to be generalised. Whether changes to gut flora are a result of disease, a cause of disease, or both in any number of possible feedback loops in the gut–brain axis, remained unclear.

Gut Flora

The gut flora is the complex community of microorganisms that live in the digestive tracts of humans and other animals. The gut metagenome is the aggregate of all the genomes of gut microbiota. The gut is one niche that human microbiota inhabit.

In humans, the gut microbiota has the largest quantity of bacteria and the greatest number of species, compared to other areas of the body. In humans, the gut flora is established at one to two years after birth; by that time, the intestinal epithelium and the intestinal mucosal barrier that it secretes have co-developed in a way that is tolerant to, and even supportive of, the gut flora and that also provides a barrier to pathogenic organisms.

The relationship between gut flora and humans is not merely commensal (a non-harmful coexistence), but rather a mutualistic relationship. Human gut microorganisms benefit the host by collecting the energy from the fermentation of undigested carbohydrates and the subsequent absorption of short-chain fatty acids (SCFAs), acetate, butyrate, and propionate. Intestinal bacteria also play a role in synthesizing vitamin B and vitamin K as well as metabolising bile acids, sterols, and xenobiotics. The systemic importance of the SCFAs and other compounds they produce are like hormones and the gut flora itself appears to function like an endocrine organ; dysregulation of the gut flora has been correlated with a host of inflammatory and autoimmune conditions.

The composition of human gut flora changes over time, when the diet changes, and as overall health changes.

Enteric Nervous System

The enteric nervous system is one of the main divisions of the nervous system and consists of a mesh-like system of neurons that governs the function of the gastrointestinal system; it has been described as a “second brain” for several reasons. The enteric nervous system can operate autonomously. It normally communicates with the central nervous system (CNS) through the parasympathetic (e.g. via the vagus nerve) and sympathetic (e.g. via the prevertebral ganglia) nervous systems. However, vertebrate studies show that when the vagus nerve is severed, the enteric nervous system continues to function.

In vertebrates, the enteric nervous system includes efferent neurons, afferent neurons, and interneurons, all of which make the enteric nervous system capable of carrying reflexes in the absence of CNS input. The sensory neurons report on mechanical and chemical conditions. Through intestinal muscles, the motor neurons control peristalsis and churning of intestinal contents. Other neurons control the secretion of enzymes. 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. More than 90% of the body’s serotonin lies in the gut, as well as about 50% of the body’s dopamine; the dual function of these neurotransmitters is an active part of gut-brain research.

The first of the gut-brain interactions was shown to be between the sight and smell of food and the release of gastric secretions, known as the cephalic phase, or cephalic response of digestion.

Gut-Brain Integration

The gut-brain axis, a bidirectional neurohumoral communication system, is important for maintaining homeostasis and is regulated through the central and enteric nervous systems and the neural, endocrine, immune, and metabolic pathways, and especially including the hypothalamic-pituitary-adrenal axis (HPA axis). That term has been expanded to include the role of the gut flora as part of the “microbiome-gut-brain axis”, a linkage of functions including the gut flora.

Interest in the field was sparked by a 2004 study (Nobuyuki Sudo and Yoichi Chida) showing that germ-free mice (genetically homogeneous laboratory mice, birthed and raised in an antiseptic environment) showed an exaggerated HPA axis response to stress, compared to non-GF laboratory mice.

The gut flora can produce a range of neuroactive molecules, such as acetylcholine, catecholamines, γ-aminobutyric acid, histamine, melatonin, and serotonin, which are essential for regulating peristalsis and sensation in the gut. Changes in the composition of the gut flora due to diet, drugs, or disease correlate with changes in levels of circulating cytokines, some of which can affect brain function. The gut flora also release molecules that can directly activate the vagus nerve, which transmits information about the state of the intestines to the brain.

Likewise, chronic or acutely stressful situations activate the hypothalamic-pituitary-adrenal axis, causing changes in the gut flora and intestinal epithelium, and possibly having systemic effects. Additionally, the cholinergic anti-inflammatory pathway, signalling through the vagus nerve, affects the gut epithelium and flora. Hunger and satiety are integrated in the brain, and the presence or absence of food in the gut and types of food present also affect the composition and activity of gut flora.

That said, most of the work that has been done on the role of gut flora in the gut-brain axis has been conducted in animals, including the highly artificial germ-free mice. As of 2016, studies with humans measuring changes to gut flora in response to stress, or measuring effects of various probiotics, have generally been small and cannot be generalised; whether changes to gut flora are a result of disease, a cause of disease, or both in any number of possible feedback loops in the gut-brain axis, remains unclear.

The history of ideas about a relationship between the gut and the mind dates from the nineteenth century. The concepts of dyspepsia and neurasthenia gastrica referred to the influence of the gut on human emotions and thoughts.

Gut-Brain-Skin Axis

A unifying theory that tied gastrointestinal mechanisms to anxiety, depression, and skin conditions such as acne was proposed as early as 1930. In a paper in 1930, it was proposed that emotional states might alter normal intestinal flora which could lead to increased intestinal permeability and therefore contribute to systemic inflammation. Many aspects of this theory have been validated since then. Gut microbiota and oral probiotics have been found to influence systemic inflammation, oxidative stress, glycaemic control, tissue lipid content, and mood.

Research

Probiotics

A 2016 systematic review of laboratory animal studies and preliminary human clinical trials using commercially available strains of probiotic bacteria found that certain species of the Bifidobacterium and Lactobacillus genera (i.e. B. longum, B. breve, B. infantis, L. helveticus, L. rhamnosus, L. plantarum, and L. casei) had the most potential to be useful for certain central nervous system disorders.

Anxiety and Mood Disorders

As of 2018 work on the relationship between gut flora and anxiety disorders and mood disorders, as well as attempts to influence that relationship using probiotics or prebiotics (called “psychobiotics”), was at an early stage, with insufficient evidence to draw conclusions about a causal role for gut flora changes in these conditions, or about the efficacy of any probiotic or prebiotic treatment.

People with anxiety and mood disorders tend to have gastrointestinal problems; small studies have been conducted to compare the gut flora of people with major depressive disorder and healthy people, but those studies have had contradictory results.

Much interest was generated in the potential role of gut flora in anxiety disorders, and more generally in the role of gut flora in the gut-brain axis, by studies published in 2004 showing that germ-free mice have an exaggerated HPA axis response to stress caused by being restrained, which was reversed by colonising their gut with a Bifidobacterium species. Studies looking at maternal separation for rats shows neonatal stress leads to long-term changes in the gut microbiota such as its diversity and composition, which also led to stress and anxiety-like behaviour. Additionally, while much work had been done as of 2016 to characterise various neurotransmitters known to be involved in anxiety and mood disorders that gut flora can produce (for example, Escherichia, Bacillus, and Saccharomyces species can produce noradrenalin; Candida, Streptococcus, and Escherichia species can produce serotonin, etc.) the interrelationships and pathways by which the gut flora might affect anxiety in humans were unclear.

In one study, germ-free mice underwent faecal transplants with microbes from humans with or without major depressive disorder (MDD). Mice with microbes from humans with MDD displayed more behaviours associated with anxiety and depression than mice transplanted with microbes from humans without MDD. The taxonomic composition of microbiota between depressed patients and healthy patients, as well as between the respective mice, also differed. Germ-free mice in another study also displayed behaviours associated with anxiety and depression as compared to mice with normal microbiota, and had higher levels of corticosterone after exposure to behavioural tests. Using rodents in microbiome and mental health studies allows researchers to compare behaviour and microbial composition of rodents to humans, ideally to elucidate therapeutic application for mental disorders.

Additionally, there is a link between the gut microbiome, mood disorders and anxiety, and sleep. The microbial composition of the gut microbiome changes depending on the time of day, meaning that throughout the day, the gut is exposed to varying metabolites produced by the microbes active during that time. These time-dependent microbial changes are associated with differences in the transcription of circadian clock genes involved in circadian rhythm. One mouse study showed that altering clock gene transcription by disrupting circadian rhythm, such as through sleep deprivation, potentially has a direct effect on the composition of the gut microbiome. Another study found that mice that could not produce the CLOCK protein, made by a clock gene, were more likely to develop depression. Stress and sleep disturbances can lead to greater gut mucosal permeability via activation of the HPA axis. This in turn causes immune inflammatory responses that contribute to the development of illnesses that cause depression and anxiety.

Autism

Around 70% of people with autism also have gastrointestinal problems, and autism is often diagnosed at the time that the gut flora becomes established, indicating that there may be a connection between autism and gut flora. Some studies have found differences in the gut flora of children with autism compared with children without autism – most notably elevations in the amount of Clostridium in the stools of children with autism compared with the stools of the children without – but these results have not been consistently replicated. Many of the environmental factors thought to be relevant to the development of autism would also affect the gut flora, leaving open the question of whether specific developments in the gut flora drive the development of autism or whether those developments happen concurrently. As of 2016, studies with probiotics had only been conducted with animals; studies of other dietary changes to treat autism have been inconclusive.

Parkinson’s Disease

As of 2015, one study had been conducted comparing the gut flora of people with Parkinson’s disease to healthy controls; in that study people with Parkinson’s had lower levels of Prevotellaceae and people with Parkinson’s who had higher levels of Enterobacteriaceae had more clinically severe symptoms; the authors of the study drew no conclusions about whether gut flora changes were driving the disease or vice versa.

Book: Avoiding Anxiety in Autistic Children: A Guide for Autistic Wellbeing

Book Title:

Avoiding Anxiety in Autistic Children: A Guide for Autistic Wellbeing.

Author(s): Luke Beardon.

Year: 2020.

Edition: First (1st)

Publisher: Sheldon Press.

Type(s): Paperback and Kindle.

Synopsis:

One of the biggest challenges for the parent of any autistic child is how best to support and guide them through the situations in life which might cause them greater stress, anxiety and worry than if they were neurotypical.

Dr Luke Beardon has put together an optimistic, upbeat and readable guide that will be essential reading for any parent to an autistic child, whether they are of preschool age or teenagers. Emphasising that autism is not behaviour, but at the same time acknowledging that there are risks of increased anxiety specific to autism, this practical book gives insight into the nature of the anxiety experienced by autistic people, as well as covering every likely situation in which your child might feel anxious or worried. It will help you to prepare your child for school, to monitor their anxiety around school, and also to be informed about the educational choices available to your child. It will give you support to help make breaktimes less stressful for them and how to help them navigate things like eating at school and out of the house.

Educationally, this book will take you and your child right up to the point of taking exams and leaving school; socially and emotionally it will cover all the challenges from bullying, friendships, relationships, puberty and sex education. It will give suggestions for alternatives in the scenarios that might cause anxiety or confusion in your child; it will also give a full understanding of your child’s sensory responses and such behaviours as masking, or echopraxia.

As the parent of an autistic child, you may find their path to adulthood different to the one you had expected to take, but as this book makes clear, autism should be celebrated and affirmed. Avoiding Anxiety in Autistic Children helps you to do just that, with practical strategies that will help happiness, not anxiety, remain the over-riding emotion that colours your child’s memories of their early years.

Book: Women and Girls with Autism Spectrum Disorder: Understanding Life Experiences from Early Childhood to Old Age

Book Title:

Women and Girls with Autism Spectrum Disorder: Understanding Life Experiences from Early Childhood to Old Age.

Author(s): Sarah Hendrickx.

Year: 2015.

Edition: First (1st)

Publisher: Jessica Kingsley Publishers.

Type(s): Paperback and Kindle.

Synopsis:

The difference that being female makes to the diagnosis, life and experiences of a person with an Autism Spectrum Disorder (ASD) has largely gone unresearched and unreported until recently. In this book Sarah Hendrickx has collected both academic research and personal stories about girls and women on the autism spectrum to present a picture of their feelings, thoughts and experiences at each stage of their lives.

Outlining how autism presents differently and can hide itself in females and what the likely impact will be for them throughout their lifespan, the book looks at how females with ASD experience diagnosis, childhood, education, adolescence, friendships, sexuality, employment, pregnancy and parenting, and aging. It will provide invaluable guidance for the professionals who support these girls and women and it will offer women with autism a guiding light in interpreting and understanding their own life experiences through the experiences of others.

What is World Autism Awareness Day?

Introduction

World Autism Awareness Day is an internationally recognised day on 02 April every year, encouraging Member States of the United Nations (UN) to take measures to raise awareness about people with autistic spectrum disorders including autism and Asperger syndrome throughout the world.

Background

It was designated by the UN General Assembly resolution (A/RES/62/139).

World Autism Awareness Day”, passed in council on 01 November 2007, and adopted on 18 December 2007. It was proposed by the UN representative from Qatar, Her Highness Sheikha Mozah Bint Nasser Al-Missned, Consort of His Highness Sheikh Hamad Bin Khalifa Al-Thani, the Emir of the State of Qatar, and supported by all member states.

This resolution was passed and adopted without a vote in the UN General Assembly, mainly as a supplement to previous UN initiatives to improve human rights.

World Autism Day is one of only seven official health-specific UN Days. The day itself brings individual autism organisations together all around the world to aid in things like research, diagnoses, treatment, and acceptance for those with a developmental path affected by autism.

Components

The original resolution had four main components:

  • The establishment of the second day of April as World Autism Awareness Day, beginning in 2008.
  • Invitation to Member States and other relevant organisations to the UN or the international societal system, including non-governmental organisations and the private sector, to create initiatives to raise public awareness of autism.
  • Encourages Member States to raise awareness of autism on all levels in society.
  • Asks the UN Secretary-General to deliver this message to member states and all other UN organisations.

Themes

For the past years, each World Autism Awareness Day has focused on a specific theme determined by the UN:

  • 2012: “Launch of Official UN “Awareness Raising” Stamp”.
  • 2013: “Celebrating the ability within the disability of autism”.
  • 2014: “Opening Doors to Inclusive Education”.
  • 2015: “Employment: The Autism Advantage”.
  • 2016: “Autism and the 2030 Agenda: Inclusion and Neurodiversity”.
  • 2017: “Toward Autonomy and Self-Determination”.
  • 2018: “Empowering Women and Girls with Autism”.
  • 2019: “Assistive Technologies, Active Participation”.
  • 2020: “The Transition to Adulthood”.

Notable Initiatives

Onesie Wednesday

In 2014, WAAD coincided with Onesie Wednesday, a day created by the National Autistic Society to encourage people in England, Wales and Northern Ireland to show their support for anyone on the autistic spectrum. By wearing a onesie or pyjamas, participants are saying, “it’s all right to be different”.

Outcomes

United States

In a 2015 Presidential Proclamation, President Obama highlighted some of the initiatives that the US government was taking to bring rights to those with autism and to bring awareness to the disorder. He highlighted things like The Affordable Care Act, which prohibits health insurance companies from denying coverage based on a pre-existing condition such as autism. He also pointed out the recent Autism CARES Act of 2014, which provides higher level training for those who are serving citizens on the autism spectrum.