The Cruciality of Empathy and a Message of Hope for Those With Mental Illness and Other Misunderstood Conditions

I do not have any special degrees I can flash to show you my intellectual superiority on this subject. I am simply an expert in this: experience as someone who has suffered with severe mental-illness and a few rare conditions that are still being misdiagnosed/not diagnosed at all in many due to lack of awareness in the medical community. What I suffer isn’t all of me as an identity but such conditions have significant effects on many people and the problems therein deserve to be addressed. It has affected my functioning to varying degrees and has even made me ponder thoughts of not being here anymore. It has been a cage of both wonder and torment. However, from what I’ve gone through I’ve derived not only self-compassion that I once barely had any of, but deep compassion and empathy for others.

In today’s world we are met with ongoing crises, all of which vary across different geographical areas. We are continually being faced with the uncertainty of our own existence and that of others. Mass chaos, suffering, calamity, confusion, and mortality. So what is it we all do share? Our humanity.

It is through our humanity that we can foster understanding and compassion for others that are different from us. We will never, neurologically, be able to fully understand another person’s perspective but we can all work toward getting as close as possible to this through deep discussion and most importantly, listening. There is a difference between hearing and listening. You have probably encountered many people in your life who could hear what you said yet did not fully grasp or come to terms with the weight of what you were saying. We also have to grasp that even with our personal suffering with a condition it may not be the exact same as another individual who also has it. There are too many variables that go into how humans respond and react to difficult situations (1) but it is important for us as patients to reach out to one another and offer a receptive ear and heart. Additionally, it is important healthcare professionals also have emotional intelligence and empathy (2). And if you are a family member or friend of someone who has issues you should not only listen but arm yourselves with as much knowledge as possible.

Too often people with misunderstood conditions not only get denying or gaslighting from self-proclaimed “experts”, they are given poor advice that is oversimplified. Some insinuate that these complex areas (mental illness and medically uncertain symptoms) are due to moral failings rather than keeping a neutral and open position (as they should if they are an ethical skeptic). Platitudes regarding “be positive” and “live with it” or “get over it” are not only wrong, but unhelpful and potentially traumatic for people who are struggling to get by day to day with their troubling symptoms. I have outlined problems with a diagnosis in conventional medicine known as functional neurological disorder here. I outline reasoning, case studies, fallacies, and the ways of ethical skepticism as it is vital if we are to help our fellow person who is facing adversity. What is helpful next to a good support system is championing causes like funding of research for more rare or understudied conditions. While a positive mindset is important for one’s survival through hard times, psychology babble is not the top of the line solution. Don’t be a part of the problem.

For example, with chronic fatigue syndrome, you can find various articles and comments from patients who have felt less than understood and even mocked by the healthcare professionals they were putting their trust in. This is unacceptable. There is good news recently though regarding harmful exercise guidelines no longer being recommended in the UK and Scotland. Jennifer Brea, someone I admire who suffers from craniocervical instability has been an amazing patient advocate for this patient population that has faced suicide and mass denial from healthcare professionals who are poorly versed in ethical skepticism and the scientific method. Her online activism and intelligence has been a great resource for many.

Now, onto the subject of mental-illness. Some of the misconceptions that have existed throughout the ages regarding mental illness are things such as this:

Many studies have found that the public views people with mental illness as responsible for their disorders: because of poor character or lack of moral backbone, people with disorders like schizophrenia and major depres- sion choose to have their mental illness and are to blame for the symptoms and the disabilities that result (Weiner et al. 1988; Corrigan et al. 1999, 2003; Watson et al., sub- mitted).

These types of views are absolutely absurd and ignorant but they are still persistent. It is why I, as a layperson and sponsor in the scientific method make observations along with reading as much material I can get my hands on so that I can further my understanding of the types of discussions and studies going on in those research fields. I also do the same regarding rare conditions. I have had discussions with both patients and some experts in the field and one thing I’ve learned is patient observation and research should NOT be discounted based on credentialism. Credentialism – an implication or overemphasis on academic or educational qualifications (e.g., certificates, degrees & diplomas), awards or publications as the basis of an individual’s expertise or credibility.

Be familiar with these definitions in case you encounter clear examples of it:

Demoveogenic Shift – a condition wherein amateurs of a science are proactive, well versed and investigate more depth/critical path, while in contrast the academic fellows of the discipline are habitually feckless, cocooned and privileged.

ad verecundiam – accepting as evidence for a proposition the pronouncement of someone who is taken to be an authority but is not really an authority. This can happen when non-experts parade as experts in fields in which they have no special competence.

Correlation Dismissal Error – when employing the ‘correlation does not prove causality’ quip to terminally dismiss an observed correlation, when the observation is being used to underpin a construct or argument possessing consilience, is seeking plurality, constitutes direct fingerprint evidence and/or is not being touted as final conclusive proof in and of itself.

Credulity Accusing – accusing a person of practicing pseudoscience and credulity simply because they are regarding an outlier idea. A credulist may be wrong, but as long as they are not pretending to represent Science or claim to be using the Scientific Method, they are not practicing pseudoscience; rather, are merely guilty of being receptive to an untested conclusion.

Critical Blindness – the conflation of a position of authority or influence with one’s presumed possession of a higher level of personal competence. The mental obstacle created in a person granted entitled authority before they are emotionally ready, wherein they lose their ability to create, to gracefully understand or value the dynamics of human nature, motivation and leadership; descending further into shallow and habitual negative or doubtful critical assessments of those ‘under’ or different from them, coupled with an ever growing hunger for absolute control.

Curse of Knowledge Effect – when better-informed people find it extremely difficult to think about problems from the perspective of lesser-informed people; or perceive that their burden of knowledge cannot be fathomed by lesser-capable people, rendering them unable to practice critical or evidence based thinking.

Delusions of Superiority Error – when one believes that they have special traits or talents not shared by other people. Usually these are confined to a narrow range of human abilities, and tend to center around issues of intelligence or education.

Empathy Gap – the tendency to underestimate the influence or strength of feelings, in either oneself and over-estimate it in others.

In closing, I want people who are suffering to know that there are people out there rooting for you. There is an online community who will listen and have their arms open for you. There are also researchers, even if a small group, who are rooting for you and for funding in the name of forwarding research so that we can come up with practical solutions that will actually improve your quality of life. The fact you are not an “expert” in the sense of the amount of degrees you have or being a doctor does not mean your observations, desperation, and pain have no merit, because it does. The Ethical Skeptic is someone who outlined exactly why in his scientific sponsorship post. It is a tool of the social skeptic to deny this critical pathway of the knowledge development process. Your experience as someone who actually lives with your body and brain is something no one can take from you no matter what. Furthermore, I also wanted to add in this cool piece of information regarding empathy and mirror neurons. It is thought that these neurons play a role in our ability to have empathy for other people. This ability is different between people with high levels of psychopathy and high levels of empathy. An interesting example of how skin plays a role in mirror neurons and phantom limb is when a person with phantom limb visually encounters someone else having a painful physical stimulus on their limbs the person with phantom limb can also feel it. So, what is separating us in regards to that type of pain is actually our skin and brain’s perception. I try to think that people who have clear empathy deficits simply have it due to their own bias and neurological capability (or lack thereof) . We all have different levels of emotional intelligence/empathy and our brains have been shaped by the experiences we encounter that involve ourselves and other people. But we, as a sufferer, hold a type of knowledge no person can have simply by reading schoolbooks and working in a lab. So, always remember: you are valid.

Resources for patient outreach:

I’m sure you know the feeling.

Continue reading “The Cruciality of Empathy and a Message of Hope for Those With Mental Illness and Other Misunderstood Conditions”

What is the wider significance of Cervicomedullary syndrome?


This post is somewhat speculative, but it is very clear to me that the nomenclature of psychiatric conditions is in an awful mess. Some conditions include physical symptoms, some do not, some like ADHD, are alleged to be neurobehavioural conditions but their descriptions include no information about neurological examination or neurological signs. ( These can actually be found). They also include many symptoms without making reference to the neurological paths that could generate them. The nomenclature is so bad that there is inadequate distinction between syndrome, symptoms, and actual discrete medical conditions.

More recently there has been a push to make more brain based definitions. One of those is cerebellar cognitive affective syndrome 9which overlaps many psych conditions) and it appears to me that so is “Cervicomedullary syndrome, being proposed by some neurosurgeons.

So lets go through the symptoms again- and I will make some comments beside them)



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Functional Neurological Disorders: A Potential Erroneous Category in the Land of Psychobabble and Psuedo-Theory

I made this entire post to be a great and extensive resource for those of you interested in this subject. But first and foremost I’m going to leave this for you to read about before I delve deeper into the issues at hand:

Chloe Atkins is an important figure who was mistreated and dismissed by doctors until they finally found out what she was suffering from. This is a summary about her book My Imaginary Illness:

My Imaginary Illness is the compelling story of Atkins’s decades-long battle with a disease deemed imaginary, her frustration with a succession of doctors and diagnoses, her immersion in the world of psychotherapy, and her excruciating physical and emotional journey back to wellness. As both a political theorist and patient, Atkins provides a narrative critique of contemporary medicine and its problematic handling of uncertainty and of symptoms that are not easily diagnosed or known. She convincingly illustrates that medicine’s belief in evidence-based practice does not mean that individual doctors are capable of objectivity, nor that the presence of biomedical ethics invokes ethical practices in hospitals and clinics.”

She has additional publications on bioethics and medically unexplained symptoms. More citations from her will be at the very bottom of this entire post.

I’m also going to mention David Tuller who has a wonderful post on the shaky scientific basis of FND. I implore you all to read it.

“The field of neurology has also taken to analogizing FND to “software” rather than “hardware” problems–the latter referring to known neurological disorders with recognized mechanisms. But as with MUS, FND appears to be deployed as a definitive diagnosis rather than as a tentative acknowledgement that doctors simply cannot at this moment pinpoint what the hell is going on and what is generating the troubling symptoms.”

This outlines why the FND is largely a pseudo-theory:

Moving on, functional neurological disorders as defined by the conventional criteria involve symptoms such as tremors, tingling, numbness, weakness, loss of balance, paralysis, hearing and vision problems along with many other symptoms that have not had a pinpointed physiological cause. It is a newer term that encompasses many symptoms and also includes conversion disorder. In these cases, mainstream medicine uses the testing that they have available (routine blood tests, clinical imaging technology, etc) and finds there is no currently known (emphasis on currently) organic cause that can be part of the diagnosis. I am basically going to give a background of the mainstream views on this, with citations, then I will go into other lines of reasoning and why this diagnosis is faulty.

(The following statements are concluded from the cited studies but keep in mind this is all still up for debate. Some people, like Gina ( have found that he CBT studies used for insomnia are of poor methodological quality and this could also be the case for this. I’m going to look into it and add onto this blog later on whenever I find more out about any potential methodological issues with CBT for FND). Anxiety and depression have both been associated with medically unexplained symptoms [1] and psychotherapy has shown efficacy in many with somatoform problems [2] although this is debatable. Functional neurological disorders can also co-exist with actual diseases rather than just existing by themselves; a lot of factors are supposed to be considered and investigated when making this diagnosis [3]. Between 10-30% of patients seen by neurologists have symptoms that are not currently explainable in terms of physical disease [4]. This shows just how important it is to understand this problem.

This area of research is considered very complex and researchers do not want the amount of disability or distress caused by functional neurological disorders to be underestimated or ignored, especially considering the distress and disability involved is similar to those with actual diagnosed diseases [5]. The terminology used when presenting the possibility to patients is also being carefully crafted in order to not offend them [6]. So, it does appear this name change was a way to try to get patients to “accept” the diagnosis rather than to be offended that clinicians are saying their condition is non-physical/non-organic. Ironically, it actually is still offensive when you consider everything I will outline. Funnily enough they also group the “anxiety and depression” from the symptoms (the patient’s response) within the diagnosis. So, not only does the patient have unexplained symptoms, they’re reacting to the symptoms pathologically according to the “experts.” I say this while rolling my eyes. It must be the patient’s fault! Except, it isn’t.

“Functional symptoms were previously called “hysterical”, but the term’s derogatory connotations and the ever widening meaning of the word (for example, mass hysteria, hysterical personality) make it inappropriate.5 Functional problems are sometimes called “psychogenic” or attributed to “conversion”. However, in the ICD-10 the term “psychogenic” is defined quite narrowly as signifying an association with recent trauma,11 and the term “conversion” evokes an aetiological mechanism for which we have no evidence. These models are too simplistic in most cases [7].”

Before presenting my criticisms in how the functional neurological category can be misleading in many cases, I will state that yes, this is a real category of neurological disorders and the field has complex, genuine, and interesting research even though there are epistemological issues.

Some researchers in this domain are adopting a biopsychosocial view of FNDs that takes a multifaceted approach looking at common pathways in nervous system dysfunction rather than viewing the problem as being “only psychological.” Here are other important things to note:

Functional neurological symptoms refer to neurological symptoms that are not explained by disease. They may also be called psychogenic, non-organic, somatoform, dissociative or conversion symptoms. The most common functional neurological symptoms are non-epileptic attacks and functional weakness.”

1. “Psychosomatic” can be easily confused with the term somatoform. However, psychosomatic phenomena is not the exact same same thing as somatoform/functional neurological symptoms.  Psychosomatic would involve physical illnesses that are caused or made worse by mental factors; this would include mental factors that affect the expression and course of a diagnosed physiological disease. Somatic/functional neurological symptoms would be when there is no diagnosed physiological disease and both the symptoms and the cause are all considered psychological.

2. There was past discussion about the somatoform disorder classification and how it was not optimal for diagnostic reasons [8-9].

“In the taxonomies (Diagnostic and Statistical Manual of Mental Disorder, 4th edition (DSM-IV),10 International Statistical Classification of Diseases, 10th revision (ICD-10)11) functional symptoms can be classified as manifestations of somatoform disorders (physical symptoms which suggest a general medical condition) or dissociative disorders (disruption of the usually integrated functions of consciousness, memory, identity, or perception). However, many functional neurological symptoms (like amnesia or seizures) fulfil diagnostic criteria for both categories. Perhaps because of this, the present clinical criteria in the ICD and DSM systems do not perform well diagnostically if relied upon alone.12 What is more, the term “somatoform” does not imply a positive explanation for the symptom, and there have been increasing criticisms of the somatoform classification with more emphasis being placed on symptomatology.13

With DSM–V on the horizon, discussion again has started about the classification of somatoform disorders (Wise & Birket-Smith, 2002). It has been argued that somatoform disorders are not psychiatric disorders in a strict sense. Indeed, it is not very clear that unexplained physical symptoms are caused by psychological factors. It is clear, however, that there is a strong relationship with anxiety and depression, given that half of the patients in general practice with anxiety or depression suffer from a somatoform disorder as well. The relationship could be due to anxiety and depression causing (awareness of) physical symptoms, or physical symptoms causing anxiety and depression, or there may be a more complex relationship such as a circular causality. Furthermore, a third factor, such as consulting behaviour, could be related to both. In addition to patients with comorbid disorders, many more patients suffer from a somatoform disorder without anxiety or depression. From our study it is evident that both somatoform disorders and anxiety and depression come with substantial functional impairment and that the combination is even worse. A somatoform presentation seems to result from a complex interplay of perception and attribution of symptoms, resulting in unproductive illness behaviour. It has been demonstrated repeatedly that a cognitive–behavioural approach can be effective in alleviating this burden (Kroenke & Swindle, 2000). The inclusion of a well-defined category of somatoform disorders in DSM–V is needed to facilitate further research on the effective treatment of such patients.”

Now after an update, it is called somatic symptom disorder rather than somatoform disorder. Somatic symptom disorders can involve a wide range of symptoms involved with the whole body in addition to the excessive worry caused by the perceived symptoms, whereas functional neurological disorders are those that more specifically have symptoms that mimic neurologically based problems.

“A somatic symptom disorder formerly known as a somatoform disorder,[1][2][3] is any mental disorder which manifests as physical symptoms that suggest illness or injury, but which cannot be explained fully by a general medical condition or by the direct effect of a substance, and are not attributable to another mental disorder (e.g., panic disorder).[4]

In the newest version of DSM-5 (2013) somatic symptom disorders are recognized under the term Somatic Symptom and Related Disorders:

-Somatic Symptom Disorder: This will take over many of what was formerly known as Somatization Disorders, and Hypochondriasis

-Factitious disorder: Can be either imposed on ones self, or to someone else (Formally known as Factitious Disorder by proxy).

-Conversion disorder

-Illness anxiety disorder: A somatic symptom disorder involving persistent and excessive worry about developing a serious illness. This disorder has recently gone under review and has been altered into three different classifications.[citation needed]

-Somatoform disorder Not Otherwise Specified (NOS)[12]

Included among these disorders are false pregnancy, psychogenic urinary retention, and mass psychogenic illness (so-called mass hysteria).

Somatization disorder as a mental disorder was recognized in the DSM-IV-TR classification system, but in the latest version DSM-5, it was combined with undifferentiated somatoform disorder to become somatic symptom disorder, a diagnosis which no longer requires a specific number of somatic symptoms.[13]”

The classifications and distinctions can be quite confusing for anyone unfamiliar with this part of psychiatry and neurology, but it is worth reading about over time if you want to understand how it is being used.

Here, I will present a syllogism example that can identify specific flawed reasoning where it may exist in the mind of a neurologist, psychiatrist, or other doctor.

⁃ Somatic and functional neurological disorders  often involve co-existence with anxiety, depression, and other psychiatric factors as initiating causes of physically felt symptoms in the absence of a known organic cause.

⁃ This person I am evaluating (and based on our testing abilities) has unexplained physically-felt symptoms and they also have anxiety, depression, and/or other psychiatric symptoms.

⁃ Therefore, the anxiety, depression, and/or other psychiatric underpinnings must be the cause of the physical symptoms the patient describes.

Is there anything wrong with these premises and the conclusion when considering all of the possible factors and interpretations? The answer is yes. Some researchers have pointed out that it is difficult to know what caused what (physical symptoms resulting in psychological symptoms, or the other way around) but the issue here is when causation is automatically assumed by a doctor. “Your stress is causing the symptoms you perceive.” This would be a good example of correlation does not imply causation. Another key question to ask is “What is within conventional medicine’s testing abilities and is it adequate enough for the extent of the problem?” While certain diseases and structural problems can be ruled out, they do not account for all possible explanations. For example, mitochondrial dysfunction is not routinely tested for and it can cause both psychological and physical symptoms [10]. Moreover, there are rare diseases and biochemical abnormalities that may exist that are not screened for in routine conventional testing [11]. This includes mitochondrial testing, cytokine measurements, xenobiotic exposure evaluations, and CSF pressure (in cases of IIHWOP), craniocervical instability, and probably more. While some of these are still not understood for their potential role in associations or clinical usage for functional neurological and somatic symptoms, it is important that it is investigated so we understand if some type of exposure or biochemical factor (like heavy metals, unexplored metabolic factors, etc) may have had impact on nervous system function. While our measuring capabilities may not be perfect or complete, they can help us go a step forward if they are considered. Furthermore, I must also mention the fact that at one point ulcerative colitis was considered “psychosomatic” until the actual immune factors were identified. This is due to the fact unknown etiology often sparks psychological theories.

These psychological theories can cause problems especially in situations where something physical actually is involved, but remains to be found and properly investigated. I found an article that was very interesting and discussed how secondary neuronal damage can have psychiatric manifestions. These researchers found important overlaps in brain insult symptoms and neuropsychiatric symptoms.

“However, 40% of neuropsychiatric signs and symptoms were found to be commonly shared by traumatic, infectious, toxic, oncogenic, and degenerative brain insults, suggesting that the same or similar brain regions/structures can be possibly affected by different acute and chronic brain insults.”

They also discussed limitations to our imaging technology on picking up certain changes in the brain.

“A neuropsychiatric disorder should have its morphological alter-ations in the brain. Any brain insult can certainly cause histo-morphological, biochemical, or molecular biological alterations in some parts of the brain, such as the limbic system, basal ganglia system, the brainstem, the basal forebrain, the cerebellum, and the cerebral cortex. Unfortunately, these alterations at the cellular and molecular level are usually not easy to detect by using traditional diagnostic imaging techniques (e.g., ultrasound, X-rays, CT, and MRI), because tiny morphological changes (such as neuronal cell death or loss) in deep brain structures (such as the limbic system and basal ganglia system) can be often covered by other normal neural tissue layers of the brain. Much of the neuronal damage in deep brain structures can be seen only under a microscope after death (13).”

Some of the symptoms they also looked at in this analysis also included somatic symptoms:

“Somatoform disorders are a group of neuropsychiatric disorders characterized by physical symptoms that suggest physical illness or injury. However, the cause for the symptoms cannot be fully explained by a general physical illness because physical exami-nations and clinical lab tests do not indicate the presence of a physical illness (101). This has led to the hypothesis that the physical symptoms of these patients’ experience may be from a neuropsychiatric source associated with brain damage (102). They may be relevant to the damage to some parts of the cerebral cortex (such as dorsolateral prefrontal, insular, rostral anterior cingulate, premotor, parietal cortices, and parahippocampal gyrus) (103, 104). Because the cerebral cortex controls sensory–motor coupling, sensory feed-back system, and somatic sensation, cortical damage may cause increased sensitivity to internal physical sensations and pain. The increased sensitivity to somatic feelings may predispose patients to produce somatoform symptoms (105, 106).”

“If a patient has neuropsychiatric signs and symptoms of unknown origin, physicians and psychiatrists should be aware that potential neuronal damage can possibly exist in the patient’s brain and not simply conclude that the patient has a psychological problem associated with social/environmental factors. Necessary treatment aimed at slowing down the process of neuronal damage and attenuating individual symptoms or clusters of neuropsy-chiatric and neurological disorders may help improve recovery of neurobehavioral functions. The clinical symptom-comparing approach used in the present study to identify the same clin-ical manifestations may be a useful tool for investigating the causes of neuropsychiatric disorders and other complex diseases of unknown origin.”

So yes, even somatoform symptoms may possibly be rooted in unseen neuronal damage.

Furthermore, a 2005 systematic review concluded that there was a misdiagnosis rate of 5% for FNDs (conversion disorder) since 1970. Is this number entirely accurate? That can depend on interpretation/inclusion and exclusion criteria, but it is still important to note nonetheless. It is being said that functional disorders should be based on positive signs and strict criteria rather than only being based on (some) negative test results (exclusionary diagnosis) [12]. This could be misleading if further needed tests end up showing association with a real illness. Rare diseases can be misdiagnosed as psychiatric and psychological and this must be taken into consideration. Functional neurological disorders could co-exist with an organic illness as well and one existing does not automatically discredit the other.

Pertinently, Harvard Ph.D. student Jennifer Brea is a director of a documentary titled Unrest; she is another person who has suffered at the hands of false assumption. She has chronic fatigue syndrome (myalgic encephalomyelitis) and was diagnosed by a neurologist with the psychiatric conversion disorder. Conversion disorder is grouped with functional neurological disorders. There has been controversy surrounding the conversion disorder diagnosis based on oversimplification [13].

“One of the most common conditions bringing patients to neurologists, FND involves a constellation of neurologic symptoms — including weakness, tremors, walking difficulties, convulsions, pain and fatigue — not explained by traditional neurologic diagnoses. This condition has also been called conversion disorder, reflecting one theory that patients were converting emotional distress into physical symptoms, but Perez notes that this now appears to be an oversimplified view of a complex neuropsychiatric condition. The research team hopes that advancing the neurobiological understanding of FND will increase awareness and decrease the stigma — including skepticism about the reality of patients’ symptoms — often associated with this condition.

Previous functional MRI studies have suggested that a group of brain structures forming part of what is called the salience network — which are involved in detecting important bodily and environmental stimuli, as well as integrating emotional, cognitive and sensory-motor experiences — showed increased activity in FND patients during a variety of behavioral and emotion-processing tasks. The current study is one of the first to examine structural relationships between components of the salience network and the physical and mental health of patients with FND.”

Even if this somehow was the case for her (unlikely), it would still not disprove all neurobiological cause.

Edit: she has biological issues (not surprising) that were finally identified and treated:

Furthermore, the neurologist who diagnosed her claimed there was some “past trauma” she does not remember. There is no evidence for this statement and it is presented as unfalsifiable. An ethical skeptic has to ask “Is this considered proof by non-falsifiability?”

Jennifer also had a history of viral infection and was given prescriptions accordingly. Yet, this was not considered or accepted as a possible sign of an etiological event.

An NIH researcher, Brian Walitt, is another example of a researcher who has assumed that fibromyalgia and chronic fatigue syndrome are somatoform. In the following 2015 paper this statement is made:

“The discordance between the severity of subjective experience and that of objective impairment is the hallmark of somatoform illnesses, such as fibromyalgia and chronic fatigue syndrome.”

To claim that CFS/ME and fibromyalgia are somatoform is a bit of stretch; this broad of a conclusion cannot be made considering the state of evidence and what is currently unknown. It wasn’t until recently that it was discovered that cytokine signature was associated with chronic fatigue syndrome. The reason this information wasn’t being collected on patients in clinical practice is because the tests aren’t offered, and as Montoya (one of the researchers) says regarding what is offered by mainstream medicine, “those tests aren’t measuring the right things.”

This evidence alone disproves the notion that chronic fatigue syndrome patients have a disease of purely “psychological origin.” What is more likely is that chronic fatigue syndrome is a disease involving multiple etiological links and pathways varying in subgroups. For example, CFS/ME has also been connected to intracranial hypertension without papilledema in some CFS patients. If the investigators involved in this study had not looked into this, what would our current state of knowledge be? Each investigator that asks the right question leads us further and further down the knowledge development process. We cannot assume answers before questions are even asked.

What needs to be both understood and avoided is pro-innovation bias, the argument from ignorance, probabilistic fallacy, and the availability heuristic.

Pro-innovation bias is “the tendency to have an excessive optimism towards technology or science’s ability to shed light into a subject or advance understanding, while often failing to identify its limitations and weaknesses, and habitually dismissing all other methods (The Ethical Skeptic, n.d.).” Simply put, any excessive optimism or confidence in our current understanding of this issue may be overplayed. In turn, this can lead to conclusions that were made too quickly before more biological bases could even be discovered or explored.

The argument from ignorance asserts that a proposition is true because it has not yet been proven false, or is false because it has not been shown to have any evidence. A functional neurological disorder diagnosis could in many cases be based on an argument from ignorance. A proposition regarding somatic/functional neurological symptoms may be assumed to be true (because it has not been proven false). This is also because the alternative explanations have not yet been found due to scientific obscurity.

Additionally, this situation can relate to the probabilistic fallacy and availability heuristic. The probability fallacy involves “the presumption that one holds enough data to determine what is probable and improbable in a field of a set of data” and the availability heuristic involves “adjudicating an answer to a question according to only the information which is available at the time (The Ethical Skeptic, n.d.).” Although current and past symptom history is considered in functional neurological disorder diagnoses, this diagnostic “answer” may still only be serving the overall information known at the time in the field of science and medicine.

Provisional Knowledge – the contrivance of a series of purposed provisional arguments, into a stack of probable explanations wherein we ignore the increasing unlikelihood of our conclusions and simply consider the stack of plurality to be proscribed; and eventually by Neuhaus’s Law, prescribed (The Ethical Skeptic, n.d.)

We also have to play close attention to psychologism. This is “when psychology plays the sole or central role in underpinning facts or explaining a non-psychological fact or principle expressed as constituting accepted knowledge. Suffers from the weakness that psychological principles enjoy a perch which can never be falsified, therefore they are at risk of standing as pseudoscience (The Ethical Skeptic, n.d).” Michael Loughlin, a senior philosophy lecturer at Manchester Metropolitan University has explored this problem in regards to how ambiguities in diagnostic terms and psychological inference can be fallacious when perceiving and categorizing symptoms since they can have possible underlying (and unseen) physical causes.

An important issue here is that assumptions are being used for specious proclamations and it is harming patients. An example of this in the case of a patient with chronic fatigue syndrome, Karina Hansen, a danish woman who was taken forcibly from her loving parents and forced to undergo psychiatric treatment for an assumed functional neurological disorder. Another example is of a case study where a woman with prion disease died after she was originally diagnosed with conversion disorder and major depression. Below will be the case history (if you find this too long you can scroll down and skip over it or look at the provided link to the PDF).

“Ms. A was a 49-year-old Caucasian woman who had never married and who had been a communications product engineer. Before onset of her symptoms, she had never seen a psychiatrist, never been diagnosed with a psychiatric disorder, and never been treated with a psychotropic medication. Her medical history was notable only for a febrile illness that may have been an encephalitis of uncertain etiology after a trip to South America when she was in her 20s. There was no family history of psychiatric illness, epilepsy, or neurological or neurodegenerative disorders.

Ms. A had grown up as the youngest of three children. She described her relationship with her two brothers as an adult as “distant.” Her relationship with her parents was reported to have been “good,” although additional details were lacking, and both parents were deceased. She had no history of physical or sexual abuse, but she felt that she had been excessively teased by her brothers while growing up, which left residual resentment even late into her adult life. She did not date frequently in either her teens or 20s. She had a number of heterosexual romantic relationships but described these as superficial and brief. She noted that she had always been sexually interested in women, but until just before the onset of the symptoms leading to hospitalization, she had never had a same-sex romantic relationship. The revelation of her homosexuality to her family was poorly received. She described it as “cold,” and she felt criticized and ashamed. Ms. A had begun her employment with a communications company as a telephone operator and had advanced over the next 20 years until she became a high-level manager in research and development.

Ultimately, she was recruited into an upper-level management position with a competitor in the field. She traveled frequently to Europe as part of her new job. During this transition in her career, she met a woman with whom she hoped to have a fulfilling romantic relationship and thus estranged herself from her family. In the context of these psychosocial stressors and after a flight from Europe, she developed an acute onset of lower-back pain while lifting her laptop computer out of an overhead bin. Soon after she saw a chiropractor for lower-back pain; upon examination, the practitioner noted some weakness of the lower extremities. She received no benefit from the chiropractic visits and began to note the onset of new symptoms. These included a tremor “all over [her] body” and weakness in “big muscle groups.” This made ambulation difficult and was the beginning of a slow deterioration in gait. She made an appointment with her primary care physician.

A workup included magnetic resonance imaging (MRI) of her spine, which showed a mild lumbar right-paramedian bulge that was judged to be inadequate to explain her symptoms. Her laboratory tests included a CBC, a full metabolic panel, including liver function tests—all of which were found to be within normal ranges—a measurement of erythrocyte sedimentation rate (4), and a rheumatoid factor check (negative result). These results were obtained almost 2 months after Ms. A’s original lower-back strain. Ms. A’s medical and emotional needs became overly burdensome to her partner, which led to the end of their romantic relationship. Ms. A continued to experience weakness in her lower extremities and ambulation difficulties.

Her physician ordered an MRI of the brain, which was normal except for evidence of chronic sinusitis in the left maxillary sinus. An MRI of her cervical spine was also performed, and the results were found to be normal. Additionally, a lumbar puncture was performed as the diagnostic considerations expanded to include multiple sclerosis, encephalitis, neurosyphilis, subacute sclerosing panencephalitis, and acute idiopathic polyneuritis. Results of tests regarding CSF glucose, cell cytology, protein, gram stain, immunoglobulin M, immunoglobulin G, fluorescent treponemal antibody absorption, and immunoglobin banding were all negative. Despite reassurance that these symptoms would likely remit, Ms. A continued to experience more weakness and ataxia. She was seen by another internist and diagnosed with atypical multiple sclerosis.

She was given a trial of methylprednisolone sodium succinate and noted a brief period of symptom improvement. She was seen by a neurologist 1 month later, and an EEG was ordered. Again, the result was unrevealing. Five months after her initial symptoms, Ms. A complained of diplopia, difficulty swallowing, and frequency of urination in addition to her symptoms of leg weakness, tremor, and gait difficulties. She saw another neurologist whose differential diagnosis included Creutzfeldt-Jacob disease. She was then seen by an associate of a national authority on prion disease, who felt that Creutzfeldt-Jakob disease was a “low-probability” diagnosis, but a measurement of blood mercury level was recommended, which was also found to be negative. At this point Ms. A’s treating physician began to seriously consider that these symptoms might have a psychological component, which led to a psychiatric evaluation. About 6 months from the onset of her symptoms, Ms. A completed a neurocognitive and psychological battery of tests.

The results were as follows: score of 30/30 on the Mini-Mental State Examination (MMSE), a score of 33/33 on the Blessed Dementia Scale (5), and a Sensory Perceptual Screening (6)examination performed without errors. She completed the Wechsler Memory Scale—Revised (7). Her score fell within the average to high-average range, and she was judged to have high-average intellectual abilities. Also of note was that her receptive and expressive language abilities were found to be intact, her conversational speech was fluid and nonphasic, her digit repetition was high average, her oral calculations were average, and her attention and concentration were normal. The only abnormal finding in this test battery was on the MMPI-2, which showed elevated depression.

Although Ms. A complained of weakness and an unstable gait, results of formal neurologic examinations continued to be completely normal. In addition, Ms. A’s complaints of waxing and waning strength and difficulty walking were difficult to explain. At this time, she was given axis I diagnoses of major depression and conversion disorder. Ms. A was given fluoxetine for depression and buspirone for anxiety. She was thereafter discharged to a residential psychiatric facility. Nearly 8 months after the first appearance of lower-back strain, Ms. A was seen by a specialist in dissociative disorders and psychosomatic illness. He hypnotized Ms. A and noted that she was highly hypnotizable and that, under hypnosis, her symptoms improved. She continued to decompensate and was transferred from the residential facility to a skilled nursing facility secondary to functional deterioration and an inability to complete activities of daily living without assistance.

This deterioration continued until Ms. A was again hospitalized, this time on the Behavioral Medicine Unit at Stanford University Hospital. At that time, she was confined to a wheelchair. She complained of waxing and waning dysarthria and difficulty swallowing, an ataxic-like gait, and tremors that would move over her entire body, which she would refer to as “convulsions.” She also had occasional complaints of diplopia, for which she would compensate by closing one eye, and frequent squinting. She continued to experience subjective weakness in her lower extremities, which varied in degree, although it was always present. At this time, both Ms. A and her family agreed that her mood was normal. Her score on the MMSE at admission was 24/30; she appeared to be poorly motivated to complete the test. Her insight was judged to be good, and she was reported to say that she was motivated to determine the cause of her disability so she could return to work. She admitted that being ill had brought her family back to her and that her ex-lover was again in frequent contact, both of which pleased her deeply. Upon examination her tremors were noted to wax and wane depending on the content of her conversation.

Her diagnoses at admission were conversion disorder and major depression, single episode, moderate, nonpsychotic, and in remission with a regimen of fluoxetine and buspirone. Psychological testing was ordered, as was a follow-up neurology consultation. Upon completion of neurological and psychometric evaluations, Ms. A’s primary diagnosis remained conversion disorder. Supporting this diagnosis were fluctuating and at times bizarre symptoms: waxing and waning memory deficits, an inability to ambulate without assistance despite adequate strength, back pain, eye squinting, and tremor, but no evidence of spasticity or cerebellar abnormalities.

There was also some concern over factitious elements, such as a new complaint of life-long auditory and visual hallucinations. Ultimately, it was decided to proceed with a behaviorally oriented rehabilitation program. This involved aggressive physical therapy, occupational therapy, and participation in groups and activities, with the focus on treating Ms. A’s functional disability. Furthermore, with the intent of both confirming and treating the conversion disorder, it was explained to Ms. A that in the setting of such an intensive rehabilitation program, her functional ability should improve if it was simply related to an underlying medical etiology, such as the apparent severe muscle deconditioning she had experienced.

It was also explained to Ms. A that if she did not improve after undergoing such an intensive rehabilitation program, it would be owing to either a lack of participation or motivation on her part or because her condition was purely the result of a psychological disturbance. That is to say, improvement would confirm a medical etiology. This behavioral approach to treating conversion disorder was based on a review of the literature and the apparent success of the use of this “double-bind” model (3).

The neurology service was consulted soon after Ms. A was hospitalized. They found her to have normal conjugate eye movements without nystagmus, although she complained of diplopia. Her palate lifted symmetrically, her gag reflex was intact, and a fluctuating dysarthria in her speech was described as “clear” at times. She was noted to have decreased muscle bulk on the anterior tibialis muscles bilaterally and a slight contracture of the left Achilles tendon, both attributed to deconditioning. Her muscle strength was intact, with bilaterally symmetric deep tendon reflexes. She had intermittent tremors of her trunk and extremities, both at rest and with movement, without an apparent pattern. She had no cerebellar abnormalities; e.g., heel-to-shin and finger-to-nose movements were intact. While standing Ms. A was unable to place her left heel to the floor, was unsteady, and was unable to stand unassisted. She appeared to be cognitively intact, although her affect ranged from tearful to “flattened.” Noting her prior workup and neurologic evaluations, the neurology service assessed the observed tremors and other symptoms as highly elaborated and “functional” in nature.

There was noted a lack of cooperation with the funduscopic examination, which was complicated by Ms. A’s frequent blinking. The neurology service emphasized that at that time there was no evidence of nervous system disease, concurred with a diagnosis of conversion disorder, and recommended continued behaviorally based treatments. With great encouragement, Ms. A was at times able to ambulate somewhat better and at other times was only able to ambulate with two-person support. Her speech would fluctuate in terms of intelligibility, her tremors would wax and wane, and her ability to perform on the MMSE would change as well. Some of the variability was clearly associated with anxiety about issues and concerns expressed in the content of her speech. She clearly responded to decreased nursing attention with vocalizations but not always with words, sometimes moaning plaintively.

While eating she was observed to throw her head back, causing her to choke on her food; however, with consistent reinforcement, she would keep her chin down while chewing and have no difficulty. Because of concerns over her apparent swallowing difficulties, a videofluoroscopic study was performed and an occupational therapy swallowing examination completed. Both showed normal swallowing reflexes but noted that she would tilt her head back and choke at times. This was considered to be volitional behavior.

There were also attempts at managing her condition with psychotropic medication. Ms. A had had a good response to fluoxetine for her depression, and this treatment was continued and the dose increased. The buspirone therapy was continued, and olanzapine was added at a dose up to 10 mg, given at night, mostly for episodes of agitation and concern that Ms. A was at times psychotic. None of these medication changes appeared to change her course of illness. Approximately 6 weeks after Ms. A’s admission, the psychiatry service noted waxing and waning primitive reflexes. In addition, she began to exhibit progressively more disinhibited behavior, such as throwing food and smearing it on her face, along with choking sounds. She developed an exaggerated startle response to innocuous stimuli. Another MRI and EEG were performed, and again the neurology service was consulted. Ms. A had an essentially normal examination.

The service noted slurred speech but felt it was functional and that no evidence of dysarthria was present. Ms. A knew the date but appeared to be disoriented to place. The neurology service did not note any disconjugate gaze but raised questions about subtle right nasolabial fold flattening, oral dyskinesias, and uncoordinated tongue movements. There also was a concern over a subtle right lower-extremity rigidity that had not been noted previously. Additionally, mild, right-greater-than-left intention tremor was noted. Ms. A’s repeat MRI of the head resulted in a normal scan without evidence of ventricular enlargement or expanded sulci. The neurology team noted that the buspirone may have caused her tremor, referring to it as tardive dyskinesia, and thought both fluoxetine and olanzapine may have contributed to it as well. They recommended simplification of the medication regimen. Earlier in her hospitalization, Ms. A had been administered an MMPI-2. The results of the entire neuropsychological battery were now considered to be invalid because of her excessive endorsement of symptoms.

In addition, a Rorschach test given Ms. A was deemed unscorable. She tended to tell long, convoluted stories about the inkblots and could not be redirected. She used what appeared to be neologisms (e.g., “torcle bug” and “buldar”), but when she was questioned, she would laugh and say that she had made them up by combining words. Ms. A was dysarthric and difficult to understand. She tended to avoid responding to questions with direct answers and appeared to be somewhat disinhibited; e.g., she asked the female examiner out on a date.

Given the lack of information gained from administration of these tests, the examiner requested copies of the raw data from Ms. A’s previous neuropsychological testing. Her MMPI-2 results, taken 4 months earlier, were notable only for depression and lacked the expected elevation in somatic preoccupation, denial, repression, and endorsement of neurological symptoms that is often found in individuals with conversion disorder.

Subsequently, psychological testing was readministered, and this time it was considered to be valid. Ms. A was given the shorter Millon Clinical Multiaxial Inventory—III (8), the Rorschach test, and the Thematic Apperception Test. The results of the Millon Clinical Multiaxial Inventory—III were considered to be valid, but Ms. A appeared to answer it with a bias toward magnifying her symptoms, as it indicated the presence of a significant mental disorder. Her profile suggested a personality disorder with narcissistic, avoidant, and paranoid features. Her Rorschach test results had 19 scorable responses and, this time, was notable for linear responses and an absence of neologisms. Ms. A exhibited considerable effort and demonstrated complexity in her thought process, as well as an ability to synthesize information. She had some difficulty with perceptual accuracy and demonstrated a tendency to become easily disorganized.

Ms. A continued to fare poorly, her grooming was very poor, and her ability to perform simple activities of daily living was severely impaired. Despite aggressive behavioral strategies to treat a presumptive conversion disorder, no progress was seen. Repeated neurologic consultations were inconclusive. An MRI and EEG showed no abnormality. After exhaustive review of Ms. A’s care, strategies to improve her function, and attempts to define a possible medical etiology, it was reluctantly agreed that no progress had been made in the prior 6 weeks of intensive therapies. Plans were made to have her moved to a skilled nursing facility. Ms. A’s response to this proposed move was dramatic. There was an increase in nonverbal vocalizations, choking, disinhibited outbursts, difficulty following directions, and tearfulness. She began to look more abulic, with more frequent and severe difficulties with chewing and swallowing. With the expected discharge date looming, another EEG was ordered. It was decided to place a nasogastric tube for feeding. However, less than 24 hours after insertion, it was taken out by Ms. A. Another was placed, with a similar result. Faced with the difficulties of having Ms. A undergo even a minor procedure for the presumed conversion disorder, her unwillingness to allow the nasogastric tube to remain in place, and ambivalence about proceeding to percutaneous endoscopic gastrostomy placement in an individual with a psychosomatic illness, we decided to initiate another trial of oral feedings. That day Ms. A ate both lunch and dinner without significant difficulty.

Ms. A was found later that night in cardiopulmonary arrest. It occurred almost 90 minutes after dinner, which had been observed by nursing staff and described as uneventful. After dinner that night, Ms. A had been heard choking; although her oropharynx had been examined and was found to be clear of food and debris. She was found cyanotic approximately 30 minutes later, without respiration or pulse. Suction performed during cardiopulmonary resuscitation revealed small bits of food—apparent evidence of aspiration. Ms. A was presumed to have asphyxiated because of an obstructed airway. It was thought possible at the time that Ms. A may have moved some food into her chair and later put it into her mouth and choked, suffering asphyxiation, cardiopulmonary collapse, and near-death. She was resuscitated and sent to the intensive care unit, where about 36 hours later she was declared brain dead by EEG. Ironically, the EEG ordered earlier in the week was read at the same time as the EEG from the ICU. The former was noted to be abnormal and interpreted as showing excessive theta activity in bilateral temporal areas that was consistent with an encephalopathy. The EEG report specifically mentioned the possibility of a rapid neurodegenerative process in the differential. Ms. A was removed from life support after a lengthy meeting with her family, and she expired shortly thereafter.

The family granted permission for an unrestricted autopsy. On general autopsy, Ms. A was found to have acute and organizing bronchopneumonia, with fragments of vegetable material in the bronchus consistent with prior aspiration. The results of gross examination of the external brain and coronal sections was found to be entirely normal, with no evidence of inflammation, neoplasm, atrophy, or white matter changes.

However, microscopic examination revealed changes indicative of prion disease; namely, sections of the frontal, hippocampal, and occipital cortices showed moderate neuronal loss, reactive astrocytosis, and variably sized vacuoles within the neuropil, also know as spongiform change (Figure 1A). No kuru-type plaques were seen; no inflammation was observed. The underlying white matter showed patchy myelin loss and spongiform change. In addition, many of the sections revealed evidence of acute ischemic/hypoxic injury, with shrunken neurons displaying hyperchromatic, indistinct nuclei and eosinophilic cytoplasm (Figure 1B). Sections of the midbrain and brainstem also showed spongiform change, as well as neuronal dropout and gliosis in the substantia nigra and olivary nuclei. A section of the cerebellum showed a normal-appearing granular cell layer, loss and acute ischemic/hypoxic injury of the Purkinje neurons, and mild spongiform change in the molecular layer. The underlying cerebellar white matter had mild spongiform change, and the dentate nucleus showed gliosis and neuronal loss.

In compliance with an ongoing surveillance program sponsored by the American Association of Neuropathologists and the Centers for Disease Control and Prevention, tissue was sent for immunodiagnostic studies to collaborators at the newly formed National Prion Disease Pathology Surveillance Center in Cleveland. Western immunoblot analysis revealed the presence of the pathogenic, protease-resistant isoform of prion protein, which confirmed the diagnosis of prion disease (Figure 2). Of interest, this sensitive detection method (9) discerned the protease-resistant isoform of prion protein, as evidenced by the unique three-band pattern revealed after digestion with proteinase K in the comparison tissue from another patient with Creutzfeldt-Jakob disease (lane 1) and in the frontal cortex from Ms. A (lane 4). It found no protease-resistant isoform of prion protein in the cerebellar tissue (lane 3). This might suggest a sampling or technical error or that levels of the prion protein in the cerebellum were possibly too low for detection.”

Conclusions from this presented case study:

“A remarkable aspect of this case was the nearly unani- mous opinion by the neurology and psychiatry services that this patient’s presentation was conversion disorder and was not organic until after she had coded and was in the intensive care unit. This case provides an excellent teaching example of why the physician needs to sustain a suspension of belief or disbelief and seriously consider in every patient whether an entirely psychological or entirely biological explanation will identify the current diagnosis and appropriate interventions.

The belief that this patient had a conversion disorder also appeared to dissuade the consulting neurologists from reconsidering some of their findings. Signs such as an apparent dyskinesia of the tongue, a flattened affect, at least one frontal release sign, functional evidence of disin- hibition, and loss of appropriate social behaviors may have been minimized by the consulting service.

This case report is, to the best of our knowledge, the first report in the literature of a patient, who, upon death, was diagnosed with Creutzfeldt-Jakob disease and who had symptoms that were thought to represent a primary diag- nosis of a psychosomatic illness. This report also contains, to our knowledge, the first serial psychometric examina- tion of a patient with Creutzfeldt-Jakob disease. Despite the use of different psychometric instruments, there was a clear pattern of development of impaired defenses and primitive personality characteristics that were associated with clinical decline and progression of the disease.
In addition to the visible effects of the neurodegenera- tive process on motor control and cerebellar function, we argued that the neurodegeneration of frontal cortices and subcortical structures affected

Ms. A’s personality and possibly created a vulnerability for the elaboration of symptoms concordant with pathologic illness behavior. More subtle effects that may have affected interhemi- spheric communication, dominance, or interference of parietal motor control may have contributed to this bio- logic vulnerability as well (35, 36). This case provides a small window into the neurobiology of personality and perhaps into conversion itself. It also reveals the power of our biases and the intersection of neurobiology and psy- chological models of psychiatric illness.”

While I understand that psychological explanations may seem sexy and tempting to psychiatrists and even some neurologists, I still highly recommend suspending judgement before making declarations and using them to justify medical kidnappings and erroneous diagnoses.

In closing, some major points to outline are (1) yes, functional neurological disorders and somatic symptoms are real and need as much research as possible on the topic, (2) professionals in the field of psychiatry and neurology need to openly discuss the limits to some of their neurological disorder diagnoses especially concerning functional neurological disorders and somatic symptoms, (3) while the criteria is very specific and researchers call for positive diagnoses rather than just diagnoses based on exclusion, they can still be falsely made when it is assumed that science and medicine already have the needed resources to identify every single pathophysiological/biochemical problem related to symptoms of disease, and (4) the diagnostic manual needs to include a disclaimer that states that a functional neurological disorder diagnosis may in fact be innacurate because our testing methods/detection capabilities are not complete and science may advance the field in such a way that contradicts the assumed causes involved in the diagnosis. This diagnosis will likely be proven to to be misleading once science sheds light on misunderstood and unexplored issues.

Similarly to this issue of assumption, I have also outlined the psychiatric fallacy wherein psychiatrists use fallacious reasoning and fail to properly investigate or identify potential biological causes of commonly diagnosed mental disorders [14]. It is up to the patient population and ethical scientists and skeptics to weigh the current state of evidence and openly discuss their questions, concerns, findings, and observations. The below image will also visually demonstrate an important concept of the knowledge development process.

The larger circle contains smaller circle sections tha relate to a specific time frame of information and knowledge. As each section moves outward, we see that the circle gets bigger and years add together. The 20 year circle contains the smaller 10 year circle within it, the 30 year circle contains the 10 and 20 year circles within it, the 40 year circle contains the 10, 20, and 30 year circles within it, and this continues to go on and on. Each circle contains knowledge from different years combined within it based on the time and the extent of development. We cannot assume that our circle represents the entire whole and that the circle will not grow in size over time as new information is collected. When people within each time frame assume their section has all of the answers, they are suffering from myopia. Each section has critical importance and plays a part in the entire circle’s growth, size, and intelligence.

I am also going to add (adding this to this post in 2020) that a friend brought up that it’s even an assumption to claim that somatoform conditions even exist, and I have to agree to an extent. We really don’t know all of the true causes (of a patient’s symptoms) or how many are misdiagnosed and have something misunderstood by science. This category of psychiatric diagnosis is clouded with assumption, questionable conclusions, and stigma.
















Chloe Atkins’ additional publications:

The Psychiatric Fallacy 

What do I mean when I say “psychiatric fallacy?” I am talking about the erroneoussness of some of the most prominent assumptions held by some psychiatrists and the field of psychiatry. Moving on from the accumulation of information in the past, modern science has made major breakthroughs in our understanding of the possible underlying biological and environmental basis of many behavioral and mood disorders. The surface was originally just scratched while the biological hell beneath was grossly misunderstood.

You would think that given today’s knowledge on the involvement of inflammation and neuroexcitotoxicity in mental dysfunction (Najjar S, et al., 2013) that some of this information would have already seeped its way into modern mainstream clinical practice, but this has not been the case. Instead, we have pervasive myths that still fill the atmosphere of psychiatric facilities and practices. Keep in mind that these are very specific and pertain to specific instances; I am not claiming that psychiatry as a whole is wrong or that it doesn’t provide any benefit to patients. That would be an equally preposterous assumption.

Firstly, many psychiatrists wrongly assume that certain disorders only have behavioral relevance. This makes sense given their training in understanding the identification, classification, and drug/psychotherapy treatment of behavioral disorders based on symptoms. However, they have failed to be properly educated on the potential role that neuroinflammation, environmental xenobiotics, and other biological abnormalities can have on the surfacing  psychological symptoms in many patients [1]. 

Secondly, the biological basis of some neuropsychiatric disorders has clinical relevance and once recognized properly can potentially generate attention and awareness while also producing new information to be added to curriculum and continuing education. Funding for drug therapies that target biochemical/mitochondrial/inflammatory abnormalities and funding for lab testing that a patient may need could also be possible once this scientific basis and possibilitity is further elucidated. 

In regards to the link between inflammation and depression, there are still issues to consider for immune altering drug treatments since inflammation is protective against invaders and immune altering drugs may affect this process in ways that are not wanted. It is specifically chronic inflammation that plays the pathological role. However, once immunomodulators are developed for this they have to carefully be used and studied for their effects on the immune system and how they will work long term [2]. This would also apply for other neurological disorders that have been associated with underlying biological factors, such as OCD, anxiety, ADHD, schizophrenia, and autism.

Thirdly, although there is are still a lot of questions to be asked and studies to be completed, there is enough evidence thus far to at least partially educate providers about the current state of information and how it may help their patients. This would include learning about the role that diet and nutrition potentially have in disorders like depression. For example, there has already been a randomized control trial (RCT) that found a healthier diet had a positive influence on the participants’ depression and could potentially be used for other people with this mental disorder. Nutrition is being understood to play a vital role in depression and other psychiatric diseases (O’Neil, Quirk, and Jacka, 2014; Asha and Rao, 2008). In addition to this, the gut-brain axis is being studied for its role in anxiety, depression, and other mental disorders (Berding K, et al. Nutr Rev. 2016; Evrensel and Ceylan, 2015; Foster JA, et al. Trends Neurosci. 2013; Scirocco and Severi, 2015; Mayer, Knight, and Tillisch, 2014). Inflammation has also been connected to suicidal behaviors (Erhardt and Postolache, 2015). The possible cause and effect relationship between diet, inflammation, and suicide needs to be further evaluated. There are researchers  proposing a new “bio-psychosocial” perspective which looks at these interactions (Desseilles F, et al. Sante Ment Que. 2012). Another interesting study I thought I would mention is one that looked at the interaction between unhealthy behaviors (fast food, tobacco usage, alcohol, lack of exercise, etc) and its role in violent behaviors and mental health problems in Pakistani adolescents (Shah and Shafique, 2015). 

Fourthly, it is the duty of healthcare providers to provide the best quality of life possible for their patients. Informed consent and the education of patients is absolutely imperative in this. Patients deserve to know the possible side effects of anti-depressants and the possible ineffectiveness. In the cases where anti-depressants don’t provide benefit, a deeper exploration should go into the patient’s lifestyle and environment, including  their diet. 

In autism, there is emerging evidence that NAC may have efficacy; this review compared its usage to SSRIs. NAC has been shown to alter neuroexcitoxicity through its effects on glutamate. In schizophrenia, the role of inflammation and immune dysfunction is also being explored. Along with this we have adjunct therapies being studied that use supplements as an add on to drugs. An example of this would be NAC plus clozapine (Francis and Castle, 2016). Other nutritional interventions have also been studied. One I find particularly interesting is the article by Arroll, Wilder, and Neil:

“Similarly, the benefits of folate supplementation on negative symptoms were only revealed once the sample was sub-grouped by genotype; those patients who had at least one copy of the low-functioning variant of the methylenetetrahydrofolate reductase (MTHFR) gene showed a greater improvement in negative symptoms compared to the placebo group. Indeed this variant has been associated with the onset of schizophrenia [83].”

A fifth and final point to be made is there needs to be close attention to the link between obstructive sleep apnea and behavioral disorders in both children and adults (Lal C, et al. Chest. 2012; Beebe & Gozal, 2002). Unfortunately, there are flaws in our current testing methods for sleep disordered breathing that also need to be addressed (D.E. Wardly, 2014).

In closing, there is still much to be learned about mental disorders and their association with dietary, inflammatory, and immunological factors. There is accumulating evidence on these relationships and it is important that it is discussed in the field of psychiatry where the primary practice is to prescribe drugs. Drugs are not effective in every case and the subgroups within these different mental health conditions need to be analyzed with an interdisciplinary approach. This would involve looking at drug responders and non-responders along with their biomarkers. We must ask when treating symptoms with drugs is necessary and when there are cases where a root pathophysiological cause can be properly targeted.  

The exciting research looking at how social and economic environments induce epigenetic changes with inflammation and methylation also goes to show that there are a wide array of overlaps between the biological effects of people’s upbringing as well (social factors). 

And interestingly enough, similar types of biological changes can also be seen with xenobiotic and infectious exposures along with diet. It is important that absolutely everything is taken into consideration with mental health. This involves exploring and understanding the field of systems biology all the way to understanding the work from geniuses such as Carl Jung. We must continue to follow the scientific method and denounce true pseudoscience and pseudoskepticism which seeks to hinder this very process.


The artwork used in the featured image is by Cameron Gray. 

Obstructive Sleep Apnea and elevated ICP: The Next Big Autism Puzzle Piece 

I am typing this primarily for the education of readers who are interested in autism causation. As we all know, autism is multi-faceted and a spectrum; children from the “low”, “middle”, and “high” ends have variation in their symptomatology and the possible underlying causes. It is being established that autism involves neuroinflammation, mitochondrial dysfunction, and oxidative stress. It is a heterogenous disorder that has a genetic component but is not a “genetic disease” in the sense there is a consistent single-gene finding. Rather, there are 206 genes associated with autism (Autworks, n.d.).

Moreover, there are many associated factors and causes of autism which affect normal growth and development of the brain:

  • Metals (Adams et al., 2013; Al-Ayadhi, 2005; Blaurock-Busch, Amin, & Rabah, 2011; Hill et al., 2015; Rossignol, Genuis, & Frye, 2014).
  • 2, 3, 7, 8 tetrachlorodibenzo-p-dioxin (TCCD, dioxin) (Nishijo et al., 2014).
  • Organophosphates and pyrethroids (De Felice et al., 2014; De Felice, Scattoni, Ricceri, & Calamandrei, 2015; Shelton et al., 2014).
  • Air pollutants (Rossignol et al., 2014, Shen et al., 2010, Becerra, Wilhelm, Olsen, Cockburn, & Ritz, 2013).
  • Urban emissions (von Ehrenstein, Aralis, Cockburn, & Ritz, 2014).
  • High-risk behavior while pregnant like drug and substance abuse (Davis et al., 1992; Drahota, Chavira, & Stein, 2010; Ornoy, Weinstein-Fudim, & Ergaz, 2015).
  • Pharmaceutical drugs (Avella- Garcia et al., 2016; Bauer & Kriebel, 2013; Christensen et al., 2013; Harrington et al., 2014; Ornoy et al., 2015).
  • Flame retardants (Braun et al., 2014; Hertz-Picciotto et al., 2011).
  • Endocrine disrupting chemicals (Kajta & Wojtowicz, 2013; Lichtensteiger et al., 2014; Rossignol et al., 2014; Sobolewski et al., 2014).
  • Hexavalent chromium (Talbott et al., 2015).
  • Pharmaceutical agents that induce or delay labor (Cook, 1990; Croen et al., 2011).
  • Maternal infections/autoimmune disease (Ornoy et al., 2015; Estes & McAllister, 2016).

Other associated factors:

  • Zinc deficiency (Bjorklund, 2013).
  • Low iron (Chen et al., 2013).
  • Low vitamin D during pregnancy or childhood (Mazahery et al., 2016).
  • Abnormal neurotransmitter/hormone levels (Quaak, Brouns, & Van de Bor, 2013; Tordjman et al., 2013; Tostes, et al., 2012; Braam et al., 2010; Braam et al., 2013; Quaak et al., 2013; Tordjman et al., 2013; Tostes, et al., 2012).
  • Genetic polymorphisms affecting melatonin (Braam et al., 2010; Braam et al., 2013) and MTHFR (Frustaci et al., 2012; Irena et al., 2015; Pu, Shen, & Wu, 2013) which contributes to reduced glutathione, dysfunctional mitochondria, and imbalance in neurotransmitters.
  • Oxidative stress (Frustaci et al., 2012; Irena et al., 2015).
  • Chronic neuroinflammation (El- Ansary & Al-Ayadhi, 2012; Pardo, Vargas, & Zimmerman, 2005, Zimmerman et al., 2005).
  • Auto-antibodies and brain proteins/ Autoimmunity (Elamin & Al-Ayadhi, 2014; Piras et al., 2014).
  • Folate/methionine/homocystine metabolism (Frustaci et al., 2012).
  • Mitochondrial dysfunction (Rossignol & Frye, 2012).
  • Cholesterol and fatty acid metabolism (Aneja & Tierney, 2008; Schengrund et al., 2012; Wang, 2014).
  • Immune system dysfunction (Filiano et al., 2016; Streit, Mrak, & Griffin, 2004).
  • Dysbiosis/microbiota-gut-brain axis (Randolph-Gips, 2011; Finegold, 2008; Kantarcioglu, Kiraz, & Aydin, 2016).

(Sources/list collected from the work of Heather Rhodes, DHS).

Moving onward, there is still a gap in our knowledge regarding what I think is a major part of the autism puzzle. It has been identified and explained by medical doctor and researcher Deborah Wardly but needs more discussion in the public sphere and by scientists. This connection involves OSA, intracranial hypertension, and autism. Her ASD/OSA hypothesis incorporated over 90 pieces of the autism puzzle and how it is connected to sleep disordered breathing and intracranial hypertension. First and foremost, I want to give you more background information on what intracranial hypertension and obstructive sleep apnea is.

Intracranial Hypertension

Intracranial hypertension is when there is increased pressure inside of the skull; this happens when cerebral spinal fluid (CSF) is too high.

Intracranial hypertension can have several causes including systemic diseases of infectious etiology, venous sinus thrombosis, dural fistula, certain endocrine and metabolic disorders, tumors, obstructive sleep apnea, and certain drugs.1 The “idiopathic” diagnosis is made when there are no known identifiable causes. Pseudotumor cerebri is considered by the mainstream to be a rare disease and is said to occur in 28/100,000 people a year and mostly affects those who are obese and female. The “rare” label is debatable considering 91, 041 per year (90K/year) is considered by some scientists to actually be significant. There is still much argument over this disease considering the pathology and etiology is not completely understood.2 The presentations of intracranial hypertension usually include headaches, dizziness, vision loss, double vision, nausea, and pulsatile tinnitus.3 It is said to be rare but this is a highly debatable claim. The possible issue is under-reporting due to not all cases presenting with optic nerve swelling. Idiopathic intracranial hypertension can occur without visual symptoms but it is considered to not be common. However, if people have IIHWOP (Idiopathic Intracranial Hypertension Without Papilledema) and are diagnosed with typical migraines and never receive a lumbar puncture, this will go under the radar. It has been stated by some researchers that the rates of IIHWOP are unknown.4

Sleep apnea


Sleep apnea is a disorder where someone repeatedly stops breathing during sleep or has shallow breathing during this time. It has significant impacts on brain function and leads to higher morbidity and mortality.5 When left untreated in children, obstructive sleep apnea can lead to learning, behavioral, and other health problems.6  Unfortunately, there are problems related to the diagnosis of OSA because sleep study results can be inaccurate. The American Academy of Sleep Medicine had a statement that allowed sleep labs to use different criteria regarding hypopnea (overly shallow breathing) and this resulted in different interpretations and diagnoses depending on what criteria was used.7 Parents can also miss the signs of sleep disordered breathing in their children and SDB can even lead to ADHD, so noticeable excessive sleepiness is not necessary for the existence of sleep apnea either. It was demonstrated through a study that the 2007 AASM criteria diagnosed only 19% of a study group with sleep disordered breathing while 99% of the study group were diagnosed properly when Stanford criteria was used. This is very significant. Esophageal manometry is also more sensitive for detecting SDB but is not commonly used or studied for its correlation with behavioral disorders.

Furthermore, OSA can be an underlying factor in autism and treatment can result in behavioral improvement.8 It is extremely important that proper sleep studies are put into place so we can have accurate diagnoses and treatment plans related to sleep disordered breathing and the resulting biological effects. OSA can co-exist in some patients with intracranial hypertension (through a possible common cause, jaw anatomy) and the overlaps between autism and sleep disordered breathing have been identified alongside the findings that suggest elevated ICP may be related autism:

Pertinently enough, sleep is also known to clear the brain of waste products. Lack of sleep leads to significant cognitive problems and health issues which are possibly related to this. Sleep is needed to flush out toxins and dysfunction of this process can have consequences. Cerebral spinal fluid is managed by the glymphatic system with the brain’s neuroglia; this is an area of research that is currently a hot topic given it was first published in 2015 in Nature that the lymphatic system was connected to the brain and potentially related to numerous neurological disorders.

“The scientists examined layers of tissue, known as meninges, that cover the brain and contain blood vessels and cerebrospinal fluid. While searching for structures associated with the meninges, the researchers noticed vessel-like patterns. These vessels contained markers of the lymphatic system. By injecting dye into anesthetized mice and tracking its path, they found that the vessels carried fluid and immune cells from the cerebrospinal fluid, along veins in the sinuses, and into nearby deep cervical lymph nodes. The researchers surmise that these vessels may serve as a second step in the drainage of fluid from the brain, after it’s drained into the cerebrospinal fluid through the glymphatic system.”

Additionally, this year it was also reported that elevated extra-axial CSF in infants was associated with later diagnosis of autism:

“A national research network found that many toddlers diagnosed with autism at two years of age had a substantially greater amount of extra-axial cerebrospinal fluid (CSF) at six and 12 months of age, before diagnosis is possible. They also found that the more CSF at six months — as measured through MRIs — the more severe the autism symptoms were at two years of age.”

Although this is extra-axial CSF (rather than just CSF on outside of the brain which is more related to intracranial hypertension), the authors still think this has to do with improper CSF flow. 

Cerebral spinal fluid protects the central nervous system. It’s main purpose is to protect the brain from trauma, supply nutrients, and carry out waste products. However, when it becomes too elevated, we obviously run into some very serious problems. The glymphatic system will be a huge part in understanding intracranial hypertension of idiopathic origin and other secondary causes. The glymphatic system has been more seriously studied and considered since it was first published about in 2015; this means that much more research is needed so we can understand the lymphatic system’s role in neurological disorders as a whole. We must ask the right questions such as “Why are people presenting with symptoms of a brain tumor without having an actual tumor? Why do they present with symptoms of head trauma even without an identifiable physical cause? Why does the brain end up increasing the CSF as if it has been injured? What possible toxicants can lead to blood-brain barrier disruption and affect the immune and glymphatic system to the point there is CSF build up?”

This is something I also wanted to bring attention to since I have not seen any other articles from anyone discussing it. I found a case study that found increased intracranial pressure following DTP immunization. The authors here noted that there is a problem with under-reporting of adverse events following vaccines because of the difficulty connecting the vaccine to the negative reaction. However, when it happens within 24-48 hours, people should be suspicious of the connection. The question remains, can vaccines contribute to chronic CSF build up and through what mechanisms does this happen? Can this occur slowly over time with repeated exposures and go unidentified due to the time gaps? 

In closing, there are several problems we still face concerning the treatment of autism. With OSA and intracranial hypertension, we possibly have under-diagnosis due to the lack of studies on the issue and the inaccurate sleep testing that is offered. The autism community needs to actively study and talk about these connections. Both conventional and non-conventional health professionals have grossly underestimated the link between obstructive sleep apnea and autism as well. Routine screening for sleep disorders should be done in patients who present with behavioral problems that have been linked to obstructive sleep apnea and sleep disordered breathing. Additionally, more sensitive and accurate testing with well defined criteria (like Stanford’s) should be used. It is unfortunate that there are not non-invasive ways of measuring ICP, although they are being discussed and suggested.9 This has lead to great difficulty in getting diagnoses for elevated intracranial pressure that may be associated with autism. Still, this problem requires further research so that we can better understand, treat, and manage the possible elevated ICP and sleep disordered breathing in those with ASD.











Misinformation Espoused by Proud Social Skeptics (Academics and Otherwise)

I’m sure if you live on planet earth and are up to date with the vaccine debate you know who Dorit Reiss is. She is omnipresent on the internet; if you bring up vaccine risks, bet the person next to you 20 bucks that she will show up and see how long it takes before that prediction comes true (wink). For the purpose of this post I will be identifying some of the misinformation she has posted on twitter.


“Autism isn’t encephalitis” she says, as she compares photos of a normal brain to an autistic and encephalitis stricken brain. Firstly, she fails to differentiate between encephalitis and encephalopathy. When researchers discuss brain inflammation in autism they are not always speaking about encephalitis induced by a viral or bacterial infection. I cannot comment entirely upon the images shown because she cites no source and has failed to respond to my request for the citations used for the comparison (needed to determine the accuracy of methodology), but I can prove how the images are misleading and that in fact brain inflammation is associated with autism. Vaccine-induced encephalitis does happen as well, but what is much more common in autism is chronic neuroinflammation.


Neuroinflammation is inflammation of the nervous tissue. It may be initiated in response to a variety of cues, including infection, traumatic brain injury, toxic metabolites, or autoimmunity.”










Dorit fails to understand how underlying neuroinflammation can influence and directly cause certain behaviors. These behaviors fall under DSM-5 criteria used in autism diagnoses. Pseudo-skeptics fail miserably at separating underlying biological abnormalities from neurobehavioral disorders. This is something that they maintain in their arguments for the purpose of avoiding the grim reality and defending interest groups. Moreover, Dorit is using complexifuscation:

Complexifuscation – the introduction of similar signals, inputs or measures, alongside a control measure or an experimental measure, in an attempt to create a ‘cloud of confusion or distraction’ around the ability to effect observation, control or measure of a targeted set of data. Preemption of a phenomena with in-advance flurries of fake hoaxes, in order obscure the impact, or jade the attention span of a target audience, around a genuine feared phenomena

Dorit has succeeded at creating a cloud of confusion and distraction surrounding the topic of autism etiology and pathophysiology. Researchers and even parents want a specific set of data studied on autism biomarkers including the presence of neuroinflammation. She solely defines autism by behavioral characteristics and signals while separating it from underlying medical/biological problems that cause those exact same characteristics to come into being. By doing this she has been able to obfuscate the true causes of those very behavioral disorders in a statistically significant part of the population.

In addition to that, Dorit also uses misleading memes such as this one:



(This meme is misleading and disingenuous for several reasons that are outlined here and here).

Pertinently, (something else she also conveniently ignores) is that the peer-reviewed journal EHP came out with a project known as TENDR (Targeting Environmental Neuro-Developmental Risks) and they discuss the very risks that environmental exposures pose to children’s brain health.

CONCLUSION: Based on these findings, we assert that the current system in the United States for evaluating scientific evidence and making health-based decisions about environmental chemicals is fundamentally broken. To help reduce the unacceptably high prevalence of neurodevelopmental disorders in our children, we must eliminate or significantly reduce exposures to chemicals that contribute to these conditions. We must adopt a new framework for assessing chemicals that have the potential to disrupt brain development and prevent the use of those that may pose a risk. This consensus statement lays the foundation for developing recommendations to monitor, assess, and reduce exposures to neurotoxic chemicals. These measures are urgently needed if we are to protect healthy brain development so that current and future generations can reach their fullest potential.

Pseudo-skeptics and con artists such as Dorit can deny facts as much as they want and further fuel their cognitive dissonance; this however does not change the scientific evidence or the reality that children and their parents currently face when it comes to disability. There are also societal consequences to this that branch out and affect multiple areas of existence and potential prosperity. We are not claiming that all neurobehavioral problems have the same cause; rather, we want the public to be educated on the current state of knowledge regarding causes that have been identified and associated with these issues. This includes potential causes that are still being studied. We find that it is absolutely necessary that parents have the ability and right to avoid certain exposures where there is doubt and a lack of solid conclusive evidence of their safety. We favor the precautionary principle over interest groups’ opinions and shoddy (poorly designed) studies that reach specific conclusions too hastily. We also favor transparency, plurality, and the scientific method over proof gaming, the argument from ignorance, and the existential fallacy of data.

In closing, genetic and environmental factors both have a place in determining behavioral and social skills. Autism is multifactorial and epigenetic—involving an interaction between a genetic background and environmental exposures (triggers). Various phenotypes have been identified and the classifications are supported by scientific evidence. I recommend reading James Weiler’s evidence-based book “The Environmental and Genetic Causes of Autism” for further edification. Some important messages from his book are on the importance of adhering to the scientific method and always asking questions. An important question to ask yourself now would be “Where do we all go from here?”


Scientific Consensus or Political Consensus? 

In scientific debates surrounding controversial topics we commonly hear the claim that scientists are the experts who shape consensus based on the facts and available evidence. If anyone questions the “evidence” or the conclusions of this consensus (including other scientists and health professionals) they are anti-science, pseudoscience peddling loons (or any other number of pejoratives frequently used). 

Once we understand the conceptualization of social skepticism and what it derives from we can further understand the edifice of psuedo-skepticism and its faulty interpretation of reality (what is subjective and mistaken as objective). 

The first mistake is to assume that scientists somehow dictate scientific reality. Scientists describe, measure, investigate, identify, and study phenomena. Through experimental investigation, and most importantly, asking questions, we build upon our knowledge base and can establish facts. The scientific method is a process and establishing facts requires rigorous science, question formulation, and laborious investigation. “Facts” must be differentiated between the social skeptic version:

¡fact! – lying through facts. Data or a datum which is submitted in order to intimidate those in a discussion, is not really understood by the claimant, or rather which is made up, is not salient or relevant to the question being addressed, or is non-sequitur inside the argument being made. The relating of a fact which might be true, does not therefore mean that one is relating truth.

Social skeptics use this quite often when citing studies that they have never even fully reviewed in order to claim that the said ¡facts! support their conclusion. They even throw ¡facts! around when people are merely asking questions. It is a way that they attempt to halt discussion on the issue under the guise of the so-called “facts” already being established and accepted (thus being incontrovertible and free from criticism). 

I will provide an example. Here is a citation that has been thrown around with ¡facts! but is poorly designed and lead to questionable conclusions. 

Jain, A., Marxhall, J., Buikema, A., Bancroft, T., Kelly, J., Newschaffer, C. (2015). Autism occurrence by MMR vaccine status among US children with older siblings with and without autism. Journal of the American Medical Association, 313(15). doi:10.1001/jama.2015.3077.

The people using this do not necessarily understand the research methods and how the data is being used. When an independent scientist reviewed this study she found issues with the statistical testing. The authors also ignored statistically significant findings in the 5 year old group. It is another study being used in support of a specific conclusion but the avenue to this conclusion is flawed within itself. 

With regards to consensus, here are some definitions to start with for a better understanding:

Consensus – is the collective judgment, position, and opinion of the community of scientists composing a particular field of study. It is not a popularity poll among scientists in general or even necessarily inside the field of study in question. Consensus can only be claimed when multiple opposing explanatory alternatives have been researched in objective detail, and a reasonable body of those scientists who developed the field of opposition alternatives, have been convinced of the complimentary alternative’s superiority. Just because a null hypothesis exists, and only that hypothesis has been researched, does not provide a basis for a claim to consensus, no matter how many scientists, or those pretending to speak for science in the media, favor the null hypothesis.

Consensus Appeal to Authority – in so far as scientists speak in one voice, and dissent is not really allowed, then appeal to scientific consensus is the same as an appeal to authority.

Interestingly enough, those claiming to represent the side of consensus don’t have a complete grasp on the meaning of consensus. 
Here, I will speak specifically about the contention that vaccine safety is proven and agreed upon through the consensus of experts. On the issue of vaccine safety, have multiple opposing explanatory alternatives been researched in objective detail? Specific parts have indeed been researched and the purported safety of vaccines has not only not been proven, it has been proven otherwise.1 Other specific parts have not been researched objectively in detail. For example, to this date, there are no robust long-term prospective unvaccinated versus vaccinated studies looking at total health outcomes in US children who have followed the full schedule versus children who have not been vaccinated. There aren’t randomized control trials on the vaccine schedule either because it is claimed that it is “unethical” to do that type of study and leave children without vaccines. Vaccines are also labeled as biologicals instead of pharmaceuticals – with this classification they have been able to avoid the FDA research standard. The studies used to “prove” safety and refute causation are epidemiological and by methodology cannot even do what they are claiming.2 

All scientific work is incomplete—whether it be observational or experimental. All scientific work is liable to be upset or modified by advancing knowledge. That does not confer upon us a freedom to ignore the knowledge we already have, or to postpone the action that it appears to demand at a given time.3

Within the framework that social skeptics have created the core of their argument is a consensus appeal to authority. Once you understand and identify this (you can do this easily in a debate—pick any social media website and bring up the topic of vaccines and count how many times this is used) you will see how banal pseudo-skeptics are, yet how crafty and sophisticated they are with rhetoric, the deceptive usage of language, misrepresentation of data, method, science, and assumption. Some of them are better at it than others but you will see similar tactics even amongst the varying degrees of developed sophistication within the social skeptic crowd. 

Another example would be the statement “The dose makes the poison.” Here we can identify it as falling under these terms:

Ingens Vanitatum Argument – citing a great deal of irrelevance. A posing of ‘fact’ or ‘evidence’ framed inside an appeal to expertise, which is correct and relevant information at face value; however which serves to dis-inform as to the nature of the argument being vetted or the critical evidence or question being asked.

Ambiguity – the construction or delivery of a message in such words or fashion as to allow for several reasonable interpretations of the context, object, subject, relationship, material or backing of the intended message.

“The dose makes the poison” is both misleading and true depending on the context. At face value it is correct and relevant but it ultimately disinforms those who are asking questions and bringing up specific arguments about the various factors involved in a poison (a substance that causes injury, illness, or death, especially by chemical means). “The dose makes the poison” is also ambiguous. One reasonable interpretation of this is that “dose makes the poison” translates to “low doses are not poisonous.” If you have a debate over environmental exposures “dose makes the poison” is usually used when the claimant is arguing that the levels of chemicals (xenobiotics) we encounter are in “too low” of doses to cause any possible harm to an organism. When discussing aluminum adjuvants we also hear social skeptics say that “the dose makes the poison.” You want to know something both interesting and ironic about this? The dose does make the poison with al adjuvants; however, it is actually the low doses in vaccines that are more harmful—the exact opposite of what they are claiming. They are not clear in their statement either and should modify it to fit the true intended meaning, but this is not what they do, and there is a reason for this. It is successfully sophistical. 

Crepeaux (paper): Non-linear dose-response of aluminium hydroxide adjuvant particles: Selective low dose neurotoxicity

The low toxicity of the higher dosages appears to be a consequence of dosage-dependent inflammation at the injection site. The high dosages caused intense inflammation at the injection site, forming “granulomas”. The 200 mcg/Kg dosage did not produce granulomas. Granulomas are hard nodules in tissue produced in response to injury, infection or foreign substances. Its a way the body “walls off” injured tissue and prevents the spread of infection or toxins. The granulomas apparently prevented Al adjuvant particles from leaving the injection site. This explains why the 200 mcg/Kg dosage affected the brain and behavior, while the higher dosages did not.

(The aluminum adjuvant used was Alhydrogel. This is used in the tetanus, Hep A, Hep B, HiB, pneumococcal, meningococcal, and anthrax vaccines. This study found that the lower dosages were actually more toxic than the higher doses used.)

It is also stated that the “consensus” is that aluminum adjuvants are safe and you ingest more aluminum than you inject (Ingens Vanitatum Argument – the second statement is true, but there is a difference in mechanisms, kinetics, and affected tissues). 
Ingested aluminum cannot be compared to injected aluminum since injected aluminum is more metabolically available and ingested aluminum has lower absorption (0.1-0.4% and .5-5% for al citrate). Again, “the dose makes the poison” is a common and inaccurate one-liner/argument people have regarding this issue, but it is overly simplistic and not aligned with modern science on the kinetics of aluminum adjuvants. 

The reason that there are vaccine-injuries is because of several factors, many involving genetic susceptibility. We do not entirely understand every single susceptibility factor involved—but we do understand some of them. We have enough science to further support the precautionary principle in this matter. More unbiased scientific research is needed of course, but even then, the science already available is overwhelmingly crucial yet remains unacknowledged and even denied by people and health authorities who wish to vigorously defend the vaccine schedule. Aluminum adjuvants are not safe for everyone and comparing them to ingested aluminum is highly misleading. You cannot scientifically compare studies of ingested water-soluble aluminum salts such as Al-lactate or AlCl3 to establish safety regarding injected aluminum adjuvants made of aluminum hydroxide/aluminum phosphate nanoparticles. The chemicals and route of administration are both different and the well designed animal studies thus far have shown that low doses of al adjuvant cause brain inflammation. 

(This information was collected from VaccinePapers, a highly recommended evidence-based science website with citations. On this link you can learn more about the study and how the childhood vaccine schedule poses a risk with the amount of aluminum that is injected.)

The analyses used in support of aluminum adjuvant safety (Mitkus and Keith) are also scientifically flawed. These are used by the FDA and other health authorities, and in turn, this is used by other major health organizations who misinform doctors that aluminum adjuvants are completely safe. The very people claiming to be experts are getting their information from other “experts” who are using pseudoscience. Having the label or status of an expert does not somehow negate the unsound evidence being used in support of a specific conclusion. The evidence should be objectively studied and analyzed—and it has been. It is found to be erroneous. You can learn more about that here as well. 

There is the issue of al adjuvant toxicity, but there is also the issue of immune activation (including postnatal) and its role in brain injury. We know that immune activation (from infections) during pregnancy has been associated with schizophrenia and autism. What wasn’t entirely understood in the beginning was how vaccination could also activate the immune system in such a way to also cause damage. Now the science on cytokines, neurons, glial cells, purkinje cells, and microglial activation has given us more information on why immune activation causes damage to the fetal brain and how immune activation is related to conditions such as autism. 

It is an incredibly heated and complex debate, but the existing science shows that vaccines can and do in fact cause damage. If someone presents the false and specious dilemma to you that you must be either “pro-vaccine” or “anti-vaccine”, they are being dishonest. Not everyone is arguing that vaccines have never prevented disease or that they are not needed. Many vaccine skeptics are simply giving the facts and showing the holes that exist in the research that claims vaccines are safe and effective. 90% of infectious disease mortality was also on the decline before vaccines were even introduced – another fact that is rarely mentioned by those who claim to be “pro-vaccine”. 

For clarity: Guyer et al, “Annual Summary of Vital Statistics: Trends in the Health of Americans During the 20th Century”, PEDIATRICS, 2000.

“Once again, nearly 90% of the decline in infectious disease mortality among US children occurred before 1940, when few antibiotics or vaccines were available.”

If someone makes the claim that vaccines are responsible for saving all of those lives from infectious disease, they are wrong.
People are afraid to not vaccinate because of the threat of infectious disease and the supposed herd immunity that mass vaccination gives, but they should also be afraid of risks that do in fact exist and are not disclosed to parents. You have to understand each disease and vaccine available before you come to a complete conclusion on what to do for your child; you also have to understand the risks, which for many, far outweigh the benefits. You can learn more about the science of each vaccine and its ingredients here. You cannot force someone to vaccinate when there is a risk to their child that will negatively affect them the rest of their life. Unfortunately, the risks are usually unknown and unheard of until after the event of vaccine injury occurs. It is also unethical to tell everyone to vaccinate when there is experimental and observational evidence that vaccines cause damage to a genetically vulnerable sub-population (which major organizations have refused to properly study in order to prevent other people from being harmed). 

IOM, pg. 127

What is even more unethical is when proper research is blocked or never completed because social skeptics, health organizations and biased scientists assume that vaccine safety is already proven and anyone who suggests otherwise should be shamed and ridiculed. The scientists, doctors, and parents who do speak out are considered “anti-vaccine loons” even when they bring up valid concerns. The fact that a majority of health organizations and doctors state that vaccines are completely safe does not make it so. What would make that statement a fact would be if the scientific evidence supported it, but the scientific evidence in favor of that conclusion is actually lacking and distorted because of biased and poorly designed studies. Immunity is a very complex subject and every person does not respond exactly the same; the “one size fits all” approach does not work when it comes to vaccination. It isn’t that we want vaccination to be stopped—it’s that we want vaccine injuries to be stopped. We want the at-risk groups to be studied so that we can prevent future injuries in people who also share that susceptibility. We also don’t know the true “benefit to risk” ratio of vaccination because adverse reactions to vaccines are not properly reported. Less than 10% are reported and physicians don’t encourage patients to report when there are visible symptoms following vaccine administration. And even when parents do take their concerns or observations to doctors, many times they are told that “It can in no way be related to the vaccination and is just a coincidence. Correlation does not imply or equal causation.” 

Furthermore, there are other problems we face when it comes to VAERS. Two variants of complexifuscation will be explained here. 

Complexifuscation – the introduction of similar signals, inputs or measures, alongside a control measure or an experimental measure, in an attempt to create a ‘cloud of confusion or distraction’ around the ability to effect observation, control or measure of a targeted set of data. Preemption of a phenomena with in-advance flurries of fake hoaxes, in order obscure the impact, or jade the attention span of a target audience, around a genuine feared phenomena.

In quotes below you will see how this was explained by a special scientist friend of mine (articulated perfectly – I could not summarize this any better than the given description). 

Hiding Through Data Flood 
“The VAERS database of vaccine injury is one example. – There are tens of thousands of vaccine injuries each year, and in order to mask this statistic, the Department of Health and Human Services has created a database where not only are those injuries recorded, but EVERY side effect of a vaccine is also reported. So rashes, slight fevers, ‘didn’t feel good’ reports come in by the hundreds of thousands and squelch out both the usefulness of the database and the ability to spot ‘permanent disability through encephalopathy’ data. It is a way of killing an idea by tendering the appearance of giving it overwhelming attention.

Hiding Through Cladistic Categorization
“Autism is a great example here. In this method of counter-intelligence, you take a threatening data trend, and in order to mask its growth – you start identifying subcategories inside the malady so that old numbers are apples-to-oranges in comparison to new numbers. You cannot track the 1970’s ‘autism’ stats versus the 2010’s autism because there are so many gradiations now. Incumbent in the Cladistic Complexifuscation tactic, is the built in excuse when any growth is observed = ‘Well it is simply a case of increase in diagnosis, ability to detect and maladies which used to not be included, which are now included.” This is how Steven Novella attempts to diffuse the topic.”

Moreover, as I have stated before, there are also no well designed prospective studies comparing total health outcomes between the vaccinated and unvaccinated so that we can better understand the effects. Pharmaceutical companies refuse to label vaccines as drugs; this makes it to where they do not have to do the same type of thorough safety studies like the ones that are completed on pharmaceuticals. It is purported that vaccines do not have negative effects and that vaccinated children are healthier in totality while unvaccinated children are dangerous. We have to move beyond the argument from ignorance that asserts that “a proposition is true because it has not yet been proven false, or is false because it has not been shown to have any evidence” and the existential fallacy of data “the implication or contention that there is an absence of observation or data supporting an idea, when in fact no observational study at all, or of any serious import has been conducted by science on the topic at hand.” 

We constantly see doctors and nurses claiming they are the experts (next in line to the scientists who support the conclusions they espouse) and that we unqualified plebs better take a step back. Unfortunately for them, their claims are rooted in erroneous conclusions and social skepticism. This means that what they are saying is not “settled science” but rather deceptive rhetoric influenced by deep indoctrination and a lack of information. No amount of adverting to asserted consensus or authority will change the scientific method or epistemological accuracy. 

The nurses and people in medical school who make these claims have been taught how to administer vaccines and/or that vaccines are life saving, safe, and effective, and that that’s all there is to it. They are given courses in immunology and microbiology as well. However, they are not given the facts about the 1986 National Childhood Vaccine Injury Act, the national vaccine injury compensation table of injuries, the science of aluminum adjuvant neurotoxicity, thimerosal neurotoxicity (thimerosal is still in multi-dose flu shots), the science of immune activation and its role in brain disorders, or how to discern the difference between sound research methods, biased science, and research flaws/manipulation. They are given one side of information and in many cases misinformation in regards to safety. You cannot expect to see the whole picture if you take advice and listen to people who only give one specific side of regurgitated one-liners. Aside from the pretentiousness and hubris of these purported “experts”,  we also have to understand most of these people genuinely think they are doing the right thing. 

In closing, it is essential that you understand the differences between political consensus that is derived from deception and scientific consensus that is formed through the proper usage of the scientific method. Political consensus has to do with the politicization of science and agenda driven misinterpretations of data, information collection, and epistemological solecism that is used in order to cite a false consensus that would not even exist if scientists were given the complete information from both sides (along with being properly informed about the lack of data on the given subject and the reasons why you shouldn’t jump to a conclusion precipitately and wrongfully). Political consensus covers the social and political dimension of subjective interpretation in social skepticism and pop science. The antithesis to this is scientific consensus that properly follows the scientific method through arriving at conclusions based on time, objective understanding free of human bias, meticulous consideration, and at the apex—ethical skepticism.



Human Studies that Indicate Autism/Vaccine Link

Click to access DNA_Contaminants_in_Vaccines_Can_Integrate_Into_Childrens_Genes.pdf

Click to access IJVV-04-00072.pdf



Definitions worth learning:

Appeal to Tradition (argumentum ad antiquitam) – a conclusion advertised as proven scientifically solely because it has long been held to be true.

Appeal to Probability – the false contention of a skeptic that the most probable, simple, or likely outcome in a set of highly convoluted but unacknowledged assumptions, is therefore the compulsory or prevailing conclusion of science.

Appeal to Ridicule – an argument is made by presenting the opponent’s argument in a way that makes it appear ridiculous.

Appeal to Scientific Democracy – the contention that if the majority of scientists believe something to be true, regardless of epistemological merit, then it must be assumed as true.

Appeal to Scientists Fallacy
– an argument that is misrepresented to be the premise held true on the part of the prevailing group of scientists; or concludes a hypothesis (typically a belief) to be either true or false based on whether the premise leads to a more successful career in science.

Appeal to Skeptic – citing a skeptic as an authority, recitation or expert witness on a subject or observation, when a skeptic in reality provides no particular relevant expertise. In recitation rules, not qualifying as an authority. Under the Rules of Federal Evidence, skeptic testimony is the lowest ranked of any kind, being ranked under eyewitness testimony, not possessing any particular expertise other than a specious claim to know the scientific method, or lacking in the court’s Duty of Candor.

Appeal to Skepticism Position – the argument assumption or implication that an opinion possesses authoritative veracity or a proponent possesses intellectual high ground simply through allegiance to a consensus skeptical position on a topic.

Appeal to Skepticism Status – the declaration, assumption or implication that a consensus skeptical position on a topic is congruent with the consensus opinion of scientists on that topic.

Appeal to Skepticism Fallacy – the presumption or contention that taking a denial based or default dubious stance on a set of evidence or topic is somehow indicative of application of the scientific method on one’s part, or constitutes a position of superior intellect, or represents a superior critical or rational position on a topic at hand.

Appeal to Tradition (argumentum ad antiquitam) – a conclusion advertised as proven scientifically solely because it has long been held to be true.

Argument from Incredulity – the contention that because something is too difficult to imagine or possibly exist, then this is proof that it does not exist.

As Science as Law Fallacy – the implication or assumption that something is ‘innocent until proven guilty’ under the scientific method, when in fact this is an incorrect philosophy of hypothesis reduction. 

Bunk Nauseam Fallacy – the argument that a point is invalid by implying or citing incorrectly that the topic has been de-bunked many many times, and is now nothing but an irritating myth inside circles of stupidity.

Cannot be Reliably Tested Error – the malpractice of disqualifying a subject, study or researcher from science by citing that it has not been or cannot be tested or reliably repeated in testing. When in fact many conclusions of accepted science fall under such a reality. This often is achieved through blocking its access to the scientific method, ignoring the topic, conflating the scientific method with the experimental method, ignoring discovery science protocols, refusing to research/test the contention, or misrepresenting its appropriate next steps or empirical questions, and further then citing that therefore the subject has failed the necessary testing methods of science.

Cherry Picking – pointing to a talking sheet of handpicked or commonly circulated individual cases or data that seem to confirm a particular position, while ignoring or denying a significant portion of related context cases or data that may contradict that position.

The World of Autism and the False Dichotomy; It’s Not Just Black or White

1. “Autism is either environmental or it’s genetic.”

2. “You’re either pro-autistic (the qualifier being you’re a neurodiversity advocate) or you’re anti-autistic.”

3. “Vaccines either cause all autism or they do not cause autism at all.”

4. “You’re either anti-vaccine or you’re pro-vaccine.”

These are examples of false dichotomies to look for when you’re viewing discussions about autism. Let’s examine all four of them.

Firstly, what is a false dichotomy? A false dichotomy fallacy involves using two different options as if they were the only possible ones. This type of reasoning can be seen as “Either B or A” when in fact both could be false or there are more alternatives. When people use this reasoning they can also say “Claim B is true therefore claim A is false” or “Claim A is false therefore claim B is true.” It is faulty binary reasoning that can be used to obscure and avoid other possible answers that involve different factors, contexts, and conditions. It is also known as the “black-or-white” fallacy, bifurcation fallacy, and false dilemma.

Proposition number 1 states that there are two options for autism causation: genetic or environmental. This is misleading because research shows that autism involves genetics and the environment rather than just one of the two.1 An open discussion should not present itself in such a way that people cannot openly consider other factors or combinations of these factors.

Proposition number 2 states that you are either pro-autistic if you’re a neurodiversity advocate or you are anti-autistic if you are not. This only gives two options when there are actually more. To start with, we have to ask what it means to be “pro-autistic.” This can have several meanings and we will approach this statement (as an example) as if it is being specifically given by someone who is using vagueness and not clearly/thoroughly defining the meaning of the word in the given context of their statement. Does being “pro-autistic” mean that you want acceptance of autism? Does being pro-autistic mean you want people to respect those with autism? Does being pro-autistic mean that you want the healthcare of autistic people to be covered and there be adequate options for maintainence, care, and access to special education? What if you agree with most of those but you disagree with one? Are you suddenly “anti-autistic” for doing so? I have written about my position on this issue and I have replied to a neurodiversity advocate as well.2 I am not a neurodiversity advocate for several reasons, one being that I do not want to associate with a group that has largely denied the fact a statistically significant portion of autism cases are caused by environmental and genetic interactions rather than just something that is a psychologically inborn difference. Autism in its entirety is not  “positive” and we have to understand the experiences from different viewpoints rather than assuming that autism is automatically a gift. This is not to say that it isn’t a gift for some or that there aren’t positive things about autism for some people. Moreover, we should not overlook the suffering or the scientific evidence that exists so that we can instead favor a distorted view shaped by opinions and partial information. I am not “anti-autistic” because I am not a neurodiversity advocate in the same exact way that others define themselves as neurodiversity advocates. Someone framing the argument in such a black and white way is going about it through their own arbitrary interpretation rather than reasoning that considers all possible facets. I would be considered “pro-autistic” by the standard of caring about autistic people, wanting those with autism to be listened to/studied properly and advocating for autistic people to have proper access to healthcare and education. In addition to this, I also want the cases of autism caused by harmful environmental exposures to be prevented and I want those who suffer from co-morbidities to have proper treatment (including treatment for ongoing brain inflammation). There are more factors involved and ways of approaching this issue.

Proposition number 3 states that vaccines either cause all autism or they don’t cause autism at all. This does not consider all factors or possible answers. Vaccines cause autism in susceptible individuals but they don’t cause every single case of autism because autism has more than one cause.3 The fact that not all cases of autism are caused by vaccines does not mean that they don’t cause autism in a specific subgroup. One has to understand the science and circumstances which give rise to autistic behavior and how many biological factors underly autism etiology.

Proposition number 4 is one of the most commonly seen uses of the bifurcation fallacy. “You are either anti-vaccine or you are pro-vaccine.” I first encountered this reasoning when debating someone over potential vaccine risks and the research that was needed and had not been done yet. They claimed that me merely questioning vaccine safety was pushing me into the “anti-vaxx” category (celeber cavilla fallacy). They were approaching this from the position of someone who pushes the view that vaccines are completely safe and effective and hold no risks, and anyone who questions or denies this proposition must be an anti-vaxx, anti-science moron who wants infectious disease to return. The pigeonholing did not serve to help their argument. Rather, it showed that they could not look beyond “black or white” thinking or question what they’ve been told by perceived authorities. My actual position was that the at-risk subgroups needed to be studied further to mitigate the risk and there was enough science to warrant further research as well as caution. I did not claim that vaccines were never useful or harmed every single person; I was pointing out certain science and observational accounts that put into question the efficacy, safety, and “one size fits all” viewpoint of vaccine usage. We have to move beyond the two-sided “anti” and “pro” nonsense to actually analyze and interpret the arguments  being given.

The use of pigeonholing, false dilemmas, oversimplification, and making assumptions about your opponent’s position is not lending you intellectual credibility. Let’s move beyond “group think” and listen to one another so we can have objective, open and fruitful dialogue.



The Environmental and Genetics Causes of Autism


The Environmental and Genetics Causes of Autism

In Defense of Dr. Neides

Recently we have seen health professionals and other people villifying the doctor who wrote this controversial (and now removed) article:

While I am not going to address every claim by this doctor, I am going to defend him for bringing attention to this important issue—vaccine safety.

The backlash is to be expected from people who have not critically evaluated all of the existing scientific literature. They continue to believe what they are told by the WHO, FDA, and CDC regardless of what science exists that contradicts studies and statements put forth by these (and many other) organizations. Many are saying what this doctor has published is “dangerous” because it can lead people to (God forbid) question vaccine safety. Scientists, doctors, and laymen have rightfully questioned  vaccine safety because there are valid concerns. Clinical observation has time and time again implied the potential connection but further scientific data has actually shown the probable mechanisms behind vaccine-induced injury. This evidence is there for those willing to research laboriously.

Now, back to this article I am referencing. There is a plethora of ignorant comments in the comment section but I have chosen to write a reply to the comment made by Kevin Folta. I won’t go into his background as I am sure many of you already know who he is, but if you wish to look further you can make a quick Google search.
Here are snapshots of his comment:



Here is my reply:

I won’t reply to every part of your comment, Kevin, but I will point out the specific parts that are erroneous. First, let’s start with your comment that “It is well known that ethyl mercury has limited toxicokinetic properties and is eliminated from the body and poses little risk.” This assumption is false and based on pseudoscience that is pushed by the vaccine industry and many other health organizations. Ethylmercury is a mitochondrial toxin and especially injurious for those who have mild mitochondrial defects and are susceptible to its exposure. Thimerosal might be involved in the pathogenesis of autism in this subset of children. (Sharpe et al., 2013; Sharpe et al., 2012). Disorders of the mitochondria are also not rare in the autism community and individuals can acquire mitochondrial dysfunction through environmental toxins lacking a familial link. (Frye et al., 2013). 


Small amounts of thimerosal even induce changes in gene expression in the cerebellum. In the conclusion of Minami et al. (2010): “The present study helps to support the possible biological plausibility for how low-dose exposure to mercury from thimerosal-containing vaccines may be associated with autism.” It has also been long confirmed in animal studies that ethylmercury in doses from the vaccine schedule (or lower) causes damage neurologically. (Rodriques et al., 2010; Olczak et al., 2009; Qvarnstro et al., 2003; Burbacher et al., 2005; Magos et al., 1985). 

Furthermore, glutathione is the most powerful anti-oxidant in the body and has been shown to be depleted in children with autism (Rose et al., 2012). Thimerosal is shown to cause glutathione depletion, which may demonstrate exacerbation of neurotoxicity (James et al., 2005).

There is a 2014 study (Rooney, J., 2014) that documented the half-life of inorganic mercury in the human brain, which can last “several years to several decades.” It was thought before that vaccines containing ethylmercury (which is in flu vaccines as a preservative) couldn’t be compared to inorganic mercury. Inorganic Mercury is extremely neurotoxic and we now know that thimerosal containing vaccines do uptake in the brain as inorganic mercury where it can accumulate and remain for the individual’s life (Burbacher et al., 2005). The inorganic mercury concentration in the brains of ethylmercury exposed monkeys in the Burbacher study is up to 4.6 times higher than in the blood at 2 days after the last injection. The ratio increased as sacrifices were performed at a longer duration from the last dose. Furthermore, the thimerosal exposed monkeys had higher levels of mercury in the kidneys when compared to the methyl mercury monkeys. Something that vaccine advocates are quick to point out is that the ethyl mercury clears the blood at a higher rate, which is true, but both mercury compounds uptake in tissues about the same (~4-7ng/g and ~10ng/g respectively). But the total inorganic mercury concentration is much higher in the brains of thimerosal exposed monkeys. Thimerosal is still (despite evidence that warrants caution) being used in flu vaccines which are recommended to children and pregnant women. I will provide further references at the end of this comment.

When it comes to the topic of vaccine safety, there are many logical errors people use and I am going to point out a few of them (albeit there are many others). One of the first ones is an appeal to scientific democracy which involves “the contention that if the majority of scientists believe something to be true, regardless of epistemological merit, then it must be assumed as true” (The Ethical Skeptic, n.d.). Then we have an appeal to scientists fallacy which is “an argument that is misrepresented to be the premise held true on the part of the prevailing group of scientists; or concludes a hypothesis (typically a belief) to be either true or false based on whether the premise leads to a more successful career in science” (The Ethical Skeptic, n.d.). Another commonly used argument and pseudo-skeptic tactic involves the use of a consensus appeal to authority. “Insofar as scientists speak in one voice and dissent is not really allowed, then appeal to scientific consensus is the same as an appeal to authority” (The Ethical Skeptic, n.d.). Consensus that is shaped by scientific obfuscation, conflicts of interest, and shoddy scientific studies that use poor methodology is consensus that is in error. If the “consensus” on such a topic is not in line with scientific facts or the proper usage of the scientific method, it ceases to be a consensus based on actual reliable science and thus poses major issues.

The precautionary principle is of utmost importance especially when dealing with a sub-population that is at an increased risk of an adverse reaction from specific exposures. Also, I agree with the statement “First, do no harm.” But you are making this statement from a position of ignorance on the topic of thimerosal. It turns out it is you that needs a lesson in biochemistry and an understanding of how to critically evaluate the literature (including many important studies of which you have never put an eye on, considered, or weighed the evidence for).

Further reading recommendations:

Rose et al. (2014). Increased susceptibility to ethylmercury-induced mitochondrial dysfunction in a subset of autism lymphoblastoid cell lines. Journal of Toxicology. Retrieved from

“These findings suggest that the epidemiological link between environmental mercury exposure and an increased risk of developing autism may be mediated through mitochondrial dysfunction and support the notion that a subset of individuals with autism may be vulnerable to environmental influences with detrimental effects on development through mitochondrial dysfunction.”


Sharpe et al. (2013). B-lymphocytes from a population of children with autism spectrum disorder and their unaffected siblings exhibit hypersensitivity to thimerosal. J Toxicol. Retrieved from


“Cells hypersensitive to thimerosal also had higher levels of oxidative stress markers, protein carbonyls, and oxidant generation. This suggests certain individuals with a mild mitochondrial defect may be highly susceptible to mitochondrial specific toxins like the vaccine preservative thimerosal.”


Dorea JG. (2013). Low-dose Mercury Exposure in Early Life: Relevance of Thimerosal to Fetuses, Newborns and Infants. Curr Med Chem.  Retrieved from

“Major databases were searched for human and experimental studies that addressed issues related to early life exposure to TCV. It can be concluded that: a) mercury load in fetuses, neonates, and infants resulting from TCVs remains in blood of neonates and infants at sufficient concentration and for enough time to penetrate the brain and to exert a neurologic impact and a probable influence on neurodevelopment of susceptible infants; b) etHg metabolism related to neurodevelopmental delays has been demonstrated experimentally and observed in population studies; c) unlike chronic Hg exposure during pregnancy, neurodevelopmental effects caused by acute (repeated/cumulative) early life exposure to TCV-etHg remain unrecognized; and d) the uncertainty surrounding low-dose toxicity of etHg is challenging but recent evidence indicates that avoiding cumulative insults by alkyl-mercury forms (which include Thimerosal) is warranted.”


Duszczyk-Budhathoki et al. (2012). Administration of thimerosal to infant rats increased overflow of glutamate and aspartate in the prefrontal cortex: protective role of dehydroepiandrosterone sulfate. Neurochem Res. Retrieved from

“Since excessive accumulation of extracellular glutamate is linked with excitotoxicity, our data imply that neonatal exposure to thimerosal-containing vaccines might induce excitotoxic brain injuries, leading to neurodevelopmental disorders.”


Sulkowski et al. (2012). Maternal thimerosal exposure results in aberrant cerebellar stress, thyroid hormone metabolism, and motor behavior in rat pups; sex- and strain-dependent effects. Cerebellum. Retrieved from

Our data thus demonstrate a negative neurodevelopmental impact of perinatal TM exposure which appears to be both strain – and sex-dependent


Sharpe et al. (2012). Thimerosal-Derived Ethylmercury is a mitochondrial toxin in human astrocytes:  possible role of fenton chemistry in the oxidation and breakage of mtDNA. J Toxicol. Retrieved from

“These mitochondria appear to have undergone a permeability transition, an observation supported by the five-fold increase in Caspase-3 activity observed after Thimerosal treatment.”


Dorea, JG. (2011). Integrating experimental (in vitro and in vivo) neurotoxicity studies of low-dose thimerosal relevant to vaccines. Neurochem Res. Retrieved from

“Thimerosal at concentrations relevant for infants’ exposure (in vaccines) is toxic to cultured human-brain cells and to laboratory animals.”

Hooker et al. (2014). Methodological issues and evidence of malfeasance in research purporting to show thimerosal in vaccines is safe. BioMed Research International. Retrieved from

There are over 165 studies that have focused on Thimerosal, an organic-mercury (Hg) based compound, used as a preservative in many childhood vaccines, and found it to be harmful. Of these, 16 were conducted to specifically examine the effects of Thimerosal on human infants or children with reported outcomes of death; acrodynia; poisoning; allergic reaction; malformations; auto-immune reaction; Well’s syndrome; developmental delay; and neurodevelopmental disorders, including tics, speech delay, language delay, attention deficit disorder, and autism. In contrast, the United States Centers for Disease Control and Prevention states that Thimerosal is safe and there is “no relationship between [T]himerosal[-]containing vaccines and autism rates in children.” This is puzzling because, in a study conducted directly by CDC epidemiologists, a 7.6-fold increased risk of autism from exposure to Thimerosal during infancy was found. The CDC’s current stance that Thimerosal is safe and that there is no relationship between Thimerosal and autism is based on six specific published epidemiological studies coauthored and sponsored by the CDC. The purpose of this review is to examine these six publications and analyze possible reasons why their published outcomes are so different from the results of investigations by multiple independent research groups over the past 75+ years.

Adams et al. (2013). Toxicological status of children with autism vs. neurotypical children and the association with autism severity. Biol Trace Elem Res. Retrieved from

Overall, children with autism have higher average levels of several toxic metals, and levels of several toxic metals are strongly associated with variations in the severity of autism for all three of the autism severity scales investigated.

Rooney, J. (2013). The retention time of inorganic mercury in the brain – A systematic review of the evidence. Toxicology and Applied Pharmacology. Retrieved from

Evidence from such studies point to a half-life of inorganic mercury in human brains of several years to several decades. This finding carries important implications for pharmcokinetic modelling of mercury and potentially for the regulatory toxicology of mercury.

Chen et al. (2013). Effect of thimerosal on the neurodevelopment of premature rats. World J Pediatr. Retrieved from

The negative adverse consequences on neurodevelopment observed in the present study are consistent with previous studies; this study raised serious concerns about adverse neurodevelopmental disorder such as autism in humans following the ongoing worldwide routine administration of thimerosalcontaining vaccines to infants.

Olczak et al. (2011). Persistent behavioral impairments and alterations of brain dopamine system after early postnatal administration of thimerosal in rats. Behav Brain Res. Retrieved from

These data document that early postnatal THIM administration causes lasting neurobehavioral impairments and neurochemical alterations in the brain, dependent on dose and sex. If similar changes occur in THIM/mercurial-exposed children, they could contribute to neurodevelopmental disorders

Olczak et al. (2010). Lasting neuropathological changes in rat brain after intermittent neonatal administration of thimerosal. Folia Neuropathol. Retrieved from

These finding document neurotoxic effects of thimerosal, at doses equivalent to those used in infant vaccines or higher, in developing rat brain, suggesting likely involvement of this mercurial in neurodevelopmental disorders

DeSoto, C. (2007). Blood Levels of Mercury Are Related to Diagnosis of Autism: A Reanalysis of an Important Data Set. J Child Neurol. Retrieved from

We have reanalyzed the data set originally reported by Ip et al. in 2004 and have found that the original p value was in error and that a significant relation does exist between the blood levels of mercury and diagnosis of an autism spectrum disorder. Moreover, the hair sample analysis results offer some support for the idea that persons with autism may be less efficient and more variable at eliminating mercury from the blood

James et al. (2005). Thimerosal neurotoxicity is associated with glutathione depletion: protection with glutathione precursors. Neurotoxicology. Retrieved from

Although Thimerosal has been recently removed from most children’s vaccines, it is still present in flu vaccines given to pregnant women, the elderly, and to children in developing countries. The potential protective effect of GSH or NAC against mercury toxicity warrants further research as possible adjunct therapy to individuals still receiving Thimerosal-containing vaccinations

Waly et al. (2004). Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal. Mol Psychiatry. Retrieved from

The potent inhibition of this pathway by ethanol, lead, mercury, aluminum and thimerosal suggests that it may be an important target of neurodevelopmental toxins 

Citations of peer-reviewed studies from the book “The Environmental and Genetic Causes of Autism,” written by James Lyons-Weiler (AKA the Twitter troll slayer).