Written in response to Misattributions and Potential Consequences: The Case of Child Mental Health Problems and Fetal Alcohol Spectrum Disorders. John D. McLennon. Canadian Journal of Psychiatry. Vol 60, No 12, December 2015. Not published: too many words and references

1. Re. Misattributions and Potential Consequences: The Case of Child Mental Health
Problems and Fetal Alcohol Spectrum Disorders. John D. McLennon. Canadian Journal
of Psychiatry. Vol 60, No 12, December 2015
Dear Sir/Ms
Dr McLennon’s perspective requires comment and clarification.
Keywords
PAE- Prenatal Alcohol Exposure
FAS- Fetal Alcohol Syndrome
FASD- Fetal Alcohol Spectrum Disorder
DSM- Diagnostic and Statistical Manual
Phenotype
Mental Health
Epidemiology
Epigenetic
I know of no Canadian agency that has “prioritized” services for people diagnosed with
FAS….”
- Prioritize: to organize things so that the most important thing is done or dealt with
first.[1]
In Canada there are some programs relating to FASD, none of which have priority over
programs relating to other health conditions: The Province of Ontario has no programs
for FASD at all, at this time.
FASD is not a “construct”, i.e. an idea or theory not formed from empirical evidence.
There is overwhelming empirical evidence for the existence of FASD. [2,3,4]
For those who think a priori: most if not all the research that has been done on the effects
of alcohol on the developed brain surely applies to the developing brain.
FASD is not “broader” anything of FAS; rather, FAS is one of the many phenotypes of
FASD. [5]
FAS is not a label: it is a phenotype of FASD, as such the term FAS has been replaced by
“FASD with Sentinel Facial Features”. [5] This change reflects the increasing
clarification and understanding of the effects of alcohol on the developing brain.

2. The association of DSM diagnoses to FASD was established 20 years ago [6,7,8].
Confirmation of this association has continued clinically,[9] neurologically [10] and
epigenetically.[11] However, these associations have not been acknowledged by
Psychiatry, nor researched to establish further the nature of these associations.
“Problematic overlap” will always be the case until PAE is excluded or included as an
etiological factor in DSM diagnoses.
I know of no evidence that the diagnosis of FASD negatively impacts mental health
services: the reverse is not the case however. For those with FASD DSM diagnoses are
often multiple: I have seen as many as six. [12]
When the diagnosis of FASD is finally made the common reaction is one of relief: relief,
because it offers an explanation for a chaotic life that multiple symptomatic DSM
diagnoses have failed to provide.
These DSM diagnoses are made in good faith by psychiatrists. The question needs to be
asked: how could one individual fulfill the requirements for so many DSM diagnoses?
There has to be a common factor. [13]
It is likely that there will never be a pathognemonic behavior for FASD, which is a
spectrum of phenotypes.
The diagnoses in the DSM 5 are defined by behavior alone. Increasingly however,
individuals are being identified as having more than one type of DSM diagnostic
behavior. [14] What is the cause of these DSM overlaps?
Reference 5, “Identifying the behavioural phenotype in fetal alcohol spectrum disorder:
sensitivity, specificity and screening potential”, relates only to ADHD. I am not aware of
any publications that links only one DSM diagnosis specifically to FASD. On the
contrary, a number of DSM diagnoses have been linked to FASD. [7,15]
There are many non-referred population studies of FASD and PAE, some of which are of
large populations. [12,16,17]
Screening tools have been developed with great diligence. None of them include DSM
diagnoses as a criteria.
I agree, … “abnormalities in 3 of the listed domains would also be commonly found in
many children with various mental health disorders”: if they are looked for.
In my experience neuropsychological assessments are rarely done in the context of
Psychiatry, or not considered if available: in keeping with the lack of publications on the
subject.
Surely assessment of information processing, memory etc. should be routine for those
with DSM diagnoses.
I agree, …. “the fraction for whom PAE is primarily etiologic is unknown”: therefore it
needs to be explored.

3. Is it not problematic to ignore the overwhelming associations between PAE and mental
illness? [15]
“Complicating the picture is the inclusion of an etiologic variable, in this case PAE, in the
diagnostic criteria for FASD.”
Without PAE there is no FASD. This fundamental diagnostic principle is applied in
Psychiatry e.g. grouping under the common etiological factor of stress.[18,19,]
The threshold referred to is actually high in that many of the effects of PAE are not
captured. There is no threshold at which PAE will have no deleterious effect on the
developing fetus.[21]
Etiological variables are a fact of life: Epidemiology has to deal with it. [22]
“Secondary”, coming after, is a reasonable word to describe the mental disorders that
affect 98% of individuals diagnosed with FASD.
With or without PAE as an etiological factor one would expect that various mental
illnesses would always manifest postpartum, and not prepartum!
It has always been acknowledged that other environmental factors contribute to the
secondary disabilities of PAE. [7,23]
We now understand that the process of disruption of brain development by PAE is largely
through epigenetic changes of gene expression [24,25,26,27], and that manifestation of
those disruptions may occur at different times and be influenced by other environmental
factors.
So far as clinic bias is concerned: the various DSM diagnoses are not made in the few
available FASD diagnostic clinics. The DSM diagnoses are made separately by
psychiatrists and other practitioners throughout Canada, both before and after the
diagnosis of FASD is made: they make no reference to FASD. It follows that Berksonian
bias does not apply. [28]
Up to now the attribution of DSM diagnoses has not been part of the screening or
diagnostic process for FASD. However, the overwhelming associations make it
reasonable that it should be the case. [29,30,31,32] The recent updating of the Canadian
Guidelines does now include previous DSM diagnoses.[5]
The associations between FASD and DSM diagnoses satisfy the requirements of
Bradford Hill’s causal inference in epidemiologic studies, especially in the light of recent
neurological and epigenetic research. [7,29]
It should be noted that many children who are exposed to prenatal alcohol, fulfill the
requirements for the diagnosis of FASD, have been adopted at birth and have not

4. experienced abuse or neglect, yet still receive diagnoses from the DSM.[30]
We know that an early diagnosis and a positive environment mitigates the secondary
disabilities of FASD:[7] mitigate is the correct word, since in spite of positive adoptive
parental efforts significant negative outcomes may still occur, including multiple DSM
diagnoses.
Research into the effectiveness of FASD interventions for DSM comorbid symptoms is
required. I find it difficult to see how such interventions might be counterproductive for
those with DSM diagnoses.
However, the reverse is not the case, especially in relation to psychotropic medications.
Cardiac birth defects are associated with PAE/FASD. Also, there is an increased risk of
suicide. Yet ADHD is the most common other diagnosis for children with FASD, many
of whom are prescribed psychostimulants such as Ritalin.
All those diagnosed with FASD have social skills deficits. The neuropsychocgical
deficiencies required for the diagnosis are such that social skills deficits are inevitable,
but their impact can be improved. [33,34,35]
Lack of social skills may not be due to such permanent neurodevelopmental disabilities.
In such cases training and management may be different; this is all the more reason why
PAE and FASD should be excluded.
FASD Awareness and Prevention programs always emphasize the significance of risk
factors such as poverty. [36]
Pursuing the diagnosis and understanding PAE/FASD is not synonymous with ignoring
research into mental illness. On the contrary, the more research into the neurological
origins of mental illness the more associations with PAE are found.
No one is emphasizing a single risk factor model for mental illness. However any risk
model should include PAE as a risk factor: but this is not happening as is demonstrated
by the absence of references to PAS/FASD in most Psychiatric publications.
The criteria for the diagnosis of mental illness needs to be extended into the 21st
century.
It is time to move on. [37]
The day will come when the genes that control individual aspects of brain function will
be identified. Changes in gene expression will be related to clinical presentations, such as
those in the DSM5: the generation at which those changes occurred will be determined.
The agent that caused those changes, with other environmental factors, will be identified.
Then we will understand to what degree alcohol has determined the nature of mental
illness.

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