We read with interest the article describing methods for modelling count data with excess zeros compared to standard count distributions, such as Poisson1. This topic has been extensively discussed in the statistical and epidemiological literature2-3. Didactic messages given by statisticians can often lack an appreciation of the epidemiological context and sadly this article has the same shortcomings.
The primary novelty is t...
We read with interest the article describing methods for modelling count data with excess zeros compared to standard count distributions, such as Poisson1. This topic has been extensively discussed in the statistical and epidemiological literature2-3. Didactic messages given by statisticians can often lack an appreciation of the epidemiological context and sadly this article has the same shortcomings.
The primary novelty is the context in which the issue is discussed: application to counts of Activities of Daily Living (ADL-s). It is laudable that methodological issues are tackled using practical examples, but our concern is that the novel context has been largely overlooked and an educational opportunity lost. The message is too narrow in scope and arguably misleading. The reader is told that the zero-inflated Negative Binomial is the most appropriate model for the ADL-s data, yet this is likely incorrect and could lead to inappropriate models being adopted in this domain.
The Binomial distribution deals with bounded data and is extended to yield the Beta Binomial, which accommodates overdispersion. Both the Binomial and Beta Binomial distributions have zero-inflated extensions (e.g. the "zero-inflated Binomial") to account for an excess of zeros4. We were surprised to see no mention of these alternative distributions since the Poisson distribution exhibits an infinite tail and predicts counts in excess of six, albeit with low probabilities. Allowing for over-dispersion, the Negative Binomial accommodates a longer tail for the same mean. Both distributions (whether zero-inflated or not) thus possess properties that are incongruent with the nature of the data in this context.
Any count distribution assumes an increment of one has the same meaning from one to two as from five to six; for zero-inflated extensions, the increment from zero to one may have a different meaning. As each ADL-s is unique, each is likely to have a different meaning. Hence, as individuals deteriorate in their condition, some activities may become a challenge before others. Consequently, an increment of one ADL may have different meaning along the scale and it is sensible to assume an ordinal outcome5, which also accommodates differences in the increment from zero to one.
Good agreement between observed and predicted outcomes is necessary but not sufficient. Disparity between models with regard to predicted outcomes can often be negligible whilst models differ substantially in parameterisation and hence interpretation. Likelihood-based model-fit criteria are only one facet of model development; context validity and interpretability must also have a bearing and researchers must appreciate the context in which data are generated. For this reason the best model may not yet have been found. We have not investigated the dataset, nor do we feel the need to do so when proposing the ordinal model and only with no compelling evidence that increments differed might we instead propose the zero-inflated Binomial or Beta Binomial for parsimony.
References
1. Zaninotto P, Falaschetti E. Comparison of methods for modelling a count outcome with excess zeros: application to Activities of Daily Living (ADL-s). J Epidemiol Community Health 2011; 65: 205-210.
2. Lambert D. Zero-inflated Poisson regression, with an application to defects in manufacturing. Technometrics 1992; 34:1–14.
3. Gilthorpe MS, Frydenberg M, Cheng Y, Baelum V. Modelling count data with excessive zeros: The need for class prediction in zero-inflated models and the issue of data generation in choosing between zero-inflated and generic mixture models for dental caries data. Statistics in Medicine 2009; 28: 3539-3553.
4. Vieira AMC, Hinde JP, Demetrio CGB. Zero-inflated proportion data models applied to a biological control assay. Journal of Applied Statistics 2000; 27:373–389.
5. Lall R, Campbell MJ, Walters SJ, Morgan K and MRC CFAS Co-operative. A review of ordinal regression models applied on health-related quality of life assessments. Stat Methods Med Res 2002; 11: 49-67.
There is much evidence linking learning and behaviour problems in
childhood to refined oils in the maternal diet during pregnancy and
lactation, particularly linoleic acid in both cis and trans forms which
may impair fetal brain development. A lower IQ in these children would
not be surprising.
I have seen no evidence, however, linking fresh natural fats to any
of these problems. Diets high in refined sugars...
There is much evidence linking learning and behaviour problems in
childhood to refined oils in the maternal diet during pregnancy and
lactation, particularly linoleic acid in both cis and trans forms which
may impair fetal brain development. A lower IQ in these children would
not be surprising.
I have seen no evidence, however, linking fresh natural fats to any
of these problems. Diets high in refined sugars tend to be high in
refined oils as well -- the two go together -- so I think it's important
to stress that "high fat" in this case refers only to processed oils, not
the healthy fats naturally present in fresh whole foods.
I would be pleased to provide references re linoleic acid and effects
on offspring to anyone wishing to contact me at the address above.
The authors conclusions that the media did not 'over-hype' the swine
flu nondemic are reached as a result of a methodology that directed them
towards that conclusion; an analysis solely of the UK print media.
I travelled to New Zealand on 11 May - two weeks after the first
cases emerged - and arrived in Melbourne on the 5th June, a time when this
was arguably the swine flu capital of the world. Yes...
The authors conclusions that the media did not 'over-hype' the swine
flu nondemic are reached as a result of a methodology that directed them
towards that conclusion; an analysis solely of the UK print media.
I travelled to New Zealand on 11 May - two weeks after the first
cases emerged - and arrived in Melbourne on the 5th June, a time when this
was arguably the swine flu capital of the world. Yes, it was apparent that
there was flu circulating and I fell victim to it, but the print media
response was far more measured and balanced than it was here. The joys of
the internet meant that I was following the print media in the UK closely,
as well as reading the major daily newspapers in both Australia and New
Zealand.
I suspect that an analysis of the UK print media v that of other
countries may expose our response to this nondemic for the hysteria that
it was.
There is much to like in the argument presented by Clare Bambra. Epidemiology (and public health generally) has much to learn from the social sciences and the reverse is also true. And Bambra is surely correct to raise concerns about the associated risks including the "engrained caution and purism of epidemiology" and the excessive deference to experimental research designs before acting.
However, in order to effectively mana...
There is much to like in the argument presented by Clare Bambra. Epidemiology (and public health generally) has much to learn from the social sciences and the reverse is also true. And Bambra is surely correct to raise concerns about the associated risks including the "engrained caution and purism of epidemiology" and the excessive deference to experimental research designs before acting.
However, in order to effectively manage and profit from "the interface between social science and epidemiology" it is essential that epidemiologists and their public health colleagues engage with the broad range of social science including, and perhaps especially, political science. In many discussion of the linkage between epidemiology and the social sciences there are repeated references to the insights of psychology, economics and sociology but few if any direct references are made to political science. This is ironic given the sheer size of the political science enterprise. It is also tragic insofar as the goal of much of the writing on the social and economic determinants of health is to encourage action on these determinants often, if not primarily, by means of the state. Political science has much to say about the why, what and how of state action.
Fore example, having highlighted the association between social inequality and poor health, while it is reasonable to call, as Bambra does, for income redistribution, this is but the start. Contemporary political science (including political theory) can offer a great deal of insight into why inequality is on the rise (e.g., Pierson, Paul, and Jacob S. Hacker. 2010. Winner-Take-All Politics: How Washington Made the Rich Richer--and Turned Its Back on the Middle Class. New York: Simon & Schuster.), why this varies between states, what alternative exist for ensuring more redistribution, and how to counter the inevitable arguments that this would be unfair or unwise (e.g., Cohen, G. A. 2008. Rescuing Justice and Equality. Cambridge, Mass.: Harvard University Press).
I suggest the findings of Xu, et al., are caused by increased
testosterone within urban populations. A report comparing rural areas and
a large city found that testosterone is higher in the large city (Folia
Histochem Cytobiol. 2001;39 Suppl 2:38-9).
It is my hypothesis that the "secular trend," the increase in size
and earlier puberty occurring in children, is caused by an increase in the
percentage of individu...
I suggest the findings of Xu, et al., are caused by increased
testosterone within urban populations. A report comparing rural areas and
a large city found that testosterone is higher in the large city (Folia
Histochem Cytobiol. 2001;39 Suppl 2:38-9).
It is my hypothesis that the "secular trend," the increase in size
and earlier puberty occurring in children, is caused by an increase in the
percentage of individuals of higher testosterone. More specifically, I
suggest this is due to an increase in the percentage of mothers of higher
testosterone with time within the population. This exposes more fetuses to
increased maternal testosterone with time within the population. This
causes permanent effects in the fetus which persist throughout the life
span. I suggest this is the cause of the parallel increases in morbidity
occurring within the population, such as obesity, cancer, breast cancer,
diabetes, etc., including prematurity, small for gestational age, etc.,
including less obvious gross effects which later contribute to "failing
schools" and other adverse behavioral outcomes in children.
I have come to the conclusion that the "increase in testosterone" may
partially be due to a reduction in "sex hormone binding globulin (SHBG)"
as a number of phenomena explained by the secular trend may be based on
changes in SHBG. A decrease in SHBG increases free testosterone levels.
I suggest increased testosterone may be higher in the lower
socioeconomic levels. Increased testosterone has been connected with
reduced learning ability, reduced impulse control, and sexuality. All of
these reduce the ability to obtain gainful employment and participation in
a society increasingly dependent upon advanced educational achievement and
personal control. This would concentrate this type of individual within...
I suggest increased testosterone may be higher in the lower
socioeconomic levels. Increased testosterone has been connected with
reduced learning ability, reduced impulse control, and sexuality. All of
these reduce the ability to obtain gainful employment and participation in
a society increasingly dependent upon advanced educational achievement and
personal control. This would concentrate this type of individual within
these levels and they would exhibit reduced intelligence and shorter life
spans.
I agree with the previous responder that the age of 5 and the battery
of tests used here seem inadequate to detect many of the impacts of
prenatal alcohol exposure.
Even so, I still find it remarkable that this study fails to find
statistically significant (after adjustment for confounders) impacts of
heavy maternal drinking in this sample to date.
This may have resulted from the relatively young age...
I agree with the previous responder that the age of 5 and the battery
of tests used here seem inadequate to detect many of the impacts of
prenatal alcohol exposure.
Even so, I still find it remarkable that this study fails to find
statistically significant (after adjustment for confounders) impacts of
heavy maternal drinking in this sample to date.
This may have resulted from the relatively young age of the study
group, inadequately sensitive measures, significant levels of 1st
trimester "before I knew I was pregnant" alcohol exposure in the "not
during pregnancy" group, optimistic self-reports of "light drinking," or
the obvious confounding effects of socioeconomic status and environmental
influences.
Regardless, if this study is unable to find a specific impact of
heavy drinking, how is it adequate to rule out impacts from light
drinking?
The authors do note some of these limitations in the discussion, but
frustratingly these have not come across so clearly in the media coverage.
From the press reports of this and the previous paper, it would seem that
FAPs (Fetal Alcohol Powers) have been discovered.
I think this conclusion, and even milder statements such as "At age
5, children of women who were light drinkers during pregnancy do not have
higher risk of socioemotional or cognitive deficits than those of women
who did not drink at all in pregnancy" are very premature, and in fact
irresponsible, in light of current knowledge of alcohol as a neurotoxin,
and one without a reliably described safe lower limit of exposure.
Can we please keep these concerns in mind when interpreting this
study, and future reports from this cohort, to the media?
The findings by Kelley at al. (2010) were found in newspapers and TV
shows and presented as evidence that light drinking during pregnancy may
not be harmful after all. The study cannot be used as a dependable
indication that low amounts of alcohol are beneficial to children, because
the amount of alcohol consumed was measured by a self-report of the
mother. Self-reported data on alcohol consumption does not produce
accu...
The findings by Kelley at al. (2010) were found in newspapers and TV
shows and presented as evidence that light drinking during pregnancy may
not be harmful after all. The study cannot be used as a dependable
indication that low amounts of alcohol are beneficial to children, because
the amount of alcohol consumed was measured by a self-report of the
mother. Self-reported data on alcohol consumption does not produce
accurate findings, as found in previous studies1,2. In addition to this,
due to the use of a non-experimental design in the study by Kelley et al.
(2010), there could have been a number of intervening variables that
remain undiscovered and account for the absence of association between
these two variables. The authors point to several that they accounted for
to some degree, but understate the fact that causal inference is
impossible, rather than just limited as they indicated. Yet, the authors
use wording in the abstract conclusion of "not increased risk" which also
overstates the findings. This wording implies that they somehow showed a
cause-and-effect relationship between prenatal alcohol exposure and
postnatal behavioral problems. A more cautious wording would have been
better to prevent misunderstanding by the readers.
The authors downplay the observation that mothers in their light
drinking category had children who had fewer behavioral problems than
mothers who did not drink at all. In other words, light drinking during
pregnancy is beneficial, if their findings are any indication. The
question is why did the authors not state that light drinking by the
mother during pregnancy is beneficial for children? The answer might be
that it would put a spotlight on the flaws in the study methodology.
One other point is that negative effects of prenatal alcohol cannot
accurately be studied unless the study is lifelong. Studying the child in
question, at the age of five does not demonstrate later consequences that
could emerge clear into adulthood. Finally, one drink once a week during
pregnancy may not have the same effects on one woman as it does another
due to genetic, dietary, and other differences. For these reasons,
pregnant women and health care workers should not yet take any actions
whatsoever based on this study. Until a well-executed experimental study
with random assignment is conducted on this important topic, the answer
will remain unknowable. Light drinking during pregnancy must be soundly
discouraged - not encouraged -- until proven otherwise.
The SDQ is only a brief screening tool. It is questionable that its
reliability extends to the highly charged questions of alcohol consumption
during pregnancy and the effects on the child.
The BAS is not comprehensive "were more specific abilities need
investi...
The SDQ is only a brief screening tool. It is questionable that its
reliability extends to the highly charged questions of alcohol consumption
during pregnancy and the effects on the child.
The BAS is not comprehensive "were more specific abilities need
investigating other diagnostic scales can be used to provide more detail"
FASD [ fas and arnd ] is truly a spectrum from the death of the fetus
to the articulate and intelligent individual who never the less has the
secondary disabilities of FASD to varying degrees.
The secondary disabilities are drug and alcohol problems, disrupted school
experience, confinement, difficulty maintaining employment and living
independently. In addition 94% will eventually be given mental health
diagnoses. Adaptive and executive functioning are effected resulting in
many issues e.g. money management.
In order to identify the less effected all domains of brain function
need to be evaluated, with subtests.
I have seen many times adolescents and adults who are articulate and
intelligent yet have chaotic lives, impacting others and society in
general. They were never fully evaluated but when they are, as above, then
significant deficiencies of brain function are found that account for
their difficulties.
The evidence is that the sooner the effects of alcohol on the
developing fetus is established the less the secondary disabilities.
There is research that shows low levels of alcohol exposure cause
deficiencies in brain function.
It is true the research is limited; a reflection of denial by the majority
of politicians and professionals.
Although the MCS is an ongoing longitudinal study I am left with the
distinct and alarming impression that the two papers to date, and the
response of the media, promote the consumption of alcohol during pregnancy
rather than the urgent need for more research into the effect on the
developing fetus of low levels of alcohol.
I leave the reader with a question-
If it is all right to expose the fetus to alcohol during pregnancy is it
all right to give the same amount of alcohol to the infant?
Barry Stanley, MB Ch.B, F.R.C.S[C]
references provided on request
I am a Senior Audiologist by profession who qualified with a British Masters degree (University College London, 2004) and an American Doctorate degree (NOVA Southeastern University, 2006), both in Audiology. I have practised Clinical Audiology for more than six years and I work closely with Otolaryngology doctors/surgeons both in clinical procedures and research. At present (2010), I am pursuing a Master...
I am a Senior Audiologist by profession who qualified with a British Masters degree (University College London, 2004) and an American Doctorate degree (NOVA Southeastern University, 2006), both in Audiology. I have practised Clinical Audiology for more than six years and I work closely with Otolaryngology doctors/surgeons both in clinical procedures and research. At present (2010), I am pursuing a Masters degree in Public Health at Manchester University Medical School.
I read with both interest and controversial scepticism on the large scale population-based study on the 'Prevalence and Characteristics of hearing problems in a working and non-working Swedish population' recently published in J Epidemiol Community Health 2010:64:453-460. I wish to highlight potential erratum or flaws concerning the said 'health issue' of hearing problems, in-hope of inferring a meaningful interpretation of the study's findings that are relevant to Public Health Practice.
Firstly, the definition of 'hearing problems' in the study, as referenced to the World Health Organisation's (WHO) statement of "being among the top 10 most common burdens of disease in medium and high income countries", was intended to refer to the pathophysiology of sensorineural / cochlear or inner ear hearing loss (Mathers and Loncar, 2006; Mathers et al, 2000).
According to the WHO published definitions (Mathers and Loncar, 2006; Mathers et al, 2000) and to the Professional bodies of the British Academy of Audiology (BAA) and the American Speech-Language Association (ASHA), sensorineural hearing loss refers to 'a permanent and irreversible damage to the sensory hair cells found inside the peripheral end organ in hearing' called the cochlea that is predominantly caused by natural deterioration in old-age (presbyacusis), by noise-damage, and also by ototoxic medications. These aetiologies can concur at the same time and synergistically worsen sensorineural hearing loss (e.g. old aged patients with previous occupational or recreational noise-exposure). Other less common causes of sensorineural hearing loss include congenital, syndromal, or hereditary causes, idiopathic sudden hearing loss, or Otoneurotological pathologies coupled with vestibular symptoms (e.g. Acoustic tumours).
Not so relevant to the scope of this definition are the "conductive hearing loss" cases, which refer to middle ear pathologies managed by doctors / surgeons specialising in Otolaryngology. More irrelevant, are the "central processing disorders", which refer to problems along the neuro-auditory or cognitive pathways, or psychological difficulties and/or mental alertness or orientation issues, unless it is a Psychiatric, Psychological, or Mental Health disorder at hand.
In the study however, the first outcome measure used in the questionnaire was a subjectively self-reported difficulty "to hear what is said in a conversation between several persons" (Hasson et al, 2010). The question is vague and presents a big dilemma because it may refer to a 'one-off incident of not hearing something' (e.g. absent-mindedness), a 'normal phenomenon of missing one word or two in a conservation', or anything referring to central auditory processing issues of speech-in- noise problems without proper clinical documentation or diagnostic evidence of dysfunction or impairment.
Secondly, tinnitus that is typically considered as clinically relevant and debilitating to the patient is a constant, non-ceasing, continuous tinnitus day and night, which may occur unilaterally or bilaterally and in varying degrees of loudness and frequency / type such as buzzing, swooshing, whistle, etc (British Tinnitus Association).
In the study however, the second outcome measure in the questionnaire was a subjective self-reported questionnaire on tinnitus "lasting more than 5minutes" (Hasson et al, 2010). It is clinically considered a normal phenomenon to have 'Spontaneous Tinnitus' in healthy individuals, which occurs and disappears spontaneously. Individuals truly suffering with debilitating tinnitus report of constant tinnitus that affects their sleep and/or daily activities (McKenna and Gardner, 2009).
Given the above flaws in the pathophysiology definition of hearing problems, there are dilemmas arising in the interpretation of the studied 'public health issue' and to the recommendations for interventions or preventions.
The intended objective of the study was to compare the prevalence of hearing problems and tinnitus in the working and non-working population by grouping the samples from one common population source in Sweden. It is not surprising to find very closely similar prevalence results in both the working and non-working groups's (proportion or percentage %) distribution of tinnitus and severity and discomfort of tinnitus, and prevalence of hearing loss and of hearing problems (see Hasson et al, 2010; Table 1 and 2). Also, no test of population heterogeneity or comparative difference was conducted between the working and non-working groups. There is no statistical test to demonstrate any difference between the two groups, which poses a serious flaw to the conclusion that hearing problems (tinnitus and hearing loss) are "by far more prevalent than previously estimated" when it is not supported by any found evidence showing a higher prevalence. Therefore, there is a high probability that both the working and the non-working populations may be homogenous groups belonging to the same population and sharing the same characteristic risks or self-reported complains of "hearing problems" as outcome measure.
There is also vagueness in the Public health related recommendation that "tailored preventive interventions need to be implemented at individual, organisational as well as societal levels" (Hasson et al, 2010). It is common knowledge to healthcare practitioners, and public health experts that both the working and non-working populations are at risk to hearing problems when exposed to noise or individuals who incur age-related problems
From a health protection point of view, there are already existing organisational and societal preventative interventions targeted at occupational and recreational damaging noise exposure. Existing measures and policies in the European Legislation already address environmental noise pollution (EU Directive 2002/49/EC), occupational health risks for work environments (EU Directive 2003/10/EC) and recreational risks to young adults, e.g. music players / disco club noise risks (EU Scientific Committee on Emerging and Newly Identified Health Risks SCENIHR, 2008).
From a healthcare provision and policy point of view, there remains no surgical or medical treatment to 'cure' constant tinnitus or permanent sensorineural hearing loss, except for middle ear pathologies and infections managed by Otolaryngology surgeons or doctors. No prevention can avoid risks or problems of age-related hearing difficulties, except by interventions of providing hearing aids use. Limitations and cost-benefit analysis coupled to diagnostic and rehabilitative interventions are considered in these respects.
Finally however, the study generated two important new findings which are - the link between socioeconomic (employment) status and self-reported hearing problems, and the highlighted findings for young adults aged below 40. The results found a "clear socio-economic gradient in the prevalence of hearing problems, where lower status is more affected", as well as finding that "approximately every fifth of young adult below 40 years of age to have either tinnitus or hearing loss"(Hasson et al, 2010). These may be of high importance for demographic targeting in Health Promotions or Health Communications for raising public awareness for occupational and recreational risks in noise-induced hearing loss
Bibliography:
1. Hasson D, Theorell T, Westerlund H, Canlon B. Prevalence and
Characteristics of hearing problems in a working and non-working Swedish
population. J Epidemiol Community Health 2010; 64:453-460
2. Mathers CD, Loncar D. Projections of global mortality and burden
of disease from 2002 to 2030. PLoS Med 2006;3(11):e442 (also found online:
http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0030442;
accessed 11th October 2010).
3. Mathers C, Smith A, Concha M. Global Burden of hearing loss in
the year 2000. Global Burden of Disease. Geneva: World Health
Organization, 2000:1-30 (also found online:
http://www.who.int/healthinfo/statistics/bod_hearingloss.pdf; accessed
19th October 2010).
4. British Academy of Audiology website: Accessed 19th October 2010.
(http://theloop.netplan.co.uk/~admin9/index.php?option=com_content&task=view&id=68&Itemid=96)
5. American Speech-Language Hearing Association website: Accessed
19th October 2010. (http://asha.org/)
6. British Tinnitus Association website: Accessed 10th October 2010
(http://www.tinnitus.org.uk/)
7. McKenna L and Gardner C (2009). Good Night Sleep Tight. British
Tinnitus Association (also found online:
http://www.tinnitus.org.uk/files/good%20night%20sleep%20tight.pdf;
accessed 17th October, 2010)
There is much evidence linking learning and behaviour problems in childhood to refined oils in the maternal diet during pregnancy and lactation, particularly linoleic acid in both cis and trans forms which may impair fetal brain development. A lower IQ in these children would not be surprising.
I have seen no evidence, however, linking fresh natural fats to any of these problems. Diets high in refined sugars...
Sir,
The authors conclusions that the media did not 'over-hype' the swine flu nondemic are reached as a result of a methodology that directed them towards that conclusion; an analysis solely of the UK print media.
I travelled to New Zealand on 11 May - two weeks after the first cases emerged - and arrived in Melbourne on the 5th June, a time when this was arguably the swine flu capital of the world. Yes...
I suggest the findings of Xu, et al., are caused by increased testosterone within urban populations. A report comparing rural areas and a large city found that testosterone is higher in the large city (Folia Histochem Cytobiol. 2001;39 Suppl 2:38-9).
It is my hypothesis that the "secular trend," the increase in size and earlier puberty occurring in children, is caused by an increase in the percentage of individu...
I suggest increased testosterone may be higher in the lower socioeconomic levels. Increased testosterone has been connected with reduced learning ability, reduced impulse control, and sexuality. All of these reduce the ability to obtain gainful employment and participation in a society increasingly dependent upon advanced educational achievement and personal control. This would concentrate this type of individual within...
I agree with the previous responder that the age of 5 and the battery of tests used here seem inadequate to detect many of the impacts of prenatal alcohol exposure.
Even so, I still find it remarkable that this study fails to find statistically significant (after adjustment for confounders) impacts of heavy maternal drinking in this sample to date.
This may have resulted from the relatively young age...
The findings by Kelley at al. (2010) were found in newspapers and TV shows and presented as evidence that light drinking during pregnancy may not be harmful after all. The study cannot be used as a dependable indication that low amounts of alcohol are beneficial to children, because the amount of alcohol consumed was measured by a self-report of the mother. Self-reported data on alcohol consumption does not produce accu...
2288 Rougecrest Drive, Oakville, Ontario. Canada. L6H 6N2 tel. 905 257 7869 e-mail bstanley3@cogeco.ca
6th. October, 2010.
Dear Editor.
The SDQ is only a brief screening tool. It is questionable that its reliability extends to the highly charged questions of alcohol consumption during pregnancy and the effects on the child. The BAS is not comprehensive "were more specific abilities need investi...
Dear Editor
I am a Senior Audiologist by profession who qualified with a British Masters degree (University College London, 2004) and an American Doctorate degree (NOVA Southeastern University, 2006), both in Audiology. I have practised Clinical Audiology for more than six years and I work closely with Otolaryngology doctors/surgeons both in clinical procedures and research. At present (2010), I am pursuing a Master...
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