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Biomedical subjects

Marco Procopio

Publications and source records attributed to Marco Procopio.

9 recordsLinked to original sources
PubMed2005

Seasonality of birth in epilepsy: a Southern Hemisphere study.

A consistent pattern has emerged from research in Northern Hemisphere populations indicating differences in the seasonality of birth between patients with epilepsy and the general population. This is the first study using similar methodology to look at Southern Hemisphere data. The population studied is composed of patients discharged from Australian hospitals with a diagnosis of epilepsy, in the period 1998-1999. The results show a significantly higher incidence of epilepsy in the patients born during the Australian winter and summer and a deficit of patients born during the spring and fall. This pattern is consistent with the Northern Hemisphere findings. This study provides further evidence of the existence of a seasonal aetiological agent(s) for epilepsy acting in the perinatal period.

Adult↗
PubMed2005

The hormonal environment in utero as a potential aetiological agent for schizophrenia.

There is consistent evidence in the literature that the foetal neurodevelopmental period is crucial for the genesis of schizophrenia later in adult life. There are also strong indications that the schizophrenic illness has sexually dimorphic features. A hypothesis consistent with both findings is that sexual hormones may act as aetiological agents for schizophrenia during the foetal period influencing the neurodevelopment in a differential way in males and females. The aim of this study is to verify this hypothesis exploiting the correlation between fingers' length in adults and hormonal concentrations in utero, which has been demonstrated in previous studies. More specifically, the literature shows that the lengths of the second and fourth finger in adults are proportional to the foetal concentrations of respectively oestrogens and androgens. When the sample of patients suffering from schizophrenia analysed in this study was compared with healthy subjects, it was observed that the average length of the second digit in the female schizophrenic sample resulted significantly shorter than in the female controls. There was no significant difference when the male schizophrenic sample was compared with male controls. The result of the study is, therefore, compatible with the hypothesis that oestrogenic hormones protect female foetuses from damage during the neurodevelopment in utero and ultimately give more benign characteristics to the schizophrenic illness in women.

Adult↗
PubMed2005

Does god play dice with schizophrenia? A probabilistic model for the understanding of causation in mental illness.

While the pure sciences have moved over the XX century from the certainties of the Laplacian mechanistic models to probabilistic ones, such as quantum physics, the attempts to explain the causation in mental illness are still stuck to deterministic frameworks which are deceptively reassuring, but also too simplistic to approach problems of such a complexity. The deterministic approach has led to several false leads that have affected research in the aetiology in mental illness, especially schizophrenia, and only moving to probabilistic models will allow an understanding of the causal processes. In this paper is challenged the almost universally accepted assumption that, to explain the lack of complete concordance amongst identical twins in schizophrenia, there is the need to resort to environmental aetiological agents. It is described instead how, using a probabilistic framework, a polygenic model without threshold can satisfactorily explain the data available so far without having to resort to environmental factors. The genes predisposing to schizophrenia, probably through a derailment of the neurodevelopment, would have a normal distribution in the general population, while the liability for the illness will increase exponentially with the number of risk genes, with a small minority of the population being at high risk. The average genetic liability to develop schizophrenia in individuals who later are affected by the disorder is around 50%. The adoption of a probabilistic model for the understanding of the inheritance of schizophrenia has therefore far reaching consequences, revolutionizing the interpretation of the twin studies, allowing a consistent model which does not require environmental interventions in the aetiology of schizophrenia and offering a framework to make sense of findings from the epidemiological research which are not satisfactorily explained by the deterministic models adopted so far.

Genetic Predisposition to Disease↗
PubMed2005

Misattributed paternity. A bias in the family studies in schizophrenia?

One of the few consistent findings originating from the research in schizophrenia is the high familiality in the transmission of the disease. Data from family studies have been used in the attempt to disentangle the genetic from the environmental components of this familiality. The analysis of this body of research has led several groups to the conclusion that there is a higher heritability of schizophrenia through the female rather than the male lineage and that the concordance for the illness is higher among DZ twins than siblings. These assumptions have generated a flurry of hypotheses on the aetiology of schizophrenia. This article demonstrates that the above findings can instead be explained as the result of an artefact originating from the uncertainty in the paternity of the probands. None of the studies has in fact considered that, in some populations, up to 30% of children are not genetically related to their putative fathers. This issue is potentially important for the genetic studies in all pathologies, but has a particular relevance for schizophrenia, due to the high profile acquired by family studies in the research for the aetiology in this illness. The conclusions reached in most family studies in schizophrenia should therefore be reappraised.

Female↗
PubMed2005

The multiple outcomes bias in antidepressants research.

Despite the widespread use of antidepressant medication, there are no signs that the burden of depression and suicide is decreasing in the industrialised world. This is generating mounting scepticism on the effectiveness of this class of drugs as an approach for the treatment of mood disorders. These doubts are also fuelled by the increasing awareness that the literature on antidepressants is fundamentally flawed and under the control of the pharmaceutical companies. This article describes systematically for the first time what is probably the most insidious and misleading of the biases that affect this area of research: the "multiple outcomes bias". Most trials on the effectiveness of antidepressants, instead of first establishing a hypothesis and then trying to demonstrate it, following the scientific method, start instead "data mining", without a clear hypothesis, and then select for publication, amongst a multitude of outcomes, only the ones that favour the antidepressant drug, ignoring the others. This method has obviously no scientific validity and is very misleading, allowing the manipulation of the data without any overt fraudulent action. There is the need to generate new research, independently funded and with clear hypotheses established "a priori ". What is at stake is not only the appraisal of the balance between benefits and potential damage to the patients when using this class of medications, after the realisation that they are not as harmless as believed. It is also to establish whether the research on antidepressant medication has gone on a "wild goose chase" over the last half century, concentrating almost exclusively on molecules that modify the monoaminergic transmission at synaptic level and virtually ignoring any other avenue.

Antidepressive Agents↗