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Thread: Inflammation and academic performance, (Jan 2016 paper)

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    Inflammation and academic performance, (Jan 2016 paper)

    Of interest:

    n=494

    http://www.ncbi.nlm.nih.gov/pubmed/26778777

    "Results showed that three of the four inflammatory biomarkers (CRP,
    IL-6 and WBC) and the inflammatory index were negatively associated
    with all academic indicators (β values ranging from -0.094 to -0.217,
    all P< 0.05) independent of confounders including body fat percentage.
    Indeed, youth in the highest tertile of the inflammatory index had
    significantly lower scores in all academic indicators compared with
    youth in the middle tertile (scores ranging from -0.578 to -0.344) and
    in the lowest tertile (scores ranging from -0.678 to -0.381). "

    Clearly, a wide range of factors can contribute to increased inflammation, such as obesity, diabetes, chronic illness, etc. In any case it is an interesting indication of a possible (but not proven of course) mechanism. It would be useful to follow-up, since technology could be used to treat these issues or provide additional support to these youth.

    Also, this could be another mechanism by which poverty contributes to academic performance.
    Last edited by warwick; 01-22-2016 at 06:08 PM.

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    Follow-up

    Reference:
    http://www.ncbi.nlm.nih.gov/pubmed/26686654



    Abstract
    The occurrence of cognitive disturbances upon CNS inflammation or infection has been correlated with increased levels of the cytokine tumor necrosis factor-α (TNFα). To date, however, no specific mechanism via which this cytokine could alter cognitive circuits has been demonstrated. Here, we show that local increase of TNFα in the hippocampal dentate gyrus activates astrocyte TNF receptor type 1 (TNFR1), which in turn triggers an astrocyte-neuron signaling cascade that results in persistent functional modification of hippocampal excitatory synapses. Astrocytic TNFR1 signaling is necessary for the hippocampal synaptic alteration and contextual learning-memory impairment observed in experimental autoimmune encephalitis (EAE), an animal model of multiple sclerosis (MS). This process may contribute to the pathogenesis of cognitive disturbances in MS, as well as in other CNS conditions accompanied by inflammatory states or infections.
    Illustrative paper of a possible mechanism by which TNF causes cognitive impairment. Another early paper that needs to be replicated.

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    I looked into some recent research, and there doesn't seem to be strong evidence for treatments to address the problem. That is, no treatments have been proven by double blind, randomized clinical trials. However, anti-inflammatory drugs such as aspirin et al may be helpful as well as a variety of known anti-oxidant supplements. But, none of these have been proven over the longer term.
    Last edited by warwick; 01-22-2016 at 07:06 PM.

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    I'm a bit hesitant to wholesale accept the premise that higher levels of inflammation are correlated with poorer academic performance.

    This could be a chicken-egg paradigm; quite possible that some of the individuals with higher inflammatory marker counts compared to their cohorts were experiencing this as a result of poor academic performance.

    Psychological (or indeed any sort of significant acute or chronic) stress will lead to hypothalamic-pituitary-adrenal (HPA) axis over-activation. Many students have issues with time management or prioritisation skills. It's likely a chunk of these "inflamed" under-achievers have behavioural and/or social reasons for their phenotype.

    Additionally, the association could be a red herring result. Students with pre-existing morbidities which predispose one towards inflammation (e.g. depression, any of the various affective spectrum disorders like fibromyalgia, chronic fatigue syndrome etc.)

    I'm also unsure why they've only used CRP, IL-6, TNF-a and total white cell count for their inflammatory markers... Could've thrown in erythrocyte sedimentary rate (ESR) at least (it's a better marker for chronic stress than CRP, for the unaware). Serum endocrine markers from the HPA axis would've also been a good idea to rule out confounding (discussed above). IL-1 would've been a good inclusion as well given its' popularity in the literature. From memory, IL-1 plays a role in adaptive immunity signalling, so that (plus the HPA axis endocrine markers) would've nicely allowed the authors to build a more robust picture.

    The data looks fairly clear, but the inferences look somewhat speculative without addressing some of the confounding factors here. Interesting nonetheless!

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    Quote Originally Posted by DMXX View Post
    I'm a bit hesitant to wholesale accept the premise that higher levels of inflammation are correlated with poorer academic performance.

    This could be a chicken-egg paradigm; quite possible that some of the individuals with higher inflammatory marker counts compared to their cohorts were experiencing this as a result of poor academic performance.

    Psychological (or indeed any sort of significant acute or chronic) stress will lead to hypothalamic-pituitary-adrenal (HPA) axis over-activation. Many students have issues with time management or prioritisation skills. It's likely a chunk of these "inflamed" under-achievers have behavioural and/or social reasons for their phenotype.

    Additionally, the association could be a red herring result. Students with pre-existing morbidities which predispose one towards inflammation (e.g. depression, any of the various affective spectrum disorders like fibromyalgia, chronic fatigue syndrome etc.)

    I'm also unsure why they've only used CRP, IL-6, TNF-a and total white cell count for their inflammatory markers... Could've thrown in erythrocyte sedimentary rate (ESR) at least (it's a better marker for chronic stress than CRP, for the unaware). Serum endocrine markers from the HPA axis would've also been a good idea to rule out confounding (discussed above). IL-1 would've been a good inclusion as well given its' popularity in the literature. From memory, IL-1 plays a role in adaptive immunity signalling, so that (plus the HPA axis endocrine markers) would've nicely allowed the authors to build a more robust picture.

    The data looks fairly clear, but the inferences look somewhat speculative without addressing some of the confounding factors here. Interesting nonetheless!
    Here's one search example:
    http://www.ncbi.nlm.nih.gov/pubmed/?...ines+cognition

    Diseases/Disorders:
    A. Schizophrenia:
    http://www.ncbi.nlm.nih.gov/pubmed/26037944

    B. Bipolar disorder: Toxoplasma gondii infection, cognitive status and bipolar disorder
    Cognitive deterioration among bipolar disorder patients infected by Toxoplasma gondii is correlated to interleukin 6 levels.
    http://www.ncbi.nlm.nih.gov/pubmed/25863913
    Among deteriorated patients (defined by scores above 0.10 according to Weschler׳s definition), the IL-6 mRNA expression was twice greater (p=0.01).
    C. Influence of socioeconomic status trajectories on innate immune responsiveness in children.
    http://www.ncbi.nlm.nih.gov/pubmed/22685596
    OBJECTIVES:
    Lower socioeconomic status (SES) is consistently associated with poor health, yet little is known about the biological mechanisms underlying this inequality. In children, we examined the impact of early-life SES trajectories on the intensity of global innate immune activation, recognizing that excessive activation can be a precursor to inflammation and chronic disease...SES was inversely associated with innate immune responsiveness (p=0.003), with persistently low-SES children exhibiting responses more than twice as intense as their high-SES counterparts.
    D. Inflammation and social cognition
    Inflammation impairs social cognitive processing: A randomized controlled trial of endotoxin.(2015)
    http://www.ncbi.nlm.nih.gov/pubmed/25770082
    We found that endotoxin (vs. placebo) led to decreases in performance on the RME test from baseline to the peak of inflammatory response, indicating that acute inflammation can lead to decreases in the ability to accurately and reliably comprehend emotional information from others. Given that deficits in ToM are implicated in neuropsychiatric disorders, including those which may have an inflammatory basis, these results may have implications for understanding the links between inflammation, social cognition, and neuropsychiatric disorders.
    So, a set of possibilities, is that either an innate disposition (perhaps genetic immune response) or an environmental stimulus can exacerbate certain types of illness and impair the patient. The question is whether something like poverty can have a persistent effect, and to what degree that is caused by the environment.
    (correlational/or a cause)
    Last edited by warwick; 01-24-2016 at 04:58 PM.

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    Academic performance is a complex phenotype, so we should expect some interplay between genetics, epigenetics, shared environment and broader environment for sure.

    Prolonged inflammation no doubt contributes to a host of physiological processes (of which we could consider cognition to be one), so that finding isn't a surprise. The links you've kindly share all support the broad correlation here.

    I just don't think the authors are in a position to explicitly identify pre-educational environment as the single factor responsible for the high inflammation (and then the poorer performance).

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    It's all unproven and somewhat speculative, but the environmental explanations of lasting behavioral changaes are certainly interesting:

    Another example (except in this case environmental impacts on stress and GR gene:

    http://www.ncbi.nlm.nih.gov/pubmed/24690014
    The Tutsi genocide and transgenerational transmission of maternal stress: epigenetics and biology of the HPA axis.
    Transmission of parental post-traumatic stress disorder (PTSD) to offspring might be explained by transmission of epigenetic processes such as methylation status of the glucocorticoid receptor (GR) gene (NR3C1).

    Mothers exposed to the genocide as well as their children had lower cortisol and GR levels and higher MR levels than non-exposed mothers and their children. Moreover, exposed mothers and their children had higher methylation of the NR3C1 exon 1F than non-exposed groups.

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    Of course; as is the case with many things in medical genetics these days... We're left guessing what the future puzzle pieces even look like.

    Fantastic, had no idea about other studies looking at epigenetic transmission of stress responses in humans. I'm aware of a study on WWII descendants from the Netherlands who survived a Nazi siege of their town and developed a "thrifty" phenotype in response to nutritional deprivation at the hands of the Nazis.

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    Quote Originally Posted by DMXX View Post
    I'm a bit hesitant to wholesale accept the premise that higher levels of inflammation are correlated with poorer academic performance.

    This could be a chicken-egg paradigm; quite possible that some of the individuals with higher inflammatory marker counts compared to their cohorts were experiencing this as a result of poor academic performance.

    Psychological (or indeed any sort of significant acute or chronic) stress will lead to hypothalamic-pituitary-adrenal (HPA) axis over-activation. Many students have issues with time management or prioritisation skills. It's likely a chunk of these "inflamed" under-achievers have behavioural and/or social reasons for their phenotype.

    Additionally, the association could be a red herring result. Students with pre-existing morbidities which predispose one towards inflammation (e.g. depression, any of the various affective spectrum disorders like fibromyalgia, chronic fatigue syndrome etc.)

    I'm also unsure why they've only used CRP, IL-6, TNF-a and total white cell count for their inflammatory markers... Could've thrown in erythrocyte sedimentary rate (ESR) at least (it's a better marker for chronic stress than CRP, for the unaware). Serum endocrine markers from the HPA axis would've also been a good idea to rule out confounding (discussed above). IL-1 would've been a good inclusion as well given its' popularity in the literature. From memory, IL-1 plays a role in adaptive immunity signalling, so that (plus the HPA axis endocrine markers) would've nicely allowed the authors to build a more robust picture.

    The data looks fairly clear, but the inferences look somewhat speculative without addressing some of the confounding factors here. Interesting nonetheless!
    I'm also hesitant to accept the hypothesis. I myself have a host of inflammatory diseases, including asthma, allergies, arthritis, and the beginnings of atherosclerosis. But I was always the top of my class in school.

    One data point does not make a trend, but it's something. I suppose I could be a special case exception, but if so then I'm a pretty far-flung outlier.

    I have also been diagnosed with a pretty severe case of hyperhomocysteinemia due to a genetic defect in my vitamin B metablism. Perhaps that is a confounding factor. It may be that all contributing factors have not been considered in the study, and it is not the inflammation itself causing the low performance, but some other factor causing both the low performance and the inflammation. Most likely there are a wide range of causes of inflammation, but only some subset are linked to academic performance. The one that causes inflammation in myself may not be the one linked to academic performance.

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    Quote Originally Posted by warwick View Post
    It's all unproven and somewhat speculative, but the environmental explanations of lasting behavioral changaes are certainly interesting:

    Another example (except in this case environmental impacts on stress and GR gene:

    http://www.ncbi.nlm.nih.gov/pubmed/24690014
    The Tutsi genocide and transgenerational transmission of maternal stress: epigenetics and biology of the HPA axis.
    I recall a study that found a link between women exposed to famine and their granddaughters being overweight. It's fascinating that environmental factors can influence gene expression and even be transmitted from one generation to another.

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