Was I Wrong?
In honor of The Neurocritic's 10th anniversary, I'd like to announce a new occasional feature:
Was I Wrong?
In science, as in life, we learn from our mistakes. We can't move forward if we don't admit we were wrong and revise our entrenched theory (or tentative hypothesis) when faced with contradictory evidence. Likewise, it's possible that some of the critiques in this blog are no longer valid because additional evidence shows that the authors were correct. And vindicated. At least for now...
I've been collecting possible instances of this phenomenon for months, and I'll preview two of these today.
(1) In November 2015, I said that Obesity Is Not Like Being "Addicted to Food". Drugs of abuse are consistently associated with decreases in D2 dopamine receptors, but D2 receptor binding in obese women is not different from that in lean participants (Karlsson et al., 2015). Conversely, μ-opioid receptor (MOR) binding is reduced, which supports lowered hedonic processing. After the women had bariatric surgery, MOR returned to control values, while the unaltered D2 receptors stayed the same.
However, a recent study in mice “points to a causal link between striatal dopamine signaling and the outcomes of bariatric interventions” (Han et al., 2016). How relevant is this new finding for clinical studies in humans?
(2) In another post, I poo-pooed the notion that there is One Brain Network for All Mental Illness. However, a subsequent paper in Molecular Psychiatry claimed that common psychiatric disorders share the same genetic origin (Pettersson et al., 2015). If so, could this result in common brain
In the future, I'll take a closer look at these and other examples to see if I should revise my opinions.
posted by The Neurocritic @ 11:56 PM
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6 Comments:
Obesity may correlate to discovered or discoverable genes in a pattern of neurons in a network. If that pattern is unique to an individual despite similarities in patterns of individuals, then the pattern is a correlate of an intangible, imperceptible individual predisposition towards obesity. The causal predisposition is correlate of perceptible neuro-genetic pattern. Pattern alone is a cause only if it is necessary and sufficient condition in all cases of obesity. Additional cause of predisposition is unconscious desire of knower of body in mind to experience obesity in mind involving sense impressions of body in mind creating body image. Knower in mind identifies with body image. Only in mind are body and obesity experienced as body image both with joy and sorrow and pleasure and pain for which experience body is born with the predisposition.
I still think you're right about the futility in searching for a "mental illness" brain network. To me, there are just too many steps between genotype and phenotype for it to be so simple. Shared genes may simply indicate broad dysfunction in the brain that manifests in unique ways depending on environmental input and gene-x-gene interactions - hence their different clinical presentations.
I think you're still probably right about the futility of searching for a "mental illness" network. There are simply too many steps between genotype and phenotype for it to be so simple. Also, shared genetic origin seems to indicate genes that promote broad dysfunction in the brain that manifest uniquely in different disorders (depending on environmental input and interaction with other genes). That is, I would still reasonably expect the brain to look different for two mental disorders even if the disorders appear to be caused by the same genes (as may be the case for anxiety & depression). Otherwise, their outcomes would be theoretically indistinguishable, right?
good
It is necessary that energy movement in brain and also in synthesizing genes looks different for two mental disorders as may be the case for anxiety & depression. The disorders are so named by behavior of body observed in own mind or that of the psychiatrist. Mind is intangible (non material) and so is feeling of anxiety or depression. Their correlation is to intangible predispositions that create in mind anxiety and depression correlated to looked at phenotype behavior, looked at energy movement in brain and genes and also to 'not looked at but only felt in mind' and intangible anxiety and depression. The energy movements looked at and phenotype behavior looked at are co-created as looked at events. What creates them are the intangible predispositions correlated to them and they create them with power of life as moving energy in neurons. Feelings and images in mind which is consciousness, are intangible but their tangible correlates are called genoneuro types and pheno types. All that are tangible are known in mind by perception but only after creation by intangible energy (psychic and material coming together)with creation conforming to predispositions correlated to the perceived genoneuro types and pheno types which are unrefined sets of perceivable and tangible correlations
Obesity may correlate to discovered or discoverable genes in a pattern of neurons in a network. If that pattern is unique to an individual despite similarities in patterns of individuals, then the pattern is a correlate of an intangible, imperceptible individual predisposition towards obesity. The causal predisposition is correlate of perceptible neuro-genetic pattern. Pattern alone is a cause only if it is necessary and sufficient condition in all cases of obesity. Additional cause of predisposition is unconscious desire of knower of body in mind to experience obesity in mind involving sense impressions of body in mind creating body image. Knower in mind identifies with body image. Only in mind are body and obesity experienced as body image both with joy and sorrow and pleasure and pain for which experience body is born with the predisposition.
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