Moreover, it has a seamless flow of causality from genetic etiology right through to symptomology and disease progression.
No unexplained risk, correlation, or probability.
After 225 YEARS of disease hypothesis, NO such physiological causal model has ever emerged and ever will.
I challenge any biologist, biomedical researcher or specialist physician (or ANYONE ELSE) to provide hard evidence that supports such a complete causal model of addiction.
This mutation complex disallows chloride osmosis through the cell walls. This leads to a number of symptoms, the most devastating of which is a build up of mucosa in the lungs...
→ which leads to chronic respiratory infection
→ which leads to lung scaring
→ which leads to a decline in lung function
→ which leads to eventual death
Now THAT’S a disease with an extremely complex, yet SCIENTIFICALLY PROVEN, genetic etiology, disease entity, symptomology and prognosis.
A very complex genetic anomaly that occurs anywhere throughout the CFTR gene located on the long (q) arm of chromosome 7 at position 31.2, from base pair 116,907,253 to base pair 117,095,955.
More than 1000 mutant combinations can occur - the most common of which is the ΔF508 mutation complex.
The problem with genetic, metabolic or any other reductive, physio-pathological causal model for addictive behaviour is that it involves a leap of faith. All these so called genes associated with addiction are mere weak correlates that do not demonstrate a seamless flow of causality from the genetic anomaly to addictive behaviour.
As such, they are inadequate and invalid causal explanations.
You cannot explain human behaviour through reductionism.
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[4]
Moreover, it has a seamless flow of causality from genetic etiology right through to symptomology and disease progression.
No unexplained risk, correlation, or probability.
After 225 YEARS of disease hypothesis, NO such physiological causal model has ever emerged and ever will.
I challenge any biologist, biomedical researcher or specialist physician (or ANYONE ELSE) to provide hard evidence that supports such a complete causal model of addiction.
Until then, addiction IS NOT a disease.
Hammersley1967 1 month ago
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[3]
This mutation complex disallows chloride osmosis through the cell walls. This leads to a number of symptoms, the most devastating of which is a build up of mucosa in the lungs...
→ which leads to chronic respiratory infection
→ which leads to lung scaring
→ which leads to a decline in lung function
→ which leads to eventual death
Now THAT’S a disease with an extremely complex, yet SCIENTIFICALLY PROVEN, genetic etiology, disease entity, symptomology and prognosis.
(Continued in [4])
Hammersley1967 1 month ago
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[2]
My wife has cystic fibrosis...
A very complex genetic anomaly that occurs anywhere throughout the CFTR gene located on the long (q) arm of chromosome 7 at position 31.2, from base pair 116,907,253 to base pair 117,095,955.
More than 1000 mutant combinations can occur - the most common of which is the ΔF508 mutation complex.
(Continued in [3])
Hammersley1967 1 month ago
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[1]
The problem with genetic, metabolic or any other reductive, physio-pathological causal model for addictive behaviour is that it involves a leap of faith. All these so called genes associated with addiction are mere weak correlates that do not demonstrate a seamless flow of causality from the genetic anomaly to addictive behaviour.
As such, they are inadequate and invalid causal explanations.
You cannot explain human behaviour through reductionism.
Consider the following:
(Cont. in [2])
Hammersley1967 1 month ago