Paul Saladino· MD
basically they're saying here a byproduct of linoleic acid metabolism for hne is the worst thing in the world for humans it's
The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
basically they're saying here a byproduct of linoleic acid metabolism for hne is the worst thing in the world for humans it's
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our studies demonstrate that acute and repeated exposure of adipocytes with physiological low concentrations of hne for hne which is a byproduct of linoleic acid metabolism is sufficient to promote oxidative stress impaired adipogenesis alter the expression of adipocynes like adiponectin or p par gamma agonists which lead to adipocyte hyperplasia and increase lipolytic gene expression and increase free fatty acid release
acute and repeated exposure to physiological low concentrations of h e is sufficient to promote oxidative stress impaired adipogenesis they alter the expression of adipocynes like adiponectin and increase lipolytic gene expression and increase flea fatty acid release
increased levels of linoleic acid in the diet lead to increased levels of linoleic acid in the adipocytes the fat cells and increased levels of linolenic acid and adipocytes lead to increased levels of 4h and e 4 hydroxynol it's pretty well established fat cells cause big fat cells cause metabolic dysfunction excess linoleic acid causes for hne for hne causes big fat cells
4h and e does appear to impair adipocyte biology and this is something i talk about with ben bickman and the they show that with physiologic low concentrations of h e sufficient to promote oxidative stress impaired adipogenesis that was something i got really interested in alter the expression of adipocynes which are the hormones signaling the fat cells to actually divide impaired dipogenesis leads to adipocyte hypertrophy and increased lipolytic gene expression and increased free fatty acid release this i believe is some of the main central pathology around metabolic dysfunction
our studies demonstrate that acute and repeated exposure of adipocytes fat cells with physiologic low concent ations of h& is sufficient to promote oxidative stress impaired adipogenesis that is at the center of metabolic dysfunction when your adipocytes cannot divide they become overly swollen and they release free fatty acids that is called osy hypertrophy versus adite hyperplasia they alter the expression of adipokines and increase lipolytic gene expression to increase free fatty acid release that is metabolic function right there and is connected with a breakdown product of linolic acid known as for hydroxy nonanol
these results provide an insight into the role of hne induced oxidative stress in the regulation of adipocyte differentiation and adipocyte and adipose dysfunction taken together these data indicate a potential role for hne promoting diverse effects toward adipocyte homeostasis and adipocyte differentiation which may be important to the pathogenesis observed in obesity and metabolic syndrome
basically what they're saying is that hne causes impaired adipogenesis hne does not allow the fat cells to divide that leads to hypertrophy and broken fat cells