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.
there's good evidence that the breakdown products of linolenic acid are associated with that phenotyping and fat cells these are things like 4h and e 13 hod e or protein code and so linoleic acid is polyamory effect so we see okay the breakdown parts of linoleic acid are associated with that pathological king type
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our studies demonstrate that acute and repeated exposure of adipocytes fat cells with physiologically low concentrations of hne a toxic aldehyde from the breakdown of linoleic acid are sufficient to promote subsequent oxidative stress impaired adipogenesis that is the hyperplasia that I was talking about alter the expression of adipokines and increase lipolytic gene expression and increase free fatty acid release
four hydroxyone and all that's hne causes impairment of human subcutaneous or depogenesis an induction of adipocyte insulin resistance
the takeaway from this study is that hne comes almost exclusively from the breakdown of linoleic acid in the human body or outside of the human body as we saw in the studies looking at french fries
there's pretty good evidence that hne for hydroxy known and all the breakdown product of linoleic acid is a major culprit in what causes broken and fat cells
where does linoleic acid come from in the human body it comes from what we eat we don't make any linoleic acid in the human body that's why it's considered quote essential
acute and repeated exposure of adipocytes fat cells with physiologically low concentrations of hne a toxic aldehyde from the breakdown of linoleic acid are sufficient to promote subsequent oxidative stress impaired adipogenesis that is the hyperplasia that I was talking about alter the expression of adipocins and increase lipolytic gene expression and increase free fatty acid release
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
causes oxidative stress up regulates lipolytic gene expression increases free fatty acids and leads to broken fat cells and insulin resistance that compound comes from linoleic acid in the human body or outside of the human body if it's in a high linoleic acid oil that is being heated
probably linoleic acid breaks down into hne that product that we know is problematic from French fries h e has all sorts of problems in humans probably hne is one of the single greatest drivers of fat cells turning into broken fat cells and broken fat cells lie at the root of metabolic dysfunction insulin resistance
four hydroxy nonanol causes impairment of human subcutaneous adipogenesis and induction of a diosy insulin resistance again this is a hypothesis this is not proven but I think the conclusions here are pretty clear that a breakdown product of linolic acid for hydroxy nonanol that's where it comes from is involved in the long-term progression toward pathological insulin resistance
there are Downstream products of linolic acid metabolism like 4& that are worsening that process again