Paul Saladino· MD
When adipocytes are “broken” by PUFAs, insulin signaling from carbohydrates can worsen this process. In a state of excess PUFAs, carbs can worsen metabolic dysfunction but they don’t initiate this process.
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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.
When adipocytes are “broken” by PUFAs, insulin signaling from carbohydrates can worsen this process. In a state of excess PUFAs, carbs can worsen metabolic dysfunction but they don’t initiate this process.
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the problem is your body fat is dysfunctional because it's full of these poof --is
how they're chemically different they're less stable there are so much less stable that you can see it on your counter when you take out your butter it doesn't melt on
i believe it's primarily driven by a long-term process which begins with excess polyunsaturated fatty acids
excess omega-6 seed oils hold the door open the adipocyte creating inappropriate insulin sensitivity which allows them to take on more and more fat
The problem arises creating pathological insulin resistance when our fat cells break I think most people who have read the literature would agree with this and how do our fat cells get broken well they get broken by a couple of mechanisms I think the most common one is excess polyunsaturated fatty acids I've done lots of podcasts on polyunsaturated fatty acids and the way that they are incorporated into the cell membranes of fat cells the downstream collateral damage from their byproducts of breakdown spoken about this with Tucker Goodrich and Jeff knobs for hne other oxidative products of linoleic acid metabolism are very closely linked to adipocyte dysfunction
even one of the papers that lane uses to suggest that seed oils improve insulin sensitivity is actually showing that they're doing something to mess with normal human metabolism that could longterm lead to pathological insulin resistance at the level of the ocy
my position is that increased amounts of linolic acid and other polyunsaturated fats accumulate in adipocytes leading to this dysfunction long term there is evidence that for hn for hydroxy nool a breakdown product of UGES it linolic acid will cause adipocytes to dysfunction and to behave pathologically just like they do in insulin resistance