A trial balloon, for those who do not claim English as their primary language, is a term relating to "floating an idea", usually in hypothetical context, to gauge reaction. The notion being one of plausible deniability (I never really meant to say/do that). This is the only explanation I can come up with for why Peter/Hyperlipid is going down this whole mitochondrial dysfunction path of his. In his most recent post, he floats the following (I've numbered the steps):
- Mitochondrial dysfunction leads to cytosolic fatty acid derivative accumulation.
- This leads to chronic hyperinsulinaemia via insulin resistance.
- This leads to adipocyte distension.
- This leads to adipocyte insulin resistance.
- This leads to increased plasma FFA delivery at a given level of insulin.
- This leads to increased cytosolic FFA derivatives.
- This leads to mitochondrial ATP production being normalised.
He concludes: "The cost is increased insulin resistance. Oh, and the MECHANISM for improved ATP production is OBESITY. Call this a cost if you wish."
If I understand the premise, Peter is trying to support the notion that IR is the body's reaction to excessive fat accumulation to protect against even more fat accumulation. This is inconsistent with the fact that numerous overweight and obese become insulin resistant yet continue to pile on the pounds for years, but it sounds appealing so let's go with it. Do you see the problem with the above mechanism, however? It's in the bolded statements. If increased FFA derivatives normalized mitochondrial ATP production in step 7, why doesn't the backlog of same in dysfunctional mitochondria not stimulate their own normalization back in step 1? Why would flooding mitochondria with more cytosolic FFA derivatives cause normalization. This makes no sense on its face.
Trial balloon floated.
Keep trying?? 
No comments:
Post a Comment