Insulin level, cognition, liver disease and CR

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Hi All,>There are three publications that are pdf-available below and the >first (1) introduces how insulin levels, which are measured using >plasma C peptide levels>as>an index, are associated with reduced cognition, the second (2) is >the paper>introduced in (1) and the third

Whoa, thanks for finding these first two, Al! Those are very substantial findings. I think everyone obsesses over glucose, and glycation, because it is easy to see in the "mind's eye" what glucose does directly. Pour a Coca-Cola (or Pepsi, if you are a PepsiCo fan) on yourself, and you become a sticky mess. So, it is easy to speculate that glucose can perpetrate similiar pathology at the molecular level.

But, what people often seem to fail to realize is that insulin perpetrates more "net harm" by my estimation than glucose does in "normal individuals". [ Is anyone reading posts in this group normal? ]

It is harder to explain to someone why insulin is "worse" if they have not attained a degree of comfort with abstract concepts like signal transduction and phosphorylative modification, but that does not make the issue of insulin any less important. It causes your cells to adopt a "posture" that is not conducive to health in the long-term. The way I tend to conceptualize of this effect is that it causes your cells to go "on the clock" in terms of their "survival clock". It would seem that nature has built very intricate "gearworks" inside the cell, and it "knows" that things may mess up and become dysregulated with time.

In fact, it counts on it. So it has built a kind of "planned obsolescence" (to borrow a term used to disparigingly describe Detroit's decision to build cars that broke down quickly "on purpose" to foster further sales) into its overall strategy for maintaining tissue level homeostasis, in order to prevent the generation of aberrant "immortal" cancer cells. By purposely linking a hormone associated with eating with the gradual attenuation of normal physiology activity, nature has "engineered" a way of balancing the growth associated with one' s nutritional state with the appropriate level of "attenuated growth capacity" that is described as "aging". It is evidence that nature "concedes" that it is "imperfect", and so it made its cells fragile, and when "growing", as in the "hyperinsulinemic" (more accurately, "hyper-PI3K-Akt-mTOR......" ], it has orchestrated a "sensitization" to natural, pro-aging influences so as to effect further stabilization,

differentiation, and eventually, death.

I think this may general framework can be elaborated with more specifics from the developmental biologists, but it is one way to make sense of the findings. The longitudinal influences of insulin are going to be quite negative when viewed from this framework, and this is in spite of the "acute" "cytoprotective" influences sometimes associated with insulin. This implies that insulin's anabolic, "cytoprotective" influences are not very compatible with "longitudinal health", and this distinction may involve stem cell dynamics, developmental biology, and "senescence" in very interesting ways.

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T.

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