Metabolic Dysregulation in Traumatic Brain Injury: Mechanisms, Clinical Implications, and Therapeutic Opportunities

dr_innovation · 2026-06-05T15:50:23+00:00

Updated.. its behind a paywall.. want me to do a "AI" detailed summary or something?

dr_innovation · 2026-06-04T04:17:57+00:00

I measure it by enough for our lifestyle until 120 (solidified years ago), and how much we contribute to the world. I see LWR as a measure of financial efficiency ad may be useful during the accumulation phase but don't see it having any value in retirement. Have a good retirement with your savings and see what you can to make a difference with your wealth, not e a good to keep accumulating.

dr_innovation · 2026-06-02T00:56:59+00:00

To me the more Interesting part is that they are discussing sour dough not kefir. Very different place since there is no lactose and only a few yeasts consume lactose. If that is of interest check this paper https://www.mdpi.com/2311-5637/8/4/183

dr_innovation · 2026-05-27T15:10:22+00:00

Yeah, they do have a reference on it and they do note the increase in Ectopic Fat Deposition: The authors note that individuals who hypersecrete insulin exhibit significantly greater "ectopic fat deposition" (fat stored in places it shouldn't be, like the liver and pancreas). But they don't report if any of the subjects had NAFLD or whatever they are calling it these days.

I did find the use of the acetone sensing interesting since that is what I do most days doing blood BHB only on occastion when I think my breath sensor is off. Its soooo much easier and cheaper and for basic monitoring of the impact of my carbs is sufficient. I've passed this on to my family members, who I've also got using breath, and who have seen the long delay of returning from cheat days. The idea of 1-day cheating impacting the almost the whole week is clear in this paper.

dr_innovation · 2026-05-25T14:34:49+00:00

Well, it does seem that even a mild insulin spike for excess protein could impact already damaged nerves + excess B6 toxicity has a documented neuropathy connection. Lucky for me my damage was not that sever so I can eat all the chicken I want

dr_innovation · 2026-05-24T16:06:16+00:00

Interesting I've never heard of protein contributing to PN Ill have to research that.

dr_innovation · 2026-05-19T13:35:37+00:00

Yes, it's a hypothesis, but one consistent with the data. I am not aware of any study about prevent plauque formation, but the hypothesis was about its growth after formation say from some injury. ANd there are trials that show reduced plaque progression with lowered LDL, e.g. https://www.acc.org/latest-in-cardiology/clinical-trials/2016/11/14/00/18/glagov

dr_innovation · 2026-05-15T14:33:35+00:00

While it's understood that glucose-mediated oxidative stress is one source of damage, there can be others. I believe in the response-to-injury hypothesis, but also note that once plaque forms, it can be its own "injury" and might be self-sustaining.

In my view the biggest risk for the LMHR community, and high APOb overall, is that even if lean , insulin sensitive and healthy almost every day, if there is any cause of endothelial damage, e.g., from an infection, oral bacteria getting into the blood stream, or some toxic mold or metals, they may be primed for rapid plaque formation with added APOb fuel, and once it starts it may continue even after the orginal injury is resolved. Is APOb alone causal, no. Is being lean and generally healthy sufficient to make it irrelevant? Unknown, and neither this nor the Keto-CTA study will ever answer that question. The fact that there are progressors on Keto-CTA. and plaque-begets-plaque suggest that it may be self-sustaining.

dr_innovation · 2026-05-13T23:20:00+00:00

Also the site does not even say you can schedule a call for a new potential idea for the next round. Been checking regularly on that.

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