How long does one have to experience cellular pathologies or mitochondrial dysfunction before becoming symptomatic to your standard? Could take decades.
How long does one have to experience cellular pathologies or mitochondrial dysfunction before becoming symptomatic to your standard? Could take decades.
How many of these “cellular pathologies” or “mitochondrial dysfunction” actually will result in clinical events, Vs remaining as merely “test abnormal values”?
We practice to help people live longer, or feel better. Not for better lab results as an end in and of itself.
It’s also scientific method 101. If one is to assert that “intervention X” is “beneficial”, the burden is on proponents of said intervention to demonstrate benefits. And when we are dealing with otherwise asymptomatic and healthy people, that burden is rightfully higher.
Steve I agree with everything you wrote. But if somebody like Chris Palmer is correct, you can add Alzheimer’s, ADHD, bipolar disorder, schizophrenia, more serious forms of anxiety and depression to the list of clinical events related to the above.
More studies are needed. I’ve never advocated for its opposite. But I see a stultified medicine environment that wants to criticize without even knowing the argument in favor.
Yes I think we agree as well. And if you can draw a causal line from tight glycemic control to a reduction of Alzheimer’s or whatever, then sign me up for sure.
What I won’t want to see is a study of a million people showing that tight glycemic control reduces A1c from 5.0% to 4.9% with 5 zeros in the P value, and have that ballyhooed as the reason why we should do this en masse.
Yes, absolutely—I think you've hit on my general objection better than I did, which is people arguing over numbers in a blood panel which are deemed apparently significant or not, as though splitting hairs (or mg/dL) is somehow doing anything. That is not MY obsession. This to me is a red herring that I see people getting stuck on.
And speaking of red herrings, we don't have an easy, wearable way to measure insulin, so instead serum glucose becomes a proxy. Only it's a lousy proxy, because one can be hyperinsulinemic for a long time before seeing the kind of variability in fasting glucose that might alert you to it.
But if a subnormal glucose response to endogenous insulin turns out to be something that you need to manage, absent diabetes mellitus, then serum glucose is one of the main things you want to keep your eyes on, given their causal relationship.
Of course, glucose isn't everything. It does nothing to measure the results of fructose metabolism, an excess of which starts with IR of the liver, causing increased production of uric acid (mine's very high without interventions) and inhibition of endothelial nitric oxide. If you're trying to get maximum glucose and insulin to the brain cells (and you are), I would argue vasoconstriction is one thing you want to avoid.
Now, if it turns out that the same thing that causes gout is also to a degree upstream of vascular dementia (remember the nitric oxide), and food intake has something to do with it, then I think all this is worth investigating. Appreciate the back-and-forth.
How long does one have to experience cellular pathologies or mitochondrial dysfunction before becoming symptomatic to your standard? Could take decades.
How many of these “cellular pathologies” or “mitochondrial dysfunction” actually will result in clinical events, Vs remaining as merely “test abnormal values”?
We practice to help people live longer, or feel better. Not for better lab results as an end in and of itself.
It’s also scientific method 101. If one is to assert that “intervention X” is “beneficial”, the burden is on proponents of said intervention to demonstrate benefits. And when we are dealing with otherwise asymptomatic and healthy people, that burden is rightfully higher.
Steve I agree with everything you wrote. But if somebody like Chris Palmer is correct, you can add Alzheimer’s, ADHD, bipolar disorder, schizophrenia, more serious forms of anxiety and depression to the list of clinical events related to the above.
More studies are needed. I’ve never advocated for its opposite. But I see a stultified medicine environment that wants to criticize without even knowing the argument in favor.
Yes I think we agree as well. And if you can draw a causal line from tight glycemic control to a reduction of Alzheimer’s or whatever, then sign me up for sure.
What I won’t want to see is a study of a million people showing that tight glycemic control reduces A1c from 5.0% to 4.9% with 5 zeros in the P value, and have that ballyhooed as the reason why we should do this en masse.
Yes, absolutely—I think you've hit on my general objection better than I did, which is people arguing over numbers in a blood panel which are deemed apparently significant or not, as though splitting hairs (or mg/dL) is somehow doing anything. That is not MY obsession. This to me is a red herring that I see people getting stuck on.
And speaking of red herrings, we don't have an easy, wearable way to measure insulin, so instead serum glucose becomes a proxy. Only it's a lousy proxy, because one can be hyperinsulinemic for a long time before seeing the kind of variability in fasting glucose that might alert you to it.
But if a subnormal glucose response to endogenous insulin turns out to be something that you need to manage, absent diabetes mellitus, then serum glucose is one of the main things you want to keep your eyes on, given their causal relationship.
Of course, glucose isn't everything. It does nothing to measure the results of fructose metabolism, an excess of which starts with IR of the liver, causing increased production of uric acid (mine's very high without interventions) and inhibition of endothelial nitric oxide. If you're trying to get maximum glucose and insulin to the brain cells (and you are), I would argue vasoconstriction is one thing you want to avoid.
Now, if it turns out that the same thing that causes gout is also to a degree upstream of vascular dementia (remember the nitric oxide), and food intake has something to do with it, then I think all this is worth investigating. Appreciate the back-and-forth.