Thoughts on this study. They found that women with fasting insulin scores in the lowest tertile (<10.3 mIU/L) had a significantly increased risk of developing dementia later. It’s a 34-year followup study on samples collected back in the late 60s. Does insulin have a U-shaped relationship to dementia risk, at least in women? Consequences for going very low carb?
Low insulin linked to increased dementia risk in women
Iced
(The amazing autoimmune 🦄)
#2
Not necessarily, it doesn’t show a direct causality just a link.
I was just reading on the bbc about a link between poor gum health and dementia. Again just a link not necessarily the cause.
Just like there was supposedly a link between being a healthy weight and eating breakfast.
Lauren_Lake
(Lauren Lake)
#3
Yes, I realize it’s just a correlation, but it does have a hazard ratio over 2. I’m trying to imagine what other factors might come into play for women with low insulin in the 60’s (before the dietary guidelines pushed all those grains).
Iced
(The amazing autoimmune 🦄)
#4
Life was so different for women in the 60s That is a hard one, so many factors both dietary and lifestyle.
I also was just thinking of the meds they used back then, they were also very different.
Iced
(The amazing autoimmune 🦄)
#5
Atomic bunny just posted this I thought it might be relevant to your thoughts.
ctviggen
(Bob M)
#8
Maybe not. This was in Sweden:
“In 1968, a representative sample of 1,622 women 38, 46, 50, 54, or 60 years of age and living in Gothenburg, Sweden, were invited to the Prospective Population Study of Women in Gothenburg.”
I have no idea what was going on in Sweden at the time.
There’s no way to get much from this study. This is what they said: “We derived a value of 10.3 mIU/L for the approximate inflection point, below which the risk of dementia is increased.”
The problem is that you’re getting a single sample of insulin and then trying to extrapolate from that over 34 years, with less than 2,000 people. My fasting insulin has been very low (<3) to very high (33), all while on low carb. Insulin is pulsatile.
And these weren’t the original values. They were values of insulin from blood that was frozen:
“Fasting insulin was measured in serum samples from 1968 stored at −20°C for 45 years and validated by comparison with values that had been analyzed at baseline in a subsample of participants using a double antibody method.23 The analysis was performed in the Clinical Chemistry Laboratory at Sahlgrenska University Hospital, Mölndal, Sweden, with Elecsys kits on a Cobas 6000 analyzer (Roche Diagnostics, Basel, Switzerland) by board-certified laboratory technicians blinded to clinical data. Because absolute values were generally low, indicating an underestimation of the original values, we performed a nonparametric analysis based on tertiles that focused on the nonlinear relationship with risk of dementia. Secondary analyses were based on calibrated insulin values that were obtained from comparison of mean values in frozen relative to fresh samples, yielding a calibration factor of 1.88.23 These calibrated insulin values were used to derive approximate cut points characterizing the nonlinear association with risk of dementia and to estimate insulin sensitivity and β-cell function according to the homeostatic model assessment (HOMA) based on the updated computer model.”
They had to do a bunch of mathematical manipulation to come up with something that made sense to them. Anytime you use a model, you’re in trouble. Is the model correct? Maybe, maybe not. (Most likely, not.)
It’s best not to waist brain cells on a study like this.
PaulL
(Bacon is a many-splendoured thing)
#10
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Insulin is essential for the metabolism of glucose by the brain.
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Dementia is caused by the defective metabolism of glucose by neurons (the result of insulin resistance, many researchers believe, hence the suggestion to call Alzheimer’s disease Type III diabetes).
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The reason many early-stage demented patients improve their cognition on ketones is that even when glucose metabolism is defective, the metabolism of β-hydroxybutyrate can remain unaffected.
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Not only that, but β-hydroxybutyrate in the brain has been shown to reduce amyloid plaque and neurofibrillary tangles, both of which seem to be involved in dementia.
So yes, the study is plausible, in the sense that low insulin in an insulin-resistant patient could indeed hamper cognition. I would not expect the same results in patients who had followed a well-formulated ketogenic diet for any length of time, especially since they would be less likely to exhibit symptoms of dementia in the first place.