7 ms·

Is diet-induced (or even diet-associated) Alzheimer's Disease a proven phenomenon in the first place? The article seems to be pretty speculative on the whole th

Is diet-induced (or even diet-associated) Alzheimer's Disease a proven phenomenon in the first place? The article seems to be pretty speculative on the whole thing, and I'm under the impression that the research on lifestyle risk factors is quite inconclusive (e.g. risk factors show up in ecological studies but produce no significant difference in controlled intervention trials).

voidlogic 11y ago
>I'm under the impression that the research on lifestyle risk factors is quite inconclusive Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/ Conclusions: "Altogether, the results from these studies provide strong evidence in support of the hypothesis that AD represents a form of diabetes mellitus that selectively afflicts the brain."
- 0xcde4c3db 11y ago
  This seems to be a much better source than the article, but I don't think it's actually claiming to show any clear connection to diet. A high-fat diet is mentioned in the description of a mouse model of type 2 diabetes (which the authors then seem to say didn't actually serve as a good Alzheimer's model), but I don't see the authors actually making a direct case for dietary influence. The article, by contrast, has a headline worded as though diet-induced Alzheimer's disease is an established phenomenon and the type 3 diabetes hypothesis is a proposed explanation of that phenomenon.
rhinoceraptor 11y ago
There is evidence of the neuroprotective effects of a ketogenic diet (low carb, moderate protein, very high fat) [1][2]. The original formulation of the ketogenic diet was for epilepsy, after all [3]. The dogma for decades has been that the brain needs glucose to function. A highly simplified and inaccurate explanation of Alzheimer's is that the brain has diminished capacity to use glucose. Luckily, the body has an alternate fuel source: ketones. The problem is most people never enter ketosis, where the body is depleted of glycogen and resorts to converting fat to ketone bodies. [1]: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2367001/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2367001/ [2]: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826507/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826507/ [3]: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133288/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133288/
- gavazzy 11y ago
  Blindly encouraging a ketogenic diet can actually be damaging. While the average person slightly benefits from a high-fat, low-carb diet, a small group of people (who have the APOE4 allele) are unable to properly digest fat and thus are greatly harmed by it. Similarly, light alcohol consumption seems to slightly benefit the majority of people. But, for those with APOE4, it causes significant harm. So, tonic for one group is toxic to another. It is far better if Alzheimer's treatment is prescribed on a case-by-case basis, based on genetic, environmental, and familial factors. This maximizes the outcomes for all, and not just the average.
  - mrfusion 11y ago
    Do you have sources for those? I've never heard that.
  - mrfusion 11y ago
    So you think apoe4's should eat a high carb diet?
    - gavazzy 11y ago
      Not necessarily high in sugar, since the insulin causes just as much damage as high fat. But a lower-fat diet would be beneficial
  - einarvollset 11y ago
    You seem to have those the exact wrong way around, or? I have never heard any evidence that people with APOE mutations are "greatly harmed" by eating a ketogenic diet. Link? Ditto for alcohol.
    - gavazzy 11y ago
      My original post is correct. APOE 4/4 is sensitive to dietary fat; high fat diets cause large LDL [0]. Further, fat causes atherosclerosis in APOE 4/4 individuals more quickly than others [1]. It would make sense that APOE 4/4 would have this effect, because it is the "defective" form of APOE. Individuals with APOE 4/4 do not clear oxidized fats from the brain as quickly as APOE 2 or 3 individuals. [0] http://jn.nutrition.org/content/134/10/2517.full http://jn.nutrition.org/content/134/10/2517.full [1] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674716/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674716/

voidlogic 11y ago

>I'm under the impression that the research on lifestyle risk factors is quite inconclusive Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/ Conclusions: "Altogether, the results from these studies provide strong evidence in support of the hypothesis that AD represents a form of diabetes mellitus that selectively afflicts the brain."

0xcde4c3db 11y ago
This seems to be a much better source than the article, but I don't think it's actually claiming to show any clear connection to diet. A high-fat diet is mentioned in the description of a mouse model of type 2 diabetes (which the authors then seem to say didn't actually serve as a good Alzheimer's model), but I don't see the authors actually making a direct case for dietary influence. The article, by contrast, has a headline worded as though diet-induced Alzheimer's disease is an established phenomenon and the type 3 diabetes hypothesis is a proposed explanation of that phenomenon.

rhinoceraptor 11y ago

There is evidence of the neuroprotective effects of a ketogenic diet (low carb, moderate protein, very high fat) [1][2]. The original formulation of the ketogenic diet was for epilepsy, after all [3]. The dogma for decades has been that the brain needs glucose to function. A highly simplified and inaccurate explanation of Alzheimer's is that the brain has diminished capacity to use glucose. Luckily, the body has an alternate fuel source: ketones. The problem is most people never enter ketosis, where the body is depleted of glycogen and resorts to converting fat to ketone bodies. [1]: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2367001/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2367001/ [2]: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826507/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826507/ [3]: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133288/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133288/

gavazzy 11y ago
Blindly encouraging a ketogenic diet can actually be damaging. While the average person slightly benefits from a high-fat, low-carb diet, a small group of people (who have the APOE4 allele) are unable to properly digest fat and thus are greatly harmed by it. Similarly, light alcohol consumption seems to slightly benefit the majority of people. But, for those with APOE4, it causes significant harm. So, tonic for one group is toxic to another. It is far better if Alzheimer's treatment is prescribed on a case-by-case basis, based on genetic, environmental, and familial factors. This maximizes the outcomes for all, and not just the average.
- mrfusion 11y ago
  Do you have sources for those? I've never heard that.
- mrfusion 11y ago
  So you think apoe4's should eat a high carb diet?
  - gavazzy 11y ago
    Not necessarily high in sugar, since the insulin causes just as much damage as high fat. But a lower-fat diet would be beneficial
- einarvollset 11y ago
  You seem to have those the exact wrong way around, or? I have never heard any evidence that people with APOE mutations are "greatly harmed" by eating a ketogenic diet. Link? Ditto for alcohol.
  - gavazzy 11y ago
    My original post is correct. APOE 4/4 is sensitive to dietary fat; high fat diets cause large LDL [0]. Further, fat causes atherosclerosis in APOE 4/4 individuals more quickly than others [1]. It would make sense that APOE 4/4 would have this effect, because it is the "defective" form of APOE. Individuals with APOE 4/4 do not clear oxidized fats from the brain as quickly as APOE 2 or 3 individuals. [0] http://jn.nutrition.org/content/134/10/2517.full http://jn.nutrition.org/content/134/10/2517.full [1] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674716/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674716/