New Article Re Nutrient Intake, Amyloid & Glucose Metabolism
Re: New Article Re Nutrient Intake, Amyloid & Glucose Metabo
Russ, thanks for the second paper. It's been a while since I looked at this stuff. BMOC is the key gene I have looked at, along with LRAT, but I see with a quick glance, there are some things I want to read in more detail.
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Re: New Article Re Nutrient Intake, Amyloid & Glucose Metabo
So, if I am understanding correctly Pal you are just guessing that there is a typo as I do not see a correction in the words in an addendum at the end of the study. Guessing as in since the table numbers for glucose metabolism do not agree with their written words. Sometimes, I tend to believe that the people that conduct these studies don't think anyone will read them for accuracy. When they make a mistake like this then I start asking what else did they screw up and is anything they did accurate or worth considering. But, I do try to be a lenient as they often times only have a Doctorate degree and not anything more.
Re: New Article Re Nutrient Intake, Amyloid & Glucose Metabo
WA, Pal's interpretation jives with the data in Table 3. For the life of me, I couldn't reconcile the abstract/summary with that. A simple typo is the best explanation, but I will still follow up with Dr. Mosconi to verify AND with questions about the contradictory information re. SFA. It was also good to be reminded of the obstacles some face absorbing Vitamin A 
I still have to check my SNPs there...
An unintended typo from a scientist put us in a tailspin.
They have NO idea how much their work means to us.
I still have to check my SNPs there...An unintended typo from a scientist put us in a tailspin.
They have NO idea how much their work means to us.-
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Re: New Article Re Nutrient Intake, Amyloid & Glucose Metabo
Now the question is if it causes increased glucose metabolism is this leading to insulin resistance and type 3 diabetes of the brain, as the sat fat reduction in glucose metabolism would indicate a protection as long as it does not become to low and the world makes sense as the vegetables have glucose in them and fat does not so they should be raising it and leading possibly to type 3 diabetes. Sugar comes from plants not fat.
Re: New Article Re Nutrient Intake, Amyloid & Glucose Metabo
Phew. And thank you to the clever clever people who saw the typo then puzzeled it out. I didn't even realise the contradiction initially or even later.
Um...can I say yipee again being woman, apoe4 with family history cos I will get the best benefit from the folate and carotene?
Is this correct?
<head spins>
Um...can I say yipee again being woman, apoe4 with family history cos I will get the best benefit from the folate and carotene?
Is this correct?
<head spins>
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Re: New Article Re Nutrient Intake, Amyloid & Glucose Metabo
The answer to your question requires further study and is not addressed in this study as they need more longitudinal studies. They also did not address some key points. What they established is there are possible different glucose metabolism a created by different diets. They did not establish if there could be other reasons for the different glucose metabolisms. What this will be able to do in the future is possibly answer your question. They did not establish if all glucose metabolisms are in the healthy range or if any or which ones are outside of the healthy range. Now we know fr other studies that higher blood glucose increases the risk of AD the higher it goes above 115 the risk goes higher. 115 appears to be the starting point of higher risk. Once they scan people at 115 and higher they can determine a safe zone high end image. Then we find the people that have diminished glucose metabolism as that is also considered a risk and establish the low zone range. Then we look at these and see where they fit and then make a determination.
On another note there was a study done that stated the higher glucose level made the ab plaques more toxic and that will be tomorrow's bedtime story of how the Prince saved the Princess from the evil toxic plaque invaders.
On another note there was a study done that stated the higher glucose level made the ab plaques more toxic and that will be tomorrow's bedtime story of how the Prince saved the Princess from the evil toxic plaque invaders.
Re: New Article Re Nutrient Intake, Amyloid & Glucose Metabo
Stavia, based upon this paper, using Pal's explanation (of a typo,) YES- E4 women with a family history did get the best boost in glucose metabolism with beta carotene and folic acid
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Re: New Article Re Nutrient Intake, Amyloid & Glucose Metabo
you will as evidenced in the small study get increased glucose metabolism perhaps as the study was too small to say 100 percent yes., it is not decided if that will benefit you as the boost may be too high causing type 3 diabetes and AD or it could boost you out of low glucose metabolism which causes AD and into the safe range based on studies of glucose metabolism and AD.
Re: New Article Re Nutrient Intake, Amyloid & Glucose Metabo
Here's a copy of the email I sent to Dr. Mosconi trying to clear up the contradictions in this paper. I'll share her reply when and if I receive one
Dear Dr. Mosconi,
I am a homozygous APOE4 carrier, writing on behalf of a group of E4 carriers https://www.apoe4.info working to hammer out an Alzheimer's prevention protocol for our population.
We were very pleased to see your recent paper, Nutrient intake and brain biomarkers of Alzheimer's disease in at-risk cognitively normal individuals: a cross-sectional neuroimaging pilot study. Obviously, this is a topic of great importance to us. However, we have a few questions regarding your conclusions that I hope you can help us clear up.
From the paper:
"β-carotene and folate were associated with reduced glucose metabolism for women, apolipoprotein E epsilon 4 (APOE4) carriers and participants with positive AD family history, but not for their risk-free counterparts."
This sentence indicates that β-carotene and folate are associated with reduced glucose metabolism for APOE4 carriers; yet the data in Table 3 contradicts this. Please clarify the effect of these nutrients on our population.
Secondly, please help us understand this part of the conclusion from your paper:
"The associations of vitamin B12, vitamin D and ω-3 PUFA with PiB retention were independent of gender, APOE and family history. The identified nutrient combination was associated with higher intake of vegetables, fruit, whole grains, fish and legumes, and lower intake of high-fat dairies, meat and sweets."
Our confusion comes from the fact that the foods that comprised the B12 group in your paper were: meat, butter, eggs; yet your conclusion recommends restricting high fat dairies and meat. Why the contradiction in the conclusion?
"Higher consumption of saturated fats was associated with lower brain glucose metabolism, albeit weakly...Specifically, women, individuals with positive family history and APOE ε4 carriers showed the strongest associations between β-carotene, folate and saturated fats on glucose metabolism as compared with their risk-free counterparts."
Lastly, given the positive effect of reduced amyloid deposition from the B12 food group, all high in saturated fat, we were struck by the contradiction advising against them (due to reduced glucose metabolism) for E4 carriers. I wonder if our population should make a distinction between the types of saturated fat? Perhaps salad dressings, processed meats and sweets have other negative attributes that could be contributing to their effect?
Once again, we are very grateful for your work. We believe that diet will play a vital role in prevention Alzheimer's for our population. Any clarification that you or your colleagues can offer would be much appreciated.
Respectfully,
Dear Dr. Mosconi,
I am a homozygous APOE4 carrier, writing on behalf of a group of E4 carriers https://www.apoe4.info working to hammer out an Alzheimer's prevention protocol for our population.
We were very pleased to see your recent paper, Nutrient intake and brain biomarkers of Alzheimer's disease in at-risk cognitively normal individuals: a cross-sectional neuroimaging pilot study. Obviously, this is a topic of great importance to us. However, we have a few questions regarding your conclusions that I hope you can help us clear up.
From the paper:
"β-carotene and folate were associated with reduced glucose metabolism for women, apolipoprotein E epsilon 4 (APOE4) carriers and participants with positive AD family history, but not for their risk-free counterparts."
This sentence indicates that β-carotene and folate are associated with reduced glucose metabolism for APOE4 carriers; yet the data in Table 3 contradicts this. Please clarify the effect of these nutrients on our population.
Secondly, please help us understand this part of the conclusion from your paper:
"The associations of vitamin B12, vitamin D and ω-3 PUFA with PiB retention were independent of gender, APOE and family history. The identified nutrient combination was associated with higher intake of vegetables, fruit, whole grains, fish and legumes, and lower intake of high-fat dairies, meat and sweets."
Our confusion comes from the fact that the foods that comprised the B12 group in your paper were: meat, butter, eggs; yet your conclusion recommends restricting high fat dairies and meat. Why the contradiction in the conclusion?
"Higher consumption of saturated fats was associated with lower brain glucose metabolism, albeit weakly...Specifically, women, individuals with positive family history and APOE ε4 carriers showed the strongest associations between β-carotene, folate and saturated fats on glucose metabolism as compared with their risk-free counterparts."
Lastly, given the positive effect of reduced amyloid deposition from the B12 food group, all high in saturated fat, we were struck by the contradiction advising against them (due to reduced glucose metabolism) for E4 carriers. I wonder if our population should make a distinction between the types of saturated fat? Perhaps salad dressings, processed meats and sweets have other negative attributes that could be contributing to their effect?
Once again, we are very grateful for your work. We believe that diet will play a vital role in prevention Alzheimer's for our population. Any clarification that you or your colleagues can offer would be much appreciated.
Respectfully,
Re: New Article Re Nutrient Intake, Amyloid & Glucose Metabo
Great letter, Julie!
