MIND diet

Alzheimer's, cardiovascular, and other chronic diseases; biomarkers, lifestyle, supplements, drugs, and health care.
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Julie G
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Re: MIND diet

Postby Julie G » Mon Feb 05, 2018 11:52 am

I agree that nuances are key to finding the best diet for our genotype. While the NORDIC diet is a move in the right direction, I have several concerns for our genotype. First is the effect that rapeseed oil, otherwise known as canola oil, may have on brain health. It’s recently been implicated in worsened cognition in AD mice as described in this study. From the abstract:
At this time point we found that chronic exposure to the canola-rich diet resulted in a significant increase in body weight and impairments in their working memory together with decrease levels of post-synaptic density protein-95, a marker of synaptic integrity, and an increase in the ratio of insoluble Aβ 42/40. No significant changes were observed in tau phosphorylation and neuroinflammation. Taken together, our findings do not support a beneficial effect of chronic canola oil consumption on two important aspects of AD pathophysiology which includes memory impairments as well as synaptic integrity. While more studies are needed, our data do not justify the current trend aimed at replacing olive oil with canola oil.

On the other hand, olive oil has consistently been found to have a positive effect on brain health and cognition. This paper suggests that it even benefits our genotype specifically.

My other concern is centered around the recommendation for cereals, crackers, and breads made with whole-grain barley, oats, and rye. As someone with a DXed gluten sensitivity, I’ve chosen to avoid all grains and replace them with vegetables, offering very similar amounts of fiber and likely higher levels of vitamins, minerals, and antioxidants. Since doing so, my health has taken a dramatic turn for the better. Lifelong widespread body pain & GI issues are gone. I know that many in the community are also avoiding grains for similar reasons, including lectin sensitivities. This avoidance makes sense when viewing the E4 gene from an evolutionary perspective. Our gene is the ancestral gene. As such, it's predated agriculture by hundreds of thousands of years. Some scientists hypothesize that the E3 and E2 variants may even have evolved to help folks better adapt to agricutural products.

Debating the nuances is complex, but likely key to finding what works best for each of us. That said, bio-individuality aside, strong signals emerge when you examine the evidence.

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Re: MIND diet

Postby Orangeblossom » Tue Feb 06, 2018 2:35 am

alangreenmd wrote:The MIND diet is excellent step in right direction in that based upon science. However MIND diet has one major problem for E4 community in that did not include APOE type. Therefore, MIND diet can be considered very good diet for the general population of E3/E2 persons in 58-95 age group for prevention of AD.

Looking at the Kivipelto 21 year study entitled, "APOE4 magnified lifestyle risk for dementia" and followed people in age group 50-71; Kivipelto found extreme difference in APOE4 carriers vs non-APOE4 carriers in risk in this middle-aged group. In particular saturated fats in highest quartile increased risk 11.3 fold compared to 1.1 for non-E4. Alcohol consumption in frequent vs never increased risk 7.4 fold in E4 carriers and DECREASED RISK 0.6 in non-E4.

This shows both alcohol and saturated fats had 10 fold greater adverse impact on E4 carriers vs non-E4 carriers in middle age group. When comes to adverse impact lifestyle and dietary factor; it's all in the details: age group and APOE type.

The previously discussed Nordic diet was extraordinary in that looked at APOE status.

The MIND diet appears very good as regards fruits, vegetables and grains. However, being E4 carrier, Kivipelto study would suggests that you should modify MIND by elimination of alcohol and decrease the amount of saturated fats and red meat.

Your approach of studying papers published in science journals is excellent. The MIND diet is good in that based upon science; just not based upon the science of risk regrading E4 carriers.

As regards diet, the single most important thing to know is BEWARE all advice not based upon long term population studies. MIND is based upon a 5 year large scale population study; so an excellent starting point.


I often see this study being used to show E4s should avoid sat fats. but if you read it in detail it states

"Dietary fat intake was determined as daily fat intake from spreads, and the amount of polyunsaturated (PUFA) and saturated (SFA) fatty acids were calculated from these data." :?

Therefore I do not think it is a good idea to generalise too much from this about it in terms of an unprocessed foods diet. Spreads are not a good way of looking at sat fat intake.

For more info about spreads and how these are negative for health I would recommend reading more on fats such as Nina Teicholz's Big Fat Surprise.

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Re: MIND diet

Postby alangreenmd » Tue Feb 06, 2018 9:18 am

Hi Julie,
Paper you posted, "Effects of canola oil consumption on memory, synapse and neuropathology in the transgenic mousw model of Alzheimer's disease, 2017 by Lauretti and Pratico, was an excellent attempt at fact-based recommendations. Unfortunately, a close look at study reveals study is a COMPLETE BUST.
They used 3xTg transgenic mice, same mice used in many Rapamycin studies I report in my website.
They did the same tests.
One big problem; They fed the control mice regular chow and the study mice canola enriched chow. At 12 months:
Weight control mice: 31.88 gm
Weight canola mice: 37.71 gm.
The Canola mice weighed 18% more than regular chow mice.

My conclusion: Fat mice are dumb mice compared to fit mice.

The problem for researchers, they were not trying to show fat mice are dumb mice; they were doing an experiment about canola oil. So they just published the report anyway.

What would be needed would be a study with olive oil, canola oil and diet adjustment so all mice get same amount calories and same weight.

As regards comment about Gluten sensitivity. Gluten sensitivity is very well defined medical disease. Most famous case is Nola Djokovic. He was struggling as number 3 tennis player in world for 5 years. He then switched to gluten free diet and for 3 years was unbeatable demolishing both Nadal and Federer. Unfortunately Djokovic recently developed a sore elbow at age 30. We would all like to know what switching to gluten free diet did for your tennis game.

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Re: MIND diet

Postby circular » Tue Feb 06, 2018 11:53 am

Martha Claire Morris, of MIND diet fame, did a recent podcast with Evolving Past Alzheimer's. You might want to have a listen. If I recall correctly she discusses working on a cookbook with her daughter. I'm not sure if it's out or soon to be out. She also has an ongoing study that sounds like it will look in depth at more variables (starting just after 18 min), including, I believe APOE.
ApoE 3/4 > Thanks in advance for any responses made to my posts.

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Julie G
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Re: MIND diet

Postby Julie G » Tue Feb 06, 2018 1:38 pm

Great comments, Alan. The interesting thing about the canola oil study is that the authors claim to have used an isocaloric diet. We communicated with them after the publication of the study. If true, it might provide some important clues.

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Re: MIND diet

Postby alangreenmd » Tue Feb 06, 2018 7:26 pm

Thanks Julie,
They said control group had regular chow and other group had "canola oil-enriched diet (50 mg/Kg, CO)". They used Mazola canola oil.
To me, standard mouse chow is pretty bland; but mix in some canola oil and it's like Dunkin donuts.

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Re: MIND diet

Postby Julie G » Tue Feb 06, 2018 8:16 pm

They said control group had regular chow and other group had "canola oil-enriched diet (50 mg/Kg, CO)". They used Mazola canola oil.
To me, standard mouse chow is pretty bland; but mix in some canola oil and it's like Dunkin donuts.

Agreed... but if the diets were truly isocaloric, meaning controlled for identical caloric intake, it shouldn't matter, right? That would indicate that something about the canola oil itself caused the weight gain.


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