Fructose Alters Brain Genes Negatively. How To Counter This From Peat Perspective?

[lollipop]

How to counter such a study from a Ray Peat perspective?

Fructose alters hundreds of brain genes, which can lead to a wide range of diseases

 

[Jayfish]

I wish they would "in rats" to headlines like these.

 

[lollipop]

I wish they would "in rats" to headlines like these.

I know. AND what people were questioning me about was it was fructose water. I always argue fructose or sweetened grain carbs like donuts, cakes, etc. are the problem. This study used pure fructose and water...

 

[ecstatichamster]

You would have to read the study. This is a press release. But it talks about altering genes. That is a surrogate endpoint. What does it mean? For morbidity or mortality? Anything? Nothing?

 

[Tarmander]

This is my opinion, but I don't think you should use peats ideas, formed into a philosophy, to counter other arguments. Not only is it kind of missing the point, but peats ideas don't really even work that well in that capacity. Plus you have to dumb him down to work that way. His articles are long, and "sugar good!" just isn't going to cut it against brain washed people who might look at an article like this and think "wow this sure sounds like high science!" Obviously you can do what you want, I'm not trying to alter what you think is best. Peat's stuff just doesn't work well as a bludgeoning device.

 

[BobbyDukes]

Why doesn't somebody show Peat the article? I'm sure he wouldn't mind.

 

[CarbAppreciator]

Since pure fructose doesn't exist in nature, I would expect a drastic change in active genes if that's all an organism is eating. I think RP said it's always good to have some glucose with the fructose. I don't remember why he said that put maybe it has to do with insulin.

 

[lollipop]

Thanks everyone for your help. I do not even try to argue using Peat's ideas. I am simply not knowledgeable enough. I always point to his website. Problem is no one takes the time to study. Frustrating imo...so I simply keep studying and let people believe what they want. I just put this here out of curiosity what you guys might say.

 

[Tarmander]

Thanks everyone for your help. I do not even try to argue using Peat's ideas. I am simply not knowledgeable enough. I always point to his website. Problem is no one takes the time to study. Frustrating imo...so I simply keep studying and let people believe what they want. I just put this here out of curiosity what you guys might say.

Ahh if that is the case I may have been misplaced in my comment.

Addressing the article...one thing i have gathered from peat is that most science is not to discover or illuminate, but to further some type of agenda. I don't see the actual study but this article is very obviously anti sugar and pro fish oil.

But does this study actually tell us anything? Not really. What was the rest of the rat diet? The usual Pufa laden grain diet? Why didn't they test other types of fat like saturated or vegetable oils?

Studies can be very easily manipulated to show what you desire. Peat may Talk about the benefits of sugar, but he often mentions the value of liver. I could probably stress myself out eating pure fructose and no fat solubles. I'm pretty sure if we sent this study to Peat he would completely ignore it.

 

[sladerunner69]

Fructose alters hundreds of brain genes, which can lead to a wide range of diseases

The problem with this study, and many similar ones resulting from corporate academia, is that it's essentially stipulation based upon a false premise. Please allow me to elaborate.

The gene mutations that the researchers observe have long been thought to eb associated with two main degenerative conditions- diabetes, and heart disease. Looking intot hese mRNA transcriptions or gene "mutations" it is apparent they they represent an increased propensity for rat glycolation of sugar, which the authors of the study seem to immediately assume is intimately connected with diabetes and heart disease. However, as true purveyors of biochemistry understand these two conditions much differently then the corporate research students, and know that diabetes results from an inefficiency in sugar metabolism, not the metabolism of sugar itself. They are actually using circular reasoning, and not exploring the base concern of the study, which should be "what causes diabetes?". The reasoning is simply: sugar intake causes diabetes> sugar intake emphasizes the transcription of a certain gene > this certain gene increases sugar intake > this gene causes diabetes.....

In other words, these transcriptome and DNA methylome changes, that the authors point to as a sign of poor health, are in fact a signs of good health. They show an increase affinity for glycolsis.
Then the DHA mediated changes are also inverted, they should be a sign of poor metabolic function, but the authors intuitively saw them as a sign of lengthended lfie span, because all the genes expressed was an icnreased concentration of DHA within the phosphorolipids of the cell wall.

The study even starts by asserting that "DHA is an important anti-oxidant that is present in too small quantities to make any difference"! How ridiculous when we know that DHA is always accompanied by free fatty acids that are responsible for significant amount of oxidative damage in the tissues!

This study helps demonstrate the common disconnect between what scientists believe or think they understand about biology, and what fundamental biochemistry dictates.

 

[DaveFoster]

The problem with this study, and many similar ones resulting from corporate academia, is that it's essentially stipulation based upon a false premise. Please allow me to elaborate.

The gene mutations that the researchers observe have long been thought to eb associated with two main degenerative conditions- diabetes, and heart disease. Looking intot hese mRNA transcriptions or gene "mutations" it is apparent they they represent an increased propensity for rat glycolation of sugar, which the authors of the study seem to immediately assume is intimately connected with diabetes and heart disease. However, as true purveyors of biochemistry understand these two conditions much differently then the corporate research students, and know that diabetes results from an inefficiency in sugar metabolism, not the metabolism of sugar itself. They are actually using circular reasoning, and not exploring the base concern of the study, which should be "what causes diabetes?". The reasoning is simply: sugar intake causes diabetes> sugar intake emphasizes the transcription of a certain gene > this certain gene increases sugar intake > this gene causes diabetes.....

In other words, these transcriptome and DNA methylome changes, that the authors point to as a sign of poor health, are in fact a signs of good health. They show an increase affinity for glycolsis.
Then the DHA mediated changes are also inverted, they should be a sign of poor metabolic function, but the authors intuitively saw them as a sign of lengthended lfie span, because all the genes expressed was an icnreased concentration of DHA within the phosphorolipids of the cell wall.

The study even starts by asserting that "DHA is an important anti-oxidant that is present in too small quantities to make any difference"! How ridiculous when we know that DHA is always accompanied by free fatty acids that are responsible for significant amount of oxidative damage in the tissues!

This study helps demonstrate the common disconnect between what scientists believe or think they understand about biology, and what fundamental biochemistry dictates.

Well said. When you use the wrong formula, every input will give you the incorrect output.

 

[tyw]

This study came up in another place on the Internet which I frequent, and I guess I can share my opinions here as well

Notes will be placed inline, Indented and tagged with [TYW NOTE]

----

Full Study doesn't prove anything wink emoticon --http://www.sciencedirect.com/.../pii/S2352396416301438

(a) This is not PUFA-controlled. I have said multiple times that PUFA + Fructose is horrible (http://high-fat-nutrition.blogspot.com/.../protons-and...).

Total fat intake was "10 g per 100 g of diet" ie: 20% fat (almost all of it likely PUFA. This is very bad on it's own)

This point alone is enough to question the veracity of the study.

(b) 15% of total calories in Fructose. This is a lot gasp emoticon Most people shouldn't do this.

NOTE: We have to assume that gene expression changes are actually significant to behaviour. They did show behavioural changes, so we can clearly see that BOTH Fructose and Fructose + DHA groups had "impaired behaviour"

but also note that ...

(c) Control Group without Fructose nor DHA did the best

All this shows is that DHA is helping to mitigate the bad effects of Fructose + PUFA. This is likely through the n-6 displacement effect of DHA.

What would happen if you just gave the control group DHA? (the fact that the researchers didn't do this is already a bias)

Or even better, what would happen if you don't give rats any PUFA to begin with wink emoticon? Look up "PUFA depletion diets", rats under these diets fared BETTER than regular rats **so long as B-vitamin deficiencies were corrected**.

DHA here just corrected for PUFA toxicity. The real problem is PUFA toxicity, not "DHA is good" or "Fructose is bad".

----

[TYW NOTE]: someone then commented something along the lines of "I imagine that a DHA-only group would have performed the best", and that "DHA is PUFA, so it can't correct its own toxicity. and long chain PUFA are "essential fatty acids" for a reason--the body has limited ability to generate them."

My response follows....
​

DHA is "bad for mitochondria" in the same sense that all PUFA is bad.

DHA can displace n-6 PUFAs from cell membranes --http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4555124/

These are Completely separate issues, and we should never complect the 2 wink emoticon

DHA or EPA in eukaryotic cell membranes have specific uses, and are arguably useful under certain contexts, and definitely more useful than common n-6 fats, precisely because of their higher unsaturation.

Do not confuse "seasonal" / temperature-dependent PUFA accumulation in eukaryotic cell membranes from the use of PUFA in mitochondrial Electron Chain Transport (which is "bad" for all the reasons that Peter @ Hyperlipid has stated).

Now, one may say that DHA and EPA are not used in ECT. This is likely true, but I cite studies which clearly show DHA / EPA integration into mitochondrial membranes very readily, with similar "bad effects" -- Docosahexaenoic Acid (DHA)

Do not confuse mitochondrial membranes from eukaryotic cell membranes wink emoticon

[TYW NOTE]: they also mentioned how DHA and PUFA are seasonally essential​

And whether or not humans have or have not consumed PUFA seasonally is besides the point. I am a practical person, and will tease out mechanics that enable good health in the current environment.

If one can live a truly natural life, that's fine, but almost no one can do that today (and it's going to be made even worse in the coming global cooling cycle wink emoticon )

The only common theme in good health, longevity, good immune function, etc .... everything that constitutes a stress-resilient, high-functioning organism .... is a high metabolism (which usually comes with mitochondrial uncoupling)

DHA, EPA, and other PUFAs actively "shut down the system" at a very basic mitochondrial level. This is the "natural response", but it is a suboptimal-to-health response in the face of true seasonal nutrient scarcity.

This is NOT the recipe for healthy living in the modern world

-----

[TYW NOTE]: continuing on the discusssion​

The researchers comment:

> "The brain and the body are deficient in the machinery to make DHA; it has to come through our diet," said Fernando Gomez-Pinilla, a UCLA professor of neurosurgery and of integrative biology and physiology, and co-senior author of the paper."

False, or at the very least, misleading -- http://tanyewwei.com/blog/dha/...

There is an inherent assumption that "we need lots of DHA", rather than questioning what the optimal dose of DHA is.

 

[tyw]

^^ A related note to my previous post:

----

Now that I remember, Peter @ Hyperlipid actually did do analysis on a study that used Fish Oil vs Corn oil against high sucrose and high protein diets -- http://high-fat-nutrition.blogspot.com/.../on-drinking...

> Fish oil combined with sucrose is the worst, corn oil is intermediate and, without sucrose, none of the fats are obesogenic.

I'll say it again -- PUFA + Sugar is a killer combo, right down to the mitochondrial level, and the more double bonds, the worse this effect. READ: DHA is the worst thing you can have with your sugar. Either one or the other.

I share Peter's sentiments grin emoticon

> I hate higher level signalling. Give me the core process any day.

----

And note Peter's other commentary on the 2nd study he cited in that post -- http://www.ncbi.nlm.nih.gov/pubmed/16783472

NOTE: this involved "purified marine n-3s". We can assume EPA and DHA were part of mix.

> Low fat group gained a gram (of bodyweight),
> added saturated fat group gained 0.6 g,
> added omega 6 group lost* 2.4g
> and omega 3 group gained 10.4g.

Note that these were diabetic mice -- ie: if you're already chronically insulin resistant, then excess n-3s do even more harm.

Also note how the low fat diet diabetic mice actually didn't gain a lot of weight wink emoticon

Saturated fat is best. In fact, it is likely protective.

Notice how the n-6 group lost weight. This is simple mechanics -- n-6 PUFAs are insulin sensitising at the michondrial level. Not that they are healthy for you, but they are insulin sensitising nonetheless.

And Peter notes how biased the study is:

> There is no other mention of the hard fact that omega 3 fats are obesogenic. Also note that in relatively normal, non hyperglycaemic db/+ mice, the omega 3s are not obesogenic. Much the same as for non-fructose fed mice in the previous study.

There is a CLEAR bias towards "n-3 fats are good" (especially applying to DHA). You MUST read the methodology of the paper and analyse it like Peter does to draw out the facts.

And those facts support the notion that PUFAs of all forms are highly dangerous in anything about required amounts. (which IMO, are practically close to zero)

 

[Tarmander]

Fructose alters hundreds of brain genes, which can lead to a wide range of diseases

The problem with this study, and many similar ones resulting from corporate academia, is that it's essentially stipulation based upon a false premise. Please allow me to elaborate.

The gene mutations that the researchers observe have long been thought to eb associated with two main degenerative conditions- diabetes, and heart disease. Looking intot hese mRNA transcriptions or gene "mutations" it is apparent they they represent an increased propensity for rat glycolation of sugar, which the authors of the study seem to immediately assume is intimately connected with diabetes and heart disease. However, as true purveyors of biochemistry understand these two conditions much differently then the corporate research students, and know that diabetes results from an inefficiency in sugar metabolism, not the metabolism of sugar itself. They are actually using circular reasoning, and not exploring the base concern of the study, which should be "what causes diabetes?". The reasoning is simply: sugar intake causes diabetes> sugar intake emphasizes the transcription of a certain gene > this certain gene increases sugar intake > this gene causes diabetes.....

In other words, these transcriptome and DNA methylome changes, that the authors point to as a sign of poor health, are in fact a signs of good health. They show an increase affinity for glycolsis.
Then the DHA mediated changes are also inverted, they should be a sign of poor metabolic function, but the authors intuitively saw them as a sign of lengthended lfie span, because all the genes expressed was an icnreased concentration of DHA within the phosphorolipids of the cell wall.

The study even starts by asserting that "DHA is an important anti-oxidant that is present in too small quantities to make any difference"! How ridiculous when we know that DHA is always accompanied by free fatty acids that are responsible for significant amount of oxidative damage in the tissues!

This study helps demonstrate the common disconnect between what scientists believe or think they understand about biology, and what fundamental biochemistry dictates.

Nice post

 

[Such_Saturation]

But let's try not to always wait for somebody else to "rebutt"

 

[Braveheart]

great post

 

[lollipop]

Fructose alters hundreds of brain genes, which can lead to a wide range of diseases

The problem with this study, and many similar ones resulting from corporate academia, is that it's essentially stipulation based upon a false premise. Please allow me to elaborate.

The gene mutations that the researchers observe have long been thought to eb associated with two main degenerative conditions- diabetes, and heart disease. Looking intot hese mRNA transcriptions or gene "mutations" it is apparent they they represent an increased propensity for rat glycolation of sugar, which the authors of the study seem to immediately assume is intimately connected with diabetes and heart disease. However, as true purveyors of biochemistry understand these two conditions much differently then the corporate research students, and know that diabetes results from an inefficiency in sugar metabolism, not the metabolism of sugar itself. They are actually using circular reasoning, and not exploring the base concern of the study, which should be "what causes diabetes?". The reasoning is simply: sugar intake causes diabetes> sugar intake emphasizes the transcription of a certain gene > this certain gene increases sugar intake > this gene causes diabetes.....

In other words, these transcriptome and DNA methylome changes, that the authors point to as a sign of poor health, are in fact a signs of good health. They show an increase affinity for glycolsis.
Then the DHA mediated changes are also inverted, they should be a sign of poor metabolic function, but the authors intuitively saw them as a sign of lengthended lfie span, because all the genes expressed was an icnreased concentration of DHA within the phosphorolipids of the cell wall.

The study even starts by asserting that "DHA is an important anti-oxidant that is present in too small quantities to make any difference"! How ridiculous when we know that DHA is always accompanied by free fatty acids that are responsible for significant amount of oxidative damage in the tissues!

This study helps demonstrate the common disconnect between what scientists believe or think they understand about biology, and what fundamental biochemistry dictates.

VERY helpful @sladerunner69 - clearly see the layered problem and false assumptions at the beginning. Thank you!

 

[lollipop]

This study came up in another place on the Internet which I frequent, and I guess I can share my opinions here as well

Notes will be placed inline, Indented and tagged with [TYW NOTE]

----

Full Study doesn't prove anything wink emoticon --http://www.sciencedirect.com/.../pii/S2352396416301438

(a) This is not PUFA-controlled. I have said multiple times that PUFA + Fructose is horrible (http://high-fat-nutrition.blogspot.com/.../protons-and...).

Total fat intake was "10 g per 100 g of diet" ie: 20% fat (almost all of it likely PUFA. This is very bad on it's own)

This point alone is enough to question the veracity of the study.

(b) 15% of total calories in Fructose. This is a lot gasp emoticon Most people shouldn't do this.

NOTE: We have to assume that gene expression changes are actually significant to behaviour. They did show behavioural changes, so we can clearly see that BOTH Fructose and Fructose + DHA groups had "impaired behaviour"

but also note that ...

(c) Control Group without Fructose nor DHA did the best

All this shows is that DHA is helping to mitigate the bad effects of Fructose + PUFA. This is likely through the n-6 displacement effect of DHA.

What would happen if you just gave the control group DHA? (the fact that the researchers didn't do this is already a bias)

Or even better, what would happen if you don't give rats any PUFA to begin with wink emoticon? Look up "PUFA depletion diets", rats under these diets fared BETTER than regular rats **so long as B-vitamin deficiencies were corrected**.

DHA here just corrected for PUFA toxicity. The real problem is PUFA toxicity, not "DHA is good" or "Fructose is bad".

----

[TYW NOTE]: someone then commented something along the lines of "I imagine that a DHA-only group would have performed the best", and that "DHA is PUFA, so it can't correct its own toxicity. and long chain PUFA are "essential fatty acids" for a reason--the body has limited ability to generate them."

My response follows....
​

DHA is "bad for mitochondria" in the same sense that all PUFA is bad.

DHA can displace n-6 PUFAs from cell membranes --http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4555124/

These are Completely separate issues, and we should never complect the 2 wink emoticon

DHA or EPA in eukaryotic cell membranes have specific uses, and are arguably useful under certain contexts, and definitely more useful than common n-6 fats, precisely because of their higher unsaturation.

Do not confuse "seasonal" / temperature-dependent PUFA accumulation in eukaryotic cell membranes from the use of PUFA in mitochondrial Electron Chain Transport (which is "bad" for all the reasons that Peter @ Hyperlipid has stated).

Now, one may say that DHA and EPA are not used in ECT. This is likely true, but I cite studies which clearly show DHA / EPA integration into mitochondrial membranes very readily, with similar "bad effects" -- Docosahexaenoic Acid (DHA)

Do not confuse mitochondrial membranes from eukaryotic cell membranes wink emoticon

[TYW NOTE]: they also mentioned how DHA and PUFA are seasonally essential​

And whether or not humans have or have not consumed PUFA seasonally is besides the point. I am a practical person, and will tease out mechanics that enable good health in the current environment.

If one can live a truly natural life, that's fine, but almost no one can do that today (and it's going to be made even worse in the coming global cooling cycle wink emoticon )

The only common theme in good health, longevity, good immune function, etc .... everything that constitutes a stress-resilient, high-functioning organism .... is a high metabolism (which usually comes with mitochondrial uncoupling)

DHA, EPA, and other PUFAs actively "shut down the system" at a very basic mitochondrial level. This is the "natural response", but it is a suboptimal-to-health response in the face of true seasonal nutrient scarcity.

This is NOT the recipe for healthy living in the modern world

-----

[TYW NOTE]: continuing on the discusssion​

The researchers comment:

> "The brain and the body are deficient in the machinery to make DHA; it has to come through our diet," said Fernando Gomez-Pinilla, a UCLA professor of neurosurgery and of integrative biology and physiology, and co-senior author of the paper."

False, or at the very least, misleading -- http://tanyewwei.com/blog/dha/...

There is an inherent assumption that "we need lots of DHA", rather than questioning what the optimal dose of DHA is.

Very helpful @tyw thank you! This study caused a shake up and fight in another health FB group I am in. Was hard for me to scientifically refute, though intuitively felt it was wrong. Loved your two additions to the conversation! Thank you!

 

[paymanz]

i haven't read article but 2 thing comes in mind

from what others said they feed them fructose by mixing it with their water(usually its their method for studies like this on sugar and salt..)so by this way the animal ingest some fructose whenever is thirsty! but is not necessarily hungry!
so its different from when you freely choice to eat some sugary food.

and the second point is that-as mentioned above- fructose alone can not absorbed well and gets fermented and produce endotoxins and other metabolites.and they used fructose not sucrose.ray recommends natural sugars i think.

 

[tara]

(b) 15% of total calories in Fructose. This is a lot gasp emoticon Most people shouldn't do this.

Many people here probably do get at least half their calories from sugars in various forms, likely often at least 15% fructose. (Many also probably get less.) Peat seems to generally favour sugars over starches when good quality is available, and reasonably high sugar/carb intake.