Coconut Oil Leads To Dementia?

[Badger]

A few days ago I saw on TV a Dr. Oz show examining coconut oil. Dr. Michael Roizen, MD, an anesthesiologist, say he worked years ago at the CDC , and they routinely triggered dementia in rats feeding them coconut oil. He emphatically proclaimed that people should not eat coconut oil due to such a risk. Another MD, Mark Hyman, who was brought on to counter Roizen, shot back that such results were from low-grade inferior coconut oil, and would not happen with virgin, high-quality coconut oil. Roizen replied with an analogy that if you take high or low quality cocaine, it's still cocaine, that is, it's still a poison, which he is implying about coconut oil. Roizen said the mechanism for this outcome from eating coconut oil is that it brings inflammation into the brain, leading to dementia. Almost got the sense he was saying that it somehow bores pathways into the brain for inflammation to emerge in.

Any comments on this, is coconut oil really a dementia promoter? Until this show, I have heard anecdotal stories of just the opposite: that it lessens dementia or eliminate it.

 

[dookie]

That is a pretty amazing statement. Are there any studies at all to back this up, or is this just this one guys anecdotal experience?
What else did they feed the rats? Was it a diet consisting of only coconut oil, or very high in fat?
Has this been published anywhere at all?

Don't forget the @haidut tag when you are posting controversial things like this :)

 

[Dhair]

A few days ago I saw on TV a Dr. Oz show

I would recommend that you stop watching this garbage.

 

[yerrag]

If it's the CDC, you can chuck that to fake medical news easily as well. It has no credibility at all.

How did they conclude coconut oil triggered dementia? Did they do a brain scan and saw something? Did the rats forget who their offsprings are, and forget their names? Or did they fail to find their address in rat alley?

 

[Badger]

I'm just reporting what I saw on the segment. I eat coconut oil daily so it was concerning to see this, but I think Roizen is likely smearing it.

This Dr. Oz segment originally aired in October 2017, which starts at this link below. When Dr. Roizen starts, he agrees with the American Heart Association claim, I think made then, that coconut oil, like all saturated fats, causes heart disease, hence don't consume it:

Can Coconut Oil Cause Heart Disease?
Can Coconut Oil Cause Heart Disease?

This next segment has Roizen referring to coconut oil as causing dementia, and some lab nearby his lab causing it in mice. It starts at 0:50:
The Conflicting Science Behind Coconut Oil

That is a pretty amazing statement. Are there any studies at all to back this up, or is this just this one guys anecdotal experience?
What else did they feed the rats? Was it a diet consisting of only coconut oil, or very high in fat?
Has this been published anywhere at all?

Don't forget the @haidut tag when you are posting controversial things like this :)

 

[Badger]

See 2nd video segment I posted in reply to Dookie.

If it's the CDC, you can chuck that to fake medical news easily as well. It has no credibility at all.

How did they conclude coconut oil triggered dementia? Did they do a brain scan and saw something? Did the rats forget who their offsprings are, and forget their names? Or did they fail to find their address in rat alley?

 

[Such_Saturation]

cough cough











Coconut oil attenuates the effects of amyloid-β on cortical neurons in vitro. - PubMed - NCBI

Coconut oil protects cortical neurons from amyloid beta toxicity by enhancing signaling of cell survival pathways. - PubMed - NCBI

 

[Badger]

Oops, I was in error, Roizen made his claim about cocount oil and mice dementia in connection to his work at NIH, not CDC.

If it's the CDC, you can chuck that to fake medical news easily as well. It has no credibility at all.

How did they conclude coconut oil triggered dementia? Did they do a brain scan and saw something? Did the rats forget who their offsprings are, and forget their names? Or did they fail to find their address in rat alley?

 

[Badger]

I found Roizen's blog where he writes in detail about coconut oil causing dementia in mice:

Is A Diet With Coconut Oil Really Very Risky For Your Brain?
Is A Diet With Coconut Oil Really Very Risky For Your Brain?
Here's some key quote:
"So in this blog, I hope to inform you why I am so cautionary about coconut oil; it has nothing to do with fats in your blood leading to heart disease or not, but rather that researchers in the lab next to mine at NIH in the early 70’s used coconut oil to accelerate brain dysfunction, Alzheimer’s and dementia in animals. And more recently that paper published in a respected peer reviewed journal recently indicated coconut oil accelerates the inflammatory changes in multiple sclerosis that lead to nervous system dysfunction. Multiple sclerosis is a disease thought to be caused by or accelerated by nervous tissue inflammation just like dementia and Alzheimer’s disease are.

The recent paper that triggered my desire to remind you of my three concerns about coconut oil use is an abstract (from April, 2017) by a different group (a different group means the data are reproducible by others than those who made the original observation—meaning the original observation is much more likely to be real rather than a statistical aberration). That abstract confirms a 2015 publication in the journal Immunity. I won’t discuss the confirming abstract cause it is only an abstract rather than a full peer reviewed scientific paper (abstracts are not scrutinized or vetted to even 10% of the degree papers are). In that memory triggering paper (memory triggering for me) on the effects of dietary coconut oil on MS, entitled “Dietary Fatty Acids Directly Impact Central Nervous System Autoimmunity via the Small Intestine”, coconut oil added to soybean oil in a typical rat diet made the rat’s equivalent of your immune system attack the protective sheath (myelin) that covers your nerve fibers. That inflammatory attack causes the equivalent of communication problems between your brain and the rest of your body.
Now this side effect relating to accelerating the development of dementia caused by coconut oil in mice and rats and guinea pigs oil isn’t a minor acceleration—it is the human equivalent of bringing it on 16 to 20 years earlier—so instead of 14% of US women developing serious degrees of memory problems at age 83, that 14% would develop them at age 63 to 67 or so if they had used coconut oil as the major fat in their food choices. This earlier development would cost the US an additional 100 billion dollars a year in medical costs by 2024 if just 35% of Americans chose to use coconut oil as their main fat."

"In 2015, a study was published in another prestigious and peer reviewed journal, Hippocampus (2015; 25:1567-1576), entitled “A high fat diet impairs learning that is dependent on the dorsal hippocampus but spares other forms of learning”. That study indicates that adding saturated fat to soybean oil required 8 weeks and specific tests that depend on the hippocampus in these rats to find important changes in learning from diet. You’ll note these studies on memory change, even in rats or mice or guinea pigs , require a long time to complete as they need the inflammation to develop and then destroy the neuronal connections that cause what we know as memory or human brain functioning. Your hippocampus is the only organ where size matters in the human body, as size shrinks as memory and learning problems occur in humans.

That hippocampal size and inflammation reference relates to the 2008 study by Granholm and colleagues in the Journal of Alzheimer’s Disease (Effect of a Saturated Fat and High Cholesterol Diet on Memory and Hippocampal Morphology in the Middle Aged Rat, 2008;14: 133-145) that showed that 8 weeks of a diet with hydrogenated coconut oil (most coconut oil is hydrogenated or saturated in nature and as you might buy it) added to the normal diet was associated with inflammation in key to memory hippocampal nervous tissues. But they used middle aged not young rats, and gave the equivalent of 20 or more years of the diet. So I urge you if you do your own research, or if you are a doc in the field, before you advocate something like coconut oil, to make sure the studies you are basing your recommendations on are long enough and look for the changes well enough to insure that what they advocate isn’t short term beneficial and long term hazardous. Short term or poor choice of study variables can be misleading. For example, it is widely verified in scientific study and now generally accepted that sugar and/or insulin inserted up the nose of an Alzheimer’s patient improve mental functioning in the short term but cause long term problems. These docs advocating coconut oil would not advocate long term diets high in sugar. Were they so careful before advocating coconut oil?

Granholm and her research partner, Linnea Freeman, in a 2012 paper in the Journal of Cerebral Blood Flow and Metabolism (2012; 32; 643-53) indicated that the inflammation associated with hydrogenated coconut oil (like the kind you might use in cooking) causes inflammatory vascular changes and breaks down that key area of the blood-brain barrier in their rat model. Now they gave the rats 10% coconut oil, the equivalent of 160 calories or less than 3 tablespoons for a human, and found inflammatory and disruptive changes in one of the proteins key for the tight junctions and thereby functioning of the blood-brain barrier. But they changed the diet of the rats for 6 months to see this effect, the equivalent of about 15 year period for you. But this break down of the blood brain barrier and inflammation in the hippocampus that Granholm and Freeman reported is exactly what the researchers in the laboratory next to mine in 1973-5 found. The researchers in the laboratory next to ours in the National Institutes of Mental Health at NIH in that period were early in trying to understand dementia. They administered coconut oil after causing an inflammatory stimulus (a bacterial skin infection as I recall). That process led to the mice in their studies not being able to learn maze navigation, as I remember it (not the focus of my research just down the hall; we were trying to understand consciousness and how anesthetics caused anesthesia). In the meantime genetic models of dementia in rats and mice were developed. That’s why I worry the data are too old for the young docs of today to be aware of that model of accelerated dementia associated with a coconut oil diet plus inflammation."

"Because it is rich in the medium-chain fatty acids (MCFAs) it is supposed to be different than other saturated fats that are made of fatty acids with more than 12 or 14 carbons so called Long-term fatty acids (LCFAs). The LCFA’s largely come with amino-acids such as carnitine (plentiful in red meat, pork, and even some fish like cod), lecithin and choline (cheese and egg yolks) that select for bacteria inside your intestine. Those bacteria produce inflammation in your arteries, immune system, and brain (to name just a few areas). That inflammation caused by the poop those bacteria produce relates not to the fat changes they produce but to the amino acids that certain bacteria love. Those bacteria then produce poop as they go after the C, H and O’s of the red meat, cheese, egg yolks or peanuts (yes they have problems too) that contains the inflammation stimulating substance."

"And if your doc advocates coconut oil, ask to see the long term studies that look at learning and inflammation in the brain. And then send em to me. "

 

[Such_Saturation]

8 weeks of a diet with hydrogenated coconut oil (most coconut oil is hydrogenated or saturated in nature and as you might buy it) added to the normal diet was associated with inflammation in key to memory hippocampal nervous tissues. But they used middle aged not young rats, and gave the equivalent of 20 or more years of the diet. So I urge you if you do your own research, or if you are a doc in the field, before you advocate something like coconut oil, to make sure the studies you are basing your recommendations on are long enough and look for the changes well enough to insure that what they advocate isn’t short term beneficial and long term hazardous.

That's way more than what a dementia patient usually lives

 

[Travis]

I found Roizen's blog where here writes in detail about coconut oil causing dementia in mice:

Is A Diet With Coconut Oil Really Very Risky For Your Brain?
Is A Diet With Coconut Oil Really Very Risky For Your Brain?
Here's some key quote:
"So in this blog, I hope to inform you why I am so cautionary about coconut oil; it has nothing to do with fats in your blood leading to heart disease or not, but rather that researchers in the lab next to mine at NIH in the early 70’s used coconut oil to accelerate brain dysfunction, Alzheimer’s and dementia in animals. And more recently that paper published in a respected peer reviewed journal recently indicated coconut oil accelerates the inflammatory changes in multiple sclerosis that lead to nervous system dysfunction. Multiple sclerosis is a disease thought to be caused by or accelerated by nervous tissue inflammation just like dementia and Alzheimer’s disease are.

The recent paper that triggered my desire to remind you of my three concerns about coconut oil use is an abstract (from April, 2017) by a different group (a different group means the data are reproducible by others than those who made the original observation—meaning the original observation is much more likely to be real rather than a statistical aberration). That abstract confirms a 2015 publication in the journal Immunity. I won’t discuss the confirming abstract cause it is only an abstract rather than a full peer reviewed scientific paper (abstracts are not scrutinized or vetted to even 10% of the degree papers are). In that memory triggering paper (memory triggering for me) on the effects of dietary coconut oil on MS, entitled “Dietary Fatty Acids Directly Impact Central Nervous System Autoimmunity via the Small Intestine”, coconut oil added to soybean oil in a typical rat diet made the rat’s equivalent of your immune system attack the protective sheath (myelin) that covers your nerve fibers. That inflammatory attack causes the equivalent of communication problems between your brain and the rest of your body.
Now this side effect relating to accelerating the development of dementia caused by coconut oil in mice and rats and guinea pigs oil isn’t a minor acceleration—it is the human equivalent of bringing it on 16 to 20 years earlier—so instead of 14% of US women developing serious degrees of memory problems at age 83, that 14% would develop them at age 63 to 67 or so if they had used coconut oil as the major fat in their food choices. This earlier development would cost the US an additional 100 billion dollars a year in medical costs by 2024 if just 35% of Americans chose to use coconut oil as their main fat."

"In 2015, a study was published in another prestigious and peer reviewed journal, Hippocampus (2015; 25:1567-1576), entitled “A high fat diet impairs learning that is dependent on the dorsal hippocampus but spares other forms of learning”. That study indicates that adding saturated fat to soybean oil required 8 weeks and specific tests that depend on the hippocampus in these rats to find important changes in learning from diet. You’ll note these studies on memory change, even in rats or mice or guinea pigs , require a long time to complete as they need the inflammation to develop and then destroy the neuronal connections that cause what we know as memory or human brain functioning. Your hippocampus is the only organ where size matters in the human body, as size shrinks as memory and learning problems occur in humans.

That hippocampal size and inflammation reference relates to the 2008 study by Granholm and colleagues in the Journal of Alzheimer’s Disease (Effect of a Saturated Fat and High Cholesterol Diet on Memory and Hippocampal Morphology in the Middle Aged Rat, 2008;14: 133-145) that showed that 8 weeks of a diet with hydrogenated coconut oil (most coconut oil is hydrogenated or saturated in nature and as you might buy it) added to the normal diet was associated with inflammation in key to memory hippocampal nervous tissues. But they used middle aged not young rats, and gave the equivalent of 20 or more years of the diet. So I urge you if you do your own research, or if you are a doc in the field, before you advocate something like coconut oil, to make sure the studies you are basing your recommendations on are long enough and look for the changes well enough to insure that what they advocate isn’t short term beneficial and long term hazardous. Short term or poor choice of study variables can be misleading. For example, it is widely verified in scientific study and now generally accepted that sugar and/or insulin inserted up the nose of an Alzheimer’s patient improve mental functioning in the short term but cause long term problems. These docs advocating coconut oil would not advocate long term diets high in sugar. Were they so careful before advocating coconut oil?

Granholm and her research partner, Linnea Freeman, in a 2012 paper in the Journal of Cerebral Blood Flow and Metabolism (2012; 32; 643-53) indicated that the inflammation associated with hydrogenated coconut oil (like the kind you might use in cooking) causes inflammatory vascular changes and breaks down that key area of the blood-brain barrier in their rat model. Now they gave the rats 10% coconut oil, the equivalent of 160 calories or less than 3 tablespoons for a human, and found inflammatory and disruptive changes in one of the proteins key for the tight junctions and thereby functioning of the blood-brain barrier. But they changed the diet of the rats for 6 months to see this effect, the equivalent of about 15 year period for you. But this break down of the blood brain barrier and inflammation in the hippocampus that Granholm and Freeman reported is exactly what the researchers in the laboratory next to mine in 1973-5 found. The researchers in the laboratory next to ours in the National Institutes of Mental Health at NIH in that period were early in trying to understand dementia. They administered coconut oil after causing an inflammatory stimulus (a bacterial skin infection as I recall). That process led to the mice in their studies not being able to learn maze navigation, as I remember it (not the focus of my research just down the hall; we were trying to understand consciousness and how anesthetics caused anesthesia). In the meantime genetic models of dementia in rats and mice were developed. That’s why I worry the data are too old for the young docs of today to be aware of that model of accelerated dementia associated with a coconut oil diet plus inflammation."

"Because it is rich in the medium-chain fatty acids (MCFAs) it is supposed to be different than other saturated fats that are made of fatty acids with more than 12 or 14 carbons so called Long-term fatty acids (LCFAs). The LCFA’s largely come with amino-acids such as carnitine (plentiful in red meat, pork, and even some fish like cod), lecithin and choline (cheese and egg yolks) that select for bacteria inside your intestine. Those bacteria produce inflammation in your arteries, immune system, and brain (to name just a few areas). That inflammation caused by the poop those bacteria produce relates not to the fat changes they produce but to the amino acids that certain bacteria love. Those bacteria then produce poop as they go after the C, H and O’s of the red meat, cheese, egg yolks or peanuts (yes they have problems too) that contains the inflammation stimulating substance."

"And if your doc advocates coconut oil, ask to see the long term studies that look at learning and inflammation in the brain. And then send em to me. "

Could be fear, uncertainly, and doubt. Ian Prior will tell you that even a diet of 50% coconut, in humans, leads to good health with practically zero cardiovascular disease:

Prior, Ian A. "Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies." The American journal of clinical nutrition (1981)​

But cardiovascular disease appears to have little to do with lipids (Pauling, 1991).

Now for the coconut oil dementia rats: What is going on with this? I mean . . . WTF is going on with this, really?

Granholm, Ann-Charlotte. "Effects of a saturated fat and high cholesterol diet on memory and hippocampal morphology in the middle-aged rat." Journal of Alzheimer's Disease (2008)​

The very first paragraph lets us know exactly what's going on:

'Diets rich in cholesterol and/or saturated fats have been shown to be detrimental to cognitive performance. Therefore, we fed a cholesterol (2%) and saturated fat (hydrogenated coconut oil, Sat Fat 10%) diet to 16-month old rats for 8 weeks to explore the effects on the working memory performance of middle-aged rats.' —Granholm​

The Raney catalyst used to hydrogenate coconut oil consists of nickel on an aluminum scaffold. The Raney particles are made small to increase the surface area for dihydrogen (H₂) adsorption and to lower the time for complete hydrogenation. These micron‐sized aluminum and nickel particles are filtered‐out afterwards, but some do remain and they can be detected.

Aluminum can leads to an autoimmune myelin condition since microtubule‐associated proteins, which support the myelin in nerves, are highly phosphorylated. The aluminum ion has a natural affinity for phosphate, and has been shown to aggregate phosphorylated proteins such as τ in vitro. The aluminum ion (Al³⁺) is trivalent, and can form a three‐membered phosphate crosslink. This ion has historically been implicated—more than anything else—directly in the etiology of Parkinson's, Alzheimer's, and ALS. Aluminum has been detected in the brains and spinal cords of such people by electron dispersive spectroscopy, neutron activation analysis, LAMMA spectroscopy, and solochrome azurine staining. Aluminum has been also been linked epidemiologically to Alzheimer's through analysis of drinking water, and proved directly to cause dementia in case of the Waterford Poisoning Incident (aluminum sulfate is used a flocculant in some city water supplies). Thousands of cases of diabetic encephalopathy show the same . . . because this only happens when aluminum can be found in the dialysate fluid.

The only thing ever shown to replicate the neurofibrillary tangles seen in Alzheimer's has been injections of aluminum chloride. ​

Hydrogenated coconut oil would be expected to retain more Raney catalyst than all other oils due to its high viscosity. This could contribute enough aluminum to cause the characteristic neurological changes seen in the rats. Indeed, nothing else even makes sense; there is no way that caprylic, myristic, or palmitic acids can cause dementia.

 

[tca300]

" stick with fats that you can love and that love you back like the odd omegas® in avocados, chia seeds, walnuts, and canola oil (all omega3’s), or in extra virgin olive oil (omega-9) or in salmon or ocean trout ( both a lot of omega-3’s and 7’s). " Is A Diet With Coconut Oil Really Very Risky For Your Brain?


......... will do.. I'm sure the lipid peroxidation, thyroid suppression, and benign metabolites of those PUFAs do a brain good.

 

[yerrag]

Could be fear, uncertainly, and doubt. Ian Prior will tell you that even a diet of 50% coconut, in humans, leads to good health with practically zero cardiovascular disease:

Prior, Ian A. "Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies." The American journal of clinical nutrition (1981)​

But cardiovascular disease appears to have little to do with lipids (Pauling, 1991).

Now for the coconut oil dementia rats: What is going on with this? I mean . . . WTF is going on with this, really?

Granholm, Ann-Charlotte. "Effects of a saturated fat and high cholesterol diet on memory and hippocampal morphology in the middle-aged rat." Journal of Alzheimer's Disease (2008)​

The very first paragraph lets us know exactly what's going on:

'Diets rich in cholesterol and/or saturated fats have been shown to be detrimental to cognitive performance. Therefore, we fed a cholesterol (2%) and saturated fat (hydrogenated coconut oil, Sat Fat 10%) diet to 16-month old rats for 8 weeks to explore the effects on the working memory performance of middle-aged rats.' —Granholm​

The Raney catalyst used to hydrogenate coconut oil consists of nickel on an aluminum scaffold. The Raney particles are made small to increase the surface area for hydrogen adsorption and lower the time it takes for complete hydrogenation. These micron‐sized aluminum and nickel particles are always filtered‐out afterwards, but some do remain and they can be detected.

Aluminum can leads to an autoimmune myelin condition since microtubuleassociated proteins, which support they myelin, are highly phosphorylated. The aluminum ion has a natural affinity for phosphate, and has been shown to aggregate phosphorylated proteins such as τ in vitro. Hydrogenated coconut oil would be expected to retain more Raney catalyst than all other oils due to its high viscosity.

Now that is some cause for concern.

 

[Badger]

So what's upshot of this regarding coconut oil and dementia? Does it mean we should not consume coconut oil that's been hydrogenated?

Could be fear, uncertainly, and doubt. Ian Prior will tell you that even a diet of 50% coconut, in humans, leads to good health with practically zero cardiovascular disease:

Prior, Ian A. "Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies." The American journal of clinical nutrition (1981)​

But cardiovascular disease appears to have little to do with lipids (Pauling, 1991).

Now for the coconut oil dementia rats: What is going on with this? I mean . . . WTF is going on with this, really?

Granholm, Ann-Charlotte. "Effects of a saturated fat and high cholesterol diet on memory and hippocampal morphology in the middle-aged rat." Journal of Alzheimer's Disease (2008)​

The very first paragraph lets us know exactly what's going on:

'Diets rich in cholesterol and/or saturated fats have been shown to be detrimental to cognitive performance. Therefore, we fed a cholesterol (2%) and saturated fat (hydrogenated coconut oil, Sat Fat 10%) diet to 16-month old rats for 8 weeks to explore the effects on the working memory performance of middle-aged rats.' —Granholm​

The Raney catalyst used to hydrogenate coconut oil consists of nickel on an aluminum scaffold. The Raney particles are made small to increase the surface area for dihydrogen (H₂) adsorption and to lower the time for complete hydrogenation. These micron‐sized aluminum and nickel particles are filtered‐out afterwards, but some do remain and they can be detected.

Aluminum can leads to an autoimmune myelin condition since microtubule‐associated proteins, which support the myelin in nerves, are highly phosphorylated. The aluminum ion has a natural affinity for phosphate, and has been shown to aggregate phosphorylated proteins such as τ in vitro. The aluminum ion (Al³⁺) is trivalent, and can form a three‐membered phosphate crosslink. This ion has historically been implicated, more than anything else, directly in the etiology of Parkinson's, Alzheimer's, and ALS. Aluminum has been detected in the brains and spinal cords of such people by electron dispersive spectroscopy, neutron activation analysis, LAMMA spectroscopy, and solochrome azurine staining. Aluminum has been also been linked epidemiologically to Alzheimer's through analysis of drinking water, and proved directly to cause dementia in case of the Waterford Poisoning Incident (aluminum sulfate is used a flocculant in some city water supplies). Thousands of cases of diabetic encephalopathy show the same, because this only happens when aluminum can be found in the dialysate fluid.

The only thing ever shown to replicate the neurofibrillary tangles seen in Alzheimer's has been injections of aluminum chloride. ​

Hydrogenated coconut oil would be expected to retain more Raney catalyst than all other oils due to its high viscosity. This could contribute enough aluminum to cause the characteristic neurological changes seen in the rats. Indeed, nothing else even makes sense; there is no way that caprylic, myristic, or palmitic acids can cause dementia.

 

[tca300]

Could be fear, uncertainly, and doubt. Ian Prior will tell you that even a diet of 50% coconut, in humans, leads to good health with practically zero cardiovascular disease:

Prior, Ian A. "Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies." The American journal of clinical nutrition (1981)​

But cardiovascular disease appears to have little to do with lipids (Pauling, 1991).

Now for the coconut oil dementia rats: What is going on with this? I mean . . . WTF is going on with this, really?

Granholm, Ann-Charlotte. "Effects of a saturated fat and high cholesterol diet on memory and hippocampal morphology in the middle-aged rat." Journal of Alzheimer's Disease (2008)​

The very first paragraph lets us know exactly what's going on:

'Diets rich in cholesterol and/or saturated fats have been shown to be detrimental to cognitive performance. Therefore, we fed a cholesterol (2%) and saturated fat (hydrogenated coconut oil, Sat Fat 10%) diet to 16-month old rats for 8 weeks to explore the effects on the working memory performance of middle-aged rats.' —Granholm​

The Raney catalyst used to hydrogenate coconut oil consists of nickel on an aluminum scaffold. The Raney particles are made small to increase the surface area for dihydrogen (H₂) adsorption and to lower the time for complete hydrogenation. These micron‐sized aluminum and nickel particles are filtered‐out afterwards, but some do remain and they can be detected.

Aluminum can leads to an autoimmune myelin condition since microtubule‐associated proteins, which support the myelin in nerves, are highly phosphorylated. The aluminum ion has a natural affinity for phosphate, and has been shown to aggregate phosphorylated proteins such as τ in vitro. The aluminum ion (Al³⁺) is trivalent, and can form a three‐membered phosphate crosslink. This ion has historically been implicated—more than anything else—directly in the etiology of Parkinson's, Alzheimer's, and ALS. Aluminum has been detected in the brains and spinal cords of such people by electron dispersive spectroscopy, neutron activation analysis, LAMMA spectroscopy, and solochrome azurine staining. Aluminum has been also been linked epidemiologically to Alzheimer's through analysis of drinking water, and proved directly to cause dementia in case of the Waterford Poisoning Incident (aluminum sulfate is used a flocculant in some city water supplies). Thousands of cases of diabetic encephalopathy show the same . . . because this only happens when aluminum can be found in the dialysate fluid.

The only thing ever shown to replicate the neurofibrillary tangles seen in Alzheimer's has been injections of aluminum chloride. ​

Hydrogenated coconut oil would be expected to retain more Raney catalyst than all other oils due to its high viscosity. This could contribute enough aluminum to cause the characteristic neurological changes seen in the rats. Indeed, nothing else even makes sense; there is no way that caprylic, myristic, or palmitic acids can cause dementia.

Son of a b... back to <10% fat for me.

 

[Koveras]

The Raney catalyst used to hydrogenate coconut oil consists of nickel on an aluminum scaffold. The Raney particles are made small to increase the surface area for dihydrogen (H₂) adsorption and to lower the time for complete hydrogenation. These micron‐sized aluminum and nickel particles are filtered‐out afterwards, but some do remain and they can be detected.

Aluminum can leads to an autoimmune myelin condition since microtubule‐associated proteins, which support the myelin in nerves, are highly phosphorylated. The aluminum ion has a natural affinity for phosphate, and has been shown to aggregate phosphorylated proteins such as τ in vitro. The aluminum ion (Al³⁺) is trivalent, and can form a three‐membered phosphate crosslink. This ion has historically been implicated—more than anything else—directly in the etiology of Parkinson's, Alzheimer's, and ALS. Aluminum has been detected in the brains and spinal cords of such people by electron dispersive spectroscopy, neutron activation analysis, LAMMA spectroscopy, and solochrome azurine staining. Aluminum has been also been linked epidemiologically to Alzheimer's through analysis of drinking water, and proved directly to cause dementia in case of the Waterford Poisoning Incident (aluminum sulfate is used a flocculant in some city water supplies). Thousands of cases of diabetic encephalopathy show the same . . . because this only happens when aluminum can be found in the dialysate fluid.

The only thing ever shown to replicate the neurofibrillary tangles seen in Alzheimer's has been injections of aluminum chloride. ​

Hydrogenated coconut oil would be expected to retain more Raney catalyst than all other oils due to its high viscosity. This could contribute enough aluminum to cause the characteristic neurological changes seen in the rats. Indeed, nothing else even makes sense; there is no way that caprylic, myristic, or palmitic acids can cause dementia.

Implying that this popular oil around here may not be ideal?

Coconut Oil (92 degree)

 

[yerrag]

It's the hydrogenation, not the coconut then? But then, how much more hydrogenation is done on PUFAs? 100x?

 

[haidut]

That is a pretty amazing statement. Are there any studies at all to back this up, or is this just this one guys anecdotal experience?
What else did they feed the rats? Was it a diet consisting of only coconut oil, or very high in fat?
Has this been published anywhere at all?

Don't forget the @haidut tag when you are posting controversial things like this :)

I need to see at least one study. Don't wan to dismiss automatically anything, but such a wild claim unreported by anybody else requires equally "wild" evidence to take seriously.

 

[Travis]

The Raney catalyst used to hydrogenate oils is basically nickel on an aluminum support. You would actually expect micron‐sized particles of aluminum to be found in hydrogenated coconut oil. In fact, I distinctly remember seeing determinations of this in the past.

I will find some numbers shortly so we know how much aluminum to expect from hydrogenated coconut oil.

 

[raypeatclips]

The Raney catalyst used to hydrogenate oils is basically nickel on an aluminum support. You would actually expect micron‐sized particles of aluminum to be found in hydrogenated coconut oil. In fact, I distinctly remember seeing determinations of this in the past.

I will find some numbers shortly so we know how much aluminum to expect from hydrogenated coconut oil.

So the regular unrefined coconut oil that's easily available in shops that has like 2% PUFA wouldn't have this problem?