High-Fructose-High-Coconut-Oil Diet Disregulates Leptin, Stearoyl-CoA Desaturase, And Spatial Memory

grenade

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This study is in rats.

The authors postulate that stearoyl-CoA desaturase (an enzyme that unsaturates saturated fatty acids) increases as a possible "protection" against obesity and other ill-effects seen in the rats (elevated insulin, elevated glucose, etc.)

A High-Fructose-High-Coconut Oil Diet Induces Dysregulating Expressions of Hippocampal Leptin and Stearoyl-CoA Desaturase, and Spatial Memory Deficits in Rats

It's interesting as when I was on a super high sugar diet from fruits and juices (regardless of how much saturated fat I consumed), I had memory issues, gained a lot of weight, and horrible hunger.

Now that I dropped most of the sugar and upped the saturated fats (dairy and red meat, primarily), everything appears to be beginning to normalize, slowly but surely.

I wonder what people's thoughts are, as this is sort of runs counter to what some Peat might say.
 

X3CyO

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Ive experienced that phenomenon. Mainly on high amounts of sugar. Partially when eating high amounts of fat.

It could be a lot of things depending on who you listen to. Too low phosphorus.
Too high cholesterol not converting.

Im dropping both sugar and fat.
 
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grenade

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Interesting point.

One thing I forgot to mention is that brain tissues seem to become unsaturated with certain unsaturated fatty acids.

This seems to be completely opposite of what Peat says - that eating primarily saturated fats and “keeping the stress hormones at bay” with plentiful carbohydrate is a sure way to slowly saturate the tissues overtime.
 

Luann

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That's really interesting. I can't wait to hear interpretations and thoughts on this one.

I wonder how well rats do on mostly fructose instead of glucose.
 
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grenade

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Randle Cycle.

Not in conflict with anything Ray talks about.

Didn’t Peat himself say that you can consumed up to a certain % of saturated fat (I think he said 60% of calories) and still be healthy? I don’t remember him qualifying it with “but there must be a majority of carbs or fat, not an even mix.”

Also, how does that explain the process of unsaturation seen in the brain when rats consume equally large amounts of saturated fat and fructose?
 

jitsmonkey

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instead of asking for conjecture
why not just ask him directly
he'll give you the answer you're looking for
and then you can post it here.
 
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grenade

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#1 - I don’t have his contact info.
#2 - I’d hate to bother an elderly gentleman who’s already bombarded by those who’ve found him on the internet, and whose only means of replying to these people is over a dial-up connection in Mexico.
#3 - The reason I posted this is because I was curious of what the community thinks and wanted to discuss the study with you all (this is a forum, after all). Thus far, two other posters are eager in hearing more discussion, too.
 

Kartoffel

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As I see it the only thing that this study shows is that soybean oil makes you fat while coconut oil will make you leaner. Their interpretation of memory and learning improvements is ridiculous.



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nwo2012

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Reminds me of EFA proving experiment of the Burrs. Without checking for nutrient deficiencies how would you know whether the higher metabolic rate brought on by the increased sarurated fat and fructose consumption led to nutrient deficiencies or nor? Also the low protein content would confound this. Peat says at most fat 30ish% of intake.
As I see it the only thing that this study shows is that soybean oil makes you fat while coconut oil will make you leaner. Their interpretation of memory and learning improvements is ridiculous.



View attachment 10177

Thanks, saves me wasting much time on the usual. Some random member here posts some crap from an abstract without fully reading AND understanding the data some random mainstream authors with a saturated fat and fructose axe to grind postulate. Simply reading the study's introduction shows what the authors already believe about saturated fat and fructose. So much for so called unbiased studies.
They simply wave their dicks around in agreement like good little pets to the system.
 
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grenade

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As I see it the only thing that this study shows is that soybean oil makes you fat while coconut oil will make you leaner. Their interpretation of memory and learning improvements is ridiculous.

View attachment 10177

I’m not sure how to interpret he memory / learning improvements parameters, so i can’t comment. In regards to leanness, the soybean oil group experienced an increase in bodyweight and adiposity, while the CO group only experienced an increase in adiposity (higher than the soybean oil group.) So it looks like lean mass was lost and fat mass was gained in the CO group.

Reminds me of EFA proving experiment of the Burrs. Without checking for nutrient deficiencies how would you know whether the higher metabolic rate brought on by the increased sarurated fat and fructose consumption led to nutrient deficiencies or nor? Also the low protein content would confound this. Peat says at most fat 30ish% of intake.


Thanks, saves me wasting much time on the usual. Some random member here posts some crap from an abstract without fully reading AND understanding the data some random mainstream authors with a saturated fat and fructose axe to grind postulate. Simply reading the study's introduction shows what the authors already believe about saturated fat and fructose. So much for so called unbiased studies.
They simply wave their dicks around in agreement like good little pets to the system.

In the EFA deficiency experiment, did they observe symptoms regarding obesity, glucose control, insulin control, etc.? From my memory, that experiment observed skin issues, most notably.

The CO group in this study had 32% of its food be comprised of CO, with the rest being fructose, protein, micronutrients, etc. Good point on the low protein content.

See my response to Kartoffel - adiposity increased the most in the CO group. It’s right there in the graph he attached.
 

Kartoffel

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Reminds me of EFA proving experiment of the Burrs. Without checking for nutrient deficiencies how would you know whether the higher metabolic rate brought on by the increased sarurated fat and fructose consumption led to nutrient deficiencies or nor? Also the low protein content would confound this. Peat says at most fat 30ish% of intake.


Thanks, saves me wasting much time on the usual. Some random member here posts some crap from an abstract without fully reading AND understanding the data some random mainstream authors with a saturated fat and fructose axe to grind postulate. Simply reading the study's introduction shows what the authors already believe about saturated fat and fructose. So much for so called unbiased studies.
They simply wave their dicks around in agreement like good little pets to the system.

Yes, most of these studies are designed to show exactely what the authors want to show, not to present and analyze what their actual data means. For example, in this study they an indicator like this adiposity index to make the reader believe that the coconut oil group was actually obese compared to the soybean oil, eventhough the coconut oil group weighed 10% less. These tricks are so obviously fraudulent and embarrassing that they give you an impression of how corrupt all these researchers are. They all know that what they do is bull**** but they keep doing it nevertheless because you don't get funding for coming to the conclusion that saturated fat and sucrose might be protective and healthy.
 

Kartoffel

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See my response to Kartoffel - adiposity increased the most in the CO group. It’s right there in the graph he attached.

Well, if you think that this is an accurate way to calculate adiposity I can't argue with that:

The adiposity index was calculated with the following equation: relative total body fat weight (%) = [the sum of the weight of abdominal and epididymal fat pads (g)/final body
weight (g)] × 100%.
 
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grenade

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Yes, most of these studies are designed to show exactely what the authors want to show, not to present and analyze what their actual data means. For example, in this study they an indicator like this adiposity index to make the reader believe that the coconut oil group was actually obese compared to the soybean oil, eventhough the coconut oil group weighed 10% less. These tricks are so obviously fraudulent and embarrassing that they give you an impression of how corrupt all these researchers are. They all know that what they do is bull**** but they keep doing it nevertheless because you don't get funding for coming to the conclusion that saturated fat and sucrose might be protective and healthy.

Well, if you think that this is an accurate way to calculate adiposity I can't argue with that:

The adiposity index was calculated with the following equation: relative total body fat weight (%) = [the sum of the weight of abdominal and epididymal fat pads (g)/final body
weight (g)] × 100%.

From my understand, this is very similar to to what we humas to measure bodyfat percentage - your typical fat pinch tests. And they’re quite accurate as long as measurer knows how to follow the protocol.

Except, in this case, they WEIGH the rats’ fat, which seems to be even more accurate than the pinch tests that we as humans use.

So, it appears pretty reasonable to say the CO group had higher adiposity (because the researchers proved that they had a greater percentge of bodyweight be comprised of bodyfat).
 

Kartoffel

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Those insulin and glucose numbers don't look too good for the coconut oil group.

Of course blood glucose and insulin were high. They fed them 50% pure fructose and 37% fat. A diet like this, especially with very little protein, will flood the blood with triglycerides and FFA that will suppress glucose oxidation. The study doesn't provide any reason to assume that the lower levels in the soybean oil were beneficial. PUFA have been demonstrated to lower blood glucose, but that's no reason to think they are healthy.

PLoS One. 2017 Jul 13;12(7):e0179542. doi: 10.1371/journal.pone.0179542. eCollection 2017.
Effects of coconut oil on glycemia, inflammation, and urogenital microbial parameters in female Ossabaw mini-pigs.
Newell-Fugate AE1,2, Lenz K3, Skenandore C1, Nowak RA2, White BA2,4, Braundmeier-Fleming A3,4,5.
Author information
Abstract

Forty percent of American women are obese and at risk for type II diabetes, impaired immune function, and altered microbiome diversity, thus impacting overall health. We investigated whether obesity induced by an excess calorie, high fat diet containing hydrogenated fats, fructose, and coconut oil (HFD) altered glucose homeostasis, peripheral immunity, and urogenital microbial dynamics. We hypothesized that HFD would cause hyperglycemia, increase peripheral inflammation, and alter urogenital microbiota to favor bacterial taxonomy associated with inflammation. We utilized female Ossabaw mini-pigs to model a 'thrifty' metabolic phenotype associated with increased white adipose tissue mass. Pigs were fed HFD (~4570 kcal/pig/day) or lean (~2000 kcal/pig/day) diet for a total of 9 estrous cycles (~6 months). To determine the effect of cycle stage on cytokines and the microbiome, animals had samples collected during cycles 7 and 9 on certain days of the cycle: D1, 4, 8, 12, 16, 18. Vaginal swabs or cervical flushes assessed urogenital microbiota. Systemic fatty acids, insulin, glucose, and cytokines were analyzed. Pig weights and morphometric measurements were taken weekly. Obese pigs had increased body weight, length, heart and belly girth but similar glucose concentrations. Obese pigs had decreased cytokine levels (IL-1β, TNF-α, IL-4, IL-10), arachidonic acid and plasma insulin, but increased levels of vaccenic acid. Obese pigs had greater urogenital bacterial diversity, including several taxa known for anti-inflammatory properties. Overall, induction of obesity did not induce inflammation but shifted the microbial communities within the urogenital tract to an anti-inflammatory phenotype. We postulate that the coconut oil in the HFD oil may have supported normal glucose homeostasis and modulated the immune response, possibly through regulation of microbial community dynamics and fatty acid metabolism. This animal model holds promise for the study of how different types of obesity and high fat diets may affect metabolism, immune phenotype, and microbial dynamics

Except, in this case, they WEIGH the rats’ fat, which seems to be even more accurate than the pinch tests that we as humans use.

They didn't weigh the rat's (total) fat, they weighed their abdominal and epididymal fat. It's common knowledge that PUFA tend to decrease abdominal and liver fat while increasing it in all other fat tissues. To put that into perspective, "lean" rats are considered to have around 13-14% body fat, obese rats around 30%. Their adiposity index is a cheap, fraudulent trick to fool readers.
 
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CLASH

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Didnt read the study yet but I saw this:

@grenade
“In the EFA deficiency experiment, did they observe symptoms regarding obesity, glucose control, insulin control, etc.? From my memory, that experiment observed skin issues, most notably.

The CO group in this study had 32% of its food be comprised of CO, with the rest being fructose, protein, micronutrients, etc. Good point on the low protein content.

See my response to Kartoffel - adiposity increased the most in the CO group. It’s right there in the graph he attached.“

Pretty sure most animals cant digest pure fructose by itself. Alot of studies show pure fructose leading to endotoxin, hyperlidpidemia and fatty liver. Dont think its the coconout oil.
 

Peater Piper

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Of course blood glucose and insulin were high. They fed them 50% pure fructose and 37% fat. A diet like this, especially with very little protein, will flood the blood with triglycerides and FFA that will suppress glucose oxidation.
Percentages of fructose and fat were the same in the soybean group. I assume because soybean oil is so high in PUFA, it didn't impair glucose oxidation as significantly as the CO group. Still, 20-weeks isn't a short study for rats, and it's hard to say the CO group looked any better in any health category by the end except for in overall body weight (and we could actually look at that as a failure to thrive). Still, it was definitely an extreme dietary approach, and in rats which aren't always comparable to humans, so I doubt we can really draw any real conclusions. I don't believe fructose and saturated fat are a great combo though, which is kind of anti-Peat, but there's plenty of evidence they don't play well together, at least in the same meal, and can lead to long term problems when used in combination.
 

Kartoffel

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I assume because soybean oil is so high in PUFA, it didn't impair glucose oxidation as significantly as the CO group.

What makes you say that? I can't see anything supporting that in the study
 

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