Tyw. Said Something That Makes Alot Of Sense!

Drareg

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I don't want to make this back and forth discussion worse, I hope what I post makes it better. First I have gotten alot of good information from Tyw, and there is a dispute or whatever you want to call it with pufa. Below is from what RP has said:

Essential fatty acids (EFA) are, according to the textbooks, linoleic acid and linolenic acid, and they are supposed to have the status of "vitamins," which must be taken in the diet to make life possible. However, we are able to synthesize our own unsaturated fats when we don't eat the "EFA," so they are not "essential." The term thus appears to be a misnomer. [M. E. Hanke, "Biochemistry," Encycl. Brit. Book of the Year, 1948.]


Just saying

This is a great quote, if the body is producing on its own a lot of confusion will be observed by researchers. They don't know this?
 
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Well she did have pregnancy diabetes but don't worry they quickly made her quit all simple sugars :cool

afd (1).jpg
 

tyw

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Thanks! But I meant the other discussion linked.

OK. That study demonstrates the effect even better -- Effect of added fat on the plasma glucose and insulin response to ingested potato given in various combinations as two meals in normal individuals. - PubMed - NCBI

This was 50g carb and 50g fat (as butter), either alone or combined, first thing in the morning, and then with the second meal at noon.

First, this is definitely a high fat intake, so the commentary above about this still holds.

Then we have Four combinations:
(1) potato for the first meal, potato for the second meal;
(2) potato for the first meal, potato with fat for the second meal;
(3) potato with fat for the first meal, potato for the second meal; and
(4) potato with fat for the first meal, potato with fat for the second meal

The statement:

When the first meal contained potato only, the glucose area response to the second meal was significantly less when the second meal contained fat.​

is referring to the often observed "fat lowers GI" mechanic.


The statement:

fat ingestion had no effect on the glucose area response to the second meal when fat was present in the first meal​

implies that the fat immediately in a meal blunts glucose absorption, but that fat in a meal prior blunts glucose clearance. In other words, you have fat do


The statement:

when both meals contained fat, a decrease in the glucose area response did not occur with the second meal.​

implies that glucose clearance was inhibited by a high level of fat intake.


The statement:

The glucose area responses all were greater after the second meal compared with those after the first meal​

implies that glucose clearance was poorer at noon, after having already eaten. More available dietary fuel and without the "glucose sink" of an overnight fast affects clearance. Physical activity would also affect this.


Then the statements:

The insulin area responses to the first and second meals were similar after ingestion of potato or potato with fat.

When both meals contained fat, a decrease in the glucose area response did not occur with the second meal.​


Implies that Insulin did not change, yet glucose clearance was poorer. This is exactly the meaning of insulin resistance.

....
 

Amazoniac

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OK. That study demonstrates the effect even better -- Effect of added fat on the plasma glucose and insulin response to ingested potato given in various combinations as two meals in normal individuals. - PubMed - NCBI

This was 50g carb and 50g fat (as butter), either alone or combined, first thing in the morning, and then with the second meal at noon.

First, this is definitely a high fat intake, so the commentary above about this still holds.

Then we have Four combinations:
(1) potato for the first meal, potato for the second meal;
(2) potato for the first meal, potato with fat for the second meal;
(3) potato with fat for the first meal, potato for the second meal; and
(4) potato with fat for the first meal, potato with fat for the second meal

The statement:

When the first meal contained potato only, the glucose area response to the second meal was significantly less when the second meal contained fat.​

is referring to the often observed "fat lowers GI" mechanic.


The statement:

fat ingestion had no effect on the glucose area response to the second meal when fat was present in the first meal​

implies that the fat immediately in a meal blunts glucose absorption, but that fat in a meal prior blunts glucose clearance. In other words, you have fat do


The statement:

when both meals contained fat, a decrease in the glucose area response did not occur with the second meal.​

implies that glucose clearance was inhibited by a high level of fat intake.


The statement:

The glucose area responses all were greater after the second meal compared with those after the first meal​

implies that glucose clearance was poorer at noon, after having already eaten. More available dietary fuel and without the "glucose sink" of an overnight fast affects clearance. Physical activity would also affect this.


Then the statements:

The insulin area responses to the first and second meals were similar after ingestion of potato or potato with fat.

When both meals contained fat, a decrease in the glucose area response did not occur with the second meal.​


Implies that Insulin did not change, yet glucose clearance was poorer. This is exactly the meaning of insulin resistance.

....
But do you know how butter compares to fats of similar compositions? Unfortunately that first study by Mary Gannon that you mentioned didn't include butter..
 

tyw

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But do you know how butter compares to fats of similar compositions? Unfortunately that first study by Mary Gannon that you mentioned didn't include butter..

TBH. I doubt there would be much difference. The study by Gannon et. al. had lard with composition, 45% MUFA, 11% PUFA, 39% SFA. Regular butter would be 26% MUFA, 4% PUFA, 62% SFA.

This provides a similar comparison between Lard vs Safflower oil, and Butter vs Safflower oil, and one would think that the differences (if any) would be more pronounced with butter instead of lard.

I think the main factor is more a case of gastric emptying and other carbohydrate absorption inhibition mechanics, which come about with any sort of fat consumption, rather than having to do with specific composition of said fat.

However, even in this single meal study, there were no differences in glucose response (all topped off at about 150mg/dL), whereas there were differences in insulin response, with the more saturated Lard showing a definite 25% average increase in insulin (when combined with potato), and also a huge variance (look at those error bars ..... and only with the lard)

This is consistent with the model that Saturated Fats cause more insulin resistance (again, more insulin + same glucose => insulin resistance).

The large variations could potentially reflect the differences in innate insulin sensitivity of the participants (who ranged from BMI 19-29, which is a large range), and the fact that only the SFA-dominant lard showed this effect, seems to indicate that it is SFA that is responsible for this sort of signalling.

Unfortunately, this yet again raises the context dependence of such mechanics, and those who are already more insulin sensitive will respond differently from those who are not.

Screen Shot 2017-03-06 at 8.25.50 am.jpg


...
 

Amazoniac

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TBH. I doubt there would be much difference. The study by Gannon et. al. had lard with composition, 45% MUFA, 11% PUFA, 39% SFA. Regular butter would be 26% MUFA, 4% PUFA, 62% SFA.

This provides a similar comparison between Lard vs Safflower oil, and Butter vs Safflower oil, and one would think that the differences (if any) would be more pronounced with butter instead of lard.

I think the main factor is more a case of gastric emptying and other carbohydrate absorption inhibition mechanics, which come about with any sort of fat consumption, rather than having to do with specific composition of said fat.

However, even in this single meal study, there were no differences in glucose response (all topped off at about 150mg/dL), whereas there were differences in insulin response, with the more saturated Lard showing a definite 25% average increase in insulin (when combined with potato), and also a huge variance (look at those error bars ..... and only with the lard)

This is consistent with the model that Saturated Fats cause more insulin resistance (again, more insulin + same glucose => insulin resistance).

The large variations could potentially reflect the differences in innate insulin sensitivity of the participants (who ranged from BMI 19-29, which is a large range), and the fact that only the SFA-dominant lard showed this effect, seems to indicate that it is SFA that is responsible for this sort of signalling.

Unfortunately, this yet again raises the context dependence of such mechanics, and those who are already more insulin sensitive will respond differently from those who are not.

View attachment 4750

...
It must depend on the person, but how much fat in a starchy meal do you think that might be beneficial and how much clearly interferes negatively for most people? And why?
 

Drareg

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Within the context of discussion this study is worth a look at-

http://link.springer.com/article/10.1007/s10545-014-9747-y

"Barth syndrome (BTHS, OMIM 3020660) is an X-linked disorder of cardiomyopathy (CM) and skeletal myopathy accompanied by neutropenia which was first described by Peter Barth and colleagues in 1983 (Barth et al 1983). Growth retardation and 3-methylglutaconic aciduria (3-MGCA) have also been described in BTHS (Kelley et al 1991), as well as a characteristic dysmorphology (Hastings et al 2009) and male fetal death resulting in miscarriage and stillbirth (Steward et al 2010).

BTHS is caused by mutations in the tafazzin (TAZ) gene (Bione et al 1996) which encodes proteins that belong to a family of acyltransferases known as tafazzins (Schlame et al 2002). These are involved in phospholipid biosynthesis, specifically in the incorporation of linoleic acid into phosphatidylglycerol and cardiolipin (Vreken et al 2000). Cardiolipin is a mitochondrial membrane phospholipid with a tissue-specific structure (Schlame et al 2005). The most abundant form in the mitochondria of human cardiac and skeletal muscle is tetralinoleoyl cardiolipin (CL4). Deficiency of CL4 has been identified in a range of tissues in patients with BTHS (Schlame et al 2002), as well as increased concentrations of its precursor, monolysocardiolipin (MLCL) (Houtkooper et al 2009; Valianpour et al 2002a, b). These findings have also been described in TAZ deficient yeast (Li et al 2007), Drosophila (Xu et al 2006) and a knock-down mouse model of BTHS (Acehan et al 2011), and are consistent with the hypothesis that the disorder is caused by defective cardiolipin remodelling.

Over 120 mutations in the TAZ gene have been identified, occurring in all 11 exons as well as at some splice sites (Gonzalez 2013). Most are missense mutations, small deletions or insertions, but some large exon deletions and one full gene deletion have also been described. Most are predicted to result in loss of function.

Patients with BTHS exhibit considerable phenotypic variation; the features of the disorder are variable both between patients and within individual patients over time. For example, some BTHS patients never develop CM, many have CM which ameliorates with age (Rigaud et al 2013; Roberts et al 2012; Spencer et al 2006) and up to 10 % have not been identified as being neutropenic at any stage (Clarke et al 2013). No genotype/phenotype correlations have been identified.

We describe seven patients from three families with BTHS confirmed by TAZ mutation analysis who have some biochemical and clinical features which differ from other BTHS cases previously described, notably lack of severe deficiency of CL4 in leukocytes and absence of neutropenia; two are asymptomatic adults, one of whom has never had any features of BTHS."

"We have described seven subjects from three families with BTHS confirmed by the finding of a mutation in the TAZ gene. They do not have profound CL4 deficiency typical of BTHS, although increased MLCL confirms that there is an abnormality in cardiolipin remodelling. We believe this to be the first description of BTHS without severe CL4 deficiency. In two subjects, platelet or bloodspot CL4 had been measured previously and found to be normal, resulting in the diagnosis of BTHS being excluded initially. This was subsequently revised due to family history or clinical features and the finding of a MLCL/CL4 ratio significantly above the reference range; this highlights the importance of measurement of this ratio, rather than isolated assay of CL4, when performing biochemical investigation of BTHS."
 

tyw

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It must depend on the person, but how much fat in a starchy meal do you think that might be beneficial and how much clearly interferes negatively for most people? And why?

No clue TBH. When I look at other people's experiences, there is so much variation that I cannot begin to see any pattern without experimentation. I have a personal guess based on random anecdotes of single-meal experiences, that "a little fat goes a long way", and where something simple like adding a tablespoon of oil, or switching out chicken breast and including chicken thigh, seems to help people feel fuller for longer, without any brain fog or other symptoms.

Effectively, this is high carb, plus maybe 10-15g of fat, and all symptoms go away. Perhaps this falls into the 20% fat range.

I have no proof for this other than anecdote, so it comes down to self-experimentation. Personally, I can go <10% fat with zero problems, and cannot say what a maximum threshold is because of too many confounding factors (eg: when you eat something like eggs, fat goes up, but so those protein, and protein affects satiety ....)

All these mechanics are going to depend heavily on caloric content. The quip "a 50% carb, 50% calorie restricted diet, is a ketogenic diet", remains true, and if adding some fat causes the person to eat less overall that day, then insulin will already be lower, regardless of any transient insulin resistance caused.

Mechanics of Insulin resistance apply the most to chronic calorie-overloading scenarios, in which case, I am not fond of anything more than 30% fat at all (if carbs are also present).

And of course, circadian factors dominate -- a pure-carb starchy meal in the morning may not come with issues, whereas a carb + sat fat meal may (eg: bagels + cream cheese => brain fog). Whereas a pure-carb starchy meal in the evening may immediately cause issues.

And of course, physical activity factors dominate -- a pure-carb meal in the evening after 1hr of intense lifting is probably not going to be cleared pretty quick.

Therefore: Given the lack of predictability, I stand by the idea to Start with either very-low-fat or very-low-carb, and then slowly add the opposing macronutrient until a feeling of satisfaction and consistent energy is achieved.

I also think that "Carbs either earlier in the day, or at least after substantial exercise", is the way to go, with fat probably having to be reduced at those times as well.

Needless to say, I do not recommend the addition of fat be through PUFA, though the above discussions add an avenue for experimenting with MUFA.

----

@Drareg that is a good study. It shows that not all TAZ gene mutatations lead to CL4 (cardiolipin with 4 linoleic acid PUFA molecules) deficiency, and that it is precisely this lack of CL4 that leads to the complications found. The lack of 18:2 on cardiolipin is clearly the cause for the symptoms of this particular genetic disease.

.....
 

nikolabeacon

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I can only assume how butter as a satured fat(or its speciffic ratios of fats) can have different effects because it is the only fat in nature found with carbs at the same time( indeed only in milk..... with glucose(starch) and galactose....not with fructose at all nor with high glucose as well)... .

So probably butter fat can have different effects only with glucose(starch) and galactose.in 50%-50% ratios as in milk....and probably thats the scenario where high SFA is leat "harmfull"...and why there are stories where people do pretty fine with whole milk and limited fructose ....SFA ( including butter)with fructose is a different story probably...and thats probably why it is not good high fat and high fructose.....

I am not saying that higher fat and high glucose(starch) is good for sure but probably better than higher SFA and high fructose

So high SFa is reasonable probably only in milk and meat diet with limited fructose....
 

haidut

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Do the patients with Barts syndrome avoid linoleic acid? I'm guessing they eat food at times and probably get linoleic acid at some point,by the research quoted by tyw barts syndrome should not exist by this logic.

Never met anybody with Bart's syndrome so I don't know. The patients I have seen got EFA-deficient through hospital feeding them fat-free "meals" through IV infusion. It usually takes about 1 month on such diet to see Mead acid go above normal range. What is also interesting is that, just as studies on hyperthyroidism found, EFA-deficient patients see estrogen drop and androsterone, T, DHT and progesterone rise. Their androsterone:etiocholanolone ratio goes from about 1.2 to 2 or even 3 while being EFA deficient.
 

Dante

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Never met anybody with Bart's syndrome so I don't know. The patients I have seen got EFA-deficient through hospital feeding them fat-free "meals" through IV infusion. It usually takes about 1 month on such diet to see Mead acid go above normal range. What is also interesting is that, just as studies on hyperthyroidism found, EFA-deficient patients see estrogen drop and androsterone, T, DHT and progesterone rise. Their androsterone:etiocholanolone ratio goes from about 1.2 to 2 or even 3 while being EFA deficient.
Interesting, so do these hormonal changes occur solely due to being EFA-deficient( i mean do you give them anything else like aspirin or other medicines which might be causing this change) Also, do their micronutrient status also increase as in hyperthyroidism and last but not the least , do the ladies also see rise in T, DHT on being EFA deficient :) ?
 

Fractality

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Never met anybody with Bart's syndrome so I don't know. The patients I have seen got EFA-deficient through hospital feeding them fat-free "meals" through IV infusion. It usually takes about 1 month on such diet to see Mead acid go above normal range. What is also interesting is that, just as studies on hyperthyroidism found, EFA-deficient patients see estrogen drop and androsterone, T, DHT and progesterone rise. Their androsterone:etiocholanolone ratio goes from about 1.2 to 2 or even 3 while being EFA deficient.

What exactly is in those IV-infusion "meals?"
 

Wagner83

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whereas there were differences in insulin response, with the more saturated Lard showing a definite 25% average increase in insulin (when combined with potato), and also a huge variance (look at those error bars ..... and only with the lard)

This is consistent with the model that Saturated Fats cause more insulin resistance (again, more insulin + same glucose => insulin resistance).

The large variations could potentially reflect the differences in innate insulin sensitivity of the participants (who ranged from BMI 19-29, which is a large range), and the fact that only the SFA-dominant lard showed this effect, seems to indicate that it is SFA that is responsible for this sort of signalling.



View attachment 4750

...

I don't see any differences in the three graphs between potatoes + various fats, the main difference is in the potato-*only curve so lard has nothing to do with it as far as I can see. Besides are you sure lard can be considered mostly saturated given what porks are fed with ?

Therefore: Given the lack of predictability, I stand by the idea to Start with either very-low-fat or very-low-carb, and then slowly add the opposing macronutrient until a feeling of satisfaction and consistent energy is achieved.

I also think that "Carbs either earlier in the day, or at least after substantial exercise", is the way to go, with fat probably having to be reduced at those times as well.

Needless to say, I do not recommend the addition of fat be through PUFA, though the above discussions add an avenue for experimenting with MUFA.
Interesting do you think experimenting with lots of carbs/starches in the morning until noon and having a bigger meal with mostly fat in te evening would be a decent possibility or would we enter mixing glucose and fats for fuel territory (which from what you suggest wouldn't be optimal)?

Never met anybody with Bart's syndrome so I don't know. The patients I have seen got EFA-deficient through hospital feeding them fat-free "meals" through IV infusion. It usually takes about 1 month on such diet to see Mead acid go above normal range. What is also interesting is that, just as studies on hyperthyroidism found, EFA-deficient patients see estrogen drop and androsterone, T, DHT and progesterone rise. Their androsterone:etiocholanolone ratio goes from about 1.2 to 2 or even 3 while being EFA deficient.

Well then I don't see what could be wrong from going fat free, but then you have suggested the PUFA depletion diet before. Btw you make it sound like I should get some IV fat-free feeding lol :D. Why did they test for androsterone/etiocholanolone ratios though?
 
Last edited:

Drareg

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No clue TBH. When I look at other people's experiences, there is so much variation that I cannot begin to see any pattern without experimentation. I have a personal guess based on random anecdotes of single-meal experiences, that "a little fat goes a long way", and where something simple like adding a tablespoon of oil, or switching out chicken breast and including chicken thigh, seems to help people feel fuller for longer, without any brain fog or other symptoms.

Effectively, this is high carb, plus maybe 10-15g of fat, and all symptoms go away. Perhaps this falls into the 20% fat range.

I have no proof for this other than anecdote, so it comes down to self-experimentation. Personally, I can go <10% fat with zero problems, and cannot say what a maximum threshold is because of too many confounding factors (eg: when you eat something like eggs, fat goes up, but so those protein, and protein affects satiety ....)

All these mechanics are going to depend heavily on caloric content. The quip "a 50% carb, 50% calorie restricted diet, is a ketogenic diet", remains true, and if adding some fat causes the person to eat less overall that day, then insulin will already be lower, regardless of any transient insulin resistance caused.

Mechanics of Insulin resistance apply the most to chronic calorie-overloading scenarios, in which case, I am not fond of anything more than 30% fat at all (if carbs are also present).

And of course, circadian factors dominate -- a pure-carb starchy meal in the morning may not come with issues, whereas a carb + sat fat meal may (eg: bagels + cream cheese => brain fog). Whereas a pure-carb starchy meal in the evening may immediately cause issues.

And of course, physical activity factors dominate -- a pure-carb meal in the evening after 1hr of intense lifting is probably not going to be cleared pretty quick.

Therefore: Given the lack of predictability, I stand by the idea to Start with either very-low-fat or very-low-carb, and then slowly add the opposing macronutrient until a feeling of satisfaction and consistent energy is achieved.

I also think that "Carbs either earlier in the day, or at least after substantial exercise", is the way to go, with fat probably having to be reduced at those times as well.

Needless to say, I do not recommend the addition of fat be through PUFA, though the above discussions add an avenue for experimenting with MUFA.

----

@Drareg that is a good study. It shows that not all TAZ gene mutatations lead to CL4 (cardiolipin with 4 linoleic acid PUFA molecules) deficiency, and that it is precisely this lack of CL4 that leads to the complications found. The lack of 18:2 on cardiolipin is clearly the cause for the symptoms of this particular genetic disease.

.....

Barth syndrome is not a great example imo, how do we explain a mother who doesnt have the Barth gene yet the kid still gets Barth syndrome? The mother shows no signs of the disease while carrying the gene.
This is implies an environmental cause in this case.
When we look at what they currently claim the taz gene is for we see Barth syndrome, dilated cardiomyopathy (DCM), hypertrophic DCM, endocardial fibroelastosis, left ventricular noncompaction and skeletal muscle.
What's known about this gene Is currently around heart,the gene itself as Haidut pointed out will have more influence and that's what researchers are alluding to,we currently don't know it's full effect.

That aside what researchers are seeing could well be estrogen or thyroid issue for example,I would be keen to see if the mothers of kids born with Barths syndrome have had any estrogen treatment or thyroid issues,a good point to note is most of them are boys. Low cholesterol is present with Barths.
The impression the researchers are conveying is the dysfunction starts with the cardiolipin,why look at it this way only and not discuss the outside stressors causing it,essentially genetic inheritance the researchers want to convey imo.

We also see evidence of regression in some cases with Barths and with the studies shown not much effect even with the gene ,there are a lot of inconsistencies with symptoms,it doesn't say much for the "theory" overall,it's not a closed door.

The overall point is why construe the ratio as causing the problem in this context,estrogen and other issues can produce similar symptoms,at this point I would question how they "measure"this effect,when we look at this -"Cells were collected after trypsinization, centrifuged at 500 g for 5 min, washed twice with 2 ml of PBS, and stored at –80°C until analysis."
Knowing the speed of defrosting would be helpful or did they just analyse frozen?
Linoleic acid supplemention of Barth syndrome fibroblasts restores cardiolipin levels

"The results described in this report suggest that a treatment based on dietary supplementation of linoleic acid may lead to an increase of CL levels in different tissues and that this may be beneficial to BTHS patients. We have initiated a clinical trial to investigate whether the treatment described for fibroblasts in vitro can also be reproduced under in vivo conditions and whether this treatment is beneficial for the patients' condition.
To this end, the patients received a linoleic-acid enriched diet and the CL content of platelets was measured in time that revealed a definite increase in CL levels. The in vivo effect of the increase in CL will be monitored by evaluation of the cardiac output and neutrophils count".
Do you have access to this study? This quote it's at the end of the study linked.

You mentioned their is a mammal model with the different ratios and we see the same symptoms,is it possible to give me the link?

All in all this implies very little when we keep in mind we put an organism on a high speed merry go round,wash it and freeze it at -80c ,possibly defrost it? And use an inferior detection method,we then expect to see an accurate picture of "life" at its most "complex". This is death.
Fishing for cardiolipin is not that accurate in these contexts.

It does not currently offer anything categoric in relation to proof of essential PUFA .
 

Drareg

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Never met anybody with Bart's syndrome so I don't know. The patients I have seen got EFA-deficient through hospital feeding them fat-free "meals" through IV infusion. It usually takes about 1 month on such diet to see Mead acid go above normal range. What is also interesting is that, just as studies on hyperthyroidism found, EFA-deficient patients see estrogen drop and androsterone, T, DHT and progesterone rise. Their androsterone:etiocholanolone ratio goes from about 1.2 to 2 or even 3 while being EFA deficient.

At the end of the study linked the researchers start a clinical trial with humans and linoleic acid,I can't find it.

This study was not exactly Harold Hillman friendly.
" Growth media were refreshed every 48 h. Cells were collected after trypsinization, centrifuged at 500 g for 5 min, washed twice with 2 ml of PBS, and stored at –80°C until analysis".

Linoleic acid supplemention of Barth syndrome fibroblasts restores cardiolipin levels
 

haidut

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At the end of the study linked the researchers start a clinical trial with humans and linoleic acid,I can't find it.

This study was not exactly Harold Hillman friendly.
" Growth media were refreshed every 48 h. Cells were collected after trypsinization, centrifuged at 500 g for 5 min, washed twice with 2 ml of PBS, and stored at –80°C until analysis".

Linoleic acid supplemention of Barth syndrome fibroblasts restores cardiolipin levels

If you find the study on Pubmed you can click the author's name and then sort by date. If it is published, it should appear as a more recent study by the same author. Sometimes they do not publish their results, mostly for political reasons. If it is not published I guess the only option would be to email him and ask for the data/results. Usually, they are willing to provide them but may ask for promise not to quote their name when discussing it online since it is not published and peer-reviewed.
 

haidut

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I don't see any differences in the three graphs between potatoes + various fats, the main difference is in the potato-*only curve so lard has nothing to do with it as far as I can see. Besides are you sure lard can be considered mostly saturated given what porks are fed with ?


Interesting do you think experimenting with lots of carbs/starches in the morning until noon and having a bigger meal with mostly fat in te evening would be a decent possibility or would we enter mixing glucose and fats for fuel territory (which from what you suggest wouldn't be optimal)?



Well then I don't see what could be wrong from going fat free, but then you have suggested the PUFA depletion diet before. Btw you make it sound like I should get some IV fat-free feeding lol :D. Why did they test for androsterone/etiocholanolone ratios though?

They test for steroid abnormalities and often EFA-deficient people come back as HYPERthyroid, exactly as Ray said and the animal studies showed. The androsterone:etiocholanolone ratio is sometimes tested to confirm hyperthyroidism. Not very often, but since these people exhibit other steroid abnormalities like lower estrogen and increased cortisol turnover, it often leads to a full steroid panel and the higher ratio is discovered.
 

tyw

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@Drareg Barth Syndrome is a good example because the functional modification is a failure in final step of cardiolipin monitoring.

Most cases of the gene mutation gives rise to this problem in the last step of cardiolipin monitoring, which leads to very inefficient unsaturation. I already went into the process in a post in [Nov-2016] -- Haidut's Summary Of PUFA

This last step in cardiolipin monitoring is where you take a more saturated cardiolipin, and add 18:2 to it. (see linked post for details)

Again, the gene mutation reduces efficiency of this last step. This results in a lack of CL4 (linoleic acid cardiolipin).

The fact that we can over-supplement Barth fibroblasts with the PUFA 18:2, and have them recover more normal CL4 levels, is an indication that the gene mutation only reduces efficiency, and doesn't destroy cardiolipin remodelling entirely. This also means that you can have the mutation, but have a wide spectrum of CL4 compromise, ranging from very little disruption, to near complete failure.

The fact that (very) negative symptoms only exist when CL4 is low, is proof that CL4 is absolutely needed for heart function.

The fact that Barth mutation without compromise in CL4 levels does not produce negative symptoms, is proof that CL4 levels are modulating factor.

This is proof that the PUFA 18:2 is needed in cardiolipin.

.....
 

tyw

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It's a good point and often overlooked.

Have you read this?
http://superhumanradio.com/blog/why-you-may-reconsider-buttering-your-potato.html
Keep your mantra in mind: "Take just what's useful".

Nope, and it is a good read.

The mechanics on speed of gastric emptying make perfect sense, and I agree that this is a major factor.

The note that diets with 40% fat or higher do not produce this effect is interesting. ie: more than 40% fat => body learns to "flush the fat quickly" => no slowing in gastric empty => less Glycemic control benefits to eating fat.

Agree with sentiment:

The type of carbohydrate also plays a large role in determining the extent of insulin resistance. Starchy carbohydrates may be the main offender regardless of fiber content, as an interaction with fat has been observed with regular potatoes, cooked and cooled potatoes (resistant starch), legumes such as lentils, and grain breads.

On the other hand, foods with low available glucose such as fruits and fibrous vegetables appear to not be affected by dietary fat to the same extent that starches are.​

Glucose is the one that is going to be modulated by fat intake the most.

Agree with statement:

The insulin resistance effects are most pronounced with SFAs, as evidenced primarily by research using butter. Oils containing predominantly MUFA and PUFA appear to act similar to one-another, both of which are less insulinemic than SFAs.

Additionally, animal fats appear to act similar to oils, perhaps because at least half of their fat content is unsaturated.

Regardless of the fat, a reasonably “safe” upper limit of consumption appears to be about 15 grams of total fat in a meal.​


Well, if we want a possible place to experiment, it seems the "1 tablespoon of fat" rule is where it is.

These authors are also in agreement that SFA causes the most insulin resistance.

Of course, they note that this "SFA causing insulin resistance" mechanic is relevant:

If the habitual diet is greater than 35-40% calories from fat, then any potential benefit of fat on hyperglycemia may not occur and all types of fat are equally detrimental to insulin sensitivity.​

I will generally agree, but will raise another research paper which shows a benefit to MUFA vs SFA -- Substitution of saturated with monounsaturated fat in a 4-week diet affects body weight and composition of overweight and obese men. - PubMed - NCBI (PDF link).

This compares a 40% fat diet, in obese males, one which had [SFA, MUFA, PUFA] percentages of [24, 13, 3] on the SFA-rich diet, vs that with [11, 22, 7] on the MUFA-rich diet.

As we can see, relatively low PUFA in both, with more PUFA in the MUFA-rich diet, and most fats coming from SFA on the SFA-rich diet (24/40 = 60%). While there was Ad lib intake, clinical measurements of food (this was done with food samples in the lab) showed that the SFA group ate just a little bit more than the MUFA group 12,565 kJ/day vs 11,897 kJ/day => 2991kcal vs 2832kcal, which is a very small difference, certainly too small to explain fig 1:

Screen Shot 2017-03-07 at 6.51.09 am.jpg


This sorta doesn't make sense to me ..... roughly the same calorie intake, yet pretty significant body composition changes in the MUFA group, while the SFA group got fatter.

Anyway, the point being that this was a 40% fat diet with a clear difference in outcomes on SFA vs MUFA. All meals were basically carbs + fat, and is this a case where SFA-induced insulin resistance is playing a big role? Would the fact that these people are obese mean that SFA-induced insulin resistance plays an even bigger role? Dunno, but it is worth contemplating, and possibly experimenting.



I don't see any differences in the three graphs between potatoes + various fats, the main difference is in the potato-*only curve so lard has nothing to do with it as far as I can see. Besides are you sure lard can be considered mostly saturated given what porks are fed with ?

What one should be looking at is the Insulin Area Under the Curve. There is anywhere from a 10-20% increase in the Lard case vs the other 2 (depending on how we want to interpret the error bars).

But if we read the article that Amazoniac linked, more research is provided to support the idea that SFA cause more insulin resistance.

Interesting do you think experimenting with lots of carbs/starches in the morning until noon and having a bigger meal with mostly fat in te evening would be a decent possibility or would we enter mixing glucose and fats for fuel territory (which from what you suggest wouldn't be optimal)?

That is one potential meal pattern. Yes. And that is exactly what user @m_arch did to good effect.

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