Mechanism by which coconut oil promotes pregnenolone synthesis from cholesterol ?

[burtlancast]

Ray mentioned that coconut oil lowers elevated cholesterol back to normal by promoting it’s conversion to pregnenolone.

But how ?
Is it by increasing the availability of glucose to the liver cells, enabling them to convert more T4 to T3 ?
( coconut oil shuts down liver fat synthesis, thus increases the availability of glucose for other processes )

 

[haidut]

Re: How does coconut oil lower cholesterol by converting it to pregnenolone ?

Ray mentioned that coconut oil lowers elevated cholesterol back to normal by promoting it’s conversion to pregnenolone.

But how ?
Is it by promoting T3 liver conversion through it's glucose sparing effect ( it shuts down liver fat synthesis from glucose) ?

I think it's the uncoupling effects of the saturated fat on mitochondria. Cholesterol is converted into pregnenolone into the mitochondria, so I think a more active mitochondria will synthesize more pregnenolone together with more heat and less ATP.

 

[burtlancast]

Re: How does coconut oil lower cholesterol by converting it to pregnenolone ?

Here's something i came across trying to find my answer:

Ray claims coconut oil promotes the expression of the T3 receptor:

This comes from his 1993 article "MULTIPLE SCLEROSIS AND OTHER HORMONE-RELATED BRAIN SYNDROMES"

Coconut oil serves several purposes. Its butyric acid is known to increase T3 uptake by glial cells. It has a general pro-thyroid action, for example by diluting and displacing antithyroid unsaturated oils, its short- and medium-chain fatty acids sustain blood sugar and have antiallergic actions, and it protects mitochondria against stressinjury.

http://raypeat.com/articles/articles/mu ... osis.shtml

Then, he writtes it again in "Oils in context":

Butter and coconut oil contain significant amounts of the short and medium-chain saturated fatty acids, which are very easily metabolized,[60] inhibit the release of histamine,[39] promote differentiation of cancer cells,[61] tend to counteract the stress-induced proteins,[62] decrease the expression of prolactin receptors, and promote the expression of the T3 (thyroid) receptor. [63] - See more at: http://coconutoil.com/peat_oils_context ... rv2eL.dpuf

Problem is, coconut oil doesn't contain any butyric acid, according to all the sources i've checked.

Could the body convert a coconut oil ingredient to butyric acid ? Ray doesn't seem to imply it either.
The number 63 references an article proving the butyric acid effect, but doesn't cite any ingredients from coconut oil.

Other short-chain fatty acids than butyrate were found to similarly influence both nuclear receptor and extranuclear T3 levels with the following potency: butyrate > valerate > propionate >
acetate. On the contrary, ketone bodies were ineffective.

Maybe this is why he uses the word "probably" in this other article:

The short-chain fats in coconut oil probably improve tissue response to the thyroid hormone (T3), and its low content of unsaturated fats might allow a more nearly optimal function of the thyroid gland and of mitochondria. - See more at: http://coconutoil.com/peat_oils_context ... rv2eL.dpuf

So, proof or no proof ?

 

[haidut]

Re: How does coconut oil lower cholesterol by converting it to pregnenolone ?

Here's something i came across trying to find my answer:

Ray claims coconut oil promotes the expression of the T3 receptor:

This comes from his 1993 article "MULTIPLE SCLEROSIS AND OTHER HORMONE-RELATED BRAIN SYNDROMES"

Coconut oil serves several purposes. Its butyric acid is known to increase T3 uptake by glial cells. It has a general pro-thyroid action, for example by diluting and displacing antithyroid unsaturated oils, its short- and medium-chain fatty acids sustain blood sugar and have antiallergic actions, and it protects mitochondria against stressinjury.

http://raypeat.com/articles/articles/mu ... osis.shtml

Then, he writtes it again in "Oils in context":

Butter and coconut oil contain significant amounts of the short and medium-chain saturated fatty acids, which are very easily metabolized,[60] inhibit the release of histamine,[39] promote differentiation of cancer cells,[61] tend to counteract the stress-induced proteins,[62] decrease the expression of prolactin receptors, and promote the expression of the T3 (thyroid) receptor. [63] - See more at: http://coconutoil.com/peat_oils_context ... rv2eL.dpuf

Problem is, coconut oil doesn't contain any butyric acid, according to all the sources i've checked.

Could the body convert a coconut oil ingredient to butyric acid ? Ray doesn't seem to imply it either.
The number 63 references an article proving the butyric acid effect, but doesn't cite any ingredients from coconut oil.

Other short-chain fatty acids than butyrate were found to similarly influence both nuclear receptor and extranuclear T3 levels with the following potency: butyrate > valerate > propionate >
acetate. On the contrary, ketone bodies were ineffective.

Maybe this is why he uses the word "probably" in this other article:

The short-chain fats in coconut oil probably improve tissue response to the thyroid hormone (T3), and its low content of unsaturated fats might allow a more nearly optimal function of the thyroid gland and of mitochondria. - See more at: http://coconutoil.com/peat_oils_context ... rv2eL.dpuf

So, proof or no proof ?

So, if he is comparing coconut oil to butyrate and T3 both of which incouple mitochondria then I am inclined to think that coconut oil does it using the same mechanism. There is a study I posted on lauric acid (the predominant fatty acid in coconut oil) powerfully uncoupling mitochondria in liver cells, so we know it works at least in the liver.

 

[Such_Saturation]

I think I heard Ray Peat in an interview saying it not as bad to have saturated fat on the albumin which T3 also uses, or something.

 

[burtlancast]

Re: How does coconut oil lower cholesterol by converting it to pregnenolone ?

So, if he is comparing coconut oil to butyrate and T3 both of which incouple mitochondria then I am inclined to think that coconut oil does it using the same mechanism. There is a study I posted on lauric acid (the predominant fatty acid in coconut oil) powerfully uncoupling mitochondria in liver cells, so we know it works at least in the liver.

The uncoupling effect can indeed explain the increased conversion of cholesterol to pregnenolone, and thus the normalizing effects of coconut oil upon elevated cholesterol levels.

But the problem is Ray obviously seems to imply, from the extracts i've posted, that this conversion is related to the increased uptake of T3, rather than to the uncoupling effects of short-medium fatty acids.

 

[haidut]

Re: How does coconut oil lower cholesterol by converting it to pregnenolone ?

So, if he is comparing coconut oil to butyrate and T3 both of which incouple mitochondria then I am inclined to think that coconut oil does it using the same mechanism. There is a study I posted on lauric acid (the predominant fatty acid in coconut oil) powerfully uncoupling mitochondria in liver cells, so we know it works at least in the liver.

The uncoupling effect can indeed explain the increased conversion of cholesterol to pregnenolone, and thus the normalizing effects of coconut oil upon elevated cholesterol levels.

But the problem is Ray obviously seems to imply, from the extracts i've posted, that this conversion is related to the increased uptake of T3, rather than to the uncoupling effects of short-medium fatty acids.

Yeah, on that one I am confused as well. Maybe MCT act as some sort of carrier for T3 into the cell since as a hormone it is fat soluble and saturated fat goes directly to the mitochondria for oxidation, sometimes before even sugar. I am just guessing here, but if someone else has some ideas I'd like to hear them.

 

[Such_Saturation]

He said it has to do with albumin.

 

[haidut]

He said it has to do with albumin.

Meaning people with high albumin have higher T3 uptake? I know coconut oil increases albumin.

 

[burtlancast]

Here's coconut oil' s composition:

And here's a list of Straight-chain, saturated carboxylic acids:

I suppose Ray implies similar effects between similar compounds, but cannot point to a scientific article proving it.
The problem is lauric and myristic acids ( coconut oil) are 8 to 10 methyl groups larger than butyric acid or propionic acid.
Even though it looks like the article seems to point a higher effect with the larger fatty acids ( if one excepts valerate) they still constitute very small fatty acids compared to the ones in coconut oil.

 

[Such_Saturation]

I think this is similar to what he said:

While the competition by PUFA for protein binding sites blocks the effects of thyroid hormone and vitamin A, the action of PUFA on the sex steroid binding protein (SBP, or SSBG, for sex steroid binding globulin) increases the activity of estrogen. That's because the SSBG neutralizes estrogen by binding it, keeping it out of cells; free PUFA keep it from binding estrogen (Reed, et al., 1986). People with low SSBG/estrogen ratio have an increased risk of cancer. When the SSBG protein is free of estrogen, it is able to enter cells, and in that estrogen-free state it probably serves a similar protective function, capturing estrogen molecules that enter cells before they can act on other proteins or chromosomes. Transthyretin, the main transporter of thyroid and vitamin A, and albumin (which can also transport thyroid hormone) are both able to enter cells, while loaded with thyroid hormone and vitamin A. Albumin becomes more lipophilic as it binds more lipid molecules, so its tendency to enter cells increases in proportion to its fat burden. Albumin in the urine is a problem associated with diabetes and kidney disease; albumin loaded with fatty acids passes from the blood into the urine more easily than unloaded albumin, and it is the fatty acids, not the albumin, which causes the kidney damage (Kamijo, et al., 2002). It's possible that SSBG's opposite behavior, entering cells only when it carries no hormones, is the result of becoming less lipophilic when it's loaded with estrogen.

[http://raypeat.com/articles/articles/fats-functions-malfunctions.shtml]

 

[moss]

Ray mentioned that coconut oil lowers elevated cholesterol back to normal by promoting it’s conversion to pregnenolone.

But how ?
Is it by increasing the availability of glucose to the liver cells, enabling them to convert more T4 to T3 ?
( coconut oil shuts down liver fat synthesis, thus increases the availability of glucose for other processes )

Now I am a little confused about coconut oil and obviously there is still much to learn.
Forgive me if I am stating the obvious here, but I thought CO due to its stable nature, containing short and medium chain fatty acids, does not place stress on cell membranes and tissues and because the fatty chains are smaller can enter the mitochondria easier. Apparently CO does not oxidise in the body, allowing for easier conversion of T4 to T3 via the liver and I thought the mechanism by which cholesterol converts into pregnenolone and other hormones was via oxidative energy. Unlike PUFAs (the fatty acids are larger) causing great oxidative stress and cell membrane stress.

Got a little side-tracked but this may be of interest,

http://themedicalbiochemistrypage.org/s ... rmones.php

"In order for cholesterol to be converted to pregnenolone in the adrenal cortex it must be transported into the mitochondria where CYP11A1 resides. This transport process is mediated by steroidogenic acute regulatory protein (StAR). This transport process is the rate-limiting step in steroidogenesis".

http://www.cyberlipid.org/images/Steroi ... is.svg.png

 

[burtlancast]

Agreed, Moss.

Ray said it:

"An important function of coconut oil is that it supports mitochondrial respiration, increasing energy production that has been blocked by the unsaturated fatty acids. Since the polyunsaturated fatty acids inhibit thyroid function at many levels, coconut oil can promote thyroid function simply by reducing those toxic effects. It allows normal mitochondrial oxidative metabolism, without producing the toxic lipid peroxidation that is promoted by unsaturated fats.”

When added to a balanced diet, coconut oil slightly lowers the cholesterol level, which is exactly what is expected when a dietary change raises thyroid function. This same increase in thyroid function and metabolic rate explains why people and animals that regularly eat coconut oil are lean, and remarkably free of heart disease and cancer.

“Coconut oil serves several purposes. Its butyric acid is known to increase T3 uptake by glial cells. It has a general pro-thyroid action, for example by diluting and displacing antithyroid unsaturated oils, its short-and medium-chain fatty acids sustain blood sugar and have anti-allergic actions, and it protects mitochondria against stress injury.”

The red part is stated as fact, when in reality it's nothing more than conjuncture.

Also, i've googled coconut oil and cholesterol, and it seems most studies mention it changes the ratio of good cholesterol to bad cholesterol, but not the total cholesterol.

Only one study, made on animals, mentions lower cholesterol:

Despite its saturated fat content, coconut oil contains antioxidants and beneficial polyphenol compounds. Researchers in India examined the effects of virgin coconut oil in an animal study and found that it reduced total cholesterol as well as LDL and VLDL, which are bad forms of cholesterol. The researchers postulate the results may be attributed to the polyphenols present in coconut oil. The results are published in the September 2004 issue of the journal "Clinical Biochemistry."

 

[moss]

Thanks Burt

It is difficult to find detailed data on chemical composition of coconut oil but here's one.
The Chemical Composition and Biological Properties of Coconut (Cocos nucifera L.) Water.
Perhaps RP was referring to Aminobutyric acid?
According to the article (below) pg. 5148 chemical compositions of coconut oil in the Amino acids profile contains Aminobutyric acid.

mdpi.com/1420-3049/14/12/5144/pdf

 

[burtlancast]

Good find, Moss.

The article does list the saturated fatty acids in the milk, going from 6 carbons (caproic) to 20 carbons (arachidonic). But butyric, or valeric are 4 and 5 carbons, respectively.

The cited γ-Aminobutyric acid = Gabba (the neurotransmitter Ray mentions as healthy)

 

[Such_Saturation]

Good find, Moss.

The article does list the saturated fatty acids in the milk, going from 6 carbons (caproic) to 20 carbons (arachidonic). But butyric, or valeric are 4 and 5 carbons, respectively.

The cited γ-Aminobutyric acid = Gabba (the neurotransmitter Ray mentions as healthy)

Do you mean arachidic acid?

 

[Parsifal]

That's interesting. So is it possible to eat coconut oil with a sugar meal and to not feed the randle cycle if it helps the liver with glucose?

 

[tara]

post 111113 That's interesting. So is it possible to eat coconut oil with a sugar meal and to not feed the randle cycle if it helps the liver with glucose?

Not sure I've got this right, but I thought one got the benefits of coconut oil from small quantities - eg 1tsp with a meal. If this is all the fat you are getting with the meal, it would not have a big effect wrt the Randle 'Cycle'.