SFA vs Dietary Cholesterol restriction

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SFA vs Dietary Cholesterol restriction

Postby apod » Mon Apr 13, 2015 3:40 pm

I recently tested my LDL-P, which came back as borderline-high (1300's). I'm looking to modify my diet a bit to see if I can budge that number down with less saturated fat and dietary cholesterol.

Is lowering one more important than the other? What would be a realistic goal to try to keep these daily intakes under? I've probably been averaging somewhere around 30-35g SFA / 200-400mg cholesterol or so.

While grocery shopping this morning, I switched out some of my usual protein sources with seafood -- now that I'm home, I've just realized that squid has more cholesterol than eggs. (At the time I was thinking this could be a decent source of selenium / omega-3.)
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Re: SFA vs Dietary Cholesterol restriction

Postby marthaNH » Mon Apr 13, 2015 3:44 pm

Most of our authorities seem to agree that saturated fat is the place to find the solution, that dietary cholesterol is not a big part of the problem. I think there are some exceptions to that, but I think that's the advice you will hear.

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Re: SFA vs Dietary Cholesterol restriction

Postby Stavia » Mon Apr 13, 2015 4:36 pm

marthaNH wrote:Most of our authorities seem to agree that saturated fat is the place to find the solution, that dietary cholesterol is not a big part of the problem. I think there are some exceptions to that, but I think that's the advice you will hear.


cholesterol and saturated fat are completely different beasts. even though they may occur together in food, then undergo completely different processes in the body.

dietary cholesterol contributes only a fraction of the body's pool of total cholesterol. The majority (~85% iirc) is synthesised by the liver. "hyperabsorption" that you may have read us discussing pertains to reabsorption of the total cholesterol pool, which is mainly that synthesised by the liver and excreted via the bile into the gut. Reducing cholesterol will not significantly reduce serum cholesterol unless you are eating gallons of it. The little bit of cholesterol in squid is IMO not an issue. I personally think your cholesterol intake is fine.

Staturated fat works differently. Fat is not cholesterol at all. IMO your sat fat intake is too high. I try to keep mine under 7 grams a day and if I pig out, it may go to 10grams max and then I feel bad. But I may be over reacting to viewtopic.php?f=6&t=1153
What do others here do about saturated fat?

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Re: SFA vs Dietary Cholesterol restriction

Postby Julie G » Mon Apr 13, 2015 5:16 pm

Stavia, help us understand exactly how SFA is different. Is it more apt to be hyper-absorbed by E4s? I sometimes wonder if our generalized condemnation of SFA is on target? Merouleau's link to Nutritional Science Isn’t Very Scientific got me thinking if we may be guilty of the same "groupthink" that has plagued public policy for many years and lead to skyrocketing rates of obesity and diabetes.
Most of our devout beliefs about nutrition have not been subjected to a robust, experimental, controlled clinical trial, the type of study that shows cause and effect, which may be why Americans are pummeled with contradictory and confounding nutritional advice.

I played skeptic and searched old cron-o-meter data and saw that I was eating around 20-30 grams of SFA a day when I was yielding LDL-Ps between 1089-1117; fairly decent for a 4/4 in ketosis. FWIW, I wasn't eating junk; but rather high quality brain food- avocados, EVOO, nuts, seeds, fatty fish, occasional free range poultry & grass-fed beef and dairy.

I think the only thing we KNOW for sure is that we should all test & tweak to gauge our response to dietary changes. Switching to a primarily plant based diet (with seafood) high in MUFA has yielded me higher LDL-Ps. For all I know, I may be hyper-absorbing phytosterols? I'm still confused and trying to work out my own puzzle :?

I think Dr. Dayspring was correct in suggesting each of us test our individual markers of cholesterol synthesis to help identify the specific foods that will increase our numbers.

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Re: SFA vs Dietary Cholesterol restriction

Postby Stavia » Mon Apr 13, 2015 7:04 pm

Juliegee wrote:Stavia, help us understand exactly how SFA is different. Is it more apt to be hyper-absorbed by E4s? I sometimes wonder if our generalized condemnation of SFA is on target?


I can look up the details exactly how it is metabolised and summarise for the group. Gimme a few hours. But what I was trying to emphasise is that saturated fat is not the same as cholesterol, they are completely different molecules but they tend to be confused by laypeople (and doctors at times lol) because they are both members of the group called "fats" as opposed to proteins and carbohydrates. I have laid out the body's management of cholesterol in a different thread, I'll get onto the saturated fat biochemistry shortly.
The hyperabsorption as far as I am aware only pertains to **STEROL molecules which are absorbed, excreted by the liver, then reabsorbed.

And I agree completely. We all need to TEST each time we make a change. We are incredibly complex.

**
Wikipedia:
Sterols of plants are called phytosterols and sterols of animals are called zoosterols. The most important zoosterol is cholesterol; notable phytosterols include campesterol, sitosterol, and stigmasterol. They look like this:
The pointy points on the rings are where the carbon atoms are joined. The usual way is not to write the C for carbon on the corners of the ring, because everyone in biochemistry knows that this is a carbon ring.

300px-Sterol_svg.png
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Re: SFA vs Dietary Cholesterol restriction

Postby Stavia » Mon Apr 13, 2015 7:23 pm

ok: saturated fats:

firstly we need to understand the building blocks here: here are the words we need to understand (Wikipedia)
In chemistry, particularly in biochemistry, a fatty acid is a carboxylic acid with a long aliphatic tail (chain), which is either saturated or unsaturated. Most naturally occurring fatty acids have a chain of an even number of carbon atoms, from 4 to 28.

What this is saying is that there are organic (found in life) compounds (complex things made out of atoms - the most important building blocks (atoms) of organic molecules(collection of atoms) are carbon, hydrogen and oxygen. They are drawn in pictures as C H and O) made up of long chains of carbon atoms in a backbone type structure, with varying amounts of hydrogen atoms sticking out of each side. Some of the types of complex things made by our bodies behave like an acid. Don't worry about this now. The word "aliphatic" is important. It means that the carbon atoms line up in a long line as opposed to when they form a ring. Which they also like to do. The most famous ring for us is in my post above - they form a ring in sterol molecules. Now this is an example of how form determines function. The ring shape and the long line shape mean sterols such as cholesterol and fatty acids such as saturated fats (aka saturated fatty acids, same thing), behave completely differently. Completely.

Carbon atoms have got four hands they can hold onto other atoms with. they need at least one to hold onto their friend on either side of the chain, or they can hold each friend's hands with two hands either side. If they hold hands with one hand only they each have two hands left over that they can hold something else. They usually hold a hydrogen atom. Hydrogen atoms only have one hand. If they are not holding a hydrogen atom they have to hold two hands between them. They cannot have an empty hand. If they are holding two hands at any place along the chain we call this an "unsaturated" fatty acid. This term is used because they could hold hands with more hydrogen so there could be more hydrogen in this molecule (a molecule is a word used for a group of atoms) so they molecule is not fully full of as much hydrogen as it could be, so we call it "unsaturated" where saturated means "full". If there is only one pair of carbons holding two hands then this is a monounsaturated fatty acid. If there is more than one pair, it is a polyunsaturated fatty acid. If there are no two hand holdings at all, this is a saturated fatty acid. Depending on where the hand holding is happening, and how long the chain is, the fatty acid has a different name.
The real name for hand holding is "single" or "double bond".
As you can see oxygen atoms have two hands.

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Re: SFA vs Dietary Cholesterol restriction

Postby Julie G » Mon Apr 13, 2015 7:27 pm

I really want to learn more here, Stavia- when you get a chance. Absolutely, no hurry! A primer on distinguishing SFA from sterols would really help me understand. Have I mentioned that you're really, really smart? :D

Here's Dr. Dayspring below. I emphasized what is confusing me:
The only thing we know is that in general the CV risk is higher in patients with E4 alleles compared to the others. We also know that as a generality those with E4 alleles tend to hyperabsorb sterols (cholesterol and xenosterols). Almost all of the cholesterol one absorbs comes from endogenous cellular production which through various pathways finds its way to the gut lumen (on average half excreted in stool, half reabsorbed). Very little ingested cholesterol gets absorbed (as it is such a tiny component on the intestinal pool of cholesterol that is available for absorption). However in patients with hyperabsorption of cholesterol (including those with E4) dietary phytosterols which can also be atherogenic are hypothetically worsening their risk with a vegan diet if they significantly raise plant phytosterol levels (campesterol and sitosterol)


He's suggesting we hyper-absorb BOTH plant & animal sterols...correct? It seems that knowing which is our "nemesis" might help us tweak our diets for optimal lipids... But understanding how SFA fits in would be uber-helpful. I truly think we're getting to the root of our issues with your help.

OMG, you've beat me to the post...THANK YOU!!!

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Re: SFA vs Dietary Cholesterol restriction

Postby Stavia » Mon Apr 13, 2015 7:31 pm

Juliegee wrote:I really want to learn more here, Stavia- when you get a chance. Absolutely, no hurry! A primer on distinguishing SFA from sterols would really help me understand. Have I mentioned that you're really, really smart? :D

Here's Dr. Dayspring below. I emphasized what is confusing me:
The only thing we know is that in general the CV risk is higher in patients with E4 alleles compared to the others. We also know that as a generality those with E4 alleles tend to hyperabsorb sterols (cholesterol and xenosterols). Almost all of the cholesterol one absorbs comes from endogenous cellular production which through various pathways finds its way to the gut lumen (on average half excreted in stool, half reabsorbed). Very little ingested cholesterol gets absorbed (as it is such a tiny component on the intestinal pool of cholesterol that is available for absorption). However in patients with hyperabsorption of cholesterol (including those with E4) dietary phytosterols which can also be atherogenic are hypothetically worsening their risk with a vegan diet if they significantly raise plant phytosterol levels (campesterol and sitosterol)


He's suggesting we hyper-absorb BOTH plant & animal sterols...correct? It seems that knowing which is our "nemesis" might help us tweak our diets for optimal lipids... But understanding how SFA fits in would be uber-helpful. I truly think we're getting to the root of our issues with your help.

OMG, you've beat me to the post...THANK YOU!!!

gonna take me a bit. its complex. gotta go to basics.

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Re: SFA vs Dietary Cholesterol restriction

Postby Stavia » Mon Apr 13, 2015 7:39 pm

ok. so now we understand what a fatty acid looks like. And that it comes in three varieties. Saturated (no double hand holding), Monounsatuarted (one double hand holding) and Polyunsaturated (more than one double hand holding).

I should digress a tad here and explain where omegas fit in. They are polyunsaturated fatty acids. There are four kinds: here is Wikipedia:
(We need a consistent way to describe these long chains: we can see from the pic above that there is an oxygen atom on one end. We call this the beginning of the molecule and start counting the carbons 1 2 3 etc from this end. The far end is the tail. Remember greek "alpha and omega'? ie alpha is beginning and omega is end? The omegas have one of their double hand holding at the tail end, and we count how far from the tail end the last hand holding is happening - either at position 3, 6, 7 or 9. These are our omega 3s omega6s omega 7s and omega 9s)


Omega-3 fatty acids (also called ω-3 fatty acids or n-3 fatty acids[1]) are polyunsaturated fatty acids (PUFAs) with a double bond (C=C) at the third carbon atom from the end of the carbon chain.[2] The fatty acids have two ends, the carboxylic acid (-COOH) end, which is considered the beginning of the chain, thus "alpha", and the methyl (CH3) end, which is considered the "tail" of the chain, thus "omega." The way in which a fatty acid is named is determined by the location of the first double bond, counted from the methyl end, that is, the omega (ω-) or the n- end.


DHA is our most important omega 3. Here is what it looks like:
360px-DHAnumbering.png


Omega-6 fatty acids (also referred to as ω-6 fatty acids or n-6 fatty acids) are a family of pro-inflammatory and anti-inflammatory polyunsaturated fatty acids[1] that have in common a final carbon-carbon double bond in the n-6 position, that is, the sixth bond, counting from the methyl end.


Omega-7 fatty acids (also referred to as ω-7fatty acids or n-7fatty acids)polyunsaturated fatty acids[1] that have in common a final carbon-carbon double bond in the n-7 position, that is, the seventh bond, counting from the methyl end.

Omega-9 fatty acids (ω−9 fatty acids or n−9 fatty acids) are a family of unsaturated fatty acids which have in common a final carbon–carbon double bond in the omega−9 position; that is, the ninth bond from the methyl end of the fatty acid.

oleic acid is am omega 9, it is 18 carbons long
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Re: SFA vs Dietary Cholesterol restriction

Postby Stavia » Mon Apr 13, 2015 7:50 pm

now that we understand what the omegas looks like, let us turn our attention to the saturated fats. Remember there are no double hand holdings at all. The only way the members of this family can differ is in their length. (The polyunsaturateds and monounstaurateds can differ both in their length and where the double hand holding is situated along the chain)

So here are some examples from Wikipedia:
Butyric acid with 4 carbon atoms (contained in butter)
Lauric acid with 12 carbon atoms (contained in coconut oil, palm kernel oil, and breast milk)
Myristic acid with 14 carbon atoms (contained in cow's milk and dairy products)
Palmitic acid with 16 carbon atoms (contained in palm oil and meat)
Stearic acid with 18 carbon atoms (also contained in meat and cocoa butter)


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