Linus Pauling Institute article implicates Saturated Fats as Unhealthy

pauljacob

Member
Joined
Mar 9, 2018
Messages
435
Butter and saturated fats are recommended by Ray Peat and many others on this forum, yet this Linus Pauling Institute article on Inflammation implicates saturated fats for diseases of the liver and whatnots. I'd ignore any other naysayers, but Linus Pauling institute is a respected source of health information. Anyone can shed some light on this please do.



Dietary fats and cholesterol
In general, epidemiological studies have found that diets high in saturated fat and trans fat are pro-inflammatory in nature (reviewed in 16). In contrast, some studies have found that adherence to a Mediterranean-style diet — a diet high in monounsaturated fats — may help reduce inflammation (17, 18). A Mediterranean diet emphasizes olive oil, fruit and vegetables, nuts, beans, fish, whole grains, and moderate consumption of alcohol. Several of these foods are important sources of essential fatty acids that are involved in inflammatory processes. Higher intakes of the omega-3 fatty acids (i.e., α-linolenic acid [ALA], eicosapentaenoic acid [EPA], and docosahexaenoic acid [DHA]) have been generally associated with decreased biomarkers of inflammation (19). Rich dietary sources of ALA include flaxseeds and their oil, walnuts and their oil, and canola oil. EPA and DHA are found in oily fish and fish oils (see the article on Essential Fatty Acids). The ratio of omega-6 to omega-3 fatty acids in the typical Western diet is about 15-20:1, yet it is estimated that humans evolved on a diet with an omega-6 to omega-3 fatty acid ratio of about 1:1 (20). Decreasing this ratio will likely reduce the prevalence and severity of various inflammatory conditions observed in Western societies (for more information on dietary fats, see the article on Essential fatty acids (21).

Low cholesterol diets may also reduce inflammation in the body. One study found that a high cholesterol diet (4 eggs/day for four weeks) increased levels of CRP and serum amyloid A (SAA), two inflammatory markers, in lean (BMI <27.5 kg/m2) subjects who were insulin-sensitive but not in lean subjects who were insulin-resistant or in obese (BMI >27.5 kg/m2) individuals; individuals in these two latter groups had elevated baseline levels of CRP and SAA (22). An 8-week intervention study in patients with primary hypercholesterolemia found that a diet low in both cholesterol (<200 mg/day) and saturated fat (5% of dietary fat from saturated fat) was linked to reduced inflammation, evidenced by a 39% reduction in CRP levels (23).
 

tankasnowgod

Member
Joined
Jan 25, 2014
Messages
8,131
Butter and saturated fats are recommended by Ray Peat and many others on this forum, yet this Linus Pauling Institute article on Inflammation implicates saturated fats for diseases of the liver and whatnots. I'd ignore any other naysayers, but Linus Pauling institute is a respected source of health information. Anyone can shed some light on this please do.

I don't think they are. Respected by who?

I think highly of Linus Pauling himself. An institute that bears his name? Not nearly as much.

Anyway, respected or not, you can always check their sources to see if you agree with their conclusions. For example, the line-

In general, epidemiological studies have found that diets high in saturated fat and trans fat are pro-inflammatory in nature (reviewed in 16). In contrast, some studies have found that adherence to a Mediterranean-style diet — a diet high in monounsaturated fats — may help reduce inflammation (17, 18).

They talk about "studies," but then simply cite three the following three Meta-Analysises.




Nothing there supports the idea that Saturated or Trans Fats are inflammatory.
 

Perry Staltic

Member
Joined
Dec 14, 2020
Messages
8,186
I think any fat in excess is going to be inflammatory. Crossing that threshold is probably easier when living a sedentary life.
 

Jessie

Member
Joined
Jul 9, 2020
Messages
1,018
Several things to keep in mind here. Any fat in excess is going to be bad, it's going to reduce CO2 and increase FAO. So Perry has a very good point.

Personally I find the debates about PUFA vs SFA to be profoundly dense. Most people don't break through their own biases regarding this debate. And even if you do, the evidence isn't so black and white either way. Firstly, almost everyone that prescribes to PUFA's being better than SFA's believe in the lipid hypothesis. And for good reason, the evidence for replacing SFA's for PUFA's to lower LDL cholesterol is basically insurmountable. PUFA's will unquestionably lower your LDL.

Besides this, I also think there's financial reasons why PUFA's are preferred over SFA's. I don't exactly find their recommendations coincidental when there's basically a revolving door that exists in seed oil industry and the American Heart Association (AHA). I'm not saying there's some big conspiracy here, why go to that extreme when a simple case of making as much money as possible perfectly explains it.

Now, lets look at some basic reasons why SFA's may not be as bad as people think they are. A good opening case would be the point Broda Barnes laid out in his book Solve:Riddle of Heart Attacks. Mammalian organisms' adipose tissues are mostly saturated and monounsaturated. When their PUFA concentrations being to rise, their risk for cancer exponentially increases.

Another good argument for SFA's and against PUFA's runs adjacent to Barnes's point. That being, what happens if you put a mammal on a no fat diet (of very, very lowfat)? Arguably the best way to "resaturate" your cells is to eat a diet that mostly or very nearly all carbohydrate. Why? Because when we consume glucose in excess of what we can burn or store as glycogen it gets convert into saturated fat, not unsaturated fat. So if you give your body no fat at all, it will make saturated fats but not fats like linoleic acid. If someone is arguing that PUFA's are better, then I guess they're also indirectly saying that rudimentary human physiology is inherently incorrect.

Third: the picture to disease, as we all know, is just fundamentally bigger than the lipid hypothesis. The mechanical nature of this hypothesis is just not good science. Yes, we know there's a correlation to high LDL and a increased propensity to get atherosclerotic plaque. But this tells us absolutetly nothing about the pathology of this disease. Furthermore, should we even be viewing atherosclerosis as the disease itself? It seems more like a mid-late stage symptom of the disease. If you could magically remove all the cholesterol from your blood, thus preventing atherosclerosis, it wouldn't mean that you don't have heart disease anymore.

Conventional medicine isn't even designed to catch heart disease in it's early stages because heart disease is a problem of energy deficiency and this can't be detected by them until later symptoms begin to show up. So, since we know heart disease is caused by energy deficiency, how do fats such as PUFA and SFA compare to each to other in regards to energy production? The answer is there is no comparison. PUFA's unquestionably have a much bigger impact on suppressing energy production than SFA's do. PUFA's cause leakage of electrons, PUFAs inhibit pyruvate dehydrogenase, PUFA's block transport proteins from taking thyoid hormone up into the cells, PUFA's poison the liver reducing it's ability to convert T4 into T3, etc.

Lets also not forget that, even though PUFA's may reduce total LDL, there's also the question of the cholesterol esters themselves. If your cholesterol esters are mostly unsaturated, they will be much more susceptible to oxidation. I'm not sure if lower LDL is a good tradeoff if I'm also increasing it's susceptibility to oxidation. The extent to which SFA's block energy production is simply are you eating them at the expense of carbohydrate.

To close out my case, I would like to briefly mention the question of endotoxin. There is some evidence to suggest that SFA's are better at pulling endotoxin into the bloodstream when compared to PUFA's. This could also be why some people's LDL shoots up after eating saturated fat. Whenever there's an immune response your cholesterol will always go high. But if this happens, it's still not a compelling case in my opinion to implicate SFA. I think this just proves saturated fats are good at pulling things into the serum. In healthy individuals, this is a good thing because it mean enhanced vitamin and mineral uptake. Unfortunately, if you're unhealthy, and have bad bacterial overgrowth, saturated fat could also potentially pull the bad stuff into the serum as well.

At any case, this seems to be a problem stemming from intestinal endotoxin, not a problem associated with saturated fat. This would also conveniently explain why stuff like meta analysises are so inconsistent (i.e some say SFA's cause disease, some say there's an inverse associations, etc.). It could be that SFA's are effecting different populations of people in different ways based on their metabolic health. At the end of the day, I think Peat's idea is generally the best and safest option. Focus primarily on carbs, and when you do eat fat, make it saturated.
 

Sefton10

Member
Joined
Oct 19, 2019
Messages
1,593
Several things to keep in mind here. Any fat in excess is going to be bad, it's going to reduce CO2 and increase FAO. So Perry has a very good point.

Personally I find the debates about PUFA vs SFA to be profoundly dense. Most people don't break through their own biases regarding this debate. And even if you do, the evidence isn't so black and white either way. Firstly, almost everyone that prescribes to PUFA's being better than SFA's believe in the lipid hypothesis. And for good reason, the evidence for replacing SFA's for PUFA's to lower LDL cholesterol is basically insurmountable. PUFA's will unquestionably lower your LDL.

Besides this, I also think there's financial reasons why PUFA's are preferred over SFA's. I don't exactly find their recommendations coincidental when there's basically a revolving door that exists in seed oil industry and the American Heart Association (AHA). I'm not saying there's some big conspiracy here, why go to that extreme when a simple case of making as much money as possible perfectly explains it.

Now, lets look at some basic reasons why SFA's may not be as bad as people think they are. A good opening case would be the point Broda Barnes laid out in his book Solve:Riddle of Heart Attacks. Mammalian organisms' adipose tissues are mostly saturated and monounsaturated. When their PUFA concentrations being to rise, their risk for cancer exponentially increases.

Another good argument for SFA's and against PUFA's runs adjacent to Barnes's point. That being, what happens if you put a mammal on a no fat diet (of very, very lowfat)? Arguably the best way to "resaturate" your cells is to eat a diet that mostly or very nearly all carbohydrate. Why? Because when we consume glucose in excess of what we can burn or store as glycogen it gets convert into saturated fat, not unsaturated fat. So if you give your body no fat at all, it will make saturated fats but not fats like linoleic acid. If someone is arguing that PUFA's are better, then I guess they're also indirectly saying that rudimentary human physiology is inherently incorrect.

Third: the picture to disease, as we all know, is just fundamentally bigger than the lipid hypothesis. The mechanical nature of this hypothesis is just not good science. Yes, we know there's a correlation to high LDL and a increased propensity to get atherosclerotic plaque. But this tells us absolutetly nothing about the pathology of this disease. Furthermore, should we even be viewing atherosclerosis as the disease itself? It seems more like a mid-late stage symptom of the disease. If you could magically remove all the cholesterol from your blood, thus preventing atherosclerosis, it wouldn't mean that you don't have heart disease anymore.

Conventional medicine isn't even designed to catch heart disease in it's early stages because heart disease is a problem of energy deficiency and this can't be detected by them until later symptoms begin to show up. So, since we know heart disease is caused by energy deficiency, how do fats such as PUFA and SFA compare to each to other in regards to energy production? The answer is there is no comparison. PUFA's unquestionably have a much bigger impact on suppressing energy production than SFA's do. PUFA's cause leakage of electrons, PUFAs inhibit pyruvate dehydrogenase, PUFA's block transport proteins from taking thyoid hormone up into the cells, PUFA's poison the liver reducing it's ability to convert T4 into T3, etc.

Lets also not forget that, even though PUFA's may reduce total LDL, there's also the question of the cholesterol esters themselves. If your cholesterol esters are mostly unsaturated, they will be much more susceptible to oxidation. I'm not sure if lower LDL is a good tradeoff if I'm also increasing it's susceptibility to oxidation. The extent to which SFA's block energy production is simply are you eating them at the expense of carbohydrate.

To close out my case, I would like to briefly mention the question of endotoxin. There is some evidence to suggest that SFA's are better at pulling endotoxin into the bloodstream when compared to PUFA's. This could also be why some people's LDL shoots up after eating saturated fat. Whenever there's an immune response your cholesterol will always go high. But if this happens, it's still not a compelling case in my opinion to implicate SFA. I think this just proves saturated fats are good at pulling things into the serum. In healthy individuals, this is a good thing because it mean enhanced vitamin and mineral uptake. Unfortunately, if you're unhealthy, and have bad bacterial overgrowth, saturated fat could also potentially pull the bad stuff into the serum as well.

At any case, this seems to be a problem stemming from intestinal endotoxin, not a problem associated with saturated fat. This would also conveniently explain why stuff like meta analysises are so inconsistent (i.e some say SFA's cause disease, some say there's an inverse associations, etc.). It could be that SFA's are effecting different populations of people in different ways based on their metabolic health. At the end of the day, I think Peat's idea is generally the best and safest option. Focus primarily on carbs, and when you do eat fat, make it saturated.
Excellent post.
 

Greg

Member
Joined
Dec 27, 2019
Messages
23
Several things to keep in mind here. Any fat in excess is going to be bad, it's going to reduce CO2 and increase FAO. So Perry has a very good point.

Personally I find the debates about PUFA vs SFA to be profoundly dense. Most people don't break through their own biases regarding this debate. And even if you do, the evidence isn't so black and white either way. Firstly, almost everyone that prescribes to PUFA's being better than SFA's believe in the lipid hypothesis. And for good reason, the evidence for replacing SFA's for PUFA's to lower LDL cholesterol is basically insurmountable. PUFA's will unquestionably lower your LDL.

Besides this, I also think there's financial reasons why PUFA's are preferred over SFA's. I don't exactly find their recommendations coincidental when there's basically a revolving door that exists in seed oil industry and the American Heart Association (AHA). I'm not saying there's some big conspiracy here, why go to that extreme when a simple case of making as much money as possible perfectly explains it.

Now, lets look at some basic reasons why SFA's may not be as bad as people think they are. A good opening case would be the point Broda Barnes laid out in his book Solve:Riddle of Heart Attacks. Mammalian organisms' adipose tissues are mostly saturated and monounsaturated. When their PUFA concentrations being to rise, their risk for cancer exponentially increases.

Another good argument for SFA's and against PUFA's runs adjacent to Barnes's point. That being, what happens if you put a mammal on a no fat diet (of very, very lowfat)? Arguably the best way to "resaturate" your cells is to eat a diet that mostly or very nearly all carbohydrate. Why? Because when we consume glucose in excess of what we can burn or store as glycogen it gets convert into saturated fat, not unsaturated fat. So if you give your body no fat at all, it will make saturated fats but not fats like linoleic acid. If someone is arguing that PUFA's are better, then I guess they're also indirectly saying that rudimentary human physiology is inherently incorrect.

Third: the picture to disease, as we all know, is just fundamentally bigger than the lipid hypothesis. The mechanical nature of this hypothesis is just not good science. Yes, we know there's a correlation to high LDL and a increased propensity to get atherosclerotic plaque. But this tells us absolutetly nothing about the pathology of this disease. Furthermore, should we even be viewing atherosclerosis as the disease itself? It seems more like a mid-late stage symptom of the disease. If you could magically remove all the cholesterol from your blood, thus preventing atherosclerosis, it wouldn't mean that you don't have heart disease anymore.

Conventional medicine isn't even designed to catch heart disease in it's early stages because heart disease is a problem of energy deficiency and this can't be detected by them until later symptoms begin to show up. So, since we know heart disease is caused by energy deficiency, how do fats such as PUFA and SFA compare to each to other in regards to energy production? The answer is there is no comparison. PUFA's unquestionably have a much bigger impact on suppressing energy production than SFA's do. PUFA's cause leakage of electrons, PUFAs inhibit pyruvate dehydrogenase, PUFA's block transport proteins from taking thyoid hormone up into the cells, PUFA's poison the liver reducing it's ability to convert T4 into T3, etc.

Lets also not forget that, even though PUFA's may reduce total LDL, there's also the question of the cholesterol esters themselves. If your cholesterol esters are mostly unsaturated, they will be much more susceptible to oxidation. I'm not sure if lower LDL is a good tradeoff if I'm also increasing it's susceptibility to oxidation. The extent to which SFA's block energy production is simply are you eating them at the expense of carbohydrate.

To close out my case, I would like to briefly mention the question of endotoxin. There is some evidence to suggest that SFA's are better at pulling endotoxin into the bloodstream when compared to PUFA's. This could also be why some people's LDL shoots up after eating saturated fat. Whenever there's an immune response your cholesterol will always go high. But if this happens, it's still not a compelling case in my opinion to implicate SFA. I think this just proves saturated fats are good at pulling things into the serum. In healthy individuals, this is a good thing because it mean enhanced vitamin and mineral uptake. Unfortunately, if you're unhealthy, and have bad bacterial overgrowth, saturated fat could also potentially pull the bad stuff into the serum as well.

At any case, this seems to be a problem stemming from intestinal endotoxin, not a problem associated with saturated fat. This would also conveniently explain why stuff like meta analysises are so inconsistent (i.e some say SFA's cause disease, some say there's an inverse associations, etc.). It could be that SFA's are effecting different populations of people in different ways based on their metabolic health. At the end of the day, I think Peat's idea is generally the best and safest option. Focus primarily on carbs, and when you do eat fat, make it saturated.
Very informative and unbiased
 

Jbird10

Member
Joined
Mar 5, 2018
Messages
21
Excellent rebuttal Jessie. To add ... SFA raising LDL ... I remember a paleo blogger making the point that SFA raises big fluffy LDL which is not harmful, and not the small dense LDL which is. This leads to confusion when the discussion is only a simplistic SFA raises LDL. Also, I thought major orgs. were backtracking on the Lipid Hypothesis?
 

Jessie

Member
Joined
Jul 9, 2020
Messages
1,018
That's a good point about the particle size. The larger LDL is hypothesized to be less sticky and more "bouncable" within the serum. Also, speaking of Linus Pauling, I forgot to mention his work in heart disease clearly shows that it's specifically the Lp(a) that's responsible for the plaster casts themselves. In theory, all you would need to do is lower the Lp(a) and not necessarily all of the LDL. This was why he was such a fan of lysine, because it does exactly that.
 
OP
pauljacob

pauljacob

Member
Joined
Mar 9, 2018
Messages
435
I don't think they are. Respected by who?

I think highly of Linus Pauling himself. An institute that bears his name? Not nearly as much.

Anyway, respected or not, you can always check their sources to see if you agree with their conclusions. For example, the line-



They talk about "studies," but then simply cite three the following three Meta-Analysises.




Nothing there supports the idea that Saturated or Trans Fats are inflammatory.
Thank you tankasnowgod for your input. I need to keep in mind that much misinformation can be peddled out behind a reputable name.
 
Last edited:
OP
pauljacob

pauljacob

Member
Joined
Mar 9, 2018
Messages
435
I think any fat in excess is going to be inflammatory. Crossing that threshold is probably easier when living a sedentary life.
I've been a sedentary man all my life. The main reason is I'm an editor-writer by profession (now retired) , and I sit most of the day. I found out that walking a mile or two a day and working out with Kettlebells don't do much good when I sit most of the day. Currently I'm training myself to dictate instead of write and, hopefully, I can become good at it. This way I can write while jumping on a mini trampoline.
 
OP
pauljacob

pauljacob

Member
Joined
Mar 9, 2018
Messages
435
Several things to keep in mind here. Any fat in excess is going to be bad, it's going to reduce CO2 and increase FAO. So Perry has a very good point.

Personally I find the debates about PUFA vs SFA to be profoundly dense. Most people don't break through their own biases regarding this debate. And even if you do, the evidence isn't so black and white either way. Firstly, almost everyone that prescribes to PUFA's being better than SFA's believe in the lipid hypothesis. And for good reason, the evidence for replacing SFA's for PUFA's to lower LDL cholesterol is basically insurmountable. PUFA's will unquestionably lower your LDL.

Besides this, I also think there's financial reasons why PUFA's are preferred over SFA's. I don't exactly find their recommendations coincidental when there's basically a revolving door that exists in seed oil industry and the American Heart Association (AHA). I'm not saying there's some big conspiracy here, why go to that extreme when a simple case of making as much money as possible perfectly explains it.

Now, lets look at some basic reasons why SFA's may not be as bad as people think they are. A good opening case would be the point Broda Barnes laid out in his book Solve:Riddle of Heart Attacks. Mammalian organisms' adipose tissues are mostly saturated and monounsaturated. When their PUFA concentrations being to rise, their risk for cancer exponentially increases.

Another good argument for SFA's and against PUFA's runs adjacent to Barnes's point. That being, what happens if you put a mammal on a no fat diet (of very, very lowfat)? Arguably the best way to "resaturate" your cells is to eat a diet that mostly or very nearly all carbohydrate. Why? Because when we consume glucose in excess of what we can burn or store as glycogen it gets convert into saturated fat, not unsaturated fat. So if you give your body no fat at all, it will make saturated fats but not fats like linoleic acid. If someone is arguing that PUFA's are better, then I guess they're also indirectly saying that rudimentary human physiology is inherently incorrect.

Third: the picture to disease, as we all know, is just fundamentally bigger than the lipid hypothesis. The mechanical nature of this hypothesis is just not good science. Yes, we know there's a correlation to high LDL and a increased propensity to get atherosclerotic plaque. But this tells us absolutetly nothing about the pathology of this disease. Furthermore, should we even be viewing atherosclerosis as the disease itself? It seems more like a mid-late stage symptom of the disease. If you could magically remove all the cholesterol from your blood, thus preventing atherosclerosis, it wouldn't mean that you don't have heart disease anymore.

Conventional medicine isn't even designed to catch heart disease in it's early stages because heart disease is a problem of energy deficiency and this can't be detected by them until later symptoms begin to show up. So, since we know heart disease is caused by energy deficiency, how do fats such as PUFA and SFA compare to each to other in regards to energy production? The answer is there is no comparison. PUFA's unquestionably have a much bigger impact on suppressing energy production than SFA's do. PUFA's cause leakage of electrons, PUFAs inhibit pyruvate dehydrogenase, PUFA's block transport proteins from taking thyoid hormone up into the cells, PUFA's poison the liver reducing it's ability to convert T4 into T3, etc.

Lets also not forget that, even though PUFA's may reduce total LDL, there's also the question of the cholesterol esters themselves. If your cholesterol esters are mostly unsaturated, they will be much more susceptible to oxidation. I'm not sure if lower LDL is a good tradeoff if I'm also increasing it's susceptibility to oxidation. The extent to which SFA's block energy production is simply are you eating them at the expense of carbohydrate.

To close out my case, I would like to briefly mention the question of endotoxin. There is some evidence to suggest that SFA's are better at pulling endotoxin into the bloodstream when compared to PUFA's. This could also be why some people's LDL shoots up after eating saturated fat. Whenever there's an immune response your cholesterol will always go high. But if this happens, it's still not a compelling case in my opinion to implicate SFA. I think this just proves saturated fats are good at pulling things into the serum. In healthy individuals, this is a good thing because it mean enhanced vitamin and mineral uptake. Unfortunately, if you're unhealthy, and have bad bacterial overgrowth, saturated fat could also potentially pull the bad stuff into the serum as well.

At any case, this seems to be a problem stemming from intestinal endotoxin, not a problem associated with saturated fat. This would also conveniently explain why stuff like meta analysises are so inconsistent (i.e some say SFA's cause disease, some say there's an inverse associations, etc.). It could be that SFA's are effecting different populations of people in different ways based on their metabolic health. At the end of the day, I think Peat's idea is generally the best and safest option. Focus primarily on carbs, and when you do eat fat, make it saturated.
"Focus primarily on carbs, and when you do eat fat, make it saturated." This is going to be my Mantra from now on. Thank you very much, Jessie.
 

Similar threads

Back
Top Bottom