There is a sense in which swapping saturated fatty acids for linoleic acid will consistently improve insulin sensitivity and reduce risk of cancer and heart attack. Norwegian animal scientists came up with the explanation back in 2010. "Because arachidonic acid (AA) competes with EPA and DHA as well as with LA, ALA and oleic acid for incorporation in membrane lipids at the same positions, all these fatty acids are important for controlling the AA concentration in membrane lipids, which in turn determines how much AA can be liberated and become available for prostaglandin biosynthesis following phospholipase activation. Thus, the best strategy for dampening prostanoid overproduction in disease situations would be to reduce the intake of AA, or reduce the intake of AA at the same time as the total intake of competing fatty acids (including oleic acid) is enhanced, rather than enhancing intakes of EPA and DHA only. Enhancement of membrane concentrations of EPA and DHA will not be as efficient as a similar decrease in the AA concentration for avoiding prostanoid overproduction." https://pmc.ncbi.nlm.nih.gov/articles/PMC2875212/
Note that at high enough concentrations in the bloodstream, all of the unsaturated fatty acids mentioned above, including linoleic acid, will actually dampen prostanoid overproduction. Saturated fatty acid molecules are not mentioned. That's because they cannot compete with arachidonic acid molecules for membrane lipid positions normally occupied by AA and the other unsaturated fatty acid molecules. That explains this AI Overview that comes up when I do a 'Calder Linoleic Acid 2024' web search. "Recent research in 2024 suggests that linoleic acid (LA), a primary dietary n-6 polyunsaturated fatty acid, has cardiometabolic benefits rather than the previously feared harmful effects, with higher LA intakes correlating to reduced risks of heart disease, stroke, and type 2 diabetes."
Two articles about linoleic acid were pubiished in quick succession in dfferent journals. Kristina H. Jackson, William S. Harris, Martha A. Belury, & Philip C. Calder were co-authors of both articles.
The October article was entitled 'Perspective on the health effects of unsaturated fatty acids and commonly consumed plant oils high in unsaturated fat'. https://pmc.ncbi.nlm.nih.gov/articles/PMC11600290/
Both articles are excellent examples of paltering - using the truth to mislead.
For some reason Philip Calder doesn't seem to realize that their conclusions are based on an incomplete data set. Calder was president of the International Society for the Study of Fatty Acids and Lipids (ISSFAL) from 2009 to 2012. Apparently, he forgot this declaration. "All agreed that a 5-year randomized controlled trial comparing the effects of historically low (2%) with currently high (7.5%) linoleic acid intakes on cardiac endpoints would address the knowledge gap about the effects of different omega-6 PUFA intakes on the risk of heart disease." https://karger.com/anm/article/58/1/59/40551/ISSFAL-2010-Dinner-Debate-Healthy-Fats-for-Healthy
It's likely the study would have shown that 2% or less linoleic acid intake would translate into a huge reduction in mortality no matter how much saturated fat subjects consumed.
As far as I can tell, that sort of study was never funded, so the knowledge gap persists.
In his response, Dr. Adam noted that "His (Calder"s) final statement is that an increase in arachidonic acid intake up to 1.5 grams per day does not significantly change the parameters associated with inflammation, blood clotting or atherogenesis. In this very interesting observation, I was astonished by the fact that the background diet was not taken into account. Although the intake of arachidonic acid with the background diet is reported several times, the resulting metabolic consequences are not discussed.
From the data provided, it can be concluded that the background diet in all studies included in the review was a Western diet, the proportion of arachidonic acid being estimated at 200 to 400 mg per day. Our studies on healthy volunteers were carried out with formula diets and allowed a precisely defined supply of arachidonic acid over a period of 6 weeks. These studies have shown that the exclusion of arachidonic acid from the diet (vegan diet) causes a progressive decrease of this fatty acid from 11 + 3% of the total fatty acids in the cholesterol esters of the plasma to 8 + 2% after 6 weeks. The later studies on patients with rheumatoid arthritis have shown that an intake of arachidonic acid amounting to not more than 80 mg/day does not increase the concentration of arachidonic acid in the phospholipids of the plasma and in the erythrocyte lipids. From these findings I have concluded that the body's own production of arachidonic acid is around 80 mg per day. This means that the Western Diet provides approximately 2.5 to 5 times the estimated need for arachidonic acid."
An 'excessive arachidonic acid intake' web search brings up a November 2024 article entitled 'Effect of Fatty Acids on Glucose Metabolism and Type 2 Diabetes'. Excerpt: "Although managing dietary fatty acid composition is important for reducing type 2 diabetes and its related complications, the underlying mechanisms remain unclear. The general view is that fatty acids in the diet can alter cell membrane function. The fatty acid composition of the cell membrane regulates its fluidity, membrane protein incorporation, cellular activities, enzyme activities, ion permeability, receptor functions, interaction with the insulin receptor, and interaction with glucose transporters and second messengers. All these changes can alter the insulin sensitivity of tissues and organs...Elevated ratios of SFAs to PUFAs in the skeletal muscle cell membrane have been associated with decreased glucose effectiveness and insulin sensitivity, potentially increasing the risk of developing type 2 diabetes. Moreover, both the proportion and absolute quantity of fatty acids can influence plasma concentrations, underscoring their importance in determining skeletal muscle phospholipid composition...Markedly excessive consumption of SFAs, including palmitic acid, promotes both liver and visceral fat accumulation in individuals with type 2 diabetes, compared with PUFAs." https://academic.oup.com/nutritionreviews/advance-article/doi/10.1093/nutrit/nuae165/7895736
I intend to refocus my time on reading scientific research in areas in which I have long had interest, and piano music that I have been reading its history and playing for nearly 80 years. I find that I am reading almost nothing but English language articles on a screen now. Books I want to read in a more relaxed posture are piled high. I am unsubscribing from online writings, which I have enjoyed reading and learned from but that are becoming a drug; if you don't want to be tempted the temptation is best out of sight. I am a finite human with finite time. I have to conserve resources with less distraction, it will take some months to get back into what I used to do. Best wishes to you, your research is excellent.
And a relentlessly over-credulous AP to breathlessly "report" such garbage
There is a sense in which swapping saturated fatty acids for linoleic acid will consistently improve insulin sensitivity and reduce risk of cancer and heart attack. Norwegian animal scientists came up with the explanation back in 2010. "Because arachidonic acid (AA) competes with EPA and DHA as well as with LA, ALA and oleic acid for incorporation in membrane lipids at the same positions, all these fatty acids are important for controlling the AA concentration in membrane lipids, which in turn determines how much AA can be liberated and become available for prostaglandin biosynthesis following phospholipase activation. Thus, the best strategy for dampening prostanoid overproduction in disease situations would be to reduce the intake of AA, or reduce the intake of AA at the same time as the total intake of competing fatty acids (including oleic acid) is enhanced, rather than enhancing intakes of EPA and DHA only. Enhancement of membrane concentrations of EPA and DHA will not be as efficient as a similar decrease in the AA concentration for avoiding prostanoid overproduction." https://pmc.ncbi.nlm.nih.gov/articles/PMC2875212/
Note that at high enough concentrations in the bloodstream, all of the unsaturated fatty acids mentioned above, including linoleic acid, will actually dampen prostanoid overproduction. Saturated fatty acid molecules are not mentioned. That's because they cannot compete with arachidonic acid molecules for membrane lipid positions normally occupied by AA and the other unsaturated fatty acid molecules. That explains this AI Overview that comes up when I do a 'Calder Linoleic Acid 2024' web search. "Recent research in 2024 suggests that linoleic acid (LA), a primary dietary n-6 polyunsaturated fatty acid, has cardiometabolic benefits rather than the previously feared harmful effects, with higher LA intakes correlating to reduced risks of heart disease, stroke, and type 2 diabetes."
Two articles about linoleic acid were pubiished in quick succession in dfferent journals. Kristina H. Jackson, William S. Harris, Martha A. Belury, & Philip C. Calder were co-authors of both articles.
The September article was entitled Beneficial effects of linoleic acid on cardiometabolic health: an update. https://lipidworld.biomedcentral.com/articles/10.1186/s12944-024-02246-2
The October article was entitled 'Perspective on the health effects of unsaturated fatty acids and commonly consumed plant oils high in unsaturated fat'. https://pmc.ncbi.nlm.nih.gov/articles/PMC11600290/
Both articles are excellent examples of paltering - using the truth to mislead.
For some reason Philip Calder doesn't seem to realize that their conclusions are based on an incomplete data set. Calder was president of the International Society for the Study of Fatty Acids and Lipids (ISSFAL) from 2009 to 2012. Apparently, he forgot this declaration. "All agreed that a 5-year randomized controlled trial comparing the effects of historically low (2%) with currently high (7.5%) linoleic acid intakes on cardiac endpoints would address the knowledge gap about the effects of different omega-6 PUFA intakes on the risk of heart disease." https://karger.com/anm/article/58/1/59/40551/ISSFAL-2010-Dinner-Debate-Healthy-Fats-for-Healthy
It's likely the study would have shown that 2% or less linoleic acid intake would translate into a huge reduction in mortality no matter how much saturated fat subjects consumed.
As far as I can tell, that sort of study was never funded, so the knowledge gap persists.
Interesting about the knowledge gap, I hadn't heard that. Calder seems to be giving Harris the benefit of the doubt, which is a mistake.
In a 2017 paper Philip Calder wrote, "...it is important to keep in mind that, just because there is little biological impact of an increase in arachidonic acid intake or status, there may still be significant benefit from a decrease in its intake or status." https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/dietary-arachidonic-acid-harmful-harmless-or-helpful/789B73B03956B2BAC309218C215F89AB
In 2021 I sent a 2019 Review Calder co-authored to German researcher Olaf Adam. https://pubmed.ncbi.nlm.nih.gov/31130146/
In his response, Dr. Adam noted that "His (Calder"s) final statement is that an increase in arachidonic acid intake up to 1.5 grams per day does not significantly change the parameters associated with inflammation, blood clotting or atherogenesis. In this very interesting observation, I was astonished by the fact that the background diet was not taken into account. Although the intake of arachidonic acid with the background diet is reported several times, the resulting metabolic consequences are not discussed.
From the data provided, it can be concluded that the background diet in all studies included in the review was a Western diet, the proportion of arachidonic acid being estimated at 200 to 400 mg per day. Our studies on healthy volunteers were carried out with formula diets and allowed a precisely defined supply of arachidonic acid over a period of 6 weeks. These studies have shown that the exclusion of arachidonic acid from the diet (vegan diet) causes a progressive decrease of this fatty acid from 11 + 3% of the total fatty acids in the cholesterol esters of the plasma to 8 + 2% after 6 weeks. The later studies on patients with rheumatoid arthritis have shown that an intake of arachidonic acid amounting to not more than 80 mg/day does not increase the concentration of arachidonic acid in the phospholipids of the plasma and in the erythrocyte lipids. From these findings I have concluded that the body's own production of arachidonic acid is around 80 mg per day. This means that the Western Diet provides approximately 2.5 to 5 times the estimated need for arachidonic acid."
An 'excessive arachidonic acid intake' web search brings up a November 2024 article entitled 'Effect of Fatty Acids on Glucose Metabolism and Type 2 Diabetes'. Excerpt: "Although managing dietary fatty acid composition is important for reducing type 2 diabetes and its related complications, the underlying mechanisms remain unclear. The general view is that fatty acids in the diet can alter cell membrane function. The fatty acid composition of the cell membrane regulates its fluidity, membrane protein incorporation, cellular activities, enzyme activities, ion permeability, receptor functions, interaction with the insulin receptor, and interaction with glucose transporters and second messengers. All these changes can alter the insulin sensitivity of tissues and organs...Elevated ratios of SFAs to PUFAs in the skeletal muscle cell membrane have been associated with decreased glucose effectiveness and insulin sensitivity, potentially increasing the risk of developing type 2 diabetes. Moreover, both the proportion and absolute quantity of fatty acids can influence plasma concentrations, underscoring their importance in determining skeletal muscle phospholipid composition...Markedly excessive consumption of SFAs, including palmitic acid, promotes both liver and visceral fat accumulation in individuals with type 2 diabetes, compared with PUFAs." https://academic.oup.com/nutritionreviews/advance-article/doi/10.1093/nutrit/nuae165/7895736
Clearly, these researchers don't realize that saturated fats in plasma don't get elevated until after insulin resistance sets in. https://news.osu.edu/study-doubling-saturated-fat-in-the-diet-does-not-increase-saturated-fat-in-blood/
Dr. Dong Wang heh
I also subscribe to a statistician's substack, and he took this study apart, too.
https://wmbriggs.substack.com/p/butter-bs
I like Briggs.
*Briggs
No surprise that Walter Willett is one of the authors, and Harvard T.H. Chan School of Public Health is prominent among the affiliations.
I intend to refocus my time on reading scientific research in areas in which I have long had interest, and piano music that I have been reading its history and playing for nearly 80 years. I find that I am reading almost nothing but English language articles on a screen now. Books I want to read in a more relaxed posture are piled high. I am unsubscribing from online writings, which I have enjoyed reading and learned from but that are becoming a drug; if you don't want to be tempted the temptation is best out of sight. I am a finite human with finite time. I have to conserve resources with less distraction, it will take some months to get back into what I used to do. Best wishes to you, your research is excellent.
Thank, you, I can certainly relate! Best of luck.
I feel sorry for Dong D. Wang, cursed with two names for John Thomas. Does the D. stand for Dick? Maybe I'm too cynical; maybe it's DuPont.