GIven my personal arterial situation, I am interested in dietary views on saturated fat. On Jaminet's site, I searched for "saturated fat" and found one blog entry [1]. It says, "we regard saturated and monounsaturated fats as the only macronutrients that are safe in unlimited doses."
There are two references. The first is a study about cancer. The second is about CHD/CVD [2]. That study is well-known for its finding that "there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD." In its meta-analysis, 11 of the 24 CHD/CVD included studies *adjusted for serum cholesterol level*. As a comment in a later edition of the journal said, "Adjustment for serum cholesterol concentrations will inevitably bias the estimates of effect of saturated fat intake toward the null hypothesis."[3]
2. '"Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease." https://pubmed.ncbi.nlm.nih.gov/20071648/
Aerobic lipid metabolism seems straightforward enough: with CO2 and H2O as the only 'waste' products, what harm could be done? But I'm no longer as sure that Jaminet's claim — that saturated and monounsaturated fats are the only macronutrients safe in unlimited doses — extends to transportation and storage within the human body. Transportation through the blood streams requires the assistance of proteins, and it looks like things can go wrong with that. Storing lipids — whatever the saturation status — in fat tissues seems to generate inflammation and adverse hormonal responses; perhaps only above a certain threshold (a speculation I heard in a recent Peter Attia Drive podcast episode). Also, there do appear to be some human genotypes/phenotypes that have very unhealthy response to saturated fat.
I've shifted my lipid consumption a bit toward monounsaturated by relying on more macadamia nuts and reducing other nuts. 😜 This has also reduced my intake of oxalates, which have stopped showing up in my urinalyses.
I pretty much concur with that view on saturated fat you cite. Monounsaturated can come if it's sufficiently paired with saturated fat, e.g. ruminant animal fat or dairy, which tend to be roughly half/half of MUFA and SFA.
There are a ton of keto/carnivore people out there, and if the scare about SFA was true, we would've seen an epidemic of heart disease in them by now. No such thing has occurred. Personally, I've eaten what I'd consider a "high animal fat" diet for about 10 years now. I simply don't believe there is any indication that saturated fat, high cholesterol, or any of that fearmongering has any basis whatsoever.
@brec Somehow I can't seem to reply to your comment, so I'll reply to this one instead?
Yea, I've seen a lot of those studies, and I just don't think it holds up. I've seen too many dishonest studies, misrepresentations, and shenanigans in the history of the whole cholesterol saga. Plus, I'd say those people misunderstand/misrepresent causality and the true root cause. The arguments tend to be similar to "cars are causally linked to car accidents." No way! But are cars the root cause of car accidents, and is the best method of prevention to ban cars? Clearly not. The people who say these things are typically completely unwilling to discuss this productively, and so I've mainly given up. I remain unconvinced, and I suppose we'll see in 30 years who was right.
Atherosclerosis is an accretive process that (usually?) takes more than 10 years to become a functional risk. Regardless, I think there's wide variation of response to SFA consumption, specifically w/r lipid levels of LDL-C/ApoB. I am highly responsive: 13 years ago my LDL-C peaked at 296 mg/dl on a HFLC diet without drugs; a month ago it was 53 on a VLF diet with a statin + ezetimibe.
Your last sentence is a little hard to parse, but you seem to be saying that high [lipid] cholesterol has no relation to ASCVD risk. The best summary I've found about that relation is a 2017 review article. An excerpt from its abstract:
"Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C." https://academic.oup.com/eurheartj/article/38/32/2459/3745109
Contrary to what the authors repeatedly "suggest" , none of this demonstrates that LDL-C exposure causes ASCVD risk; the authors' choice of the term "suggest" correctly acknowledges this: the (alternative) hypothesis that LDL-C exposure and ASCVD risk share a common cause.
Figure 2 (roughly, RCTs with median 5 year exposure, prospective studies with median 12 year exposure, and mendelian randomizations with median 52 year exposure with respective effect magnitudes of roughly 1x, 1.5x and 3x) actually suggest a protective role for LDL-C in response to this common cause; if not, we ought to see 1x, 2.4x, 10x+.
Is not LDL-C, or a little more generally, cholesterol-laden lipoprotein particles, necessary for the development of AS lesions -- even if not sufficient? And is it not likely that the "invasion" of the endothelium and into the arterial intima by these particles is a stochastic process such that reduction of the number of possible invaders reduces ASCVD risk?
"Suggest" does appear 9 times in the article, but not in the context of causality. The authors rather use the words "cause," "causal," or "causality" in the title, the abstract-conclusion, and the conclusions section. In a response to a comment, the authors agree that LDL-C is not necessarily the only cause of ASCVD.
In Fig. 2 the exposures are to lowering of LDL-C and the log-linear effect is reduction in risk. The slope of the effect is positively associated with duration. Sorry, what is the basis of your effect magnitude estimates?
Very interesting that you noticed such dramatic improvements from cutting seed oils! I'm currently (accidentally, lol) cutting seed oils myself.
Carbs and protein through insulin, and fiber directly, cause water retention -> getting up at night to pee. If you cut out most carbs, fiber, and protein, you'll retain less water and be less thirty and pee less.
How do you know that eliminating oils was the cause of the elimination of your knee and shoulder pain?
What simple carbohydrates did you substantially reduce? Added sugars and refined flours are the canonical examples; what else, if anything? And the same "how do you know?" question as to causality.
Spoken like a fan — or future fan of — _Criticism and the Growth of Knowledge_ ! (1970, edited by Imre Lakatos and Alan Musgrave, with articles by Thomas Kuhn, Karl Popper, Imre Lakatos, Paul Feyerabend, and others.)
Let's take the Deutsch / Popper v2.0 approach for a spin. I'll address your first question in this reply and the remaining questions in a separate reply.
Here are a few possible explanations, definitely not an exhaustive list, so awaiting a superior explanation:
1. Knee and shoulder pain would have subsided without intervention. This explanation is unsatisfactory because my orthopedic surgeons told me the opposite: that each location of arthritis was degenerative and would worsen with age. Their recommendation was to reduce activity, which I now believe is counterproductive for myself (but likely correct for, say, their patients on a standard American diet).
2. Dr. Shanahan's personal anecdote is that reducing her simple carb consumption eliminated her knee pain. I've observed this myself, but it doesn't fit my timeline as an initial cause. (More on this in my reply to the remaining questions.)
Somewhere between 2016 and 2018, likely after hearing more than one acquaintance complain about arthritis, I realized "Hey, my joints feel so good I could probably take up karate again!" (I didn't resume karate because I had started speed skating, and also really wanted to return to playing baseball ... one has only so much time for physical pursuits!)
3. The timing of my realization of pain-free mobility meshes well — i.e., resolving in a year or so — with heated/refined seed oil elimination, i.e., circa 2015.
GIven my personal arterial situation, I am interested in dietary views on saturated fat. On Jaminet's site, I searched for "saturated fat" and found one blog entry [1]. It says, "we regard saturated and monounsaturated fats as the only macronutrients that are safe in unlimited doses."
There are two references. The first is a study about cancer. The second is about CHD/CVD [2]. That study is well-known for its finding that "there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD." In its meta-analysis, 11 of the 24 CHD/CVD included studies *adjusted for serum cholesterol level*. As a comment in a later edition of the journal said, "Adjustment for serum cholesterol concentrations will inevitably bias the estimates of effect of saturated fat intake toward the null hypothesis."[3]
At one time, I followed Jaminet.
1. https://perfecthealthdiet.com/category/nutrients/saturated-and-monounsaturated-fat/
2. '"Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease." https://pubmed.ncbi.nlm.nih.gov/20071648/
3. https://www.sciencedirect.com/science/article/pii/S0002916523019202?via%3Dihub
Aerobic lipid metabolism seems straightforward enough: with CO2 and H2O as the only 'waste' products, what harm could be done? But I'm no longer as sure that Jaminet's claim — that saturated and monounsaturated fats are the only macronutrients safe in unlimited doses — extends to transportation and storage within the human body. Transportation through the blood streams requires the assistance of proteins, and it looks like things can go wrong with that. Storing lipids — whatever the saturation status — in fat tissues seems to generate inflammation and adverse hormonal responses; perhaps only above a certain threshold (a speculation I heard in a recent Peter Attia Drive podcast episode). Also, there do appear to be some human genotypes/phenotypes that have very unhealthy response to saturated fat.
I've shifted my lipid consumption a bit toward monounsaturated by relying on more macadamia nuts and reducing other nuts. 😜 This has also reduced my intake of oxalates, which have stopped showing up in my urinalyses.
I pretty much concur with that view on saturated fat you cite. Monounsaturated can come if it's sufficiently paired with saturated fat, e.g. ruminant animal fat or dairy, which tend to be roughly half/half of MUFA and SFA.
There are a ton of keto/carnivore people out there, and if the scare about SFA was true, we would've seen an epidemic of heart disease in them by now. No such thing has occurred. Personally, I've eaten what I'd consider a "high animal fat" diet for about 10 years now. I simply don't believe there is any indication that saturated fat, high cholesterol, or any of that fearmongering has any basis whatsoever.
@brec Somehow I can't seem to reply to your comment, so I'll reply to this one instead?
Yea, I've seen a lot of those studies, and I just don't think it holds up. I've seen too many dishonest studies, misrepresentations, and shenanigans in the history of the whole cholesterol saga. Plus, I'd say those people misunderstand/misrepresent causality and the true root cause. The arguments tend to be similar to "cars are causally linked to car accidents." No way! But are cars the root cause of car accidents, and is the best method of prevention to ban cars? Clearly not. The people who say these things are typically completely unwilling to discuss this productively, and so I've mainly given up. I remain unconvinced, and I suppose we'll see in 30 years who was right.
Atherosclerosis is an accretive process that (usually?) takes more than 10 years to become a functional risk. Regardless, I think there's wide variation of response to SFA consumption, specifically w/r lipid levels of LDL-C/ApoB. I am highly responsive: 13 years ago my LDL-C peaked at 296 mg/dl on a HFLC diet without drugs; a month ago it was 53 on a VLF diet with a statin + ezetimibe.
Your last sentence is a little hard to parse, but you seem to be saying that high [lipid] cholesterol has no relation to ASCVD risk. The best summary I've found about that relation is a 2017 review article. An excerpt from its abstract:
"Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C." https://academic.oup.com/eurheartj/article/38/32/2459/3745109
Contrary to what the authors repeatedly "suggest" , none of this demonstrates that LDL-C exposure causes ASCVD risk; the authors' choice of the term "suggest" correctly acknowledges this: the (alternative) hypothesis that LDL-C exposure and ASCVD risk share a common cause.
Figure 2 (roughly, RCTs with median 5 year exposure, prospective studies with median 12 year exposure, and mendelian randomizations with median 52 year exposure with respective effect magnitudes of roughly 1x, 1.5x and 3x) actually suggest a protective role for LDL-C in response to this common cause; if not, we ought to see 1x, 2.4x, 10x+.
Is not LDL-C, or a little more generally, cholesterol-laden lipoprotein particles, necessary for the development of AS lesions -- even if not sufficient? And is it not likely that the "invasion" of the endothelium and into the arterial intima by these particles is a stochastic process such that reduction of the number of possible invaders reduces ASCVD risk?
"Suggest" does appear 9 times in the article, but not in the context of causality. The authors rather use the words "cause," "causal," or "causality" in the title, the abstract-conclusion, and the conclusions section. In a response to a comment, the authors agree that LDL-C is not necessarily the only cause of ASCVD.
In Fig. 2 the exposures are to lowering of LDL-C and the log-linear effect is reduction in risk. The slope of the effect is positively associated with duration. Sorry, what is the basis of your effect magnitude estimates?
Very interesting that you noticed such dramatic improvements from cutting seed oils! I'm currently (accidentally, lol) cutting seed oils myself.
Carbs and protein through insulin, and fiber directly, cause water retention -> getting up at night to pee. If you cut out most carbs, fiber, and protein, you'll retain less water and be less thirty and pee less.
How do you know that eliminating oils was the cause of the elimination of your knee and shoulder pain?
What simple carbohydrates did you substantially reduce? Added sugars and refined flours are the canonical examples; what else, if anything? And the same "how do you know?" question as to causality.
Spoken like a fan — or future fan of — _Criticism and the Growth of Knowledge_ ! (1970, edited by Imre Lakatos and Alan Musgrave, with articles by Thomas Kuhn, Karl Popper, Imre Lakatos, Paul Feyerabend, and others.)
Let's take the Deutsch / Popper v2.0 approach for a spin. I'll address your first question in this reply and the remaining questions in a separate reply.
Here are a few possible explanations, definitely not an exhaustive list, so awaiting a superior explanation:
1. Knee and shoulder pain would have subsided without intervention. This explanation is unsatisfactory because my orthopedic surgeons told me the opposite: that each location of arthritis was degenerative and would worsen with age. Their recommendation was to reduce activity, which I now believe is counterproductive for myself (but likely correct for, say, their patients on a standard American diet).
2. Dr. Shanahan's personal anecdote is that reducing her simple carb consumption eliminated her knee pain. I've observed this myself, but it doesn't fit my timeline as an initial cause. (More on this in my reply to the remaining questions.)
Somewhere between 2016 and 2018, likely after hearing more than one acquaintance complain about arthritis, I realized "Hey, my joints feel so good I could probably take up karate again!" (I didn't resume karate because I had started speed skating, and also really wanted to return to playing baseball ... one has only so much time for physical pursuits!)
3. The timing of my realization of pain-free mobility meshes well — i.e., resolving in a year or so — with heated/refined seed oil elimination, i.e., circa 2015.