Does eating eggs increase cholesterol? What are the latest scientific studies/data suggesting?

[Nutrition4Health]

https://nutritionfacts.org/video/does-dietary-cholesterol-eggs-raise-blood-cholesterol/

Get guys,

 

Long time reader, first time poster.

Anyway just watched the above video by Dr Greger from Nutritionists.org and was wondering whether the information he provides is accurate. Does anyone know?

Is it true that egg consumption increases the cholesterol in our bloodstream and throughout our body or does the body simply not absorb this excess cholesterol if we happen to eat too many eggs?

Any confirmation would be high appreciated.

 

Thanks,

Nutrition4Health

 

[sethoflagos]

5 hours ago, Nutrition4Health said:

Anyway just watched the above video by Dr Greger from Nutritionists.org and was wondering whether the information he provides is accurate. Does anyone know?

Is it true that egg consumption increases the cholesterol in our bloodstream and throughout our body or does the body simply not absorb this excess cholesterol if we happen to eat too many eggs?

Ask yourself what the phrase "went up 50 points" actually means.

It means the narrator believes his audience is too stupid to understand the actual units, how the increase relates to a normal healthy range, and how that translates to a quantifiable increased risk of serious disease.

I have fairly frequent blood tests for other reasons, but have never had my cholesterol level flagged despite getting most of my protein from eggs (I probably average about two a day). So I'm comfortable with dismissing this video as somewhat offensive, partisan rubbish.

Those who do have high cholesterol levels should heed the advice of a qualified medical practitioner who has properly assessed their health condition. 

[exchemist]

6 hours ago, Nutrition4Health said:

https://nutritionfacts.org/video/does-dietary-cholesterol-eggs-raise-blood-cholesterol/

Get guys,

 

Long time reader, first time poster.

Anyway just watched the above video by Dr Greger from Nutritionists.org and was wondering whether the information he provides is accurate. Does anyone know?

Is it true that egg consumption increases the cholesterol in our bloodstream and throughout our body or does the body simply not absorb this excess cholesterol if we happen to eat too many eggs?

Any confirmation would be high appreciated.

 

Thanks,

Nutrition4Health

 

The key thing to watch is not cholesterol, which the body makes for itself anyway, but lipoproteins which carry it in the blood, in particular LDLs, low density lipoproteins. Eggs are not high in those.  

[Sensei]

An overdose of anything is harmful. It just depends on the amount consumed.

"The dose makes the poison"

https://en.wikipedia.org/wiki/The_dose_makes_the_poison

 

Moderately eating hamburgers and fries at McD is not harmful. The key word here is moderation.

 

[TheVat]

Single food thinking is problematic for a healthy diet.  Foods operate synergistically.  Arterial plaque formation is far more affected by overall intake of soluble fiber, antiinflammatory foods (e.g. omega3 rich oils, berries, avocado, green tea, oranges, almonds, walnuts, olive oil, etc), and moderation on fried foods and animal-based saturated fats (which raise those LDLs @exchemist mentioned).  Eat well, in this way, and a couple eggs won't matter.  How about for breakfast: an egg, oatmeal with berries and walnuts, and an orange?  And go easy on whole milk, or substitute a plant milk.  

[Genady]

14 minutes ago, TheVat said:

How about for breakfast: an egg, oatmeal with berries and walnuts, and an orange?  And go easy on whole milk, or substitute a plant milk.  

Hey, that was my breakfast today.  Minus walnuts, orange, and milk, plus peanut butter.

[TheVat]

Delicious!  Adding pb to oats is one of my standard foods from youth and student days.  The natural kind (no palm oil or other hydrogenated fats) you have to stir, but it's better for you.  

[CharonY]

16 hours ago, exchemist said:

The key thing to watch is not cholesterol, which the body makes for itself anyway, but lipoproteins which carry it in the blood, in particular LDLs, low density lipoproteins. Eggs are not high in those.  

It is actually quite complicated. Originally there was the distinction between "bad" and "good" cholesterol (LDL vs HDL) and to some extent it still makes sense. Specifically LDL/HDL ratio seems to be somewhat diagnostic for cardiovascular risk, but there are quite a few caveats. There are some discussions on whether there is a functional role of LDL for e.g. atherosclerosis, or whether it is more of a side effect. 

Similarly, it was assumed that dietary intake of cholesterol would find its way into the bloodstream. However, newer findings suggest that dietary cholesterol has only an indirect impact. There is a ton of new findings, and robust discussion on that matter, but no simple answers yet. But for OP the studies suggest that cholesterol in eggs does not really have a direct impact on lipid profiles (i.e. it is not absorbed and released in the blood stream). However, high cholesterol food can apparently influence your own lipid homeostasis, but in many cases the effect was fairly moderate.

I have not seen the video, but if the persons is arguing about absorption of dietary cholesterol, they are working on rather obsolete information.

[exchemist]

1 hour ago, CharonY said:

It is actually quite complicated. Originally there was the distinction between "bad" and "good" cholesterol (LDL vs HDL) and to some extent it still makes sense. Specifically LDL/HDL ratio seems to be somewhat diagnostic for cardiovascular risk, but there are quite a few caveats. There are some discussions on whether there is a functional role of LDL for e.g. atherosclerosis, or whether it is more of a side effect. 

Similarly, it was assumed that dietary intake of cholesterol would find its way into the bloodstream. However, newer findings suggest that dietary cholesterol has only an indirect impact. There is a ton of new findings, and robust discussion on that matter, but no simple answers yet. But for OP the studies suggest that cholesterol in eggs does not really have a direct impact on lipid profiles (i.e. it is not absorbed and released in the blood stream). However, high cholesterol food can apparently influence your own lipid homeostasis, but in many cases the effect was fairly moderate.

I have not seen the video, but if the persons is arguing about absorption of dietary cholesterol, they are working on rather obsolete information.

Yes, it does seem all rather uncertain. I was told for years that even though my total LDL+HDL+triglycerides was high,  it was OK because the ratio of LDL:HDL was low. But recently I've been told, thanks to some new algorithm used by UK doctors, the total itself comes into the calculation of risk and so I've been put on statins. 

But perhaps you can clear up one point. Neither LDL nor HDL are actually cholesterol. They are colloquially called "cholesterol" because of  something to do with the way these molecules bind, transport and deposit cholesterol in the body, I think. But it is rather hard to find a clear description of what goes on, on the internet. Can you summarise how this works? 

[Phi for All]

9 hours ago, exchemist said:

Yes, it does seem all rather uncertain. I was told for years that even though my total LDL+HDL+triglycerides was high,  it was OK because the ratio of LDL:HDL was low. But recently I've been told, thanks to some new algorithm used by UK doctors, the total itself comes into the calculation of risk and so I've been put on statins.

Same here. The ratio was the important part, not the total. For years, I'd read that insulin triggered many bad things, including reducing cell receptors that call for cholesterol from the blood. Then the cells produce their own cholesterol, leaving the cholesterol borne by the LDLs to fall to the artery walls, to be retrieved by the HDLs for recirculation. Fats in the body need to hitch a ride with lipoproteins before they can travel in the bloodstream. That all made sense to me.

Now they tell us the total is what's important, and if what I'd learned earlier is true, using a total number makes no sense, except that cardiologists get to prescribe a lot of statins. The old system seemed to take into account that our diets are all so different. I really dislike the one-size-fits-all methodology.

[CharonY]

10 hours ago, exchemist said:

But perhaps you can clear up one point. Neither LDL nor HDL are actually cholesterol. They are colloquially called "cholesterol" because of  something to do with the way these molecules bind, transport and deposit cholesterol in the body, I think. But it is rather hard to find a clear description of what goes on, on the internet. Can you summarise how this works? 

The details are actually quite complicated, but I can start simple (and my apologies if it is too trivial) and maybe start with comments on some of the trickier parts.

As you mentioned, the terms LDL and HDL do not refer to the cholesterol itself. Rather, cholesterol is transported packaged by lipoproteins, the mentioned high-density lipoproteins (HDL) and low-density lipoproteins (LDL). In addition there are also very low density lipoproteins (VLDL) and intermediate density lipoproteins (IDL). 

The measurements therefore refer to the fraction of cholesterol associated with particles of specific density that circulate in the bloodstream.

To complicate matters on this level a bit, there are slightly different assays that measure the fraction of LDL in different ways (often indirectly, e.g. using the Friedewald equation, whereas direct methods often also measured IDL and VLDL). There is some data suggesting that using ApoB (which only not associated with HDL) could be a better biomarker for cardiovascular health, but that is under discussion, too.

But one way I think about VLDL- IDL-LDL is that they are different maturation steps where the very large VLDL are reduced in size and then can enter the intima.

Now, originally it was believed that LDL is a transport vehicle to move cholesterol to peripheral tissue and organs and HDL moves surplus cholesterol back to the liver. In part, the idea is then that very high LDL-cholesterol leads to deposits that can cause arteriosclerosis, for example. 

However, when trying to look at associated mechanisms, things get complicated pretty fast. For example, it was found that the vast majority of cells actually have an active lipid metabolism and most cholesterol are produced where they are used and are not necessarily delivered via LDL. Then, there is the issue that a lot of LDL cholesterol is derived from HDL and a lot of them is taken up by LDL-receptors in the liver. I.e. of the LDL is actually directed to, not away from the liver, making it questionable whether delivery to the periphery is really the main function of LDL. 

Likewise, HDL has been known to be critical for cholesterol efflux capacity (removing cholesterol from macrophages and transport to liver), but now studies suggest that LDL amplifies these efforts by HDL pathways. So taken together, the classic dichotomy of LDL vs HDL (cholesterol) has become rather questionable but we do not have a fully articulated model yet that can be used for better health prediction.

Edit: I should add that my expertise is mostly limited to biomarker analysis, and  not the clinical aspects, so it is therefore biased a bit more on the molecular/analytical side and may not reflect clinical standards. Therefore none of it should be considered medical advice of any sorts.

 

[exchemist]

25 minutes ago, CharonY said:

The details are actually quite complicated, but I can start simple (and my apologies if it is too trivial) and maybe start with comments on some of the trickier parts.

As you mentioned, the terms LDL and HDL do not refer to the cholesterol itself. Rather, cholesterol is transported packaged by lipoproteins, the mentioned high-density lipoproteins (HDL) and low-density lipoproteins (LDL). In addition there are also very low density lipoproteins (VLDL) and intermediate density lipoproteins (IDL). 

The measurements therefore refer to the fraction of cholesterol associated with particles of specific density that circulate in the bloodstream.

To complicate matters on this level a bit, there are slightly different assays that measure the fraction of LDL in different ways (often indirectly, e.g. using the Friedewald equation, whereas direct methods often also measured IDL and VLDL). There is some data suggesting that using ApoB (which only not associated with HDL) could be a better biomarker for cardiovascular health, but that is under discussion, too.

But one way I think about VLDL- IDL-LDL is that they are different maturation steps where the very large VLDL are reduced in size and then can enter the intima.

Now, originally it was believed that LDL is a transport vehicle to move cholesterol to peripheral tissue and organs and HDL moves surplus cholesterol back to the liver. In part, the idea is then that very high LDL-cholesterol leads to deposits that can cause arteriosclerosis, for example. 

However, when trying to look at associated mechanisms, things get complicated pretty fast. For example, it was found that the vast majority of cells actually have an active lipid metabolism and most cholesterol are produced where they are used and are not necessarily delivered via LDL. Then, there is the issue that a lot of LDL cholesterol is derived from HDL and a lot of them is taken up by LDL-receptors in the liver. I.e. of the LDL is actually directed to, not away from the liver, making it questionable whether delivery to the periphery is really the main function of LDL. 

Likewise, HDL has been known to be critical for cholesterol efflux capacity (removing cholesterol from macrophages and transport to liver), but now studies suggest that LDL amplifies these efforts by HDL pathways. So taken together, the classic dichotomy of LDL vs HDL (cholesterol) has become rather questionable but we do not have a fully articulated model yet that can be used for better health prediction.

Edit: I should add that my expertise is mostly limited to biomarker analysis, and  not the clinical aspects, so it is therefore biased a bit more on the molecular/analytical side and may not reflect clinical standards. Therefore none of it should be considered medical advice of any sorts.

 

Hmm, that suggests that although we have a better understanding of the complexity of the processes, the net result is we are more in the dark than before regarding what doctors should tell their patients! But thanks for the explanation. I think it could well account for why the advice I've been getting from my doctor has changed  - for the worse.  I had thought that my adherence, much of the time, to a fairly Mediterranean diet was a good thing. Perhaps it still is, but it looks as if I might need to be less liberal with the olive oil. I may try to find out more about this, now that I know a bit more what to look for.   

[CharonY]

Nutritional guidelines are necessarily simplified and there will be a lot of individual variance. Generally speaking, once on is a healthy place, it is often helpful to check from deviations a given homeostatic situation, but even that is an imperfect approach. Sometimes recommendations are actually correct, but for incorrect reasons.

[NTuft]

Here's a link to a blog post discussing a controlled feeding study (2017) looking at effects of egg consumption on blood cholesterol:

Three Eggs a Day = Doping for Your Heart Health: Larger LDL & HDL, Increased Efflux and Transport + More Benefits

Quote

...HDL function may be more important than HDL concentration...

...conducted a study to confirm and quantify the previously observed increases in HDL and LDL particle size, LCATactivity, and plasma apoAII...

...Before the dietary intervention began, the participants underwent a 2-wk washout period, during which 0 eggs/d were consumed. This baseline period was followed up by sequentially increasing intake of 1, 2, and then 3 eggs/d (large, grade A, white purchased at local supermarkets) for 4 wk each...

..."Overall, intake of ≲3 eggs/d favored a less atherogenic LDL particle profile, improved HDL function, and increased plasma antioxidants in young, healthy adults"...

@Nutrition4Health, I did not watch the video; would you clarify about what the claims are that are being made? Is he claiming that eating eggs leads to cholesterol absorption and then sustained, circulating high cholesterol levels? Because I think that is bogus.

From what I understand, the number of particles, which relates to whether LDL and HDL are small and dense vs. large and fluffy, is an issue--it can be differentiated by an NMR lipid profile. Per Cleveland (U.S.) Clinic recommendations I believe an [Ed.: NMR profile for particle quantifying/sizing should be added], an ApoB level [and also see cited study re:ApoAII], and of course circulating triglycerides are recommended to get a good picture (check recommendations, this is not advice). The cholesterol intake from egg consumption is in my opinion offset by the choline (or lecithin) content of eggs facilitating healthy fat metabolism. 

What seems to be more well established is that dietary saturated fat intake leads to increased LDL levels, which for some people may be problematic. The cholesterol hypothesis, roughly speaking, is that (LDL) cholesterol becoming oxidized and deposited in the endothelium is the mechanism of development for atherosclerosis. I do not think it is still held that dietary cholesterol is the main part of the mechanism, rather that the interplay between dietary fat and endogenous cholesterol metabolism can lead to oxidation and deposition of cholesterol plaques. The susceptibility to oxidation/inappropriate deposition I think is tied to the particle size...

As an aside, @exchemist, I do not think olive oil should be eschewed, as I think MUFA and PUFA are not shown to increase LDL "cholesterol". But yes perhaps control total fat intake--although Mediterranean ratio of <=30-40% total kCal I think is good... Again, IMO, traditional statins are very problematic in interrupting mevalonate->cholesterol, because it's then interferring with everything downstream in the steroid pathways (and muscle pain, weakness, and atrophy are underreported), let alone that cholesterol is a structural component in animal cell membranes. Perhaps look into psyllium husk, berberine, niacin (nicotinic acid) for cholesterol lowering? And do address choline/lecithin via eggs, liver, or perhaps a lecithin supplement for various things; or if you want to take statins for their anti-inflammatory and CVD protective effects it may be worthwhile investigating increasing dietary cholesterol. You may want an NMR lipid profile before even concluding that your levels are telling the tale, because the particle size/density may be more important. Friendly advice, not medical, and I should re-acquaint myself with the current literature, or any new evidence on the matter.

Edited February 14, 2023 by NTuft

[exchemist]

40 minutes ago, NTuft said:

Here's a link to a blog post discussing a controlled feeding study (2017) looking at effects of egg consumption on blood cholesterol:

Three Eggs a Day = Doping for Your Heart Health: Larger LDL & HDL, Increased Efflux and Transport + More Benefits

@Nutrition4Health, I did not watch the video; would you clarify about what the claims are that are being made? Is he claiming that eating eggs leads to cholesterol absorption and then sustained, circulating high cholesterol levels? Because I think that is bogus.

From what I understand, the particle size discrepancy as to whether LDL and HDL are small and dense vs. large and fluffy is an issue--it can be differentiated by an NMR lipid profile. Per Cleveland (U.S.) Clinic recommendations I believe an NMR profile for sizing, an ApoB level, and of course circulating triglycerides are recommended to get a good picture (check recommendations, this is not advice). The cholesterol intake from egg consumption is in my opinion offset by the choline (or lecithin) content of eggs facilitating healthy fat metabolism. 

What seems to be more well established is that dietary saturated fat intake leads to increased LDL levels, which for some people may be problematic. The cholesterol hypothesis, roughly speaking, is that (LDL) cholesterol becoming oxidized and deposited in the endothelium is the mechanism of development for atherosclerosis. I do not think it is still held that dietary cholesterol is the main part of the mechanism, rather that the interplay between dietary fat and endogenous cholesterol metabolism can lead to oxidation and deposition of cholesterol plaques. The susceptibility to oxidation/inappropriate deposition I think is tied to the particle size...

As an aside, @exchemist, I do not think olive oil should be eschewed, as I think MUFA and PUFA are not shown to increase LDL "cholesterol". But yes perhaps control total fat intake--although Mediterranean ratio of <=30-40% total kCal I think is good... Again, IMO, traditional statins are very problematic in interrupting mevalonate->cholesterol, because it's then interferring with everything downstream in the steroid pathways (and muscle pain, weakness, and atrophy are underreported), let alone that cholesterol is a structural component in animal cell membranes. Perhaps look into psyllium husk, berberine, niacin (nicotinic acid) for cholesterol lowering? And do address choline/lecithin via eggs, liver, or perhaps a lecithin supplement for various things; or if you want to take statins for their anti-inflammatory and CVD protective effects it may be worthwhile investigating increasing dietary cholesterol. You may want an NMR lipid profile before even concluding that your levels are telling the tale, because the particle size/density may be more important. Friendly advice, not medical, and I should re-acquaint myself with the current literature, or any new evidence on the matter.

I can still cycle to Wimbledon and back, up and down the hills, to buy bread, as I did before I went on statins, so I'm not worried about muscle weakness. And don't worry, I like olive oil too much to cut it back a great deal. 

[NTuft]

6 minutes ago, exchemist said:

I can still cycle to Wimbledon and back, up and down the hills, to buy bread, as I did before I went on statins, so I'm not worried about muscle weakness. And don't worry, I like olive oil too much to cut it back a great deal. 

Very well, and that can be a metric. It'd be an issue of myopathy, broadly speaking, over time, but overall I think it is a low-incidence reported side effect.

[CharonY]

20 hours ago, NTuft said:

it can be differentiated by an NMR lipid profile. Per Cleveland (U.S.) Clinic recommendations I believe an [Ed.: NMR profile for particle quantifying/sizing should be added], an ApoB level [and also see cited study re:ApoAII], and of course circulating triglycerides are recommended to get a good picture (check recommendations, this is not advice). The cholesterol intake from egg consumption is in my opinion offset by the choline (or lecithin) content of eggs facilitating healthy fat metabolism. 

I thin it should be added that there is (AFAIK) no gold standard with regard to these tests. While NMR does work at least as well as the other methods, it is not clear which one is the best. And best is defined here as yielding a measurement that is clinically predictive. It is also important to note that there is more work looking into LDL subclasses as the category is rather overly broad and fluent. And there is at least some suggestion that certain smaller types of LDL might be more diagnostic, but the measurements are even trickier, as higher specificity is needed.

 

20 hours ago, NTuft said:

What seems to be more well established is that dietary saturated fat intake leads to increased LDL levels, which for some people may be problematic.

That is actually also rather complicated. Early on, there were already suggestions that the link between saturated fat and LDL cholesterol (or specifically LDL/HDL cholesterol ratio) is not straightforward. Some studies for example suggest that reducing saturated fat in the diet hat less effect than exchanging saturated with unsaturated fat, especially cis-PUFA. There is certainly a connection somewhere but as metabolism goes, it is likely again indirect. Some data suggests that the issue with saturated fat is perhaps not really only in the realm of LDL/HDL cholesterol ratio, but perhaps by increasing the very small LDL cholesterol particles, which might be more likely to cause cardiovascular events.

Edit: I have not read the paper referenced above, but the graph shows a slight increase in LDL-cholesterol but a shift of the most problematic (small) species from 45.2 nmol/dL to 39.6. It is unclear to me whether those changes are actually clinically relevant, but I suppose that would require a study on its own.

[CharonY]

On 2/13/2023 at 1:12 PM, exchemist said:

Perhaps it still is, but it looks as if I might need to be less liberal with the olive oil. I may try to find out more about this, now that I know a bit more what to look for.   

The way I tend to think about food and health is that a) one should have limit of regular calorie intake. We do have too easy access to food and overeating clearly is associated with a wide range. From there b) the food should cover all the necessary nutrients (hence the common recommendation to have somewhat broad diet) within that rough calorie limit. 

So in this context the question would be whether you would just cut off excess olive oil and not replace it with anything else (i.e. reducing total calorie intake) which likely would have some net benefit. Conversely, if you would eat something else that contains e.g. saturated fats or instead increased carbohydrate intake, chances are that it would be more likely to be detrimental. 

In other words, I am skeptical of claims that adding something to the diet (on top) has benefits, I think it is more about the composition while eating a healthy amount.

[exchemist]

8 hours ago, CharonY said:

The way I tend to think about food and health is that a) one should have limit of regular calorie intake. We do have too easy access to food and overeating clearly is associated with a wide range. From there b) the food should cover all the necessary nutrients (hence the common recommendation to have somewhat broad diet) within that rough calorie limit. 

So in this context the question would be whether you would just cut off excess olive oil and not replace it with anything else (i.e. reducing total calorie intake) which likely would have some net benefit. Conversely, if you would eat something else that contains e.g. saturated fats or instead increased carbohydrate intake, chances are that it would be more likely to be detrimental. 

In other words, I am skeptical of claims that adding something to the diet (on top) has benefits, I think it is more about the composition while eating a healthy amount.

Indeed. But with oil, which is used for cooking and to dress salads etc, one can reduce it a little without adding anything to replace it. I had been thinking that plenty of it was a good thing, because of HDL. So I can cut it back to just what is necessary. (I don't have a problem with my weight, which has been stable for years at: 66 +/-1 kg and 1.76m in height.)  

[CharonY]

8 hours ago, exchemist said:

Indeed. But with oil, which is used for cooking and to dress salads etc, one can reduce it a little without adding anything to replace it. I had been thinking that plenty of it was a good thing, because of HDL. So I can cut it back to just what is necessary. (I don't have a problem with my weight, which has been stable for years at: 66 +/-1 kg and 1.76m in height.)  

That would be my assumption, but obviously the science is not conclusive in that regard.

[exchemist]

1 minute ago, CharonY said:

That would be my assumption, but obviously the science is not conclusive in that regard.

Understood: caveat noted. 

Edited February 16, 2023 by exchemist

[NTuft]

On 2/14/2023 at 4:52 PM, CharonY said:

I thin it should be added that there is (AFAIK) no gold standard with regard to these tests. While NMR does work at least as well as the other methods, it is not clear which one is the best. And best is defined here as yielding a measurement that is clinically predictive. It is also important to note that there is more work looking into LDL subclasses as the category is rather overly broad and fluent. And there is at least some suggestion that certain smaller types of LDL might be more diagnostic, but the measurements are even trickier, as higher specificity is needed.

[postulated +SFA=+LDL]

That is actually also rather complicated. Early on, there were already suggestions that the link between saturated fat and LDL cholesterol (or specifically LDL/HDL cholesterol ratio) is not straightforward. Some studies for example suggest that reducing saturated fat in the diet hat less effect than exchanging saturated with unsaturated fat, especially cis-PUFA. There is certainly a connection somewhere but as metabolism goes, it is likely again indirect. Some data suggests that the issue with saturated fat is perhaps not really only in the realm of LDL/HDL cholesterol ratio, but perhaps by increasing the very small LDL cholesterol particles, which might be more likely to cause cardiovascular events.

Edit: I have not read the paper referenced above, but the graph shows a slight increase in LDL-cholesterol but a shift of the most problematic (small) species from 45.2 nmol/dL to 39.6. It is unclear to me whether those changes are actually clinically relevant, but I suppose that would require a study on its own.

  Indeed this is a complicated topic. I did not read the paper either, and should have and parsed it, instead of posting the "rah-rah" blog write-up. This was a feeding study on humans, which is important as I think the usual rodent studies want to draw a parallel between a small-bodied herbivore and a large-bodied omnivore with a large gallbladder and a large brain-body ratio which brain is a cholesterol dependent construction. I don't think most any conlcusions on mechanisms of metabolism can be extended to humans, but the basic results may point toward what are conserved mechanisms.
  It looks to me that the Lipoproteins work alongside chylomicrons in the distribution and metabolism of fats. This is complicated by fats being both structural components and energetic substrates. Lipoproteins go from Very-Low Density packages distributed by the liver to Intermediate-Density, to Low-Density as they unload fatty acid cargo at peripheral tissue, dependent on binding of the Lipoprotein receptors. There is data that reducing SFA content in the diet reduces expression of LDL receptors (Reducing saturated fat intake is associated with increased levels of LDL receptors on mononuclear cells in healthy men and women). 
  Some knowledgeable people have taken evidence that the LDL receptor is saturated at very low levels as license to start statins without real indications. Again, there ought to be due diligence and it's lacking on my part here as well, but for one the materials and methods would need an investigation as to whether this saturation level is an in vitro type of tissue study or in the context of connected running metabolism. It's noteworthy that the study linked above looked at mononuclear cells, since I'm rather certain there are human population studies that show a decrease in all cause mortality and in particular suicides and infectious disease death correlating with higher levels of LDL.
  I suppose what I find most interesting about the 3 egg/day result is that estimates are that cholesterol is metabolized on the order of 1g generated by the liver per day(Ed.: with losses, I'd bet, as bile salts of cholesterol+taurine/glycine excreted]. Usual estimates are that 20% of that may come from diet, but I would speculate that that may largely be tied to average egg intake. Going from 0 eggs/d to 3/day, with a conservative estimate of 200mg cholesterol per egg, shifts the burden on the liver from ~1g/day production to .4g/day, yet there is what looks like a non-significant increase in total cholesterol; it looks like the metabolism simply shifted to acommodate the increased ingestion (assuming 100% assimilation and utilization).
  There is increasing evidence (especially if you buy into the write-ups, hook-line-and-sinker) that would exonerate SFA intake from causative in CVD. It seems to have been scapegoated in the context of metabolic syndrome or metabolic disease. I would just point out the French paradox as an entry into the topic.

On 2/15/2023 at 4:17 PM, CharonY said:

The way I tend to think about food and health is that a) one should have limit of regular calorie intake. We do have too easy access to food and overeating clearly is associated with a wide range. From there b) the food should cover all the necessary nutrients (hence the common recommendation to have somewhat broad diet) within that rough calorie limit. 

So in this context the question would be whether you would just cut off excess olive oil and not replace it with anything else (i.e. reducing total calorie intake) which likely would have some net benefit. Conversely, if you would eat something else that contains e.g. saturated fats or instead increased carbohydrate intake, chances are that it would be more likely to be detrimental. 

In other words, I am skeptical of claims that adding something to the diet (on top) has benefits, I think it is more about the composition while eating a healthy amount.

  Energy balance, the interplay between intake and expenditure, is probably more important than trying to leverage metabolic mechanisms, which are complex and seemingly geared to account for and accomodate just about any diet. You seem to point at Calorie-Restricted-Optimal-Nutrition, which I second has merit; studies on monkeys are even by visible appearance alarming in comparing overfeeding to CR. That said, the Optimal-Nutrition end requires some knowledge and application: being wary of anti-nutrients (say trans-fats, and likely some lectins or phytochemicals) and saturating would be bottlenecks(chokepoints) on metabolism by finding adequate mineral, vitamin, and vitamin-like substance sources.

On 2/16/2023 at 1:19 AM, exchemist said:

(I don't have a problem with my weight, which has been stable for years at: 66 +/-1 kg and 1.76m in height.)

  Ok now you're "trolling" for a free online physical! J/k

 

  I'm skeptical of the "Lipid hypothesis", but I know it still holds by and large in the mainstream. Which is preferred out on the science boards here at SF.net. Going into these details does seem somewhat natural from the context of the OP, but it's also a generalization of a specific question... Anyway perhaps welcome to SF, OP; not much context on what you want assessed and expecting readers to watch a video is a forlorn hope, and diverging into related topics is almost a given if you cease any follow-up or specifications on the topic at hand.

Edited February 19, 2023 by NTuft
bile salts

[CharonY]

1 hour ago, NTuft said:

It looks to me that the Lipoproteins work alongside chylomicrons in the distribution and metabolism of fats.

Chylomicrons are lipoproteins and they are produced in enterocyte. So in terms of distribution of lipids, they are basically at the source of dietary lipids, which get mobilized to adipose and muscle tissue. Cholesterol seems to be directed to the liver.

 

2 hours ago, NTuft said:

There is data that reducing SFA content in the diet reduces expression of LDL receptors (Reducing saturated fat intake is associated with increased levels of LDL receptors on mononuclear cells in healthy men and women).

I assume that was a typo (as the next sentence says the opposite), but reducing SFA content increases expression of LDL receptors. The assumption here is that LDL receptors are involved in LDL-cholesterol clearance from blood. I.e. reducing SFA increases LDL-receptors, which in turn reduce circulating LDL-cholesterol.

[NTuft]

53 minutes ago, CharonY said:

Chylomicrons are lipoproteins and they are produced in enterocyte. So in terms of distribution of lipids, they are basically at the source of dietary lipids, which get mobilized to adipose and muscle tissue. Cholesterol seems to be directed to the liver.

Yes, thank you.

53 minutes ago, CharonY said:

I assume that was a typo (as the next sentence says the opposite), but reducing SFA content increases expression of LDL receptors. The assumption here is that LDL receptors are involved in LDL-cholesterol clearance from blood. I.e. reducing SFA increases LDL-receptors, which in turn reduce circulating LDL-cholesterol.

Yes, should say increases expression. Certainly yes there is the assumption that LDL receptors are involved in LDL-C clearance. The interpretation to end the abstract from the authors is like what you suggest. It could be decreased production VLDL->IDL->LDL is sensed and signals upregulation of expression of receptors, seeing that the diets step down both fat% and SFA%: 34%(15%)[0,0], 29%(9%)[-5%,-6%], 25%(6%)[-9%,-9%]. I presume both numbers are % of total energy, and the latter not a %SFA of total fat, as that seems implausible.

Edited February 19, 2023 by NTuft

[genio]

Correlation does not imply causation.

It depends what kind of feed the chicken ate. Cheap eggs bioaccumulate pesticides and other POPs (persistent organic pollutants) from their conventional feed and these toxins have been shown to cause atherosclerosis.

I'm susceptible to developing atherosclerosis and I've noticed that hardboiled eggs with the green ring always clog up my arteries, while hardboiled Organic eggs that don't develop the green ring, have never clogged up my arteries regardless of how many I consumed.

Also, cell membranes contain mostly cholesterol. Cell membrane - Wikipedia

 

Edited May 8, 2023 by genio