I am interested in the biochemistry of diet and the way we have been advised to eat for the past forty years.

In researching an explanation for the relationship between dietary fat and blood cholesterol I came across the following: "It is clear that eating too much saturated fat increases the levels of cholesterol in the blood, especially our "bad" cholesterol which doctors refer to as LDL". This is from heartuk.org.uk.

"It is clear ..." - really?

I am mystified! I understand that dietary fat, other than very short chain fatty acids, does not immediately enter the blood stream but is transported via the lymphatic system as triglycerides packaged in protein assemblies called chylomicrons, finally entering the blood via lymph nodes under the armpits. Once in the blood the triglycerides are hydrolysed into fatty acids and transported to appropriate cells in albumin complexes.

Where does LDL feature in this transportation? And, by the way, why just saturated fats? Surely the small intestine doesn't differentiate between saturated and unsaturated fats, or does it?

  • $\begingroup$ Focus of your question seems twofold: a. there is a missing link between chylomicrones/saturated fat going straight to adipose tissue on one side and liver producing bad cholesterol/LDL(VLDLP) on the other side - causality? b. there is no reason to differentiate saturated from unsaturated fat: either unsaturated fats share the same fate or they pass over to the liver directly, and why should they not induce production of bad cholesterol/LDL(VLDL) $\endgroup$ Nov 1, 2021 at 11:05
  • $\begingroup$ "Surely the small intestine doesn't differentiate between saturated and unsaturated fats, or does it?" - To formulate in another question: fate of saturated and unsatured fats in instestine/enterocytes? $\endgroup$ Nov 4, 2021 at 10:30

3 Answers 3


In short: It may not be saturated fat by itself but high saturated/unsaturated fat ratio and high animal/plant fat ratio in the diet that increases the risk of heart disease.

A systematic review of the effect of dietary saturated and polyunsaturated fat on heart disease (NMCD Journal, 2017)

Reducing saturated fat and replacing it with carbohydrate will not lower cardiovascular events or CVD mortality although it will reduce total mortality. Replacing saturated fat with mono- or poly-unsaturated fats or high-quality carbohydrate [from whole-grain food] will lower cardiovascular events.

Saturated Fatty Acids and Cardiovascular Disease: Replacements for Saturated Fat to Reduce Cardiovascular Risk (PubMed, 2017)

Replacing dairy fat with carbohydrates from refined starches and added sugar was not associated with increased or decreased risk of coronary heart disease (CHD), stroke or total cardiovascular disease (CVD). However, replacing dairy fat with carbohydrate from whole grains reduced the risk of CVD, CHD and stroke. Relative to other animal fats, dairy was found to have less impact on CVD. When 5% of energy from dairy fat was replaced with animal fat from non-dairy sources, risk of CHD increased by 6%. However, when 5% of energy from dairy fat was replaced with an isocaloric amount of polyunsaturated fats, risk of CHD was reduced by 26% and CVD risk was reduced by 24% [41].

A basic explanation of the underlying mechanisms:

The liver produces low-density lipoproteins (LDL) and high-density lipoproteins (HDL). Lipoproteins are composed of triglycerids, phospholipids, cholesterol and proteins.

LDL caries cholesterol from the liver to the peripherial tissue, including arterial walls, where it can accumulate and cause atherosclerosis. This is why LDL is called "bad cholesterol" (even if LDL is only a carrier for cholesterol). HDL clears excessive cholesterol from the blood and carries it to the liver for disposal, so it is called "good cholesterol. (Heart.org.uk)"

High LDL levels are associated with an increased risk of coronary heart disease (Bentham Open).

One possible mechanism by which saturated fats increase (LDL) cholesterol (PLOS):

Saturated fat is thought to increase LDL-C primarily through down-regulation of hepatic LDL receptor activity, leading to reduced clearance of LDL particles [from the blood].

  • $\begingroup$ Why is it saturated and trans fats are bad and unsaturated cis fats are good? The only difference between the two isomers is shape: saturated and trans fats are essentially linear whereas cis fats are bent. If indeed there is a causal link between linear fats and vascular disease then surely it can only be due to their conformation? $\endgroup$
    – adlibber
    Nov 26, 2018 at 8:15
  • $\begingroup$ In medicine and nutrition, it may be enough to know what is the net result of high consumption of a certain nutrient without knowing the mechanisms. I'm sure, the exact effect of various types of fatty acids on LDL production is described in detail somewhere, but this is too much for this site, at least for me. They could know more on chemistry.stackexchange.com . The metabolism of LDL occurs in the liver, so you do not need to concentrate on what happens in the intestine and how fats come to the liver. $\endgroup$
    – Jan
    Nov 26, 2018 at 12:10
  • 1
    $\begingroup$ Fair criticism Jan but you could also say that all these questions relate to physics as well. This is a human physiological question and I felt that ‘biology’ was a more appropriate cover than ‘chemistry’. I’m not a biologist nor am I a biochemist so imagine the difficulty I’m having with this subject! i’m in fact an old retired systems engineer interested in all the noise about nutrition! $\endgroup$
    – adlibber
    Nov 26, 2018 at 15:06
  • 2
    $\begingroup$ @adlibber, It can help tremendously if you say what is the exact goal of your research? Do saturated fats increase LDL? Do they increase the risk of heart disease? Or you are strictly interested in how all this happens on biochemistry level? I had a feeling that you are trying to find a direct connection between the structure of fatty acids and LDL synthesis. While this can make sense, it can be misleading, because you need to see the whole picture: the sum of effects of all fatty acids on LDL... $\endgroup$
    – Jan
    Nov 26, 2018 at 15:11
  • 1
    $\begingroup$ @user237650 many thanks for the link. Is Kendrick correct is the big question of course! If he is then he is in agreement with my understanding obtained elsewhere and hence my original question. The BMJ came out with this a few months ago illustrating the abject confusion on the subject. My gut (excuse the pun) tells me Kendrick is right! $\endgroup$
    – adlibber
    Nov 26, 2018 at 18:17

I think you are right to question this "wisdom". In my opinion the statement from the web site that you linked is simply wrong. The idea that eating fat would make you fat dates back to the 1960s and was originally published by an MD just as offhand speculation, not any kind of science. Since then many others have just mindlessly repeated this incorrect idea.

First of all, it is physically impossible more or less for fats to be transported through the intestinal wall (see http://www.vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/absorb_lipids.html or Heinemann, T & Axtmann, G & von Bergmann, Klaus. (1994). Comparison of intestinal absorption of cholesterol with different plant sterol in man. European journal of clinical investigation. 23. 827-31.) Dietary cholesterol has to digested into more basic lipids and then transported through the intestinal wall by special molecules to be absorped by the body. So, the idea that eating eggs or whatever would give you "high cholesterol" is just an irrational idea.

Note that you will find papers with statements like 30% of dietary cholesterol is absorbed or 50% of dietary cholesterol is absorbed by the body and so forth, but these papers are either just observational papers that have no real controlled science behind them, or they are misleading. For example, it is true that 50% of dietary cholesterol gets DIGESTED and absorbed, but what gets absorbed is not cholesterol but monoglycerides and other small lipids that are the product of digestion. There are a lot of nutritional papers out there that just gloss over this and falsely imply that because cholesterol is being digested, that it is being absorbed whole, which is not true.

Virtually all serum cholesterol is synthesized by the body in the liver. The liver synthesizes cholesterol from fructose, a simple sugar that can be derived from complex sugars like cane sugar or from carbohydrates, such as wheat. Carbohydrates are first broken down into starch, then the starch is converted into sugars and the fructose component is circulated to the liver where it is converted into cholesterol or other things, such as triglycerides.

Concerning transportation of LDL: LDL is insoluble in water and cannot be transported across epithelial membranes. It must be digested into small lipids like monoglycerides with a watersoluble shell and then be transported by micelles. In the blood, triglycerides or LDL cholesterol manufactured by the liver can be transported for storage by special molecules called lipoproteins which emulsify the LDL and allow it to be transported in an aquaeous medium (the blood). In this form the LDL cannot cross any bodily membranes, but can only be placed in storage areas with direct blood contact. To be utilized as food for cells, LDL and triglycerides have to be circulated back to the liver where they are further broken down into COA, glucose and other types of molecules that cells can use as food.

  • $\begingroup$ Please add some (simple textbook) reference to "LDL is insoluble in water..." - that can't be true, as the function of the Lipoproteins is to make water insoluble fat soluble in blood, in water for transportation purposes. Please add some reference for tissue taking up cholesterol by "micelles", not by LDL-receptor (not to mention Nobel prize winners Goldstein/Brown). Did I get you wrong? $\endgroup$ Oct 31, 2021 at 10:18
  • $\begingroup$ @PeterBernhard All lipids are insoluble in water. Very first sentence in this book: ncbi.nlm.nih.gov/books/NBK305896. LDLs are not and cannot be transported across the intestinal wall for various reasons including their size. "Cholesterol is only minimally soluble in an aqueous environment and thus must be partitioned into bile salt micelles prior to absorption." direct quote from this book: ncbi.nlm.nih.gov/pmc/articles/PMC2692399. I am aware there are papers claiming dietary cholesterol can be transported across the intestinal wall whole (continued).... $\endgroup$ Oct 31, 2021 at 10:30
  • $\begingroup$ The intestinal wall has a paracellular pore size of about 10nm and only hydrophilic molecules smaller than this can traverse it. Micelles fit these restrictions. LDL, triglycerids and other large lipids are at least this large and are NOT hydrophilic, so they have no way to pass through the intestinal wall, unless they have been digested to smaller molecules and then attached to or enveloped by hydrophylic carriers such as micelles. $\endgroup$ Oct 31, 2021 at 10:39
  • $\begingroup$ My first impression of your answer was that it might be a comment to my answer, rightly questioning the premise of its second part, ie.e. more cholesterol in food means more bad cholesterol transport to cell. Actually, the question here - there are several others on Stackexchange - focuses on "more fatty acids", and even more: on saturated fatty acids input. - More fat does not mean more VDHL? Didn't you mention fat being stored away before it gets to the liver? Then "insuline" might be a worthy word. $\endgroup$ Oct 31, 2021 at 10:54
  • $\begingroup$ Highly enlightening I find "The intestinal wall". Bluntly: LDL has got anything to do with the intestinal wall, as you mentin LDL in that context. I'd be interested in your textbook or even internet reference for LDL not soluble in water or blood. How could LDL be a transporter of fatty acids? The word "acid" has it: any acid is hydrophilic. Can it be? The fat renders the LDL soluble? That is amazing and should clearly be emphasized in any textbook. Are you sure? $\endgroup$ Oct 31, 2021 at 10:59

"Why does eating saturated fat increase blood cholesterol?" From your explanatory text I understand: ... as it is transported by chylomicrones and not by LDL which is commonly known as "bad" cholesterol.

I'm paraphrasing even more: How could eating saturated fat which is not transported by LDL (termed "bad cholesterol"), and for this reason should not lead to more LDL in the blood, be held responsible for "bad cholesterol"?

There are two common misunderstandings I think your question brings up (educating, to me):

  1. Chylomicrones are not the only transporters of (saturated) fatty acids. There are the VLDL as well doing that job. The difference is termed "dietary fat" versus "endogenous fat". The liver is the body's biggest producer of (saturated) fatty acids (interestingly, the liver produces but saturated fatty acids!). This fat is transported from the liver to tissues by VLDL (Very Low Density Lipoproteins). It is no trivial knowledge that LDL is not produced by the liver "as is", only the VLDL are. However, VLDL become "bad" LDL in the bloodstream.

  2. Lipoproteins and Chylomicrones per se, as transporter molecules, incorporate cholesterol, in different amounts and percentages of total weight. From textbooks it may be easy to tell whether cholesterol is a "part" of the transporter or being transported as "package". Cp.Dr. Malcom Mkendrick (paragraph"re-cap")

  3. What might appear as some "breaking news" AD Cooper · 1997 "Chylomicrons are formed in the intestine and transport dietary triglyceride to peripheral tissues and cholesterol to the liver." Still another one: Enterocytes not only produce chylomicrones but VLDL, too.

Both Chylomicrones/chylomicrones-remnants and VLDL/"VLDL"(called LDL) resemble each other in their "later life" termed "remnant". What remains of VLDL after unloading fatty acid is termed LDL, and packed cholesterol may look like a building block of the lipoprotein (as the LDL receptor of tissue cell takes up LDL as is - no unloading). Hint: my misunderstanding taken for typical learner's was to think of LDL being sent off by the liver - not correct: it's VLDL off from the liver, and "remnancy" after unloading fatty acid at the veins' walls. So VLDL become LDL in the blood stream. There is a special page in Wikipedia not easy to find:Remnant cholesterol

These preliminary remarks are practical hints, as you may search for "why does eating saturated fat increase VLDL (very low density lipoproteins) and get some clues and discussion via google -instead of searching for "saturated fat and LDL

Why is LDL held responsible for "bad cholesterol"? Among the lipoproteins it has the highest load of cholesterol; and as a "remnant" transporter of cholesterol it does seem to unload cholesterol at arterial walls just as that same transporter (named VLDL at that point)= does with fatty acids - if tissue cells not in need of cholesterol do not express the LDL receptor (Nobel prize winners Brown and Goldstein's research on familial hypercholesteraemia).

That said, why then should reduction of dietary saturated food reduce VLDL and/or LDL (your question translated to that formula) as the only "clear" effect of saturated food is a higher production of chylomicrones which are very low in cholesterol?

Did you read my latest news up above? I think it is no common knowledge that chylomicrons are involved in cholesterol transport from the intestine to the liver. Simple inference from that: more cholesterol input (combined to saturated fat) causes more cholesterol output (combined to fat, VLDL which becomes LDL "on deliverance").

However, searching through literature, your question turns out to be valid - nothing is "clear" and undebated, and that goes for the following simple reasoning as well, recurring to basic knowledge (before I knew about chylomicrones delivering cholesterol to liver):

Effect of dietary saturated fat is that the liver will be able to synthetize and deliver to tissue cells more of so called endogenous fat as it receives more of fatty acids FROM tissues the more those tissues receive fatty adics from chylomicrones (see below about pathway from tissue TO Liver-Hint: it is not irrelevant in respect of your question that short fatty acids do not need chylomicrones for uptake from intestine, and it seems that in early scientific discussion the high amount of any kind of fat, saturated or not, was subject of debate).

Any surplus of fat the liver produces is transported to tissues (Stryer/Berg, Biochemistry) by

VLDL, the Very Low Density Lipoproteins.

The important crossroad of those pathways is at the arterial wall where VLDL unload endogenous fat from and made by the liver. VLDLs thus become "ILDL - Intermediate-Density Lipoproteins", half of which is returned to the liver for turnover, half of which, however, become LDL (how? By "unloading more fatty acids", cp. Berg/Stryer, Biochemistry).

So, this presumed mechanism is in favour of the quote cited: more saturated fat deliverd by chylomicrones will lead to more saturated fat in VLDL which, after unloading fatty acids, become "bad" LDL transporting cholesterol (only). More saturated fat input is seen here as a "commodity" the liver replenishes its production of endogenous fat with.

Let me give you some quote describing the pathways, to see how the liver receives (saturated) fatty acids taken in by chylomicrones that have delivered to storage fat tissues (not to liver!). VLDL are only needed for transportation FROM the liver, not to the liver. How might liver input of fatty acids, leading to bad LDL, be heightened by chylomicrone input?


[K.R. Feingold, Introduction to Lipids and Lipoproteins][1]

"...The exogenous lipoprotein pathway starts with the incorporation of dietary lipids into chylomicrons in the intestine. In the circulation, the triglycerides carried in chylomicrons are metabolized in muscle and adipose tissue by lipoprotein lipase releasing free fatty acids, which are subsequently metabolized by muscle and adipose tissue, and chylomicron remnants are formed (...) then taken up by the liver. The endogenous lipoprotein pathway begins in the liver with the formation of VLDL."

In Berg/Stryer,10ed., Fig. 26.16 depicts Fig 36.1 of Goodman/Gilman: The liver receives free fatty acids released into the blood by "adipose tissue", i.e. tissue cells that have received saturated fats from chylomicrones.

So, if (saturated) fat input is transported to STORAGE tissue by chylomicrones high input of fat may lead to excess, surplus storage of fat in adipose tissue, then to free fatty acids input of the liver which metabolizes to endogenous triglycerides(!) "re"-transported to storage and/or catabolic tissue. It may be a question of debate whether LDL from VLDL being turned to ILDL is a metabolic switch the aim of which is to "store as much as possible" - where, at the end of the line fat broken down in liver and re-metabolized to cholesterol by the liver (via acetyl-CoA) can be stored as cholesterol by any cell that is able to store away cholesterol,then not using cholesterol as building block of its membrane. This point alludes to the second part of my answer that differentiates between animal and plant tissue: animal cells much more than plant cells might be able to STORE cholesterol which might explain why animal fatty tissue contains roughly 100 times more cholesterol thatn plant fatty tissue, see down below.

Quote continued:

"The triglycerides carried in VLDL (annot. see quote above: triglycerides made by the liver) are metabolized in muscle and adipose tissue by lipoprotein lipase releasing free fatty acids and IDL are formed. The IDL are further metabolized to LDL, which are taken up by the LDL receptor in numerous tissues including the liver, the predominant site of uptake."

Surpringly, the liver emits LDL, but does have LDL-receptor. These LDL-receptor of the liver are said to take receive "chylomicron remnant", see, for instance, Dr. Malcom Kendrick Assuming those LDL-receptor of the liver also take up LDL that has been refused by tissue cells however, seems coherent to some basic principle of "store ("can"..) as much as you can": fat non used or stored in tissue being receivevd by the liver (free short fatty acids in blood!), liver handing its surplus back to tissue on VLDL; surplus fatty acid in liver metabolized to cholesterol, delivered to cells, cholesterol not taken up by cells returned to the liver.

Thus, deposition of bad cholesterol in veins can be seen as some last resort of storage activity, in case the liver does restrict LDL-receptors as presumably tissue cells have done before.

Thus, excess (saturated, but, as you suggest: same should apply to unsaturated) fat in food might lead to excess storage activity by bad LDL.

Refering to the distinction between saturated and unsaturated fat your question seems to focus on see, for instance, Palm Oil Consumption Increases LDL Cholesterol Compared with Vegetable Oils Low in Saturated Fat in a Meta-Analysis of Clinical Trials Ye Sun et al., This digest of empirical studies speaks in favour of saturated fat in contrast to unsaturated fat increasing "bad" (LDL) blood cholesterol. Doing quick research I did not find any explanatory theory. Here is hint: Among unsaturated fatty acids there are some that are "essential" (as vitamins are). That is mentioned here: [bmj.com] 5https://www.bmj.com/content/361/bmj.k2139 Maybe metabolism of essential unsaturated fatty acid signals a situation where there seems to be less need to turn fatty acids into cholesterol and send it to tissue cells (because those are signalled to be able to synthesize enough on their own). That's one idea.

Even if there is somehow "clear" causality in

dietary fat - chylomicrones - liver production of endogenous fat - VLDL - VLDL remnants - LDL

it seems to be debated on if there is a difference between saturated and unsaturated fat in that respect. "You're right."

In the following, I would like to show that the statement "less fat, less cholesterol" your question refers to might still be correct, in its statement of a rule of thumb, in its empirical result, especially in what regards differentiating unsaturated and saturated fat.

Content of cholesterol in food may be considered as proportional to content of saturated fatty acids.

If you exclude saturated fatty acids from your diet according to the rule quoted in question you end up with zero input of cholesterol, and you end up as a vegetarian.

This is because

  1. food from plants does not contain saturated fats - with a few exceptions: coconut and palmoil, nuts..., and

  2. food from plants does not contain cholesterol in form and relevant quantity as animal food does.

"While cholesterol averages perhaps 50mg/kg total lipid in plants, it can be as high as 5 g/ kg(or more) in animal."

This is a factor of 100!

Quote is from a paper advocating the opposite point of view (no bias):

Journal of Chemical Education J. Behrman* and V. Gopalan, Cholesterol in plants

However, "There is a widespread belief among the public and even among chemists that plants do not contain cholesterol. This error is the result (in part) of the fact that plants generally contain only small quantities of cholesterol and that analytical methods for the detection of cholesterol in this range were not well developed until recently (1). Another reason has todo with the legalities of food labeling that allow small quan-tities of cholesterol in foods to be called zero (...). The fact is that cholesterol is widespread in the plant kingdom although other related sterols, such as β-sitosterol (henceforth referred to as sitosterol), generally occur in larger quantities. No current biochemistry text that we have examined provides an accurate account of cholesterol in plants. Here is a suggested paragraph for the next generation of biochemistry texts: More than 250 steroids have been described in plants (3).Of these, perhaps sitosterol, which differs ..."

I think it's legitimate to inversely defere from this quote that food derived from plants, at least, does not contain cholesterol in amounts relevant to nutrition.

See also Athel Cornish-Bowden

From Wikipedia:

"Plants make cholesterol in very small amounts.[...] In larger quantities they produce phytosterols, chemically similar substances which can compete with cholesterol for reabsorption in the intestinal tract, thus potentially reducing cholesterol reabsorption." Wikipedia, Cholsterol

From Biology online "Because of cholesterol that provides cell membrane structural integrity and fluidity, animal cells need not to have cell walls such as that in bacterial and plant cells."

Refering to point 2 of reasoning above:

"Most animal fats are saturated. The fats of plants and fish are generally unsaturated." Wikipedia, Unsaturated Fat

Thus, avoiding saturated fat means avoiding animal fat, thus avoiding cholesterol.

Again, this reasoning is not what the quote cited in your question seems to refer to or be based on. As an empirical rule it might be correct for the reasons stated.

To sum up: Even if it must be admitted that there are relevant amounts of saturated fat in plants, reducing saturated fat in diet in any case reduces cholesterol input (even if that'd mean the exclusion of coconut, palm oil and peanuts, from the diet - in that way you'd sure still end up a veggie).

  • $\begingroup$ No references are cited to support this answer. $\endgroup$
    – Bryan Krause
    Oct 29, 2021 at 14:53
  • $\begingroup$ @Bryan Krause I added some reference and am sure to be able to add many more references. However, I have become some suspicious mind with you - personally! - and I am begging you to either withdraw comment or downvote, explain what's wrong, or - best - delete this anwer that moreover I guess is not politically correct. Can user delete answer on his own? thanks. $\endgroup$ Oct 29, 2021 at 16:34
  • $\begingroup$ Yes, users can delete their own answers. The references you've included do not seem to support the main conclusions in this answer. The first includes a quote but the citation is not sufficient for a reader to find the source of the quote, and therefore invalid. The second is also insufficient for a reader to find the source of the quote. $\endgroup$
    – Bryan Krause
    Oct 29, 2021 at 16:46
  • $\begingroup$ Hi, Bryan Hi, Thank you for your criticism, I tried to amend accordingly, and very much expanded my answer according to what the question seems to focus on. Let me know if you want me to delete the answer. There will be others. $\endgroup$ Oct 30, 2021 at 8:57
  • $\begingroup$ I gave you an upvote for trying so well to support your answer. (I didn't read the sources, so I won't comment on their appropriateness.) I can't remove downvotes; only the downvoters can do that. To notify Bryan, you need to "ping" him by using the @ character before his name (he didn't get notification of your comment.) I'll do that for you: @BryanKrause - Is this answer improved enough for you to remove your downvote? Thanks. $\endgroup$ Oct 30, 2021 at 17:43

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