What Really Happens to Saturated Fat on a Low Carb Diet?


In our last post, we went into a lot of detail about specific types of saturated fat and their effects on HDL. Here, we’ll try to summarise that information, and highlight some interesting conclusions, in simpler language.

But first, a short chemistry lesson. Nothing too hard, hopefully – we’ll just focus on the main dietary saturated fats (technically, fatty acids), the 4 “even numbered, long-chain saturated fats”.

Lauric acid – a 12 carbon saturated fat (C12:0). This is the rarest of these 4 fats. It is mainly found in the diet in coconut oil (49% auric acid) and dairy fat. Lauric acid also has some properties of  the shorter medium-chain fats (C6:0 – C:10:0), making it especially ketogenic.

Myristic acid – a 14 carbon saturated fat (C14:0). This is found in coconut oil, palm kernel oil, dairy fat, and the fats of ruminants and fish.

Palmitic acid – a 16 carbon saturated fat (C16:0). This is the most common of the saturated fats, and the second most common fat in nature after oleic acid (C18:1, a monounsaturated fat). It is found in all fats and oils.

Stearic acid – an 18 carbon saturated fat (C18:0). This is the second most common saturated fat, and is found in animal fats, cocoa butter, and palm oil.

The reality is that dietary fats, as they occur in actual foods, contain combinations of lots of different fatty acids; saturated, polyunsaturated, and monounsaturated. More, within each group they contain different combinations of each sort.

For example here’s what is in beef fat and butter*


These fats are also made in the body; they can be made from glucose and other sugars, and a shorter fat can also be converted to a longer one. Thus, palmitic acid (C16:0) is easily converted to both stearic acid (18:0) and oleic acid (18:1) in the carbohydrate fed state, myristic acid (C14:0) is less easily converted to palmitic acid (C16:0), and lauric acid (C12:0) is only with difficulty converted to myristic acid (C14:0).

The reason for these differences is that, the shorter the chain-length of a saturated fat, the quicker it is converted to energy (oxidised) and thus the less it is available for conversion to a longer fat (elongation).[1]


Dietary carbohydrate inhibits the oxidation of saturated fats and promotes their retention and elongation.[2]

This may explain why people eating low carbohydrate diets are able to eat a larger amount of energy from saturated fat without adverse effects – if indeed there are adverse effects to be experienced by saturated fats. Not only do all the blood markers of “cholesterol” improve (apart from rises in LDL cholesterol in a minority of cases), but the saturated fat content of the blood either decreases or, in a person where it was already low, stays the same.[3]

This is important because most of the health problems associated with saturated fat today are associated, not with saturated fat in the diet, but with a high level of saturated fat in the blood. High levels of palmitate and stearate are linked to insulin resistance, metabolic syndrome, and heart disease.[4,5,6] High levels of myristic acid and palmitate are linked to low levels of HDL and to NASH (non-alcoholic steatohepatitis), the inflammatory liver disease that is a dangerous consequence of NAFLD (non-alcoholic fatty liver disease).[7,8]
High plasma levels of palmitoleic acid (C:16:1 n-9), a rare monounsaturated fat formed when myristic acid is elongated to palmitate, are associated with increased future risk of new-onset type 2 diabetes.[9] This is a good indication that diets high in refined carbohydrate do play a causal role in this pathology, because levels of C16:1 drop once carbohydrate is restricted.[3]

When carbohydrate is restricted, and more fat including saturated fat eaten, the serum level of myristic acid falls more than that of palmitate, probably because its shorter chain-length means that its oxidation was less subject to carbohydrate control to begin with.[3]

It’s also the case that the shorter the chain length of a saturated fat, the more it raises HDL.[10]


And thus a very interesting set of correlations appears:

1: The shorter-chain the saturated fat, the faster it is converted to energy, and the harder it is to elongate.

2: The shorter-chain the saturated fat, the more it increases both HDL and LDL cholesterol at a normal carbohydrate intake.

3: The shorter-chain the saturated fat, the more the serum level in the blood drops when fat replaces carbohydrate

4: As a general rule, when fat replaces carbohydrate, both HDL, and the HDL: total cholesterol ratio, rise.


Mensink 2

Replacement of carbohydrate with a mixture of butter, coconut fat, olive oil and dark chocolate is predicted to improve the total to HDL cholesterol ratio

So, what is the connection? Well, it’s a mystery. So far, none of the references we’ve found actually indicates a mechanism by which some saturated fats raise HDL levels more than others.

We know that dietary fat (both saturated and monounsaturated) replacing carbohydrate increases the transport rate of ApoA-1 in liver cells, and that the decrease in triglyceride-rich VLDL with saturated fat in a low-carbohydrate diet, and the decrease in myristic acid levels, will help retain HDL in circulation long enough to do its job.[11,12]

(Interestingly, alcohol increases the transport rate of both ApoA-1 and ApoA-2, a type of HDL which has “no known function”, but which seems to be beneficial in moderate amounts, but to interfere with ApoA-1 function in larger amounts.)[13,14]
But we don’t yet have a mechanistic, nor an evolutionary, explanation as to why the chain-length of a C12-16 saturated fat and its rate of oxidation should make as much difference as it does to its effect on your HDL level. (Answers on a postcard please).

The bottom line: 
– all dietary fats are a mixture of saturated, monounsaturated, and polyunsaturated fats, and monounsaturated fat will make up the largest share of energy in the average low-carb diet (with the exception of coconut-based traditional diets), as it does in your body fat stores.
– It’s possible to eat a diet very high in lauric acid, but only if coconut or coconut oil is a major source of dietary energy. It’s impossible to eat a diet very high in myristic acid. These two fatty acids have the largest impact on HDL levels.
– Eating less carbohydrate will make less saturated fat appear in your blood between meals, even if you do eat more saturated fat, and this is most true for the lauric acid and myristic acid in your diet.
– There will also be benefits in terms of HDL (less) and reduced saturated fat in the blood (more)from a low-carb diet that is higher in monounsaturated fat, and lower in saturated fat than the average, if that’s what you like.

The bottom bottom  line: Don’t blame the butter for what the bread did!

*We have some evidence from New Zealand dairy fat expert Joycelyne Benatar that New Zealand dairy fat is, or was, higher in myristic acid than palmitic acid.[15,16] This is consistent with palmitic acid in milk being more the result of carbohydrate feeding (in grain-fed animals), or of animals being fed palm kernel expeller, and myristic acid being more the product of the synthesis of fatty acids from acetate supplied by fermentation.


[1] DeLany JP, Windhauser MM, Champagne CM, Bray GA. Differential oxidation of individual dietary fatty acids in humans. Am J Clin Nutr. 2000 Oct;72(4):905-11.

[2] Lossow WJ, Chaikoff IL. Carbohydrate sparing of fatty acid oxidation. I. The relation of fatty acid chain length to the degree of sparing. II. The mechanism by which carbohydrate spares the oxidation of palmitic acid. Arch Biochem Biophys. 1955; 57(1):23-40.

[3] Volk BM, Kunces LJ, Freidenreich DJ, et al. Effects of Step-Wise Increases in Dietary Carbohydrate on Circulating Saturated Fatty Acids and Palmitoleic Acid in Adults with Metabolic Syndrome. PLoS ONE. 2014;9(11):e113605. doi:10.1371/journal.pone.0113605.

[4] Sokolova M, Vinge LE, Alfsnes K, et al. Palmitate promotes inflammatory responses and cellular senescence in cardiac fibroblasts. Biochim Biophys Acta. 2017; 1862(2):234-245.

[5] Lu Z, Li Y, Brinson CW, Kirkwood KL, et al. CD36 is upregulated in mice with periodontitis and metabolic syndrome and involved in macrophage gene upregulation by palmitate. Oral Dis. 2016; Oct 18.

[6] Eulàlia Montell, Marco Turini, Mario Marotta et al. DAG accumulation from saturated fatty acids desensitizes insulin stimulation of glucose uptake in muscle cells. American Journal of Physiology – Endocrinology and Metabolism. 2001; 280(2): E229-E237.

[7] Tomita K, Teratani T, Yokoyama H et al. Plasma free myristic acid proportion is a predictor of nonalcoholic steatohepatitis. Dig Dis Sci. 2011 Oct;56(10):3045-52. doi: 10.1007/s10620-011-1712-0. Epub 2011 Apr 23.

[8] Martínez L, Torres S, Baulies A, et al. Myristic acid potentiates palmitic acid-induced lipotoxicity and steatohepatitis associated with lipodystrophy by sustaining de novo ceramide synthesis. Oncotarget. 2015;6(39):41479-41496.

[9] Mozaffarian D, Cao H, King IB. Circulating palmitoleic acid and risk of metabolic abnormalities and new-onset diabetes. Am J Clin Nutr 2010;92:1350–8. LINK

.[10] Mensink RP, Zock PL, Kester ADM, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr May 2003
vol. 77 no. 5 1146-1155. http://ajcn.nutrition.org/content/77/5/1146.full


[11] Brinton EA, Eisenberg S, Breslow JL. A Low-fat Diet Decreases High Density Lipoprotein (HDL) Cholesterol Levels by Decreasing HDL Apolipoprotein Transport Rates. J. Clin. Invest. 1990; 85: 144-151. 

[12] Noto, D et al. Myristic acid is associated to low plasma HDL cholesterol levels in a Mediterranean population and increases HDL catabolism by enhancing HDL particles trapping to cell surface proteoglycans in a liver hepatoma cell model. Atherosclerosis. 2016; 246:50 – 56.

[13] De Oliveira e Silva ER, Foster D, Harper MMcG, et al. Alcohol Consumption Raises HDL Cholesterol Levels by Increasing the Transport Rate of Apolipoproteins A-I and A-II.

[14] LW Castellani, Lusis AJ. ApoA-II Versus ApoA-I: Two for One Is Not Always a Good Deal. 

[15] Benatar JR, Stewart RAH. The effects of changing dairy intake on trans and saturated fatty acid levels- results from a randomized controlled study. Nutrition Journal. 2014; 13:32. LINK

[16] Palmitic acid increased from 15% to 30% of NZ dairy fat, and oleic acid increased from less than 10% to 30%, between 2011 and 2013, matching changes in palm kernel expeller use, at the expense of other saturated fats including myristic acid. Jocelyne Benatar quoted in Listener article by Jonathan Underhill, The Price of Palm Oil, 3 March 2017 LINK





  1. Zorba74 · · Reply

    It seems fairly clear that triglycerides and HDL -C clearly improve on LCHF. But If someone on LCHF diet wants to reduce LDL-C( as per conventional wisdom) are there are tweaks they should try?

  2. Hi Zorba,

    yes, that is definitely possible; here are some tweaks
    1) you could use more unsaturated fat – olive oil with lean red meat, poultry and fish, avocado and cut down on dairy fat and coconut.
    This should work – though when I tried it my LDL went up, came down again when I switched back to coconut and ghee, and I’ve heard a few other people report this – but in general, it should definitely go down
    2) LDL may be lower for some (without any increase in small dense LDL) with a few low-impact carbs in the diet – beans and lentils are probably the first choice here. Not everyone gets their most ideal ratios on keto. Some LDL-lowering mechanisms (like ApoC III clearance) are insulin-dependent and, depending on genetics and IR status might work better with more insulin flux. Insulin resistant individuals on LCHF usually get a drop in LDL if it’s high, probably because these mechanisms start to work better; it seems to be healthy individuals with better insulin sensitivity who can see it rise.

  3. Trevor Dallman · · Reply

    I was trying a low carb diet and after a few days started to suffer bad joint pain especially at night and was struggling to sleep. On researching it was suggested I was producing too much Lauric acid. I had to come off the diet and eat more carbs which got rid of my pain the next night.
    Is there any way to counter act the excess of Lauric acid?

    1. Hi Trevor,

      it seems unlikely that you could produce excess lauric acid – unless you were eating lots of coconut oil your serum level should be low, and lauric acid isn’t inflammatory; nor is it common or easy to test for this at all; maybe it was uric acid? This (not a fatty acid) is associated with gout and some people have reported developing gout on meat-heavy low carb paleo diets, though a ketogenic diet reduces the inflammation of gout.
      Eating vitamin C rich fruit on a low carb diet can lower uric acid, and I’m sure there are other hacks – does anyone have any suggestions?

      1. No personal experience, but lot of paleo adherants report anecdotal tweaks. Exhaustive discussion in the comments section here https://chriskresser.com/will-eating-a-paleo-diet-cause-gout/

  4. Sue greaves · · Reply

    On a low carb diet. No longer diabetic. Lost 3 stone. Much more energy. Cholestrol down from 5.6. To 3.2. I am the proof.

  5. chris c · · Reply

    This is fascinating stuff! You’d think people who study nutrition might know this. What are they called again? Ah yes, dieticians.

    Makes me wonder if the differences in HDL are for signalling purposes? Similarly Ron Krauss discovered different pathways which generate different sized LDL, head scratching stuff because this must have evolved for a reason. Nutrient sensing?

    One thing that may lower LDL – stop losing weight! Anecdotally LDL may increase while previously stored body fat is being metabolised and decrease again when it’s gone. Not a good way of LDL lowering though, nor is developing hyperthyroid.

  6. This study, posted by Raymund Edwards in the optimising nutrition facebook group, is really interesting


    they’ overfeeding MCTs – 150% of baseline calories, with 40%E fat – from MCTs – and DNL is producing elongation products from these in triglycerides – mostly C14 and C16, some C16:1 too.

    results are consistent with the hypothesis that ingestion of
    large amounts of MCT in a diet providing calories in excess
    of maintenance can promote substantial synthesis of
    LCFA by the liver. This synthesis of LCFA from acetate
    or from chain elongation of C8 and C10 fatty acids is energetically
    expensive, and could account for the unexpectedly
    large thermic effect of diets containing a large
    proportion of fat-calories as MCT

  7. “Replacement of carbohydrate with a mixture of butter, coconut fat, olive oil and dark chocolate is predicted to improve the total to HDL cholesterol ratio” ==> I felt personally targeted by this statement 🙂

    1. chris c · · Reply

      Worked for me too . . .

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Richard David Feinman

Richard Feinman, the Other

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