Seed Oils and Rancid Blood Lipids

I've lost count over how many times I've heard, that blood cholesterol and especially blood LDL cholesterol are bad for our health. What's more, elevated levels of blood LDL cholesterol are oftentimes stated to directly cause atherosclerosis. The evidence for this, however, is doubtful. There are two nice reviews/reevaluations of some old large-scale studies on this, which actually show, that both lower blood cholesterol and lower blood LDL cholesterol are associated with higher all-cause mortality (Ramsden et al. 2016, Ravnskov et al. 2016). This translates to a higher statistical likelihood of death, if you have lower – not higher – blood levels of cholesterol.

Evidence seems to rather show, that it's oxidised blood lipids (which includes blood cholesterol), which seem to be causally implied with atherosclerosis and related ailments (Vikram et al. 2012).

From the same publication we can see, that polyunsaturated fatty acids – chief amongst them the omega-6 fatty acids linoleic and arachidonic acid – promote atherosclerosis by being easily oxidised.

Furthermore, both products of these polyunsaturated fatty acids and from sugars are directly involved in the oxidation of LDL cholesterol particles . This means, that it's not LDL cholesterol at large, but the rancid, oxidised LDL cholesterol, which causes problems.

Atherosclerosis begins with blood lipid particles entering into the blood vessel wall. In healthy subjects, monocytes (a type of immune cell) migrate to the site in question, absorb the superfluous fat and emigrate to dispense of it. The problem arises, when danger signals, such as oxidised (rancid) LDL, keep monocytes at the cite and disallow them to emigrate. This keeps the fat in the lesion in question. Over time, the inflamed fat lesion grows in size and thus in its poor effect on vascular health (Moore et al. 2013).

In fact, these oxidised LDL cholesterol particles are taken up by macrophages. When these macrophages, gorged on oxidised LDL cholesterol, migrate into the blood vessel walls and die, it leads to atherosclerotic plaques. Blood cholesterol doesn't do this, an over-abundance of omega-6 fatty acids does.

But what's that got to do with seed oils?

Well, all commercially available seed oils – with the exception of flaxseed oil – contain high concentrations of linoleic acid, which is the same polyunsaturated acid, which is directly involved in the development of atherosclerosis (Mariamenatu and Abdu 2021).

This is only made worse by that fact, that – and this is a simplification of the biochemistry – omega-6 fatty acids tend to be pro-inflammatory and omega-3 fatty acids anti-inflammatory (Simopoulos 2002). A high omega-3/omega-6 ratio suppresses progression of many ailments, including cardiovascular diseases, cancers and other inflammatory or autoimmune diseases.

Omega-6 fatty acids are pro-inflammatory and thus are both directly involved in the formation of atherosclerotic lesions and in the increase of low-grade systemic inflammation, which itself increases the speed of progression of atherosclerosis and related ailments.

So, not only do lower levels of LDL cholesterol and general cholesterol worsen the survival of patients, but the exact seed oil, which are so often promoted as heart-healthy, are directly involved in the formation and worsening of the ailment, which is so often ascribed to LDL cholesterol.

The solution?

It seems to simply be the abstinence from seed oils, especially those with low ratios between omega-3 to omega-6 fatty acids.

We can replace these seed oils with saturated animal fats (tallow, butter, ghee) without second thought, despite the general assertion of their danger. Their consumption doesn't seem detrimental to health in any way and they even seem to be protective against cardiovascular disease (Astrup et al. 2020).

Fat from gras-fed cattle seems to be optimal, as they have a beneficial omega-3 to omega-6 ratio (Krusinski et al. 2023). Even fat from grain-fed animals is probably better than seed oils with regard to atherosclerosis, simply due to the lower concentration of polyunsaturated fatty acids.

To summarise: Oxidised LDL cholesterol, specifically, seems to be the problem. The oxidation of LDL cholesterol seems to be most easily circumvented by reducing consumption of oxidative polyunsaturated fatty acids (amongst these especially omega-6 fatty acids). That neither polyunsaturated nor omega-6 fatty acids can feasibly be eliminated – or even should be eliminated – is to be kept in mind. It's much more important to consume both in human-appropriate quantities.

Astrup, A., Magkos, F., Bier, D.M., Brenna, J.T., de Oliveira Otto, M.C., Hill, J.O., King, J.C., Mente, A., Ordovas, J.M., Volek, J.S., et al. (2020). Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations: JACC State-of-the-Art Review. Journal of the American College of Cardiology 76, 844-857. 10.1016/j.jacc.2020.05.077.

Krusinski, L., Maciel, I.C.F., van Vliet, S., Ahsin, M., Lu, G., Rowntree, J.E., and Fenton, J.I. (2023). Measuring the Phytochemical Richness of Meat: Effects of Grass/Grain Finishing Systems and Grapeseed Extract Supplementation on the Fatty Acid and Phytochemical Content of Beef. Foods 12. 10.3390/foods12193547.

Mariamenatu, A.H., and Abdu, E.M. (2021). Overconsumption of Omega-6 Polyunsaturated Fatty Acids (PUFAs) versus Deficiency of Omega-3 PUFAs in Modern-Day Diets: The Disturbing Factor for Their “Balanced Antagonistic Metabolic Functions” in the Human Body. Journal of Lipids 2021.

Moore, K.J., Sheedy, F.J., and Fisher, E.A. (2013). Macrophages in atherosclerosis: a dynamic balance. Nat Rev Immunol 13, 709-721. 10.1038/nri3520.

Ramsden, C.E., Zamora, D., Majchrzak-Hong, S.F., Faurot, K., Broste, S.K., Frantz, R.P., Davis, J.M., Ringel, A., Suchindran, C.M., and Hibbeln, J.R. (2016). Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). The BMJ 353. 10.1136/bmj.i1246.

Ravnskov, U., Diamond, D.M., Hama, R., Hamazaki, T., Hammarskjöld, B., Hynes, N., Kendrick, M., Langsjoen, P.H., Malhotra, A., Mascitelli, L., et al. (2016). Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review. BMJ Open 6, e010401. 10.1136/bmjopen-2015-010401.

Simopoulos, A.P. (2002). The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomedicine & Pharmacotherapy 56, 365-379. 10.1016/S0753-3322(02)00253-6.

Vikram, J., Koji, U., and Vasanthy, N. (2012). Pathophysiology of Lipoprotein Oxidation. In Lipoproteins, F. Sasa, and K. Gerhard, eds. (IntechOpen), pp. Ch. 16. 10.5772/50622.