Digest №9: On the Health Implications of an Animal-Based Ketogenic Diet
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Digest №9: On the Health Implications of an Animal-Based Ketogenic Diet

2026, week 15: Animal fats have got quite the bad rep, how cholesterol and LDL impact health, how animal foods influence cholesterol and LDL, and what it means.


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Bless!

At this point, we've discussed low-carb diets, especially versions of low-carb diets, which are high in animal fats. I think it appropriate to discuss such animal-derived dietary fats, as those will inevitably have to supply most of your energy needs, when transitioning from the toxic, high-carb, grain-based standard Western diet to a more human-appropriate diet with far fewer carbohydrates.

The body can readily adapt to both high fat and high carbohydrate diets. In resting metabolism, the body will then use whatever fuel source is most available, whereas increases in metabolic rate by means of intense exercise will necessitate the use of whatever fuel is most easily and quickly metabolised.1–2

This shouldn’t be surprising.

What may be surprising to some, is that the body readily produces glucose (a sugar), to keep a healthy and stable blood sugar level, even when fed exclusively with protein and fat, or when fed nothing at all – i.e. when fasting.3

Over the last decades, concerted effort has been made in campaigning against animal fats, which happen to be rich in cholesterol and saturated fat. Primarily, this effort was started and supported by Kellogg and similar sex-averse missionaries, who wanted to limit libido through food.4 The problem with this, of course, is that the food, which tanks our libido, is also incidentally extremely unhealthy for us.

But, don’t take my word for it. Let’s go over the common claims made against animal fats – specifically their components cholesterol and saturated fat – one by one and see why this scare about animal fat is simply unfounded in truth. I’m not going use such arguments as the one, that our ancestral line has been eating animals in various quantities for literal millions of years.5–6 Neither am I going to mention, that early hominids, who tried to survive on plants alone, would experience deficiencies in protein and other nutrients, thus requiring animals as food for optimal health.7

Instead, I’ll be looking at contemporary studies into the effects of animal fat consumption on human health.

The primary detriment ascribed to animal foods is, of course, that they raise both total cholesterol and the so-called ‘bad cholesterol’ (which usually refers to LDL). Naturally, the secondary claim implicit herein is, that cholesterol and LDL both be unhealthy for humans. Let’s first tackle the question of the health effect of cholesterol and LDL, before looking at whether animal foods even raise them. For if they aren’t unhealthy, then their raising shall be utterly unimportant.

The hypothesis, that animal fat – i.e. predominantly saturated fat – be unhealthy for humans, was for a long time considered proven by a dietary intervention study. The problem with that study was, that the original researchers elected to not publish a large swath of the data they generated.8 We know this, because their data has since been recovered, which has led to their reanalysis.

The reanalysed data indicated, that a higher total concentration of serum cholesterol was associated with a lower probability of death, whereas a lower total concentration of serum cholesterol was associated with a higher probability of death (graph sadly only licensable under CC BY-NC 4.0, which disallows reproduction for commercial purposes). This means, that ostensible raising of total serum cholesterol by animal foods can’t be of issue, as it’s associated with a less death not more. So, what about the so-called ‘bad cholesterol’, LDL?

One of the biggest studies (19 034 people) ever made on the supposed negative health effects of high LDL values found, that LDL values under 70 mg/dL – commonly recommended by physicians – is associated with excess all-cause mortality (see Figure 1).9 Contrarily, LDL values as high as 250 mg/dL – such values would oftentimes send physicians into a coma – are barely associated with an increase in all-cause mortality. In this particular data set, LDL levels of 130–170 mg/dL seem to be optimal for achieving the lowest possible all-cause mortality. These are still values most physicians would consider dangerously high. Turns out, such physicians are simply dangerously wrong.


Figure 2: Spline plot of all-cause mortality against serum LDL levels. Dashed lines indicate 95% confidence intervals. Taken from Liu et al. and licensed under CC BY 4.0 without changes to the material.

This means, that it would actually be good for you – or at least be associated with a lower chance of you dying – to have higher rather than lower total serum cholesterol and ‘bad cholesterol’. This doesn’t mean, that a higher LDL is necessarily entirely benign. It may worsen the development of cardiovascular disease, though this causally requires chronic vascular inflammation.10–11 It thus seems smarter indeed to simply prevent and clear up such chronic vascular inflammation – something we implicitly do with the Mosaic Method –, since without this atherosclerosis and resultant cardiovascular disease is hard to come by instead of trying to chemically restrict the normal function of LDL and other blood lipids, especially because a lower LDL concentration is associated with more not less death.

Fascinating.

One last question remains. Does animal-based food even increase total serum cholesterol and LDL? The answer to that is: it depends. Population eating different amounts of animal-based food may indeed exhibit different serum levels of cholesterol and LDL.12 This is entirely logical, as LDL and other blood lipids act as transporting vessels for long-chain fatty acids and cholesterol in the blood.13–14 The more long-chain fatty acids and cholesterol a person consumes, the more such transporting vessels should be needed.

Since LDL seems to be optimal in the concentration range of 130–170 mg/dL and perfectly healthy in the range of 80–250 mg/dL, I’d say that worrying to death about an entirely normally functioning fat transport vessel, of which our body may at time make more or less use, is inane, and just unduly stresses doctors and patients alike.

Apparently, just eat human-appropriate food and you’ll be fine.

Swift healing and lasting health, Merlin L. Marquard.

P.S.: If this digest has been valuable or simply interesting to you, you may well send it on to someone, who'd find it just as interesting. It helps spread our message of scientifically rigorous health evaluation and advisory efforts.


References

  1. Helge JW, Watt PW, Richter EA, et al. Fat utilization during exercise: adaptation to a fat-rich diet increases utilization of plasma fatty acids and very low density lipoprotein-triacylglycerol in humans. The Journal of Physiology 2001;537:1009–20. doi:10.1111/j.1469-7793.2001.01009.x
  2. Achten J, Jeukendrup AE. Optimizing fat oxidation through exercise and diet. Nutrition 2004;20:716–27. doi:10.1016/j.nut.2004.04.005
  3. Zhang X, Yang S, Chen J, et al. Unraveling the Regulation of Hepatic Gluconeogenesis. Front Endocrinol (Lausanne) 2018;9:802. doi:10.3389/fendo.2018.00802
  4. Ryan C, Jethá C. Sex at Dawn. Reprint. Harper Perennial 2012.
  5. Domínguez‐Rodrigo M. Testing meat-eating in early hominids: an analysis of butchery marks on defleshed carcases. Human Evolution 1997;12:169–82. doi:10.1007/BF02438066
  6. Clark J, Linares-Matás G. Seasonal resource categorisation and behavioral adaptation among chimpanzees: Implications for early hominin carnivory. J Anthropol Sci 2023;101:1–35. doi:10.4436/jass.10006
  7. Bunn HT, Ezzo JA. Hunting and Scavenging by Plio-Pleistocene Hominids: Nutritional Constraints, Archaeological Patterns, and Behavioural Implications. Journal of Archaeological Science 1993;20:365–98. doi:10.1006/jasc.1993.1023
  8. Ramsden CE, Zamora D, Majchrzak-Hong SF, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). The BMJ 2016;353. doi:10.1136/bmj.i1246
  9. Liu Y, Liu F, Zhang L, et al. Association between low density lipoprotein cholesterol and all-cause mortality: results from the NHANES 1999–2014. Scientific Reports 2021;11:22111. doi:10.1038/s41598-021-01738-w
  10. Ajoolabady A, Pratico D, Lin L, et al. Inflammation in atherosclerosis: pathophysiology and mechanisms. Cell Death Dis 2024;15:817. doi:10.1038/s41419-024-07166-8
  11. Libby P, Ridker PM, Hansson GK, et al. Inflammation in Atherosclerosis. JACC 2009;54:2129–38. doi:10.1016/j.jacc.2009.09.009
  12. Igl W, Kamal-Eldin A, Johansson Å, et al. Animal source food intake and association with blood cholesterol, glycerophospholipids and sphingolipids in a northern Swedish population. International Journal of Circumpolar Health 2013;72:21162. doi:10.3402/ijch.v72i0.21162
  13. Axmann M, Plochberger B, Mikula M, et al. Plasma Membrane Lipids: An Important Binding Site for All Lipoprotein Classes. Membranes 2021;11. doi:10.3390/membranes11110882
  14. Vance JE. Cellular itinerary of LDL cholesterol. Proceedings of the National Academy of Sciences2022;119:e2122584119. doi:10.1073/pnas.2122584119

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