Is the LDL response to saturated fat a sign of a healthy individual?
The BMJ article "Dietary fat and cardiometabolic health: evidence, controversies, and consensus for guidance" mentions in passing a critically important point - "evidence from clinical trials suggests that saturated fat may have little effect on LDL cholesterol levels in people with obesity".
This is true not only for obesity, but also for other factors associated with increased CVD risk, especially insulin resistance and hyperinsulinaemia. In the meta-analysis of RCTs of high-fat vs low-fat dairy foods by Benatar et al.,, there was zero change in LDL in the 12 studies on obese or overweight volunteers, and a small statistically significant difference in LDL in the 8 studies in normal subjects. The converse is also true - diets designed to lower LDL cholesterol by restricting fat or replacing saturated fat with polyunsaturated fat have little effect on LDL in the overweight or insulin-resistant. In other words, the elevation of LDL by saturated fat is in itself a marker of a metabolic state associated with a lowered risk of CVD. It is also the case that LDL can double in lean healthy subjects during a fast (when no saturated fat is consumed) but not in an obese or overweight subjects. Is it reasonable to think that a response that mainly occurs in healthy people is a cause of disease?
If we look at a population stratified by all 3 standard lipid markers, triglycerides (TG), HDL, and LDL, the Framingham Offspring Cohort, we can see that there is no increased risk of CVD associated with higher LDL levels in persons with high HDL and low TGs. Elevations in LDL due to eating saturated fat are more usually accompanied by increases in HDL and decreases in TGs than not, especially when total fat replaces carbohydrate. Improvement in the fasting ratio of TG to HDL is an effect reliably seen when fat, including saturated fat, replaces carbohydrate in the diet of persons with the metabolic syndrome - in other words, the carbohydrate-restricted diet works to improve a marker of cardiometabolic risk, the TG/HDL ratio, in the same high-risk cases where the low fat, saturated fat-restricted diet does not significantly improve LDL, and this effect is no less marked when the diet is high in saturated fat.
There are pathways whereby diets high in both saturated fat and refined carbohydrate together can plausibly increase risk, the evidence for which was well laid out by Kuipers et al. in 2011, who stated "High CHO intakes stimulate hepatic SAFA synthesis and conservation of dietary SAFA. The accumulation of SAFA stimulates chronic systemic low-grade inflammation through its mimicking of bacterial lipopolysaccharides and÷or the induction of other pro-inflammatory stimuli. The resulting systemic low-grade inflammation promotes insulin resistance, reallocation of energy-rich substrates and atherogenic dyslipidaemia that concertedly give rise to increased CVD risk."
Kuipers et al. concluded that avoidance of saturated fat accumulation, in serum and tissues, by reducing the intake of refined carbohydrates, which constitute >50% of energy from the modern diet, will be more effective in the prevention of CVD than reducing the intake of saturated fat, which only supplies <15% of energy.
A note of caution should also be sounded regarding the claim "evidence exists of the long term safety and benefit of many of the commonly consumed unsaturated plant oils".
There is in fact still no meta-analysis of prospective studies available testing the association of any, or indeed all, of the commonly consumed polyunsaturated plant oils with any disease or cause of death. All such studies for polyunsaturated fats include PUFA from nuts and other foods that have independent associations with reduced disease risk, so cannot supply good evidence about oils. There has been a meta-analyses to inform us that butter is not associated with increased CVD risk, and is associated with decreased type 2 diabetes risk, in prospective population studies. An increased consumption of polyunsaturated seed oils, often named specifically, has been an important goal of nutritional guidelines for many decades, without any such safeguard.
 Forouhi NG, Krauss RM Taubes G, Willett W.. Dietary fat and cardiometabolic health: evidence, controversies, and consensus for guidance. BMJ. 2018 Jun 13;361:k2139. doi: 10.1136/bmj.k2139.
 Flock MR, Green MH, Kris-Etherton PM; Effects of Adiposity on Plasma Lipid Response to Reductions in Dietary Saturated Fatty Acids and Cholesterol, Advances in Nutrition. 2011;2,(3):261–274, https://doi.org/10.3945/an.111.000422
 Benatar JR, Sidhu K, Stewart RAH. Effects of High and Low Fat Dairy Food on Cardio-Metabolic Risk Factors: A Meta-Analysis of Randomized Studies. Tu Y-K, ed. PLoS ONE. 2013;8(10):e76480. doi:10.1371/journal.pone.0076480.
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 Bartlett J, Predazzi IM, Williams SM, et al. Is Isolated Low HDL-C a CVD Risk Factor?: New Insights from the Framingham Offspring Study. Circulation Cardiovascular quality and outcomes. 2016;9(3):206-212. doi:10.1161/CIRCOUTCOMES.115.002436.
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 Pimpin L, Wu JHY, Haskelberg H, Del Gobbo L, Mozaffarian D. Is Butter Back? A Systematic Review and Meta-Analysis of Butter Consumption and Risk of Cardiovascular Disease, Diabetes, and Total Mortality. Schooling CM, ed. PLoS ONE. 2016;11(6):e0158118. doi:10.1371/journal.pone.0158118.
Competing interests: I am 60 years of age, lean and more-or-less active, with no history or family history of cardiovascular disease. Since soon after beginning a LCHF diet 8 years ago, I have no longer needed to visit my GP for illness or medicines as I once did frequently, and my fitness has markedly improved. However, my GP then became concerned about the rise in my LDL cholesterol level and advises me to take a statin, despite every other available marker of cardiometabolic health now being ideal..