TLDR - The vilification of saturated fat is not supported by current literature or evidence.

There is no robust evidence that current population-wide arbitrary upper limits on saturated fat consumption in the United States will prevent CVD or reduce mortality.

A few large and well-designed prospective cohort studies, which used validated questionnaires to assess diet and recorded endpoints in a systematic manner, were initiated recently. They demonstrated that replacement of fat with carbohydrate was not associated with lower risk of CHD, and may even be associated with increased total mortality (29–31).

This really should be the major lesson in the dangers of epidemiology

urthermore, a number of systematic reviews of cohort studies have shown no significant association between saturated fat intake and coronary artery disease or mortality, and some even suggested a lower risk of stroke with higher consumption of saturated fat (3,6,32,33).

FAT IS GOOD FOR YOU

in a large and the most diverse study addressing this question, the PURE (Prospective Urban Rural Epidemiological) study (35) in 135,000 people mostly without CVD from 18 countries on 5 continents (80% low- and middle-income countries), increased consumption of all types of fat (saturated, monounsaturated, and polyunsaturated) was associated with lower risk of death and had a neutral association with CVD. By contrast, a diet high in carbohydrate was associated with higher risk of death but not with risk of CVD.

Associations are not causation, but it lines up with the carbohydrate insulin model of metabolic health

the substitution of polyunsaturated for saturated fat was associated with higher CVD risk

Those that comprise the basis of dietary recommendations to limit dietary saturated fat were conducted some 40 to 50 years ago (38), and have important methodological flaws, as described further subsequently.

This is a very polite way of saying they lied and manipulated the data to fit their agenda.

there are weaknesses in the argument that a reduction in CVD risk with saturated fat restriction can be inferred from the well-documented capacity of SFAs to increase LDL cholesterol when substituted for carbohydrate or cis-unsaturated fatty acids (12). First, although it is evident that LDL particles play a causal role in the development of CVD (44,45) and that, in general, there is a relationship between lowering of LDL cholesterol and CVD benefit (45), a diet-induced reduction of LDL cholesterol cannot be inferred to result in CVD benefit without having the means for a comprehensive assessment of other biologic effects that may accompany this reduction. In this regard, it is notable that postmenopausal estrogen plus progestin therapy (46) and treatment with several cholesteryl ester transport protein inhibitors (47) result in no CVD benefit despite substantial LDL cholesterol lowering. In contrast, Mediterranean-style dietary interventions reduce CVD risk without significantly reducing LDL cholesterol (48,49). Moreover, inhibition of sodium-glucose cotransporter type 2 reduces CVD events despite an increase in LDL cholesterol levels (50).

This is a great lesson in the dangers of focusing on a intermediate metric and not outcomes. LDL is not a disease!

Large LDLs are more cholesterol-enriched but have much weaker associations with CVD risk than do smaller LDL particles (44,52), which are not reduced by saturated fat restriction in the majority of individuals

Damaged LDL is the problem… lowering healthy LDL to get the whole LDL numbers down does not resolve the issue of damaged LDL accumulating. I.E. firing all the firemen from a city reduces the number of firemen running around, but doesn’t reduce the fires

For these reasons, dietary effects on CVD risk may not be reliably reflected by changes in LDL cholesterol levels, and therefore it is imperative to develop and implement more valid surrogate markers for assessing CVD risk and monitoring diet-induced effects in research and clinical practice.

Amen! Personally I would advocate for blood pressure, insulin sensitivity (homa-ir), and tg/hdl ratio

Insulin resistance manifests functionally as carbohydrate intolerance. For example, insulin-resistant lean subjects demonstrate impaired skeletal muscle glucose oxidation, increased hepatic de novo lipogenesis, and atherogenic dyslipidemia after a high-carbohydrate meal (55). Therefore, an individual with insulin resistance has a higher propensity to convert carbohydrate to fat, which will further exacerbate the insulin-resistant phenotype.

If people with poor metabolic health (96% of all people) are carbohydrate intolerant, and carbohydrates and not a necessary nutrient, people should remove carbohydrates from their food!

however, the amount of circulating SFAs in blood is not related to saturated fat intake from the diet but instead tends to track more closely with dietary carbohydrate intake. For example, an increase in saturated fat consumption by 2- to 3-fold either has no effect or decreases serum levels of SFAs in the context of lower carbohydrate intake (62–65). Decreased accumulation of circulating SFAs in response to diets lower in carbohydrate and higher in saturated fat is partially mediated by lower production (through de novo lipogenesis), but also increased clearance. Low-carbohydrate diets consistently increase rates of whole-body fat oxidation, which includes the preferred use of SFAs for fuel. Thus, the combination of greater fat oxidation and attenuation of hepatic lipogenesis could explain why a higher dietary saturated fat intake is associated with lower circulating SFAs in the context of low carbohydrate intake.

An explanation of why saturated fat intake has been blamed for the damage carbohydrates have done.

Despite many decades of nutrition research in humans and animal models, the scientific community has not yet reached a consensus on “the one diet” (i.e., low-fat, Mediterranean) that achieves optimal metabolic health for all.

Science is not about consensus, it’s about falsifiable hypotheses that can be verified. It doesn’t matter if nobody agrees with it, it needs to be demonstrable. The problem with “consensus” is it invites cult-like philosophical faith in a untestable theory (which is what we have today with the deluge of low risk epidemiology pushing pre-selected agendas)

The highly heterogeneous outcomes of dietary intervention studies suggest that some individuals have better outcomes from specific diets than do others.

Beyond genetic phenotypes, I think this statement is more closely related to the noise in the research and the fact the interventions researched are not the most effective. i.e. a study of the standard western diet with lots of processed food vs increased fiber wont be definitive because its not the strongest lever… i.e. its the wrong question. We always need to be asking in the context of epidemiology “Compared to what”.

Obesity and type 2 diabetes are major contributors to the risk of CVD, and recent evidence suggests that the optimal diet for weight control and glycemic control depends in part on the individual’s “carbohydrate tolerance” (85), which in turn is determined by insulin resistance and insulin secretion capacity. Carbohydrate tolerance may also vary with level of exercise or fitness of the individual.

Look at how much work they are doing to not talk about ketogenic metabolism, or low carbohydrate diets.

By the 1970s, many experimental studies in animal models were conducted with dietary coconut oil of unspecified origin, which reliably caused dramatic increases in hepatic and blood cholesterol in rodents; this was taken as evidence that dietary SFAs are inherently atherogenic (95,96). However, coconut oils of the era were usually highly processed and often fully hydrogenated.

Ah yes, the flawed methodologies

Studies in rodents demonstrated that while highly processed (“refined-bleached-deodorized”) coconut oil raises serum cholesterol, virgin coconut oil does not (99,100).

Another feather in the cap of industrial processed oils are supremely unhealthy!

based on several decades of experience, a focus on total SFAs has had the unintended effect of misleadingly guiding governments, consumers, and industry toward foods low in SFAs but rich in refined starch and sugar

This really is a crime against humanity, responsible for the current epidemic of metabolic disease.