Nutrition
Reducing saturated fat intake does not lower mortality
A recent meta-analysis conducted by researchers from several universities in Japan (Yamada et al, 2025) found no reduction in mortality through lower saturated fat consumption. We explain the study's findings and their implications in detail.
There is an extensive previous meta-analysis conducted by the Cochrane group (Hooper et al, 2020), which shows consistent results for all-cause mortality and cardiovascular mortality. However, comparing the two systematic reviews, we find some relevant differences. For example, there are important studies not included in the most recent meta-analysis by Yamada et al, such as the Women's Health Initiative 2006, Ley et al, 2004, or the Women's Intervention Nutrition Study 2006. These studies are relevant because they are more recent than most of the clinical trials included in both reviews and because they have greater potential weight for the combined effect than the entire meta-analysis by Yamada et al. However, the results of these studies are consistent with the overall conclusions, finding no significant effects, so their inclusion does not change the conclusions. The reason for the exclusion of these studies from the meta-analysis by Yamada et al. is the more stringent inclusion criteria, limiting the clinical trials included to those with saturated fat restriction as a specific objective, while the Cochrane review includes studies with broader dietary interventions in which there is a reduction in saturated fat. However, the Cochrane review also includes a subgroup analysis selecting studies with the specific objective of reducing saturated fat, again without changing the conclusions.
Among the main limitations of the meta-analysis by Yamada et al. are the age of the included trials and the absence of pre-registration. However, when comparing older and more recent studies, no major differences in conclusions were found. Given the type of intervention and the impossibility of blinding participants in a nutritional protocol, no trial was rated as low risk of bias in all domains. Nevertheless, the studies cover a large sample size, and mortality is a variable less subject to bias. Although most of the interventions were carried out in secondary prevention settings, two clinical trials were primary prevention trials, with no significant differences from the effect observed in the other studies. Another relevant limitation is that a dietary intervention does not reduce saturated fat in isolation, but rather replaces some foods with others. In most studies, saturated fat was restricted by replacing it with polyunsaturated fats. However, Hooper's subgroup analysis in Cochrane shows that the conclusions do not vary significantly according to the type of replacement macronutrient. In fact, the effects found are robust, with the same conclusions being maintained in virtually all additional comparisons made: cholesterol reductions achieved, risk of bias, duration of follow-up in the various studies, sex, etc. Another limitation of the studies is that there are different saturated fatty acids, with different biological effects, and some are part of healthier foods than others.
While replacing saturated fats with unsaturated fats or certain types of carbohydrates can lower LDL cholesterol, this reduction does not necessarily translate into a lower incidence of cardiovascular events or mortality. The mechanistic logic implicitly learned in medical and health science schools is a substantial part of the problem, promoting constant inductive reasoning from the particular, beginning on the very first day of class. Evidence-based medicine requires deductive reasoning from a major premise supported by clinical consequences, reaching a conclusion through the minor premise. The opposite involves speculative reasoning based on a reductionist assumption. This does not mean that it is the only way to reason, but it must begin by studying the evidence on hard outcomes that have been systematically investigated in the first place. Psychologists dedicated to the study of logic and decision-making have been studying the well-documented problems of probabilistic reasoning in physicians for approximately 50 years. For some reason, medical schools have not sought to address this issue through specific courses on epistemology and logic applied to clinical practice. What's more, students leave university without having even systematically studied the evidence for interventions, or the entire biochemical narrative that is taken for granted. It's the same as saying that evidence-based medicine sells fewer drugs than medicine based on biochemical allegories and interventions aimed at modifying markers using reductionist inductive logic. Go figure. The same logical scheme applies to nutrition: eating good foods is more important than reducing saturated fats or cholesterol in blood tests, as reductionist reasoning dictates.
In short, controlled studies to date show that trying to reduce saturated fat in diets has no significant impact on mortality. Even if new controlled studies were to yield different results, we do not expect large absolute differences in the conclusions. Probabilistic logic makes it clear that an isolated element from a huge set of nutrients involved in a physiology driven by homeostasis must translate into small risk ratios. The difficulties in estimating effects tend to lead to overestimation of minor aspects and underestimation of what is most relevant, so the findings of these studies are more important when you consider that there are clearer ways to reduce mortality and cardiovascular risk than reducing saturated fat intake: increasing daily vegetable consumption, reducing consumption of ultra-processed products (including those marketed as containing "polyunsaturated fat"), or consuming a little extra virgin olive oil every day, to name three of the most basic. The rest is confusing the order of priorities. The overall dietary context is more important than the biochemical category of a nutrient, and the same can be said for ultra-processed foods, where it matters little whether they are produced with saturated or unsaturated fats (industrial trans fats are another matter). At ICNS, we have been exposing the reality behind the claims about fats promoted by experts who claim to represent "science" without any evidence for over a decade. The promotion of certain food products and the festival of drugs prescribed under criteria of analytical modification may have something to do with it.
PATHOPHYSIOLOGY AND MECHANISMS
Cardiovascular disease remains the leading cause of death worldwide, and its origins involve genetic, metabolic, nutritional, environmental, and lifestyle factors. For decades, the idea that saturated fats increase cardiovascular risk has been based primarily on observational studies conducted in the 20th century, which found an association between higher consumption of these fats and higher cardiovascular disease. Saturated fatty acids (saturated fats) are a type of fatty acid found in animal foods (such as meat and dairy products) and in some vegetable oils (such as coconut and palm oil). These lipids are characterized by the absence of double bonds in their carbon chain, which gives them a stable structure and makes them part of cell membranes. Saturated fats have traditionally been attributed with a hypercholesterolemic effect, as it has been observed that their consumption can increase plasma levels of total cholesterol and, in particular, LDL lipoproteins. This effect has been interpreted as a mechanism that would explain an increased cardiovascular risk. Possible pro-inflammatory effects of some of these fatty acids at the cellular level through receptors such as TLR4 have also been investigated. On the other hand, different saturated fatty acids may also have positive functions, for example at the structural level by stabilizing cell membranes and participating in the physiological and endocrine functions of lipid rafts, in addition to other biological effects by modulating the microbiota, immunity, and inflammation.STUDY
A recent systematic review and meta-analysis (Yamada et al., 2025) evaluated the impact of reducing saturated fat intake on cardiovascular disease and overall mortality. The analysis included nine randomized clinical trials involving more than 13,000 adults, mostly people with a history of myocardial infarction or stable coronary heart disease, from Europe, the United States, Australia, and India. The interventions consisted of reducing the energy intake from saturated fats through diets low in animal fats, with partial replacement by vegetable oils rich in polyunsaturated fatty acids, varying both the degree of restriction and the duration of follow-up (2 to 8 years). The control group generally maintained a usual diet, without specific restrictions. The main outcomes were cardiovascular mortality, total mortality, myocardial infarction, and major coronary events. Stroke was evaluated in fewer studies.MAIN RESULTS
The results showed that reducing saturated fat was not associated with a significant decrease in all-cause mortality or cardiovascular mortality compared with the control groups. No dose-response relationship was observed between the magnitude of the reduction in saturated fat intake and the risk of the outcomes analyzed. Excluding studies with a high risk of bias did not substantially alter the results, although most studies had methodological limitations. The results are nevertheless consistent with previous systematic reviews of controlled studies and with other lines of research showing that reducing fat in general does not reduce mortality.CONCLUSION AND CLINICAL RELEVANCE
Given that this negative view of saturated fat has been widely disseminated in medical and nutrition schools, as well as by various medical and scientific associations, we would like to make some important comments. The results of the meta-analysis by Yamada et al 2025, although the conclusion is not new compared to other systematic reviews conducted in recent years, once again question traditional recommendations based on limiting this nutrient as a central pillar of cardiovascular prevention. While there have been epidemiological studies that have shown positive associations with cardiovascular risk, these differences, apart from being small and observational in nature, are less than the potential effect of multiple uncontrolled confounding factors. Conversely, evidence from controlled studies does not support the reduction of saturated fat as an effective strategy for reducing overall mortality or cardiovascular mortality.There is an extensive previous meta-analysis conducted by the Cochrane group (Hooper et al, 2020), which shows consistent results for all-cause mortality and cardiovascular mortality. However, comparing the two systematic reviews, we find some relevant differences. For example, there are important studies not included in the most recent meta-analysis by Yamada et al, such as the Women's Health Initiative 2006, Ley et al, 2004, or the Women's Intervention Nutrition Study 2006. These studies are relevant because they are more recent than most of the clinical trials included in both reviews and because they have greater potential weight for the combined effect than the entire meta-analysis by Yamada et al. However, the results of these studies are consistent with the overall conclusions, finding no significant effects, so their inclusion does not change the conclusions. The reason for the exclusion of these studies from the meta-analysis by Yamada et al. is the more stringent inclusion criteria, limiting the clinical trials included to those with saturated fat restriction as a specific objective, while the Cochrane review includes studies with broader dietary interventions in which there is a reduction in saturated fat. However, the Cochrane review also includes a subgroup analysis selecting studies with the specific objective of reducing saturated fat, again without changing the conclusions.
Among the main limitations of the meta-analysis by Yamada et al. are the age of the included trials and the absence of pre-registration. However, when comparing older and more recent studies, no major differences in conclusions were found. Given the type of intervention and the impossibility of blinding participants in a nutritional protocol, no trial was rated as low risk of bias in all domains. Nevertheless, the studies cover a large sample size, and mortality is a variable less subject to bias. Although most of the interventions were carried out in secondary prevention settings, two clinical trials were primary prevention trials, with no significant differences from the effect observed in the other studies. Another relevant limitation is that a dietary intervention does not reduce saturated fat in isolation, but rather replaces some foods with others. In most studies, saturated fat was restricted by replacing it with polyunsaturated fats. However, Hooper's subgroup analysis in Cochrane shows that the conclusions do not vary significantly according to the type of replacement macronutrient. In fact, the effects found are robust, with the same conclusions being maintained in virtually all additional comparisons made: cholesterol reductions achieved, risk of bias, duration of follow-up in the various studies, sex, etc. Another limitation of the studies is that there are different saturated fatty acids, with different biological effects, and some are part of healthier foods than others.
While replacing saturated fats with unsaturated fats or certain types of carbohydrates can lower LDL cholesterol, this reduction does not necessarily translate into a lower incidence of cardiovascular events or mortality. The mechanistic logic implicitly learned in medical and health science schools is a substantial part of the problem, promoting constant inductive reasoning from the particular, beginning on the very first day of class. Evidence-based medicine requires deductive reasoning from a major premise supported by clinical consequences, reaching a conclusion through the minor premise. The opposite involves speculative reasoning based on a reductionist assumption. This does not mean that it is the only way to reason, but it must begin by studying the evidence on hard outcomes that have been systematically investigated in the first place. Psychologists dedicated to the study of logic and decision-making have been studying the well-documented problems of probabilistic reasoning in physicians for approximately 50 years. For some reason, medical schools have not sought to address this issue through specific courses on epistemology and logic applied to clinical practice. What's more, students leave university without having even systematically studied the evidence for interventions, or the entire biochemical narrative that is taken for granted. It's the same as saying that evidence-based medicine sells fewer drugs than medicine based on biochemical allegories and interventions aimed at modifying markers using reductionist inductive logic. Go figure. The same logical scheme applies to nutrition: eating good foods is more important than reducing saturated fats or cholesterol in blood tests, as reductionist reasoning dictates.
In short, controlled studies to date show that trying to reduce saturated fat in diets has no significant impact on mortality. Even if new controlled studies were to yield different results, we do not expect large absolute differences in the conclusions. Probabilistic logic makes it clear that an isolated element from a huge set of nutrients involved in a physiology driven by homeostasis must translate into small risk ratios. The difficulties in estimating effects tend to lead to overestimation of minor aspects and underestimation of what is most relevant, so the findings of these studies are more important when you consider that there are clearer ways to reduce mortality and cardiovascular risk than reducing saturated fat intake: increasing daily vegetable consumption, reducing consumption of ultra-processed products (including those marketed as containing "polyunsaturated fat"), or consuming a little extra virgin olive oil every day, to name three of the most basic. The rest is confusing the order of priorities. The overall dietary context is more important than the biochemical category of a nutrient, and the same can be said for ultra-processed foods, where it matters little whether they are produced with saturated or unsaturated fats (industrial trans fats are another matter). At ICNS, we have been exposing the reality behind the claims about fats promoted by experts who claim to represent "science" without any evidence for over a decade. The promotion of certain food products and the festival of drugs prescribed under criteria of analytical modification may have something to do with it.
#saturatedfats #cardiovasculardisease
References:
Yamada, S et al, 2025. Saturated Fat Restriction for Cardiovascular Disease Prevention: A Systematic Review and Meta-analysis of Randomized Controlled Trials. JMA Journal, 8(2), 395-407. https://doi.org/10.31662/jmaj.2024-0324
Hooper, L., Martin, N., Jimoh, O. F., Kirk, C., Foster, E., & Abdelhamid, A. S. (2020). Reduction in saturated fat intake for cardiovascular disease. Cochrane Database of Systematic Reviews, (8). Art. No.: CD011737. https://doi.org/10.1002/14651858.CD011737.pub3

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