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Nutritionists, clinicians and researchers know the term "saturated fat" causes more confusion than almost any other topic in nutrition. In one way or another, saturated fat has been described as either the major cause of coronary artery disease or a falsely accused nutrient that has been cleared by today's research.
Some of this confusion stems from the fact that studies (and especially studies referred to as meta-analysis) don't always seem to agree. However, when you consider the quality of each individual study, what replaced the saturated fat in the diet, and how heart disease occurs, things start to clear up.
The easiest way to summarize the information is not to state that saturated fat is uniquely toxic in every situation, nor is it harmless. Instead, the evidence shows that saturated fat typically increases LDL (low-density lipoprotein), LDL is directly involved in atherosclerosis and decreasing saturated fat will be more meaningful to some people than others based on their risk of developing cardiovascular disease.
During the last half of the 20th century, cardiovascular disease moved from being one of the least common causes of death to becoming one of the most common. As a result, there was increased focus on the relationship between diet, blood cholesterol and the development of atherosclerosis. While the primary concern was not saturated fat alone, the concern was whether saturated fat contributed to the types of lipoproteins that would increase the risk of having a heart attack or stroke.
Ancel Keys was a significant figure in the history of the diet-heart concept. His proposal suggested that saturated fat consumption would increase blood cholesterol, particularly LDL related particles, and subsequently lead to atherosclerosis. This concept came to be known as the diet-heart hypothesis.
Keys' Seven Countries Study provided significant support for his hypothesis. The study demonstrated that populations consuming more saturated fat experienced greater cholesterol levels and greater incidence of heart disease. As a result, the diet-heart concept became deeply embedded in public health policy recommendations.
Criticisms of the diet-heart concept have been voiced for decades suggesting that the case against saturated fat was exaggerated. Recent meta-analyses have continued to fuel the debate, as these analyses appear to show less or no benefit to reducing saturated fat intake. These results create the perception that the scientific community is hopelessly divided.
However, the disagreement surrounding the science is often less about the basic biology of LDL and atherosclerosis and more about which clinical trials are used in the analysis, the length of time the subjects participated in the clinical trial, the nature of the diets compared in the clinical trial, and whether the nutrient used to replace the saturated fat was truly healthier.
There is one key point to understand here. Many of the largest randomized controlled trials (RCTs) examining saturated fat have been completed decades ago. There is therefore not a large pool of recent RCTs to draw upon. Consequently, meta-analyses often draw upon overlapping sets of older studies. Therefore, small differences in the inclusion criteria of the studies can sometimes dramatically alter the outcome of the meta-analysis.
To illustrate, one meta-analysis might include a large, older study that has several design flaws, while another meta-analysis excludes the study because the intervention period was too brief or because the replacement fat contained harmful trans fats. This is not necessarily cherry-picking; it is more likely due to a systematic application of quality assessment criteria.
An example that is often cited is the Minnesota Coronary Survey. This study is well-known for several reasons including the size of the study population and the significant limitations inherent in the design. The average participant was exposed to the experimental diet for a relatively short duration. A significant number of the participants were young and therefore had a very low short-term risk of a heart attack. The experimental diet included a type of margarine that contained high amounts of trans fats. Participants did not consistently consume the experimental diet outside of the institutional setting.
Each of these issues matters. If the replacement diet contains trans fats, or if the study is too short to measure any clinically significant cardiovascular benefits, the results of the study are difficult to interpret. Because of these issues, many evidence-based reviews of higher quality often exclude older studies that continue to shape the arguments made on-line.
In general, when the results of high-quality, randomized-controlled trials are pooled together, the cumulative effect is that reducing saturated fat reduces the risk of combined cardiovascular events.
It is essential to note that this does not imply that reducing saturated fat produces a significant reduction in total mortality in every trial. Additionally, it does not imply that saturated fat is the sole dietary variable that affects cardiovascular health. It does indicate that reducing saturated fat has real-world cardiovascular implications. The explanation for this phenomenon is simple. When saturated fat is replaced with unsaturated fats, specifically polyunsaturated fats, LDL cholesterol decreases and that decrease in LDL cholesterol should reduce cardiovascular risk over time.
The saturated fat debate is often framed as if it is independent of lipoprotein biology. However, it is not. The strongest evidence supporting the limitation of saturated fat comes from the fact that saturated fat generally increases LDL cholesterol, and LDL plays a direct causal role in the development of atherosclerosis.
Multiple lines of evidence demonstrate the causal role of LDL in atherosclerotic cardiovascular disease. These include:
At this point, whether LDL plays a causal role in atherosclerotic cardiovascular disease is not highly disputed within mainstream cardiometabolic science.
Therefore, if a dietary component increases LDL cholesterol, this is an important consideration.
While observational studies cannot provide sufficient evidence on their own, they can contribute to understanding the relationships between dietary components and cardiovascular disease. Large cohorts have shown that replacing saturated fat with unsaturated fat is associated with lower risks of death and lower cardiovascular risk over time. Again, this is not conclusive evidence by itself. However, when the results of these studies align with both the biological mechanisms and the findings of clinical trials, the overall picture is strengthened.
One of the most common arguments made on-line is that elevated LDL cholesterol does not matter if everything else is in balance. If you are lean, insulin-sensitive, active and metabolically healthy, the argument suggests that elevated LDL is unimportant or of no consequence.
This is overly simplistic. Imaging studies, such as the PESA study, suggest that atherosclerotic plaque can form at LDL cholesterol concentrations > 50-60 mg/dL, even in the presence of otherwise favorable risk profiles.
This does not mean that every person with a modest elevation in LDL cholesterol who is otherwise healthy is immediately at risk. However, it does mean that LDL continues to play an important role, even in the context of otherwise good health.
This is where the nuanced approach becomes important. Reducing saturated fat is likely to be more beneficial for individuals with higher cardiovascular risk than for individuals with lower cardiovascular risk over short follow-up periods. For instance, for a young person with a low risk of cardiovascular disease, making the effort to significantly reduce saturated fat may yield little to no measurable benefit in terms of cardiovascular health over a five-year period. However, for an older adult with higher LDL cholesterol, a positive family history of cardiovascular disease, hypertension, diabetes, or existing vascular disease, the same reduction in saturated fat may make a significant difference.
This is how many preventive interventions function. Their effectiveness depends on the level of the individual's baseline risk.
Regardless of the degree of support for the case against saturated fat, the limitations of using saturated fat as the sole focus of cardiovascular prevention cannot be overlooked. Other critical elements of cardiovascular prevention include:
This is important since many individuals become focused on whether an individual’s nutrient intake is adequate and fail to consider some of the other (potentially) much stronger influences on risk.
In the end, the saturated fat debate seems to be less about real scientific controversy, and more about what appears to be a lot of noise. It appears that there is strong evidence to suggest that saturated fat is not necessarily safe for all populations, and also, that it is certainly not the only dietary concern.
A more reasonable interpretation is that saturated fat impacts our body by increasing our LDL-cholesterol levels, and that LDL-cholesterol increases plaque development. Reducing saturated fat intake, especially when saturated fat is replaced with unsaturated fat, can reduce cardiovascular risk, especially for those populations at a higher risk for developing cardiovascular diseases. While reducing saturated fat intake may have a smaller effect on individuals who are considered at a lower cardiovascular risk, this does not diminish the fact that saturated fat affects our cardiovascular system.
Using a pattern-based approach rather than absolute thinking will allow you to better understand the relationships among saturated fat intake, LDL-cholesterol levels, and cardiovascular disease. As mentioned earlier, saturated fat is just one of the potentially modifiable components within an overall cardiovascular disease risk profile, and not a single entity that represents a villain or a completely innocent nutrient.