What you know about saturated fats might be wrong

Cholesterol
Chronic diseases
Healthy eating
saturated fat image by kerdkanno
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Dietary recommendations for Canadians to limit their intake of saturated fatty acids (SFAs) to reduce their risk of cardiovascular disease (CVD) are unsupported by science. Here, we dismantle the three major premises that underlie current SFA recommendations.

Premise 1: Reducing dietary intake of SFAs will reduce levels of LDL, which leads to a reduced risk of CVD

Also known as the diet-heart hypothesis, this premise is limited by several observations. First, the causal link between serum LDL and CVD risk remains unestablished: a large RCT including 48,835 postmenopausal women demonstrated that a low SFA intervention decreased serum LDL without reducing CVD risk [1].

Second, despite the unclear relationship between serum LDL and CVD risk, many RCTs measure only markers of CVD without measuring any CVD-related outcomes [11].

Third, many RCTs do not distinguish between large buoyant (lb) vs. small dense (sd) LDL particles, even though sd-LDL particles are more atherogenic and predictive of CVD risk than total LDL and lb-LDL [2,4,11]. In fact, contrary to the diet-heart hypothesis, dietary SFAs primarily increase lb-LDL, rather than atherogenic sd-LDL [2].

Fourth, many RCTs investigating low SFA interventions replaced dietary SFAs with polyunsaturated fatty acids (PUFAs) and consistently observed reduced serum LDL and CVD risk [17-20]. However, it remains unclear whether it was the reduced SFA intake or the added cardioprotective PUFAs that actually caused the CVD benefits [11].

Finally, the remaining evidence in support of this premise is derived from observational studies. However, interpretation of causality and generalizability is strongly limited by multiple confounders (e.g. the healthy user bias), the lack of valid tools to reliably adjust for confounding variables, and methods of measuring dietary intake that are susceptible to self-reporting bias.

Overall, the diet-heart hypothesis remains unestablished and requires further investigation.

Premise 2: All SFAs have the same effects on cardiometabolic health

The blanket recommendation to limit SFA intake implies that all SFAs, regardless of type or dietary source, can be treated as a single nutrient with uniform consequences for health. This assumption is false. For example, myristic and palmitic acids increase serum LDL, but stearic acid has a neutral effect and dairy-derived pentadecanoic and heptadecanoic acids improve lipid profile and reduce CVD risk [3,4,8-11]. Treating an entire class of SFAs as if they were a single nutrient is simplistic, confounds the literature, and risks misleading the Canadian population.

Premise 3: There is no potential harm in limiting SFA intake

Research and public health have emphasized the harmful effects of overconsuming SFAs, but have largely ignored the potential risks of underconsuming SFAs. However, decreasing SFA intake has been linked to increased risk of stroke [12-14]. Further, multiple large, recent observational studies have shown that limiting SFA intake actually increased risk of CVD, likely since participants tended to replace SFA-rich foods with refined carbohydrates [11,15,16]. More research is required to justify the blanket recommendation that all Canadians limit their SFA intake to the greatest extent possible.

Making sense of the controversy

The Homeoviscous Adaptation to Dietary Lipids (HADL) model has recently emerged, arguing that LDL levels fluctuate in response to changes in dietary intakes of SFAs to maintain optimal membrane fluidity across all cells and tissues [4]. The HADL model refines our understanding of the link between SFAs and LDL by reframing elevated LDL as a feature of adaptive homeostasis, rather than a necessarily pathological marker.

People eat food, not nutrients

Blanket recommendations for Canadians to limit their intake of SFAs are unsupported by adequate evidence, and healthcare professionals should be wary that giving patients overgeneralized dietary recommendations is ineffective and potentially harmful. Instead, we advocate for comprehensive interventions that focus on the totality of the diet and are tailored to the individual’s unique biology, priorities, and lifestyle. Our team of dietitians at ÉquipeNutrition are experts at adapting our practice to the cutting edge of nutrition science and coordinating with fellow healthcare professionals to provide quality, evidence-based, and personalized nutrition therapy to help your patients achieve cardiometabolic health.

To learn more about TeamNutrition and our services, contact us here!

This article was written by our intern, Tim Leung, under the supervision of Genevieve Marchand, Dt.P.

References 

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2.    Ivanova, E. A., Myasoedova, V. A., Melnichenko, A. A., Grechko, A. V., & Orekhov, A. N. (2017). Small dense low-density lipoprotein as biomarker for atherosclerotic diseases. Oxidative medicine and cellular longevity, 2017.
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Registered Dietitian Nutritionist