Sarah Rice BSc. (Hons), MCOptom (UK), MHP, NNP

Introduction

Two recent papers have drawn attention to the contentious dietary guideline position on saturated fat restrictions, highlighting the complex relationship between saturated fat and cardiovascular disease (CVD) (1, 2).

The diet-heart hypothesis emerged in the 1950s, focusing on saturated fat as a potential driver of heart disease. Based on limited data, the 1977 Senate report influenced dietary guidelines in the US and the UK, where restrictions on saturated fats in the diet were established (3). Investigation uncovered various conflicts of interest and a lack of data which have continued to influence policy on this subject (4). A long history of papers – systematic reviews and meta-analyses, randomised trials, and observational studies – have found no benefit in reducing saturated fat intake for cardiovascular disease (CVD), cardiovascular mortality, or total mortality (2, 4, 5).

Drivers of the diet-heart hypothesis

The cornerstone of the diet-heart hypothesis is based on the potential influence of saturated fats on serum cholesterol levels, particularly LDL-c, which has historically been a key metric for assessing CVD risk. While reducing saturated fat in the diet may lower LDL-c levels, the data indicate that it is primarily the large buoyant LDL subtype that decreases (along with HDL-c), while there is no change in the more risky small dense LDL subtype (1, 5). Lowering LDL-c (which is a poor marker of CVD risk when considered in isolation) does not necessarily reduce CVD events, necessitating a more critical examination of the data (5, 6).

A closer look at saturated fat

Saturated fats contain saturated fatty acids (SFAs) that have important biological roles, such as supporting cell membrane stability, cellular signalling, and immune function. SFAs are derived endogenously and exogenously and may be classified according to their carbon chain length. These variations – short-chain, medium-chain, or long-chain SFAs – are contained in foods in different combinations, which yield different metabolic effects. Recently, C15 (pentadecanoic acid) has been investigated for its beneficial effects, and it has been suggested it may be an essential fatty acid. This SFA may be found in dairy, ruminant meat, and some plants; foods that are often associated with carbohydrate-reduced eating plans (1, 5).

Another study examining the association between low-fat versus regular dairy products in the diet and CVD (Lamarche et al., 2025) concludes, ‘Differentiating low-fat from regular-fat dairy in dietary recommendations is currently not supported by the available evidence in adults’ (7). The metabolic impact of fat in the diet is a complex interplay between individual physiology, the food matrix (whole food sources versus processed), and the amount of carbohydrate in the diet (5).

Though dietary cholesterol may be increased on a carbohydrate-reduced diet, it is not linked to increased blood cholesterol or CVD risk, and the body regulates cholesterol levels through feedback mechanisms. In acknowledgement of this, the U.S. dietary guidelines have removed limits on dietary cholesterol, stating it is ‘not a nutrient of concern for overconsumption’ (1). 

The effect of TCR on CVD risk

While TCR may include higher levels of dietary SFAs, as mentioned, the effect of saturated fat on LDL cholesterol is inconsistent, and changes in LDL-c do not reliably predict CVD risk (5, 6). In fact, increased saturated fat intake often raises HDL cholesterol, which is beneficial, and reducing dietary carbohydrates typically improves LDL subtypes and increases HDL-c, regardless of fat intake (1, 5). In addition to improved cholesterol profiles, TCR also improves other key cardiovascular risk factors, including weight, visceral fat, blood glucose, and insulin metrics (1, 6). Of note is that insulin resistance is a significant and independent risk factor for CVD, reliably improved through carbohydrate reduction (1, 6, 8).

For a small subset of individuals adopting TCR, this dietary change may increase LDL-c alongside improvements in triglycerides and HDL-c. Available evidence points to improved metabolic health and no association of LDL-c with plaque burden in this population (9); however, more data are needed, and further studies are underway. It is prudent to monitor metabolic markers and evaluate dietary effects according to personalised risk-benefit metrics, which may include coronary artery calcium (CAC) or other imaging. 

Overall, the TCR has been shown to be a safe and effective option for improving cardiometabolic health with data extending into the longer term (1, 6). Other considerations include personal preferences and competing conditions, such as the use of a ketogenic diet to manage psychiatric conditions (10).

Recent review

A recent systematic review and meta-analysis on the topic was prompted by the controversy over whether reducing SFA intake lowers CVD risk, how changes in LDL-c from lowered SFA intake relate to outcomes, and whether guidelines should set SFA targets (2). This review focused on randomised controlled trials and included nine RCTs, with a total of 13,532 adult participants (mostly in secondary prevention settings). The intervention involved restricting SFA intake, often by replacing it with unsaturated fats or other macronutrients. The primary outcomes assessed were cardiovascular mortality, all-cause mortality, myocardial infarction, and coronary artery events. The meta-analysis found no statistically significant reduction in cardiovascular mortality (OR = 0.94), all-cause mortality (OR = 1.01), myocardial infarction (OR = 0.85), or coronary artery events (OR = 0.85) with SFA reduction compared to control diets. The effect on stroke could not be evaluated due to limited data. Only one study included participants on statin therapy, and it showed no difference in outcomes. The authors conclude that current evidence from RCTs does not support recommending SFA restriction for CVD or mortality prevention, stating further clinical trials are required to justify maintaining a cap on SFA consumption and to inform on areas where data is lacking. These conclusions add to other findings, where the majority of the data show no effect of SFA intake on cardiovascular disease, cardiovascular mortality or total mortality (4, 5).

Conclusion

The totality of evidence does not support concerns around saturated fat consumption with regard to CVD risk, especially in the context of low-carbohydrate diets. Monitoring individuals’ responses to dietary changes, including various health metrics, helps guide personalised support that acknowledges patients’ preferences and any competing conditions.

Resources

A new training module, Cardiovascular Health: A Metabolic Perspective, launches on 28 August 2025. This course examines the science of insulin resistance – a key driver of inflammation, endothelial dysfunction, atherosclerosis, and hypertension. This course encourages reevaluation of cardiovascular care with evidence-based insights from leading clinicians and researchers in cardiology, nutrition, and endocrinology.

References

1. Rice, S.M. and Reynolds, D.B. (2025) ‘Practical guidelines for addressing common questions and misconceptions about the ketogenic diet’, Journal of Metabolic Health, 8(1), p. 10. Available at: https://doi.org/10.4102/jmh.v8i1.113

2. Yamada S, et al. (2025) ‘Saturated Fat Restriction for Cardiovascular Disease Prevention: A Systematic Review and Meta-analysis of Randomized Controlled Trials’ (2025) JMA Journal, 8(2). Available at:  https://doi.org/10.31662/jmaj.2024-0324.

3. Harcombe, Z. et al. (2015) ‘Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis’, Open Heart, 2(1), p. e000196. Available at: https://doi.org/10.1136/openhrt-2014-000196.

4. Teicholz, N. (2023) ‘A short history of saturated fat: the making and unmaking of a scientific consensus’, Current Opinion in Endocrinology, Diabetes, and Obesity, 30(1), pp. 65–71. Available at: https://doi.org/10.1097/MED.0000000000000791.

5. Astrup, A. et al. (2020) ‘Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations: JACC State-of-the-Art Review’, Journal of the American College of Cardiology, 76(7), pp. 844–857. Available at: https://doi.org/10.1016/j.jacc.2020.05.077.

6. Diamond, D., O’Neill, B. and Volek, J. (2020) ‘Low carbohydrate diet: are concerns with saturated fat, lipids, and cardiovascular disease risk justified?’, Current Opinion in Endocrinology, Diabetes & Obesity, Publish Ahead of Print. Available at: https://doi.org/10.1097/MED.0000000000000568.

7. Lamarche, B. et al. (2025) ‘Regular-fat and low-fat dairy foods and cardiovascular diseases: perspectives for future dietary recommendations’, The American Journal of Clinical Nutrition, 121(5), pp. 956–964. Available at: https://doi.org/10.1016/j.ajcnut.2025.03.009.

8. Bonora, E. et al. (2007) ‘Insulin Resistance as Estimated by Homeostasis Model Assessment Predicts Incident Symptomatic Cardiovascular Disease in Caucasian Subjects From the General Population: The Bruneck Study’, Diabetes Care, 30(2), pp. 318–324. Available at: https://doi.org/10.2337/dc06-0919.

9. Budoff, M. et al. (2024) ‘Carbohydrate restriction-induced elevations in LDL-cholesterol and atherosclerosis: The KETO Trial’, Metabolism, 153, p. 155854. Available at: https://doi.org/10.1016/j.metabol.2024.155854.

Diamond, D.M., Mason, P. and Bikman, B.T. (2024) ‘Opinion: Are mental health benefits of the ketogenic diet accompanied by an increased risk of cardiovascular disease?’, Frontiers in Nutrition, 11. Available at: https://doi.org/10.3389/fnut.2024.1394610.