Butter, a myth to debunk: protects against diabetes and is heart-friendly

Editorial note: this article was previously published and has been updated according to scientific and divulgative criteria. The text is for informational purposes only and does not replace professional medical advice.

IN BRIEF

• Butter is a food source of saturated fatty acids, short-chain fatty acids (like butyrate), and fat-soluble vitamins; its Intake should be evaluated in the context of the overall diet.
• While observational studies show mixed results, meta-analyses and large cohorts indicate weak or no associations between moderate butter consumption and cardiovascular risk; however, recent results suggest that replacing butter with unsaturated vegetable oils is associated with a lower risk of mortality.
• Butyric acid (butyrate), produced by the gut microbiota or present in small amounts in milk fats, has plausible biological functions supporting the intestinal barrier and metabolism; causal clinical evidence in humans is still limited.
• Nutritional recommendations advise caution: prefer unsaturated fat sources, limit but do not demonize single foods, and consider individual needs and the overall dietary context.

Abstract: what does science say?

The topic concerns three related areas: butter composition (fats, vitamins, traces of butyrate), plausible biological effects of butyrate and short-chain fatty acids on the gastrointestinal tract and metabolism, and epidemiological evidence linking butter consumption to mortality, cardiovascular disease, and diabetes. Large-scale systematic reviews have shown weak or no associations between moderate butter consumption and cardiovascular risk, and some signals of reduced diabetes risk in certain observational studies; however, more recent studies on large cohorts indicate that replacing butter with non-hydrogenated vegetable oils is associated with reductions in mortality. Mechanistic studies and some interventions with butyrate in animals and small human trials indicate favorable effects on the intestinal barrier, inflammation, and metabolic parameters, but definitive clinical evidence is limited. Therefore, current science describes biological plausibility and epidemiological associations, but does not prove universal causal effects independent of dietary context and lifestyle.

Composition and biological functions of butter

Butter is a lipid-concentrated food derived from milk cream. It predominantly contains saturated fatty acids, a percentage of monounsaturated fatty acids, and traces of polyunsaturated fats, in addition to fat-soluble vitamins (A, E, and to a more limited extent D) and small lipid compounds including portions of short-chain acids and particular acids like conjugated linoleic acid (CLA). The food matrix of butter (the combination of lipids, water, and minor components) influences nutrient digestion and absorption: it differs from a pure vegetable oil, and this can also modify short-term metabolic effects. It is important to consider butter as part of an overall dietary pattern, not as a single determinant of health.

The role of butyric acid and SCFAs

Among the compounds present in milk fat and produced by the gut microbiota, butyrate (butyric acid) has attracted interest for its biological functions: it is a preferred energy source for colonocytes, contributes to the regulation of the intestinal barrier, and modulates immune responses and inflammatory processes through metabolic and epigenetic signals. Reviews on SCFAs show that these molecules participate in signaling pathways that can influence metabolism, inflammatory tone, and tissue function, but local concentration, source (microbial production vs direct ingestion), and systemic distribution are critical determinants for the final effect [1][2].

Microbiota, intestinal barrier, and extra-intestinal tissues

Products of microbial fermentation, including butyrate, influence intestinal permeability, the production of anti-inflammatory molecules, and communication with organs such as the liver, adipose tissue, and muscle through metabolic signals and specific receptors. Experimental evidence and reviews indicate that adequate levels of SCFA production promote mucosal integrity and can reduce systemic activation of inflammatory circuits related to insulin resistance and metabolic dysfunction; however, direct translation into clinical interventions is still preliminary [1][2][3].

Epidemiological evidence on mortality, heart, and diabetes

The observational literature on butter consumption is extensive and complex. A meta-analysis of over 600,000 participants concluded that the link between butter consumption and cardiovascular disease is weak or absent, with a very modest association towards increased mortality for high doses; in some studies, a slight reduction in diabetes risk was observed associated with higher butter consumption, but the results were heterogeneous [4]. More recently, analyses of large US cohorts found that higher butter consumption is associated with increased total mortality and mortality from certain causes, while Intake of unsaturated vegetable oils was associated with lower risk; the authors highlighted that the choice of replacement fat is crucial in interpreting the effects on the population [5]. Comparisons between studies are affected by differences in eating habits, measurement methods, and comparisons (e.g., butter vs. other foods), necessitating careful epidemiological interpretation.

Observational studies and meta-analyses on butter and mortality

The reference meta-analysis calculated relative risks for standardized consumption (corresponding to approximately one serving/pat of butter) and showed generally mild associations: some studies indicated a slight increase in mortality for very high doses, while others showed no significant effects on cardiovascular events. These results support a modest effect dependent on the overall dietary context rather than a strong, independent effect of butter [4].

Recent data and comparison with vegetable oils

An analysis of updated cohorts highlighted that the energetic replacement of butter with unsaturated vegetable oils (e.g., olive oil, canola oil, soybean oil) is associated with measurable reductions in total and cause-specific mortality; this does not contradict the biological plausibility of butyrate but strengthens the evidence that the profile of substitute fatty acids matters greatly in public health translation [5].

Nutritional aspects: vitamins, lactose, CLA, and performance

Butter contains fat-soluble vitamins (A, E, and partly D), mainly present in the fat fraction; in practical terms, it can contribute, to a small extent, to the Intake of these vitamins in a varied diet. Lactose is present in reduced quantities compared to whole milk, so some people with mild intolerance tolerate butter better than milk. Conjugated linoleic acid (CLA), present as a minor component in milk fats, has been studied for possible effects on body composition, metabolism, and inflammation: reviews of trials indicate modest effects on fat mass and insulin resistance in specific contexts, but this evidence is not sufficient to recommend supplementation or targeted butter consumption for these purposes [6][7].

Vitamins and lactose tolerance

Vitamins A and E are naturally present in butter and can contribute to daily Intake, especially when the diet is limited. The European Food Safety Authority (EFSA) and other institutional sources list dairy products among the food sources of retinol (vitamin A), while emphasizing that levels can vary depending on animal feed and production processes [8].

CLA, physical activity, and performance

Clinical studies and meta-analyses on CLA (generally from supplementation) suggest modest effects in reducing fat mass and improving insulin sensitivity in specific subgroups; however, the majority of evidence does not support the use of butter as a performance 'supplement': the overall energy contribution and lipid profile must be evaluated within the individual nutritional plan [9].

What it means in practice

For the general population, the practical message is one of balance and context. Butter is neither a 'miraculous' food nor a universal 'poison': consumed in moderate portions and included in a diet rich in vegetables, fruits, whole grains, legumes, fish, and unsaturated vegetable oils, it has not been shown to solely cause a strong increase in cardiovascular risk. If one chooses to reduce butter, replacement with unsaturated vegetable oils (e.g., raw olive oil) is supported by evidence linking such replacements to lower mortality in the observed population [5][7]. In practical terms: evaluate the total fat content and type of fats in the overall diet; prefer unsaturated fats for cooking and seasoning when the goal is cardiovascular health; for those who engage in long-duration sports, butter can be a dense caloric source but must be considered within the overall energy plan. In cases of clinical conditions (familial hypercholesterolemia, known cardiovascular disease, advanced type 2 diabetes), it is advisable to discuss the appropriate quantity and food substitutions with a healthcare professional.

KEY POINTS TO REMEMBER

• Butter contains saturated fats, fat-soluble vitamins, and small amounts of short-chain acids; its effect on health depends on the dietary context.
• Observational evidence and meta-analyses show generally weak associations between moderate butter consumption and CVD; replacement with unsaturated vegetable oils is associated with mortality benefits in large cohorts [4][5].
• Butyrate has plausible biological functions on the intestinal barrier and inflammation, but clinical evidence in humans is preliminary and varies between healthy and metabolic subjects [1][3].
• There are no simple universal rules: prefer recognized dietary patterns (e.g., Mediterranean), limit but do not demonize single foods, and adapt choices to personal conditions.

Limitations of the evidence

It is crucial to distinguish observational studies from causal evidence: cohort studies can show associations but do not uniquely prove that a food causes an effect. Meta-analyses aggregate data with different methods and depend on the quality and homogeneity of the included studies; moreover, residual confounders (lifestyle, dietary pattern, socioeconomic status) can influence the results. Heterogeneity in Intake measures (food questionnaires, time intervals), in the choice of comparisons (butter vs. average diet or butter vs. vegetable oils), and in the studied populations limits general applicability. Randomized clinical interventions, especially long-term ones with objective measures of exposure and outcome, are still scarce for defining direct causal effects of butter on long-term risk [10]. Furthermore, biological mechanisms (for example, the role of microbiota-produced metabolites like butyrate) are plausible, but their translation into clinical effects depends on dose, duration, bioavailability, and individual metabolic state. For these reasons, clinical recommendations prioritize the adoption of overall healthy dietary patterns rather than exclusive focus on a single food.

Editorial conclusion

Butter cannot be described with a clear 'good' or 'bad' judgment without considering the total diet, the type of individual, and practical alternatives. Current science documents biological plausibility (for example, through the actions of butyrate and SCFAs) and epidemiological associations that vary depending on the chosen comparison. For most people, the most prudent approach is to use butter in moderation and, when possible, prefer non-hydrogenated vegetable oils for dressing and cooking if the goal is cardiovascular disease prevention. Individual decisions regarding quantity and frequency should be discussed with a healthcare professional in the context of medical history and nutritional goals.

Editorial note

This article is an updated version of a previously published text. The update was carried out following criteria of transparency, source verification, and institutional divulgative language. The information reported here is for informational purposes and does not replace personalized medical consultation.

SCIENTIFIC RESEARCH

1. Liang C-W, Cheng H-Y, Lee Y-H, et al. Effects of conjugated linoleic acid and exercise on body composition and obesity: a systematic review and meta-analysis. Nutrition Reviews. 2023. https://doi.org/10.1093/nutrit/nuac060
2. Gao Z, et al. Short-chain fatty acids and their association with signalling pathways in inflammation, glucose and lipid metabolism. International Journal of Molecular Sciences. 2021;21(17). https://doi.org/10.3390/ijms21176356
3. Bouter KE, et al. Differential metabolic effects of oral butyrate treatment in lean versus metabolic syndrome subjects. Clinical and Translational Gastroenterology. 2018;9:e155. https://doi.org/10.1038/s41424-018-0025-4
4. Pimpin L, Wu JHY, Haskelberg H, Del Gobbo L, Mozaffarian D. Is butter back? A systematic review and meta-analysis of butter consumption and risk of cardiovascular disease, diabetes, and total mortality. PLoS ONE. 2016;11(6):e0158118. https://doi.org/10.1371/journal.pone.0158118
5. Zhang Y, et al. Butter and Plant-Based Oils Intake and Mortality. JAMA Internal Medicine. 2025;185(5):549–560. https://doi.org/10.1001/jamainternmed.2025.0205
6. Soedamah-Muthu SS, et al. Dairy consumption and risk of type 2 diabetes mellitus: a meta-analysis of cohort studies. European Journal of Clinical Nutrition. 2011. https://doi.org/10.1038/ejcn.2011.62
7. Sacks FM, Lichtenstein AH, Wu JHY, et al.; American Heart Association. Dietary fats and cardiovascular disease: a presidential advisory from the American Heart Association. Circulation. 2017;136(3):e1–e23. https://doi.org/10.1161/CIR.0000000000000510
8. EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA). Scientific opinion on the tolerable upper intake level for preformed vitamin A and β‑carotene. EFSA Journal. 2024. https://doi.org/10.2903/j.efsa.2024.8814
9. Nature Metabolism. Short-chain fatty acids as potential regulators of skeletal muscle metabolism and function. 2020. https://doi.org/10.1038/s42255-020-0188-7
10. Harcombe Z, et al. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ. 2015;351:h3978. https://doi.org/10.1136/bmj.h3978

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