Diet and belly fat reduction: salmon, walnuts, and the role of fats

Editorial note: [This article was previously published and has been updated according to scientific and informative criteria. It is for informational purposes only and does not replace professional medical advice. For personal questions, consult your doctor or a qualified healthcare professional.]

IN BRIEF

• The quality of fats in the diet (saturated vs. polyunsaturated) can influence where body fat accumulates—not just how much weight is gained.
• Controlled clinical overfeeding studies indicate that saturated fats tend to increase liver and visceral fat more than polyunsaturated fats, even with similar weight gain. [1]
• Polyunsaturated fat intake is associated with less visceral fat accumulation and, in some studies, a greater increase in lean mass compared to saturated fats. [1][3]
• Replacing saturated fats with polyunsaturated fats is consistent with a reduction in cardiovascular risk in reviews and meta-analyses, but the effects depend on what is being replaced. [4][5]
• The evidence has limitations: many studies are short or conducted under experimental conditions (overfeeding) and do not replace individual clinical recommendations.

Abstract: what does science say?

The type of dietary fat affects not only plasma lipid parameters but also the distribution of adipose tissue. Controlled experimental studies in healthy adults show that a caloric excess primarily from saturated fats promotes a more marked increase in liver and visceral fat compared to an equivalent excess from polyunsaturated fats. Some evidence suggests that polyunsaturated fats can promote a greater increase in lean mass during overfeeding. Proposed mechanisms include changes in adipose tissue gene expression, hepatic lipid synthesis, and the production of toxic lipids (e.g., ceramides). Systematic reviews and recommendations from scientific societies recommend reducing saturated fats in favor of unsaturated fats for cardiovascular prevention, but the impact on metabolic diseases depends on the context, quantity, and substitute alternative.

Types of fats and why they matter

Dietary fats are distinguished into different chemical categories with non-identical metabolic effects. Saturated fatty acids (SFAs) are found in some animal products like butter and fatty meats, and in some tropical oils; polyunsaturated fatty acids (PUFAs), particularly n-6 (e.g., linoleic acid) and n-3 (e.g., fatty acids found in fish), are abundant in vegetable oils, nuts, and fish. Clinical research has shown that it is not only the total amount of fat that influences health, but also its composition: unsaturated fats tend to improve the plasma lipid profile compared to saturated fats and can modulate metabolic and inflammatory processes at the organ level. Scientific societies generally recommend reducing the proportion of SFAs in the diet and, when possible, replacing them with unsaturated sources such as seed oils, nuts, and fish, taking into account the overall dietary pattern and total calories. Important: the final effect depends on what is removed from the diet to compensate (refined carbohydrates, proteins, other fats) and the overall quality of the adopted dietary model.

Experimental evidence: overfeeding studies

Controlled studies that added calories in the form of different types of fat provide direct data on the possible effects of lipid quality on body fat distribution. A randomized trial in lean adults compared 7 weeks of overfeeding with extra calories from saturated fats versus polyunsaturated fats; despite similar weight gain, those who consumed more SFAs showed a greater increase in liver and visceral fat, while those who consumed PUFAs showed a greater increase in lean mass. These results indicate that the composition of fats can guide the destination of lipid deposits in the body. [1]

The Uppsala–Karolinska study: design and main results

The work conducted in collaboration between Uppsala and Karolinska Universities (an overfeeding trial with muffins enriched with palm oil or sunflower oil) involved young, normal-weight adults overfed for seven weeks. Assessments included magnetic resonance imaging to measure visceral and liver fat and gene expression analysis in adipose tissue. The main results showed that caloric excess from SFAs increased liver and visceral fat more significantly than the same calories from PUFAs, while PUFAs were associated with a relative increase in lean mass. These effects were associated with changes in the expression of metabolic genes. [1]

Replications, related studies, and population variations

Further trials and metabolomic analyses linked to the same research program have confirmed metabolic differences between SFA-rich and PUFA-rich diets, including metabolic signals related to lipid metabolism and the production of certain bioactive molecules. In overweight populations or in studies of different durations, the magnitude and sometimes the direction of effects can vary: some studies on overweight subjects have not replicated the effect on lean tissue, suggesting that baseline status, age, and other variables influence the response. [3][2]

Plausible biological mechanisms

The mechanisms explain why the type of fat can guide lipid deposition. Saturated fats promote the formation of bioactive lipids such as ceramides, molecules linked to metabolic liver dysfunction and insulin resistance; this has been observed in studies that measured changes in circulating lipid species and in the liver after SFA overfeeding. [2] PUFAs, on the other hand, appear to modulate the activity of metabolic pathways involved in lipid oxidation and gene regulation in adipose tissue and the liver, with potentially protective effects on visceral accumulation and glucose management. Alterations in adipose tissue gene expression and in local endocrine signals (adipokines) have been documented as correlated with the type of fat consumed, providing biological plausibility to clinical observations. [1][3]

Implications for metabolic and cardiovascular risk

The localization of body fat—particularly the increase in visceral and liver fat—is associated with a higher risk of type 2 diabetes and cardiovascular diseases compared to weight gain alone. Consequently, foods and nutritional patterns that promote hepatic or visceral accumulation are considered potentially harmful from a metabolic perspective. Systematic reviews and meta-analyses of randomized and observational studies have shown that replacing SFAs with PUFAs is associated with a reduction in coronary events and improvements in the lipid profile; major scientific societies recommend replacing SFAs with unsaturated fats as a strategy for cardiovascular prevention. [4][5][6]

What this means in practice

For the general public, the practical message is not prescriptive but guiding: the quality of fats in the diet can influence not only weight, but also where fat is deposited and how metabolism responds. Dietary choices that prioritize sources of polyunsaturated and monounsaturated fats (fatty fish like salmon, nuts, seeds, non-tropical vegetable oils) over sources rich in saturated fats (butter, fatty cuts of red meat, some industrial products containing hydrogenated fats or saturated oils) are consistent with available evidence for reducing cardiometabolic risk. However, it is essential to consider the overall diet: replacing SFAs with refined carbohydrates does not produce benefits; it is better to opt for substitutions with unsaturated fats or protein sources and whole carbohydrates. Choices should be adapted to one's health status, dietary preferences, and overall caloric balance. Consulting a healthcare professional provides personalized guidance.

KEY POINTS TO REMEMBER

• The quality of fats (saturated vs. polyunsaturated) influences body fat distribution and metabolism, beyond just the amount of energy consumed. [1]
• Overfeeding with saturated fats has been linked to a more marked increase in liver and visceral fat compared to PUFAs. [1][2]
• Replacing SFAs with PUFAs is consistent with a reduction in cardiovascular risk in reviews and long-term trials. [4][5]
• Effects vary based on context: baseline status, duration, calorie quantity, and what is removed from the diet to compensate. [3][7]
• Experimental evidence provides plausibility but does not replace individual clinical evaluation.

Limitations of the evidence

It is important to distinguish between different levels of evidence: observational studies show associations useful for generating hypotheses but do not prove causality; randomized clinical trials are more robust for evaluating causal effects but can be short, conducted under artificial conditions (e.g., overfeeding), and with limited numbers of participants. Many studies on the effect of fat type are short-term or aim to test metabolic responses under conditions of caloric excess; transferring these results to long-term recommendations requires caution. Furthermore, results may vary by age, metabolic status, genetic background, and overall dietary composition. Therefore, the evidence should be interpreted with prudence and integrated with established guidelines and personal clinical evaluations. [1][2][4]

Editorial transparency

This article has been updated based on peer-reviewed studies and systematic reviews available in international scientific literature. The main research cited is indicated in the "SCIENTIFIC RESEARCH" section with DOIs to allow verification. No personal data or individual clinical information has been collected or included in the text. Information on conflicts of interest and original funding can be found in the individual cited articles. Authorial data for this piece: [Authorial information not provided]. ORCID authors: [not available].

Editorial note

This article was in the archive and has been updated in light of available evidence and the most recent systematic reviews consulted during the update. The purpose is informative and divulgative; it does not provide diagnoses or personalized therapeutic indications.

SCIENTIFIC RESEARCH

1. Rosqvist F, Iggman D, Kullberg J, Cedernaes J, Johansson H-E, et al. Overfeeding polyunsaturated and saturated fat causes distinct effects on liver and visceral fat accumulation in humans. Diabetes. 2014;63(7):2356–2368. https://doi.org/10.2337/db13-1622
2. Bjermo H, Iggman D, Kullberg J, Dahlman I, Johansson L, Persson L, et al. Overeating saturated fat promotes fatty liver and ceramides compared with polyunsaturated fat: a randomized trial. J Clin Endocrinol Metab. 2019. https://doi.org/10.1210/jc.2019-00160
3. Elmsjö A, Rosqvist F, Engskog M, et al. NMR-based metabolic profiling in healthy individuals overfed different types of fat: links to changes in liver fat accumulation and lean tissue mass. Nutr Diabetes. 2015;5:e182. https://doi.org/10.1038/nutd.2015.31
4. Hooper L, Martin N, Jimoh OF, Kirk C, Foster E, Abdelhamid AS. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Syst Rev. 2020;CD011737. https://doi.org/10.1002/14651858.CD011737
5. Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010;7(3):e1000252. https://doi.org/10.1371/journal.pmed.1000252
6. Sacks FM, Lichtenstein AH, Wu JHY, et al. Dietary fats and cardiovascular disease: a Presidential Advisory from the American Heart Association. Circulation. 2017;https://doi.org/10.1161/CIR.0000000000000510
7. Sevastianova K, Santos A, Kotronen A, Hakkarainen A, Makkonen J, Silander K, et al. Effect of short-term carbohydrate overfeeding and long-term weight loss on liver fat in overweight humans. Am J Clin Nutr. 2012;96(4):727–734. https://doi.org/10.3945/ajcn.112.038695
8. Zong G, Li Y, Wanders AJ, Alssema M, Zock PL, Willett WC, Hu FB, Sun Q. Intake of individual saturated fatty acids and risk of coronary heart disease in US men and women: two prospective longitudinal cohort studies. BMJ. 2016;355:i5796. https://doi.org/10.1136/bmj.i5796

For biographical details of the original authors of the cited studies, please refer to the individual articles indicated by the DOIs above. The names and roles cited in the article are taken from the original reference text: Ulf Risérus (coordinator/researcher, cited in the source material).