The Olive Wellness Institute Scientific Advisory Panel has carefully reviewed a recent publication by Wing et al in Cell Reports of a mechanistic study in mice; results from this study have been making headlines and incorrectly claiming that olive oil can make people fat. Since, when misinterpreted, findings from this study as report in this publication could both mislead the public’s understanding of olive oil’s role in human health and potentially create confusion, the Panel’s analysis below breaks down the facts on what this study means and summarises the the well-established evidence on the positive impact of olive oil on weight management and cardiovascular health.

An example of recent headlines following the Cell Reports article publication. Source: Medical Xpress

In this publication in Cell Reports by Wing et al¹, the authors inappropriately extrapolate mechanistic animal evidence to human health outcomes: (a) “This effect on fat mass is consistent with our data showing that Oleic Acid (OA) increases adipogenesis in human and mouse APCs and with the finding that plasma MUFAs have a high hazard ratio for obesity in humans”,  (b) “As OA is increasingly being incorporated into dietary fats due to purported health benefits, our finding that OA is a unique physiologic regulator of adipose biology underscores the importance of understanding how high OA consumption affects metabolic health” and (c) “The results suggest that OA consumption plays a role in human obesity.”  These statements are potentially misleading and contradict the large body of evidence that has accumulated over decades of clinical research on the numerous health benefits, including metabolic health, imparted on humans from olive oil, whose major component is oleic acid (OA).

The study by Wing et al¹  showed that high levels of dietary OA can stimulate Adipocyte Precursor Cells (APC) and adipogenesis in male mice. While this study is informative and interesting from a mechanistic standpoint, it neither reflects how humans consume olive oil or other foods containing OA nor does it weigh the proven health effects of consuming OA in humans. The authors overreach by suggesting that this is directly relevant to human obesity. Human obesity is multifactorial, while animal models are valuable for exploring biological mechanisms, the findings from these studies often cannot be directly applied to humans.

We acknowledge that the authors present some epidemiological data from human studies to generate Hazard Ratio (HR) estimates for the association between several biomarkers, including monounsaturated fatty acids (MUFA), and overweight status and obesity (Figure 1J). Of note, the MUFA-specific HR estimate is generated from data that combines all MUFA, irrespective of their source. Further, this analysis using UK Biobank data is only adjusted for sex, UK Biobank assessment center, and age. Undoubtedly, and particularly in the case of OA from olive oil, there are other variables and parameters to consider when looking at associations with obesity and overweight status, like dietary patterns and practices.

Extrapolating a single animal study to the UK Biobank data is also problematic. The mice in this study received supraphysiological exposures under lab-controlled conditions, which are not reflective of human dietary intake, where OA intake occurs in the context of food (including extra virgin olive oil). Human health outcomes are not dictated by single fatty acids in isolation. There are dietary patterns including the Mediterranean diet, food matrices, lifestyle factors, environmental factors, genetics and more that influence the diet-health relationship in humans. Plasma MUFA concentrations are largely affected by endogenous synthesis and can be elevated with insulin resistance or other metabolic dysregulation, which can be seen in overweight status and obesity. This data does not support a role for OA in obesity, rather a potential reverse causation or confounding being highly likely. Given that endogenous OA is tightly regulated, it is unclear whether dietary OA is exacerbating a dysregulated lipid system.

The authors present data about fat depot mass in mice fed Coconut Oil, that shows difference from Standard Diet (SD). This is inconclusive about the effect of OA on obesity, particularly if one compares this result to that of lard fed animals.

The potential to misinterpret the authors’ statements and conclusions from this mechanistic study could discourage consumption of a food that, based on comprehensive evidence over the last six decades, has been shown to make a significant contribution to improving human health. This published study, not being in human nutrition, should not imply that it can extrapolate its findings to the effect in humans, within the real-world context. Oils provide more than fatty acids and olive oil in particular delivers polyphenols, tocopherols, and other bioactive compounds, with randomized controlled trial evidence of a metabolic benefit in humans. In contrast, a large population-based study published last month  by Hu et al² assessed data from over 120,000 male and female participants in the Nurses’ Health Study (NHS, 1990-2010), NHSII (1991-2015), and Health Professionals Follow-up Study (HPFS, 1990-2014) and concluded that olive oil consumption is associated with less weight gain over time, especially when olive oil was used to replace either butter or margarine. The Hu et al²  study builds on a substantial body of evidence from randomized controlled trials and long-term observational research that links olive oil to improved weight management and overall health^3-8. Additional research suggests that weight gain can be reversed by substituting carbohydrates with quality “good-fat” foods such as olive oil, avocados, nuts, and seeds⁹. Olive oil might also increase and extend feelings of satiety, while improving both body composition and blood pressure¹⁰. A recent large clinical trial assessed the effect of the Mediterranean diet on health outcomes in more than 7,000 participants in Spain, randomly assigned to one of three groups: a Mediterranean diet supplemented with extra-virgin olive oil, a Mediterranean diet supplemented with nuts, or a control group that followed a low-fat diet. The study concluded that study participants who consumed a Mediterranean diet with olive oil had the most weight loss and reduction in waist circumference, when compared to the other two groups.¹¹

From a composition perspective, olive oil is primarily made up of OA, a monounsaturated fat, which is why the FDA recognizes it as an appropriate choice for heart health. Of note, OA is found in numerous other healthy plant-based oils not just olive oil. Another recent study found that replacing less healthy fats like butter with olive oil resulted in a 15% lower risk of cardiovascular disease overall and a 21% lower risk of coronary artery disease specifically¹². Olive oil also has brain health benefits. Independent research has shown that olive oil may protect against memory deficits and Alzheimer’s and even slow the decline of Alzheimer’s in people with mild cognitive issues¹³. Additionally, a recent study found that higher olive oil intake was associated with a lower risk of dementia-related death, regardless of a person’s overall diet quality¹⁴. Moreover, the antioxidants and polyphenols unique to olive oil may protect against a host of chronic diseases like cancer¹⁵, diabetes and dementia. In fact, recent studies in patients with colon¹⁶, breast¹⁷ and prostate¹⁸ cancers all saw benefits associated with olive oil consumption.

The Wing et al¹  study has indeed identified potential mechanisms of action and impact of OA on fat cells in animal models. However, extreme caution should be taken to avoid over or misinterpretation of this study’s results by extrapolation of the findings in humans. This is especially alarming in the presence of a significant body of evidence in the peer-reviewed scientific literature convincingly supporting olive oil’s health benefits, including weight management.

On Behalf of the OWI Advisory Panel

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