Editorial
The obesity paradox
La paradoja de la obesidad
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] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "La paradoja de la obesidad" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Obesity, which is measured by the Body Mass Index (BMI) ≥ 30<span class="elsevierStyleHsp" style=""></span>kg/m<span class="elsevierStyleSup">2</span>, is a complex disease that leads to a chronic low-grade inflammation of the adipose tissue and is associated with several factors, including (but not limited to) the increase of proinflammatory cytokines, release of leptin and downregulation of adiponectin, which ultimately promote the development of different metabolic alterations and diseases such as type 2 diabetes mellitus (T2DM), hypertension and dyslipidemia.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Although there is historical evidence that has associated excess weight with all-cause death in the obese population, a huge number of studies have been published in the last two decades with contradictory results, which is currently known as the “obesity paradox”.</p><p id="par0010" class="elsevierStylePara elsevierViewall">Specifically, the first study that reported beneficial effects of obesity was published in 1999 and showed that the one-year survival rate in hemodialysis patients with obesity was significantly higher compared to those with lower weight and the BMI increase in one unit reduced by 30% the relative risk of death.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Since then, the “obesity paradox”, term by which this phenomenon has been known since 2002,<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> has also been described in different pathologies and diseases such as T2DM,<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> cancer,<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> or cardiovascular diseases,<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> among many others. The obesity paradox is particularly striking in cancer, since it has been widely demonstrated that excess adipose tissue could be a modulator of both classical antitumor therapies (chemotherapy and radiotherapy) and current therapies (combined treatments and immunotherapies) due to its negative impact on the tumor microenvironment (TME), boosting tumor cell development and cancer progression. However, in recent years, it has been suggested that adipose tissue may be a factor that improves not only clinical responses, but also survival rates in both cancer murine models and oncological patients, although the mechanisms of action carried out by the interaction among treatments, adipose tissue and the TME are still unknown. Identifying those mechanisms could be of great importance to develop new therapeutic approaches.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> Altogether, different hypothesis to explain the beneficial role of obesity have arisen in a variety of diseases.</p><p id="par0015" class="elsevierStylePara elsevierViewall">First, it is believed that the anatomical distribution of adipose tissue may be crucial to explain the obesity paradox. In this sense, subcutaneous adipose tissue (SAT) could play a protective role against metabolic diseases, whereas both intra-abdominal solid organ adipose tissue and visceral adipose tissue (VAT) could be harmful. In line with this notion, it has been demonstrated a positive association between VAT and the risk of atherosclerosis in a SAT-independent manner. Importantly, there are both genetic and biological differences between these two types of adipose tissue. VAT expresses higher levels of the homeobox A4 gene (also known as <span class="elsevierStyleItalic">HoxA4</span>), <span class="elsevierStyleItalic">HoxA5</span> and the homeobox C8 gene (also known as <span class="elsevierStyleItalic">HoxC8</span>), while SAT predominantly expresses <span class="elsevierStyleItalic">HoxC9</span> or <span class="elsevierStyleItalic">HoxA10</span>.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> In addition, VAT releases higher amounts of proinflammatory cytokines compared to SAT, which could accelerate insulin resistance and the risk of atherosclerosis.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> For these reasons, some authors prefer to use the term “metabolic obesity” to refer to the anatomical location of the adipose tissue (rather than the volume), which may allow a better identification and stratification of individuals with cardiometabolic risk.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Nutrition may also play a key role in the obesity paradox since obese individuals have higher metabolic reserves that could allow to cope with the catabolic burden caused by some diseases and treatments.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> Casas-Vara et al (2012) demonstrated that the nutritional status measured by different clinical parameters (e.g., hemoglobin, lymphocyte count, serum albumin, prealbumin, and cholesterol levels) was better in obese patients with heart failure (HF) compared to their leaner counterparts. This was associated with long-term survival<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> and, therefore, obese patients may have a greater immune capacity against diseases under certain nutritional status. Related to this, glucose levels seem to be important to reveal the apparent protective effect of obesity, since an increase in BMI has been associated with a lower risk of hypoglycemia in patients with severe HF and, in turn, contributed to a lower risk of mortality.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Blood pressure may also influence on the contradictory results found in obese patients. As it is known, hypertension increases the risk of cardiovascular diseases in the obese population and, accordingly, obesity-related pulmonary hypertension has shown to increase the risk of right ventricular dysfunction. However, obesity may paradoxically confer a beneficial effect on right ventricular function and be associated with a lower risk of death, although the clinical impact of this event is still unknown.<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> In addition, the Avoiding Cardiovascular Events through Combination Therapy in Patients Living with Systolic Hypertension (ACCOMPLISH) clinical trial showed that obese subjects with hypertension responded successfully to specific treatments compared to patients with lower BMI,<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> which may explain, at least in part, why hypertension is involved in the obesity paradox.</p><p id="par0030" class="elsevierStylePara elsevierViewall">This phenomenon could also be related to age, gender, and ethnicity. Although the ageing process can imply being more prone to certain diseases and have a shorter life expectancy, it has been shown that obesity in older subjects could be associated with the same morbidities and reduced quality of life than younger adults. Furthermore, weight loss (voluntarily or unconsciously) in the elderly has been related to the loss of bone density, and obesity could be associated with a lower risk of hip fracture because the adipose tissue located in the abdominal area could cushion falls and reduce the chances of suffering fractures.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> Regarding gender and ethnicity, it has been demonstrated that accumulation of VAT (instead of SAT) is more frequent in African American women, white men, and Indian and Japanese people of both sexes.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">It is interesting to mention that BMI has been used in most of the studies in which the obesity paradox has been found. However, BMI could not be a suitable index to measure adiposity because it only considers weight and height rather than other important factors such as the anatomical location of the adipose tissue (visceral or subcutaneous) or the type of mass (fat or muscle). For those reasons, some authors use the term “BMI paradox” to explain this phenomenon.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a> Probably, it could be more suitable to consider other indexes to determine adiposity properly, such as the waist circumference, the waist-to-hip ratio, or the waist-to-height ratio (WHtR). Butt et al. (2023) recently found the obesity paradox in HF patients with BMI ≥ 25<span class="elsevierStyleHsp" style=""></span>kg/m<span class="elsevierStyleSup">2</span>; however, anthropometric measurements by the WHtR not only reflected the location and amount of ectopic adipose tissue better than BMI, but also associated adiposity with a higher risk of HF, thus suggesting the non-existence of the BMI-related obesity paradox.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">We need to consider that all the previous hypothesis that try to explain the obesity paradox may be also caused by adipokines that are released by the adipose tissue. The most known cell signaling adipokine is leptin, which play a key role in several mechanisms, including those involved in energy balance or promoting different pathologies and diseases.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a> In a similar way to obesity, leptin has also demonstrated to be beneficial in some settings, which has been called the “leptin paradox”.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a> Adiponectin is another adipocyte-secreted molecule that plays an opposite role to leptin in energy balance and its downregulation has proved to be detrimental in some diseases. However, contradictory results have also been found in obese patients, being renamed this time as the “adiponectin paradox”.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">In conclusion, although obesity has been widely demonstrated over the years to participate in the development of different diseases and the increased risk of mortality in both murine models and clinical patients, in the last couple of decades contradictory results has emerged to the point of considering the existence of a protective role of adiposity. The real reasons of such an enigmatic function of obesity against diseases and favoring long-term survival rates are still unknown and further research is needed to elucidate this phenomenon, but currently there are some hypotheses that try to explain this event. There are a variety of factors that could influence and need to be born in mind to determine the obesity paradox, such as the anatomical distribution of adipose tissue, the use of different indexes to measure obesity (e.g., BMI or WHtR), nutrition status, clinical parameters (e.g., albumin, lymphocyte count, glucose level, or blood pressure), demography, genetics, or even unidentified confounding factors. Identifying the pathways whereby the obesity paradox occurs in some patients could be of great importance to (i) better identify and stratify patients according to their fat status, (ii) establish predictive and/or prognostic clinical biomarkers, and (iii) design new drugs/investigate new therapeutic approaches to overcome certain diseases, that may ultimately improve survival rates and decrease the risk of death in those obese patients in whom the obesity paradox has not been observed.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Author contribution</span><p id="par0050" class="elsevierStylePara elsevierViewall">FS-J and CJ-C contributed to conceptualization, literature search, writing and review of the manuscript. The authors read and agreed to publish this version of the manuscript.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflicts of interest</span><p id="par0055" class="elsevierStylePara elsevierViewall">The authors declare no conflict of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:4 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Author contribution" ] 1 => array:2 [ "identificador" => "sec0010" "titulo" => "Conflicts of interest" ] 2 => array:2 [ "identificador" => "xack697214" "titulo" => "Acknowledgement" ] 3 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:3 [ "etiqueta" => "1" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">The authors contributed equally to this work.</p>" "identificador" => "fn0005" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:20 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Adiponectin-leptin ratio: A promising index to estimate adipose tissue dysfunction. 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