Diferencia entre revisiones de «Hipótesis dieta-corazón»

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Revisión del 13:54 26 dic 2022

La hipótesis dieta-corazón postula que la reducción de las grasas saturadas en la dieta reduce el colesterol sérico, disminuyendo el depósito de colesterol en la pared arterial, lo que reduce el riesgo de enfermedad cardiovascular (ECV);^[1]^[2]en concordancia con ello, las pautas dietéticas recomiendan restringir la ingesta de grasas saturadas.^[3]^[4]La gran cantidad de evidencia científica indica que el colesterol total y el colesterol LDL (lipoproteína de baja densidad), a menudo denominado 'colesterol malo', contribuyen a las enfermedades cardíacas;^[5]^[6] sin embargo, existencia evidencia que no encuentra relación de causalidad entre la ingesta de grasas saturadas y las enfermedades cardiovasculares; asimismo, hay estudios que evidencian una relación inversa entre la ingesta de grasa saturada y la salud cardiovascular; además la sustitución de grasas saturadas por grasas poliinsaturadas omega 6 no se traduce en una disminución del riesgo de padecer enfermedades cardiovasculares;^[7]en tal sentido, existen opiniones de que las pautas dietéticas globales deben reconsiderarse.^[8]

Historia

Véase también: Ancel Keys

La hipótesis de que las grasas saturadas causan CVD surgió a fines de la década de 1950, cuando los científicos observaron que estas grasas tienden a elevar la concentración de colesterol sérico total, que a su vez se consideraba un potente factor de riesgo de enfermedad cardíaca.^[9]La hipótesis dieta-corazón ganó amplia aceptación en las décadas de 1970 y 1980.^[10]

A pesar de que el público estadounidense sigue las recomendaciones para disminuir la ingesta absoluta de grasas en la dieta y específicamente disminuir la ingesta de grasas saturadas, se ha visto un aumento dramático en los últimos 40 años en las tasas de enfermedades cardiovasculares.^[4]

Numerosos metanálisis y revisiones sistemáticas de la literatura histórica y actual revelan que la hipótesis de la dieta y el corazón no estaba, y aún no está, respaldada por la evidencia.^[11]

Recomendaciones

Reino Unido recomienda, sobre las grasas saturadas, que no incluya más del 11% de nuestras calorías de alimentos y bebidas, mientras que Estados Unidos y la Organización Mundial de la Salud recomiendan menos del 10%.^[12]^[6]

Fisiología

Artículo principal: Ateroesclerosis

Algunos estudios refieren que una mayor ingesta de grasas saturadas proporciona sustratos para la síntesis de colesterol en forma de acetil-CoA.^[13]

Cuando existe un exceso de colesterol se deposita en nuestras arterias engrosando las paredes de éstas.^[14]

Zinöcker, Svendsen y Nitter han propuesto el modelo de adaptación homeoviscosa a los lípidos dietéticos (HADL), que explica los cambios en el colesterol de lipoproteínas como ajustes homeostáticos adaptativos que sirven para mantener la fluidez de la membrana celular y, por lo tanto, una función celular óptima;^[15]asimiso, de acuerdo con el modelo, la desregulación de la captación de colesterol es causada por la endotoxemia, que provoca inflamación y, por lo tanto, impide la captación de colesterol a través de los receptores de colesterol LDL.^[16]

Evidencia a favor

El Minnesota Coronary Experiment (MCE), un ensayo controlado aleatorizado realizado entre 1968 y 1973, fue el ensayo dietético más grande y quizás el más rigurosamente ejecutado para reducir el colesterol mediante el reemplazo de grasas saturadas con aceite vegetal rico en ácido linoleico. SIn embargo, posteriores hallazgos de publicación incompleta sugieren una sobreestimación de los beneficios y subestimación de los riesgos potenciales de reemplazar grasas saturadas con aceites vegetales ricos en ácido linoleico.^[17]^[18]

Evidencia en contra

De acuerdo con Ramsden, ningún ensayo controlado aleatorizado (ECA) ha demostrado que el reemplazo de grasas saturadas con ácido linoleico reduzca significativamente los eventos de enfermedad coronaria o las muertes.^[2]

Un metanálisis revisado de ECAs mostró que la sustitución de ácidos grasos (AG) saturados por AG ω6 sin aumentar simultáneamente AG ω3 no presenta indicios de beneficio e incluso es probable que aumente el riesgo de ECV^[19]

Los hallazgos del estudio Prospective Urban Rural Epidemiology (PURE), un gran estudio epidemiológico de cohortes de personas de 35 a 70 años en 18 países con una mediana de seguimiento de 7·4 años, determinaron que La ingesta alta de carbohidratos se asoció con un mayor riesgo de mortalidad total, mientras que la grasa total y los tipos individuales de grasa se relacionaron con una mortalidad total más baja. La grasa total y los tipos de grasa no se asociaron con enfermedad cardiovascular, infarto de miocardio o mortalidad por enfermedad cardiovascular, mientras que la grasa saturada tuvo una asociación inversa con el accidente cerebrovascular.^[20]^[8]

Referencias

↑ DuBroff, Robert; de Lorgeril, Michel (29 de mayo de 2019). «Fat or fiction: the diet-heart hypothesis». BMJ Evidence-Based Medicine 26 (1): 3-7. ISSN 2515-446X. doi:10.1136/bmjebm-2019-111180. Consultado el 26 de diciembre de 2022. «The concept that diet, serum cholesterol and cardiovascular disease are causally related gave rise to the diet-heart hypothesis nearly 70 years ago. This hypothesis postulates that reducing dietary saturated fat reduces serum cholesterol, thereby reducing the risk of cardiovascular disease. Today, this concept has been transformed from a hypothesis into public health policy as current guidelines recommend reducing the intake of dietary saturated fat.»
↑ ^a ^b Ramsden, Christopher E; Zamora, Daisy; Majchrzak-Hong, Sharon; Faurot, Keturah R; Broste, Steven K; Frantz, Robert P; Davis, John M; Ringel, Amit et al. (12 de abril de 2016). «Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)». BMJ: i1246. ISSN 1756-1833. doi:10.1136/bmj.i1246. Consultado el 26 de diciembre de 2022. «The traditional diet-heart hypothesis1 2 predicts that the serum cholesterol lowering effects of replacing saturated fat with vegetable oil rich in linoleic acid will diminish deposition of cholesterol in the arterial wall,3 4 slow progression of atherosclerosis,5 reduce coronary heart disease events, and improve survival.6 7 This diet-heart paradigm is supported by evidence from randomized controlled trials showing that replacement of saturated fat with linoleic acid lowers serum total cholesterol and low density lipoprotein8 9 10 11 12 and by observational evidence linking serum cholesterol to coronary heart disease events and deaths (fig 1⇓).13 Despite these compelling relations, no randomized controlled trial has shown that replacement of saturated fat with linoleic acid significantly reduces coronary heart disease events or deaths (fig 1⇓).»
↑ DiNicolantonio, James J.; Lucan, Sean C.; O’Keefe, James H. (2016-03). «The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease». Progress in Cardiovascular Diseases 58 (5): 464-472. ISSN 0033-0620. doi:10.1016/j.pcad.2015.11.006. Consultado el 26 de diciembre de 2022. «Dietary guidelines continue to recommend restricting intake of saturated fats. This recommendation follows largely from the observation that saturated fats can raise levels of total serum cholesterol (TC), thereby putatively increasing the risk of atherosclerotic coronary heart disease (CHD).»
↑ ^a ^b Gershuni, Victoria M. (1 de septiembre de 2018). «Saturated Fat: Part of a Healthy Diet». Current Nutrition Reports (en inglés) 7 (3): 85-96. ISSN 2161-3311. doi:10.1007/s13668-018-0238-x. Consultado el 26 de diciembre de 2022. «Despite the American public following recommendations to decrease absolute dietary fat intake and specifically decrease saturated fat intake, we have seen a dramatic rise over the past 40 years in the rates of non-communicable diseases associated with obesity and overweight, namely cardiovascular disease. The development of the diet-heart hypothesis in the mid twentieth century led to faulty but long-held beliefs that dietary intake of saturated fat led to heart disease. Saturated fat can lead to increased LDL cholesterol levels, and elevated plasma cholesterol levels have been shown to be a risk factor for cardiovascular disease; however, the correlative nature of their association does not assign causation.»
↑ Zinöcker, Marit Kolby; Svendsen, Karianne; Dankel, Simon Nitter (20 de enero de 2021). «The homeoviscous adaptation to dietary lipids (HADL) model explains controversies over saturated fat, cholesterol, and cardiovascular disease risk». The American Journal of Clinical Nutrition 113 (2): 277-289. ISSN 0002-9165. doi:10.1093/ajcn/nqaa322. Consultado el 26 de diciembre de 2022. «At the core of the diet–heart hypothesis lies 3-step reasoning: A dietary intervention enriched in SFAs leads to increased total and LDL cholesterol concentrations. Elevated total and LDL cholesterol concentrations are associated with atherosclerotic cardiovascular disease (ASCVD). Ergo, a diet rich in SFAs promotes ASCVD. Viewed separately, Steps 1 and 2 are well documented in the literature, although there are inconsistent findings and large individual differences both with respect to the LDL cholesterol response and its association with disease (1, 2). However, causal evidence for Step 3 is lacking (1), despite the large and still-growing number of studies that have addressed this question (3–5).»
↑ ^a ^b «¿Realmente comer grasas saturadas aumenta el colesterol y el riesgo de enfermedades del corazón?». BBC News Mundo. Consultado el 26 de diciembre de 2022.
↑ Domínguez, H.; Núñez, M. J.; Lema, J. M. (30 de octubre de 1993). «Eliminación de ácido clorogénico durante el procesado acuoso de las almendras de girasol». Grasas y Aceites 44 (4-5): 235-242. ISSN 1988-4214. doi:10.3989/gya.1993.v44.i4-5.1072. Consultado el 26 de diciembre de 2022. «En vista de la evidencia presentada se concluye que no se encuentra relación de causalidad entre la ingesta de grasas saturadas y las enfermedades cardiovasculares. Hay estudios que evidencian una relación inversa entre la ingesta de grasa saturada y la salud cardiovascular. La sustitución de grasas saturadas por grasas poliinsaturadas omega 6 no se traduce en una disminución del riesgo de padecer enfermedades cardiovasculares. Considerando estos aspectos, y teniendo en cuenta la revisión de los trabajos analizados en este artículo, entre los que se incluyen estudios del más alto rigor científico (metaanálisis y revisiones sistemáticas), se recomienda que se reconsidere en las guías dietéticas cubanas las limitaciones de la ingesta de grasa saturada para la población en general.»
↑ ^a ^b Dehghan, Mahshid; Mente, Andrew; Zhang, Xiaohe; Swaminathan, Sumathi; Li, Wei; Mohan, Viswanathan; Iqbal, Romaina; Kumar, Rajesh et al. (4 de noviembre de 2017). «Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study». The Lancet (en english) 390 (10107): 2050-2062. ISSN 0140-6736. PMID 28864332. doi:10.1016/S0140-6736(17)32252-3. Consultado el 26 de diciembre de 2022. «High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality, whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.»
↑ Astrup, Arne; Teicholz, Nina; Magkos, Faidon; Bier, Dennis M.; Brenna, J. Thomas; King, Janet C.; Mente, Andrew; Ordovas, José M. et al. (2021-10). «Dietary Saturated Fats and Health: Are the U.S. Guidelines Evidence-Based?». Nutrients (en inglés) 13 (10): 3305. ISSN 2072-6643. doi:10.3390/nu13103305. Consultado el 26 de diciembre de 2022. «The hypothesis that saturated fats cause CVD emerged in the late 1950s, when scientists observed that these fats tend to raise the concentration of total serum cholesterol, which in turn was considered a potent risk factor for heart disease. Ancel Keys, a physiologist at the University of Minnesota, postulated that saturated fats along with dietary cholesterol were the principal causes of cardiovascular disease, and his “diet-heart hypothesis” was adopted by leading groups, including the American Heart Association.»
↑ Astrup, Arne; Teicholz, Nina; Magkos, Faidon; Bier, Dennis M.; Brenna, J. Thomas; King, Janet C.; Mente, Andrew; Ordovas, José M. et al. (2021-10). «Dietary Saturated Fats and Health: Are the U.S. Guidelines Evidence-Based?». Nutrients (en inglés) 13 (10): 3305. ISSN 2072-6643. doi:10.3390/nu13103305. Consultado el 26 de diciembre de 2022. «the diet-heart hypothesis gained widespread acceptance in the 1970s and 1980s, yet the results from the totality of these trials did not provide support for the hypothesis, as many critics at the time pointed out».
↑ Gershuni, Victoria M. (1 de septiembre de 2018). «Saturated Fat: Part of a Healthy Diet». Current Nutrition Reports (en inglés) 7 (3): 85-96. ISSN 2161-3311. doi:10.1007/s13668-018-0238-x. Consultado el 26 de diciembre de 2022. «Advances in understanding the role of various lipoprotein particles and their atherogenic risk have been helpful for understanding how different dietary components may impact CVD risk. Numerous meta-analyses and systematic reviews of both the historical and current literature reveals that the diet-heart hypothesis was not, and still is not, supported by the evidence. There appears to be no consistent benefit to all-cause or CVD mortality from the reduction of dietary saturated fat. Further, saturated fat has been shown in some cases to have an inverse relationship with obesity-related type 2 diabetes.»
↑ Astrup, Arne; Magkos, Faidon; Bier, Dennis M.; Brenna, J. Thomas; de, Oliveira Otto Marcia C.; Hill, James O.; King, Janet C.; Mente, Andrew et al. (18 de agosto de 2020). «Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations». Journal of the American College of Cardiology 76 (7): 844-857. doi:10.1016/j.jacc.2020.05.077. Consultado el 26 de diciembre de 2022. «•The U.S. Dietary Guidelines recommend the restriction of SFA intake to <10% of calories to reduce CVD. •Different SFAs have different biologic effects, which are further modified by the food matrix and the carbohydrate content of the diet. •Several foods relatively rich in SFAs, such as whole-fat dairy, dark chocolate, and unprocessed meat, are not associated with increased CVD or diabetes risk. •There is no robust evidence that current population-wide arbitrary upper limits on saturated fat consumption in the United States will prevent CVD or reduce mortality.»
↑ Zinöcker, Marit Kolby; Svendsen, Karianne; Dankel, Simon Nitter (20 de enero de 2021). «The homeoviscous adaptation to dietary lipids (HADL) model explains controversies over saturated fat, cholesterol, and cardiovascular disease risk». The American Journal of Clinical Nutrition 113 (2): 277-289. ISSN 0002-9165. doi:10.1093/ajcn/nqaa322. Consultado el 26 de diciembre de 2022. «Studies have investigated whether increased SFA intake increases the endogenous synthesis of cholesterol: for example, by providing substrates for synthesis in the form of acetyl-CoA.»
↑ Cardiavant (18 de marzo de 2022). «Colesterol: ¿Por qué es un factor de riesgo cardiovascular?». Cardiavant. Consultado el 26 de diciembre de 2022.
↑ Zinöcker, Marit Kolby; Svendsen, Karianne; Dankel, Simon Nitter (20 de enero de 2021). «The homeoviscous adaptation to dietary lipids (HADL) model explains controversies over saturated fat, cholesterol, and cardiovascular disease risk». The American Journal of Clinical Nutrition 113 (2): 277-289. ISSN 0002-9165. doi:10.1093/ajcn/nqaa322. Consultado el 26 de diciembre de 2022. «SFAs play the leading role in 1 of the greatest controversies in nutrition science. Relative to PUFAs, SFAs generally increase circulating concentrations of LDL cholesterol, a risk factor for atherosclerotic cardiovascular disease (ASCVD). However, the purpose of regulatory mechanisms that control the diet-induced lipoprotein cholesterol dynamics is rarely discussed in the context of human adaptive biology. We argue that better mechanistic explanations can help resolve lingering controversies, with the potential to redefine aspects of research, clinical practice, dietary advice, public health management, and food policy. In this paper we propose a novel model, the homeoviscous adaptation to dietary lipids (HADL) model, which explains changes in lipoprotein cholesterol as adaptive homeostatic adjustments that serve to maintain cell membrane fluidity and hence optimal cell function. Due to the highly variable intake of fatty acids in humans and other omnivore species, we propose that circulating lipoproteins serve as a buffer to enable the rapid redistribution of cholesterol molecules between specific cells and tissues that is necessary with changes in dietary fatty acid supply. Hence, circulating levels of LDL cholesterol may change for nonpathological reasons. Accordingly, an SFA-induced raise in LDL cholesterol in healthy individuals could represent a normal rather than a pathologic response. These regulatory mechanisms may become disrupted secondarily to pathogenic processes in association with insulin resistance and the presence of other ASCVD risk factors, as supported by evidence showing diverging lipoprotein responses in healthy individuals as opposed to those with metabolic disorders such as insulin resistance and obesity.»
↑ Laila, Amar (2021-08). «Limitations in the “homeoviscous adaptation to dietary lipids” model». The American Journal of Clinical Nutrition 114 (2): 822-823. ISSN 0002-9165. doi:10.1093/ajcn/nqab230. Consultado el 26 de diciembre de 2022. «I read with interest the article by Zinöcker et al. (1), in which the authors proposed a model to explain the observed pathologic increase in LDL-cholesterol concentrations in response to higher SFA intake. The model de-emphasized the role of SFAs and suggested that dysregulation of cholesterol uptake is caused by endotoxemia, which causes inflammation and, therefore, prevents cholesterol uptake via LDL-cholesterol receptors. The authors’ conclusion was that, if the model is verified, recommendations should focus on reducing intake of refined carbohydrates, which increases the growth of LPS-containing gut bacteria, but not reducing intake of SFAs.»
↑ Ramsden, Christopher E; Zamora, Daisy; Majchrzak-Hong, Sharon; Faurot, Keturah R; Broste, Steven K; Frantz, Robert P; Davis, John M; Ringel, Amit et al. (12 de abril de 2016). «Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)». BMJ: i1246. ISSN 1756-1833. doi:10.1136/bmj.i1246. Consultado el 26 de diciembre de 2022. «The Minnesota Coronary Experiment (MCE), a randomized controlled trial conducted in 1968-73, was the largest (n=9570) and perhaps the most rigorously executed dietary trial of cholesterol lowering by replacement of saturated fat with vegetable oil rich in linoleic acid. The MCE is the only such randomized controlled trial to complete postmortem assessment of coronary, aortic, and cerebrovascular atherosclerosis grade and infarct status and the only one to test the clinical effects of increasing linoleic acid in large prespecified subgroups of women and older adults.»
↑ Ramsden, Christopher E; Zamora, Daisy; Majchrzak-Hong, Sharon; Faurot, Keturah R; Broste, Steven K; Frantz, Robert P; Davis, John M; Ringel, Amit et al. (12 de abril de 2016). «Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)». BMJ: i1246. ISSN 1756-1833. doi:10.1136/bmj.i1246. Consultado el 26 de diciembre de 2022. «Available evidence from randomized controlled trials shows that replacement of saturated fat with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes. MCE findings add to growing evidence that incomplete publication has contributed to overestimation of benefits, and underestimation of potential risks, of replacing saturated fat with vegetable oils rich in linoleic acid.»
↑ Ruiz-Núñez, Begoña; Dijck-Brouwer, D. A. Janneke; Muskiet, Frits A. J. (1 de octubre de 2016). «The relation of saturated fatty acids with low-grade inflammation and cardiovascular disease». The Journal of Nutritional Biochemistry (en inglés) 36: 1-20. ISSN 0955-2863. doi:10.1016/j.jnutbio.2015.12.007. Consultado el 26 de diciembre de 2022.
↑ Dehghan, Mahshid; Mente, Andrew; Zhang, Xiaohe; Swaminathan, Sumathi; Li, Wei; Mohan, Viswanathan; Iqbal, Romaina; Kumar, Rajesh et al. (4 de noviembre de 2017). «Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study». The Lancet (en english) 390 (10107): 2050-2062. ISSN 0140-6736. PMID 28864332. doi:10.1016/S0140-6736(17)32252-3. Consultado el 26 de diciembre de 2022. «The Prospective Urban Rural Epidemiology (PURE) study is a large, epidemiological cohort study of individuals aged 35–70 years (enrolled between Jan 1, 2003, and March 31, 2013) in 18 countries with a median follow-up of 7·4 years (IQR 5·3–9·3). Dietary intake of 135 335 individuals was recorded using validated food frequency questionnaires. The primary outcomes were total mortality and major cardiovascular events (fatal cardiovascular disease, non-fatal myocardial infarction, stroke, and heart failure). Secondary outcomes were all myocardial infarctions, stroke, cardiovascular disease mortality, and non-cardiovascular disease mortality. Participants were categorised into quintiles of nutrient intake (carbohydrate, fats, and protein) based on percentage of energy provided by nutrients. We assessed the associations between consumption of carbohydrate, total fat, and each type of fat with cardiovascular disease and total mortality. We calculated hazard ratios (HRs) using a multivariable Cox frailty model with random intercepts to account for centre clustering.»

[1] DuBroff, Robert; de Lorgeril, Michel (29 de mayo de 2019). «Fat or fiction: the diet-heart hypothesis». BMJ Evidence-Based Medicine 26 (1): 3-7. ISSN 2515-446X. doi:10.1136/bmjebm-2019-111180. Consultado el 26 de diciembre de 2022. «The concept that diet, serum cholesterol and cardiovascular disease are causally related gave rise to the diet-heart hypothesis nearly 70 years ago. This hypothesis postulates that reducing dietary saturated fat reduces serum cholesterol, thereby reducing the risk of cardiovascular disease. Today, this concept has been transformed from a hypothesis into public health policy as current guidelines recommend reducing the intake of dietary saturated fat.»

[:1-2] Ramsden, Christopher E; Zamora, Daisy; Majchrzak-Hong, Sharon; Faurot, Keturah R; Broste, Steven K; Frantz, Robert P; Davis, John M; Ringel, Amit et al. (12 de abril de 2016). «Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)». BMJ: i1246. ISSN 1756-1833. doi:10.1136/bmj.i1246. Consultado el 26 de diciembre de 2022. «The traditional diet-heart hypothesis1 2 predicts that the serum cholesterol lowering effects of replacing saturated fat with vegetable oil rich in linoleic acid will diminish deposition of cholesterol in the arterial wall,3 4 slow progression of atherosclerosis,5 reduce coronary heart disease events, and improve survival.6 7 This diet-heart paradigm is supported by evidence from randomized controlled trials showing that replacement of saturated fat with linoleic acid lowers serum total cholesterol and low density lipoprotein8 9 10 11 12 and by observational evidence linking serum cholesterol to coronary heart disease events and deaths (fig 1⇓).13 Despite these compelling relations, no randomized controlled trial has shown that replacement of saturated fat with linoleic acid significantly reduces coronary heart disease events or deaths (fig 1⇓).»

[3] DiNicolantonio, James J.; Lucan, Sean C.; O’Keefe, James H. (2016-03). «The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease». Progress in Cardiovascular Diseases 58 (5): 464-472. ISSN 0033-0620. doi:10.1016/j.pcad.2015.11.006. Consultado el 26 de diciembre de 2022. «Dietary guidelines continue to recommend restricting intake of saturated fats. This recommendation follows largely from the observation that saturated fats can raise levels of total serum cholesterol (TC), thereby putatively increasing the risk of atherosclerotic coronary heart disease (CHD).»

[:2-4] Gershuni, Victoria M. (1 de septiembre de 2018). «Saturated Fat: Part of a Healthy Diet». Current Nutrition Reports (en inglés) 7 (3): 85-96. ISSN 2161-3311. doi:10.1007/s13668-018-0238-x. Consultado el 26 de diciembre de 2022. «Despite the American public following recommendations to decrease absolute dietary fat intake and specifically decrease saturated fat intake, we have seen a dramatic rise over the past 40 years in the rates of non-communicable diseases associated with obesity and overweight, namely cardiovascular disease. The development of the diet-heart hypothesis in the mid twentieth century led to faulty but long-held beliefs that dietary intake of saturated fat led to heart disease. Saturated fat can lead to increased LDL cholesterol levels, and elevated plasma cholesterol levels have been shown to be a risk factor for cardiovascular disease; however, the correlative nature of their association does not assign causation.»

[5] Zinöcker, Marit Kolby; Svendsen, Karianne; Dankel, Simon Nitter (20 de enero de 2021). «The homeoviscous adaptation to dietary lipids (HADL) model explains controversies over saturated fat, cholesterol, and cardiovascular disease risk». The American Journal of Clinical Nutrition 113 (2): 277-289. ISSN 0002-9165. doi:10.1093/ajcn/nqaa322. Consultado el 26 de diciembre de 2022. «At the core of the diet–heart hypothesis lies 3-step reasoning: A dietary intervention enriched in SFAs leads to increased total and LDL cholesterol concentrations. Elevated total and LDL cholesterol concentrations are associated with atherosclerotic cardiovascular disease (ASCVD). Ergo, a diet rich in SFAs promotes ASCVD. Viewed separately, Steps 1 and 2 are well documented in the literature, although there are inconsistent findings and large individual differences both with respect to the LDL cholesterol response and its association with disease (1, 2). However, causal evidence for Step 3 is lacking (1), despite the large and still-growing number of studies that have addressed this question (3–5).»

[:0-6] «¿Realmente comer grasas saturadas aumenta el colesterol y el riesgo de enfermedades del corazón?». BBC News Mundo. Consultado el 26 de diciembre de 2022.

[7] Domínguez, H.; Núñez, M. J.; Lema, J. M. (30 de octubre de 1993). «Eliminación de ácido clorogénico durante el procesado acuoso de las almendras de girasol». Grasas y Aceites 44 (4-5): 235-242. ISSN 1988-4214. doi:10.3989/gya.1993.v44.i4-5.1072. Consultado el 26 de diciembre de 2022. «En vista de la evidencia presentada se concluye que no se encuentra relación de causalidad entre la ingesta de grasas saturadas y las enfermedades cardiovasculares. Hay estudios que evidencian una relación inversa entre la ingesta de grasa saturada y la salud cardiovascular. La sustitución de grasas saturadas por grasas poliinsaturadas omega 6 no se traduce en una disminución del riesgo de padecer enfermedades cardiovasculares. Considerando estos aspectos, y teniendo en cuenta la revisión de los trabajos analizados en este artículo, entre los que se incluyen estudios del más alto rigor científico (metaanálisis y revisiones sistemáticas), se recomienda que se reconsidere en las guías dietéticas cubanas las limitaciones de la ingesta de grasa saturada para la población en general.»

[:3-8] Dehghan, Mahshid; Mente, Andrew; Zhang, Xiaohe; Swaminathan, Sumathi; Li, Wei; Mohan, Viswanathan; Iqbal, Romaina; Kumar, Rajesh et al. (4 de noviembre de 2017). «Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study». The Lancet (en english) 390 (10107): 2050-2062. ISSN 0140-6736. PMID 28864332. doi:10.1016/S0140-6736(17)32252-3. Consultado el 26 de diciembre de 2022. «High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality, whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.»

[9] Astrup, Arne; Teicholz, Nina; Magkos, Faidon; Bier, Dennis M.; Brenna, J. Thomas; King, Janet C.; Mente, Andrew; Ordovas, José M. et al. (2021-10). «Dietary Saturated Fats and Health: Are the U.S. Guidelines Evidence-Based?». Nutrients (en inglés) 13 (10): 3305. ISSN 2072-6643. doi:10.3390/nu13103305. Consultado el 26 de diciembre de 2022. «The hypothesis that saturated fats cause CVD emerged in the late 1950s, when scientists observed that these fats tend to raise the concentration of total serum cholesterol, which in turn was considered a potent risk factor for heart disease. Ancel Keys, a physiologist at the University of Minnesota, postulated that saturated fats along with dietary cholesterol were the principal causes of cardiovascular disease, and his “diet-heart hypothesis” was adopted by leading groups, including the American Heart Association.»

[10] Astrup, Arne; Teicholz, Nina; Magkos, Faidon; Bier, Dennis M.; Brenna, J. Thomas; King, Janet C.; Mente, Andrew; Ordovas, José M. et al. (2021-10). «Dietary Saturated Fats and Health: Are the U.S. Guidelines Evidence-Based?». Nutrients (en inglés) 13 (10): 3305. ISSN 2072-6643. doi:10.3390/nu13103305. Consultado el 26 de diciembre de 2022. «the diet-heart hypothesis gained widespread acceptance in the 1970s and 1980s, yet the results from the totality of these trials did not provide support for the hypothesis, as many critics at the time pointed out».

[11] Gershuni, Victoria M. (1 de septiembre de 2018). «Saturated Fat: Part of a Healthy Diet». Current Nutrition Reports (en inglés) 7 (3): 85-96. ISSN 2161-3311. doi:10.1007/s13668-018-0238-x. Consultado el 26 de diciembre de 2022. «Advances in understanding the role of various lipoprotein particles and their atherogenic risk have been helpful for understanding how different dietary components may impact CVD risk. Numerous meta-analyses and systematic reviews of both the historical and current literature reveals that the diet-heart hypothesis was not, and still is not, supported by the evidence. There appears to be no consistent benefit to all-cause or CVD mortality from the reduction of dietary saturated fat. Further, saturated fat has been shown in some cases to have an inverse relationship with obesity-related type 2 diabetes.»

[12] Astrup, Arne; Magkos, Faidon; Bier, Dennis M.; Brenna, J. Thomas; de, Oliveira Otto Marcia C.; Hill, James O.; King, Janet C.; Mente, Andrew et al. (18 de agosto de 2020). «Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations». Journal of the American College of Cardiology 76 (7): 844-857. doi:10.1016/j.jacc.2020.05.077. Consultado el 26 de diciembre de 2022. «•The U.S. Dietary Guidelines recommend the restriction of SFA intake to <10% of calories to reduce CVD. •Different SFAs have different biologic effects, which are further modified by the food matrix and the carbohydrate content of the diet. •Several foods relatively rich in SFAs, such as whole-fat dairy, dark chocolate, and unprocessed meat, are not associated with increased CVD or diabetes risk. •There is no robust evidence that current population-wide arbitrary upper limits on saturated fat consumption in the United States will prevent CVD or reduce mortality.»

[13] Zinöcker, Marit Kolby; Svendsen, Karianne; Dankel, Simon Nitter (20 de enero de 2021). «The homeoviscous adaptation to dietary lipids (HADL) model explains controversies over saturated fat, cholesterol, and cardiovascular disease risk». The American Journal of Clinical Nutrition 113 (2): 277-289. ISSN 0002-9165. doi:10.1093/ajcn/nqaa322. Consultado el 26 de diciembre de 2022. «Studies have investigated whether increased SFA intake increases the endogenous synthesis of cholesterol: for example, by providing substrates for synthesis in the form of acetyl-CoA.»

[14] Cardiavant (18 de marzo de 2022). «Colesterol: ¿Por qué es un factor de riesgo cardiovascular?». Cardiavant. Consultado el 26 de diciembre de 2022.

[15] Zinöcker, Marit Kolby; Svendsen, Karianne; Dankel, Simon Nitter (20 de enero de 2021). «The homeoviscous adaptation to dietary lipids (HADL) model explains controversies over saturated fat, cholesterol, and cardiovascular disease risk». The American Journal of Clinical Nutrition 113 (2): 277-289. ISSN 0002-9165. doi:10.1093/ajcn/nqaa322. Consultado el 26 de diciembre de 2022. «SFAs play the leading role in 1 of the greatest controversies in nutrition science. Relative to PUFAs, SFAs generally increase circulating concentrations of LDL cholesterol, a risk factor for atherosclerotic cardiovascular disease (ASCVD). However, the purpose of regulatory mechanisms that control the diet-induced lipoprotein cholesterol dynamics is rarely discussed in the context of human adaptive biology. We argue that better mechanistic explanations can help resolve lingering controversies, with the potential to redefine aspects of research, clinical practice, dietary advice, public health management, and food policy. In this paper we propose a novel model, the homeoviscous adaptation to dietary lipids (HADL) model, which explains changes in lipoprotein cholesterol as adaptive homeostatic adjustments that serve to maintain cell membrane fluidity and hence optimal cell function. Due to the highly variable intake of fatty acids in humans and other omnivore species, we propose that circulating lipoproteins serve as a buffer to enable the rapid redistribution of cholesterol molecules between specific cells and tissues that is necessary with changes in dietary fatty acid supply. Hence, circulating levels of LDL cholesterol may change for nonpathological reasons. Accordingly, an SFA-induced raise in LDL cholesterol in healthy individuals could represent a normal rather than a pathologic response. These regulatory mechanisms may become disrupted secondarily to pathogenic processes in association with insulin resistance and the presence of other ASCVD risk factors, as supported by evidence showing diverging lipoprotein responses in healthy individuals as opposed to those with metabolic disorders such as insulin resistance and obesity.»

[16] Laila, Amar (2021-08). «Limitations in the “homeoviscous adaptation to dietary lipids” model». The American Journal of Clinical Nutrition 114 (2): 822-823. ISSN 0002-9165. doi:10.1093/ajcn/nqab230. Consultado el 26 de diciembre de 2022. «I read with interest the article by Zinöcker et al. (1), in which the authors proposed a model to explain the observed pathologic increase in LDL-cholesterol concentrations in response to higher SFA intake. The model de-emphasized the role of SFAs and suggested that dysregulation of cholesterol uptake is caused by endotoxemia, which causes inflammation and, therefore, prevents cholesterol uptake via LDL-cholesterol receptors. The authors’ conclusion was that, if the model is verified, recommendations should focus on reducing intake of refined carbohydrates, which increases the growth of LPS-containing gut bacteria, but not reducing intake of SFAs.»

[17] Ramsden, Christopher E; Zamora, Daisy; Majchrzak-Hong, Sharon; Faurot, Keturah R; Broste, Steven K; Frantz, Robert P; Davis, John M; Ringel, Amit et al. (12 de abril de 2016). «Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)». BMJ: i1246. ISSN 1756-1833. doi:10.1136/bmj.i1246. Consultado el 26 de diciembre de 2022. «The Minnesota Coronary Experiment (MCE), a randomized controlled trial conducted in 1968-73, was the largest (n=9570) and perhaps the most rigorously executed dietary trial of cholesterol lowering by replacement of saturated fat with vegetable oil rich in linoleic acid. The MCE is the only such randomized controlled trial to complete postmortem assessment of coronary, aortic, and cerebrovascular atherosclerosis grade and infarct status and the only one to test the clinical effects of increasing linoleic acid in large prespecified subgroups of women and older adults.»

[18] Ramsden, Christopher E; Zamora, Daisy; Majchrzak-Hong, Sharon; Faurot, Keturah R; Broste, Steven K; Frantz, Robert P; Davis, John M; Ringel, Amit et al. (12 de abril de 2016). «Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)». BMJ: i1246. ISSN 1756-1833. doi:10.1136/bmj.i1246. Consultado el 26 de diciembre de 2022. «Available evidence from randomized controlled trials shows that replacement of saturated fat with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes. MCE findings add to growing evidence that incomplete publication has contributed to overestimation of benefits, and underestimation of potential risks, of replacing saturated fat with vegetable oils rich in linoleic acid.»

[19] Ruiz-Núñez, Begoña; Dijck-Brouwer, D. A. Janneke; Muskiet, Frits A. J. (1 de octubre de 2016). «The relation of saturated fatty acids with low-grade inflammation and cardiovascular disease». The Journal of Nutritional Biochemistry (en inglés) 36: 1-20. ISSN 0955-2863. doi:10.1016/j.jnutbio.2015.12.007. Consultado el 26 de diciembre de 2022.

[20] Dehghan, Mahshid; Mente, Andrew; Zhang, Xiaohe; Swaminathan, Sumathi; Li, Wei; Mohan, Viswanathan; Iqbal, Romaina; Kumar, Rajesh et al. (4 de noviembre de 2017). «Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study». The Lancet (en english) 390 (10107): 2050-2062. ISSN 0140-6736. PMID 28864332. doi:10.1016/S0140-6736(17)32252-3. Consultado el 26 de diciembre de 2022. «The Prospective Urban Rural Epidemiology (PURE) study is a large, epidemiological cohort study of individuals aged 35–70 years (enrolled between Jan 1, 2003, and March 31, 2013) in 18 countries with a median follow-up of 7·4 years (IQR 5·3–9·3). Dietary intake of 135 335 individuals was recorded using validated food frequency questionnaires. The primary outcomes were total mortality and major cardiovascular events (fatal cardiovascular disease, non-fatal myocardial infarction, stroke, and heart failure). Secondary outcomes were all myocardial infarctions, stroke, cardiovascular disease mortality, and non-cardiovascular disease mortality. Participants were categorised into quintiles of nutrient intake (carbohydrate, fats, and protein) based on percentage of energy provided by nutrients. We assessed the associations between consumption of carbohydrate, total fat, and each type of fat with cardiovascular disease and total mortality. We calculated hazard ratios (HRs) using a multivariable Cox frailty model with random intercepts to account for centre clustering.»

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-La '''hipótesis dieta-corazón''' postula que la reducción de las grasas saturadas en la dieta reduce el colesterol sérico, lo que reduce el riesgo de enfermedad cardiovascular (ECV);<ref>{{Cita publicación|url=http://dx.doi.org/10.1136/bmjebm-2019-111180|título=Fat or fiction: the diet-heart hypothesis|apellidos=DuBroff|nombre=Robert|apellidos2=de Lorgeril|nombre2=Michel|fecha=2019-05-29|publicación=BMJ Evidence-Based Medicine|volumen=26|número=1|páginas=3–7|fechaacceso=2022-12-26|issn=2515-446X|doi=10.1136/bmjebm-2019-111180|cita=The concept that diet, serum cholesterol and cardiovascular disease are causally related gave rise to the diet-heart hypothesis nearly 70 years ago. This hypothesis postulates that reducing dietary saturated fat reduces serum cholesterol, thereby reducing the risk of cardiovascular disease. Today, this concept has been transformed from a hypothesis into public health policy as current guidelines recommend reducing the intake of dietary saturated fat.}}</ref>en concordancia con ello, las pautas dietéticas recomiendan restringir la ingesta de grasas saturadas.<ref>{{Cita publicación|url=http://dx.doi.org/10.1016/j.pcad.2015.11.006|título=The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease|apellidos=DiNicolantonio|nombre=James J.|apellidos2=Lucan|nombre2=Sean C.|fecha=2016-03|publicación=Progress in Cardiovascular Diseases|volumen=58|número=5|páginas=464–472|fechaacceso=2022-12-26|issn=0033-0620|doi=10.1016/j.pcad.2015.11.006|cita=Dietary guidelines continue to recommend restricting intake of saturated fats. This recommendation follows largely from the observation that saturated fats can raise levels of total serum cholesterol (TC), thereby putatively increasing the risk of atherosclerotic coronary heart disease (CHD).|apellidos3=O’Keefe|nombre3=James H.}}</ref>La gran cantidad de evidencia científica indica que el colesterol total y el colesterol LDL (lipoproteína de baja densidad), a menudo denominado 'colesterol malo', contribuyen a las enfermedades cardíacas;<ref name=":0">{{Cita noticia|título=¿Realmente comer grasas saturadas aumenta el colesterol y el riesgo de enfermedades del corazón?|url=https://www.bbc.com/mundo/vert-fut-49229783|periódico=BBC News Mundo|fechaacceso=2022-12-26|idioma=es}}</ref> sin embargo, existencia evidencia que no encuentra relación de causalidad entre la ingesta de grasas saturadas y las enfermedades cardiovasculares; asimismo, hay estudios que evidencian una relación inversa entre la ingesta de grasa saturada y la salud cardiovascular; además la sustitución de grasas saturadas por grasas poliinsaturadas omega 6 no se traduce en una disminución del riesgo de padecer enfermedades cardiovasculares.<ref>{{Cita publicación|url=http://dx.doi.org/10.3989/gya.1993.v44.i4-5.1072|título=Eliminación de ácido clorogénico durante el procesado acuoso de las almendras de girasol|apellidos=Domínguez|nombre=H.|apellidos2=Núñez|nombre2=M. J.|fecha=1993-10-30|publicación=Grasas y Aceites|volumen=44|número=4-5|páginas=235–242|fechaacceso=2022-12-26|issn=1988-4214|doi=10.3989/gya.1993.v44.i4-5.1072|cita=En vista de la evidencia presentada se concluye que no se encuentra relación de causalidad entre la ingesta de grasas saturadas y las enfermedades cardiovasculares. Hay estudios que evidencian una relación inversa entre la ingesta de grasa saturada y la salud cardiovascular. La sustitución de grasas saturadas por grasas poliinsaturadas omega 6 no se traduce en una disminución del riesgo de padecer enfermedades cardiovasculares.
+La '''hipótesis dieta-corazón''' postula que la reducción de las grasas saturadas en la dieta reduce el [[colesterol]] sérico, disminuyendo el depósito de colesterol en la pared arterial, lo que reduce el riesgo de [[Enfermedades cardiovasculares|enfermedad cardiovascular]] (ECV);<ref>{{Cita publicación|url=http://dx.doi.org/10.1136/bmjebm-2019-111180|título=Fat or fiction: the diet-heart hypothesis|apellidos=DuBroff|nombre=Robert|apellidos2=de Lorgeril|nombre2=Michel|fecha=2019-05-29|publicación=BMJ Evidence-Based Medicine|volumen=26|número=1|páginas=3–7|fechaacceso=2022-12-26|issn=2515-446X|doi=10.1136/bmjebm-2019-111180|cita=The concept that diet, serum cholesterol and cardiovascular disease are causally related gave rise to the diet-heart hypothesis nearly 70 years ago. This hypothesis postulates that reducing dietary saturated fat reduces serum cholesterol, thereby reducing the risk of cardiovascular disease. Today, this concept has been transformed from a hypothesis into public health policy as current guidelines recommend reducing the intake of dietary saturated fat.}}</ref><ref name=":1">{{Cita publicación|url=http://dx.doi.org/10.1136/bmj.i1246|título=Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)|apellidos=Ramsden|nombre=Christopher E|apellidos2=Zamora|nombre2=Daisy|fecha=2016-04-12|publicación=BMJ|páginas=i1246|fechaacceso=2022-12-26|issn=1756-1833|doi=10.1136/bmj.i1246|cita=The traditional diet-heart hypothesis1 2 predicts that the serum cholesterol lowering effects of replacing saturated fat with vegetable oil rich in linoleic acid will diminish deposition of cholesterol in the arterial wall,3 4 slow progression of atherosclerosis,5 reduce coronary heart disease events, and improve survival.6 7 This diet-heart paradigm is supported by evidence from randomized controlled trials showing that replacement of saturated fat with linoleic acid lowers serum total cholesterol and low density lipoprotein8 9 10 11 12 and by observational evidence linking serum cholesterol to coronary heart disease events and deaths (fig 1⇓).13 Despite these compelling relations, no randomized controlled trial has shown that replacement of saturated fat with linoleic acid significantly reduces coronary heart disease events or deaths (fig 1⇓).|apellidos3=Majchrzak-Hong|nombre3=Sharon|apellidos4=Faurot|nombre4=Keturah R|apellidos5=Broste|nombre5=Steven K|apellidos6=Frantz|nombre6=Robert P|apellidos7=Davis|nombre7=John M|apellidos8=Ringel|nombre8=Amit|apellidos9=Suchindran|nombre9=Chirayath M}}</ref>en concordancia con ello, las pautas dietéticas recomiendan restringir la ingesta de grasas saturadas.<ref>{{Cita publicación|url=http://dx.doi.org/10.1016/j.pcad.2015.11.006|título=The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease|apellidos=DiNicolantonio|nombre=James J.|apellidos2=Lucan|nombre2=Sean C.|fecha=2016-03|publicación=Progress in Cardiovascular Diseases|volumen=58|número=5|páginas=464–472|fechaacceso=2022-12-26|issn=0033-0620|doi=10.1016/j.pcad.2015.11.006|cita=Dietary guidelines continue to recommend restricting intake of saturated fats. This recommendation follows largely from the observation that saturated fats can raise levels of total serum cholesterol (TC), thereby putatively increasing the risk of atherosclerotic coronary heart disease (CHD).|apellidos3=O’Keefe|nombre3=James H.}}</ref><ref name=":2">{{Cita publicación|url=https://doi.org/10.1007/s13668-018-0238-x|título=Saturated Fat: Part of a Healthy Diet|apellidos=Gershuni|nombre=Victoria M.|fecha=2018-09-01|publicación=Current Nutrition Reports|volumen=7|número=3|páginas=85–96|fechaacceso=2022-12-26|idioma=en|issn=2161-3311|doi=10.1007/s13668-018-0238-x|cita=Despite the American public following recommendations to decrease absolute dietary fat intake and specifically decrease saturated fat intake, we have seen a dramatic rise over the past 40 years in the rates of non-communicable diseases associated with obesity and overweight, namely cardiovascular disease. The development of the diet-heart hypothesis in the mid twentieth century led to faulty but long-held beliefs that dietary intake of saturated fat led to heart disease. Saturated fat can lead to increased LDL cholesterol levels, and elevated plasma cholesterol levels have been shown to be a risk factor for cardiovascular disease; however, the correlative nature of their association does not assign causation.}}</ref>La gran cantidad de evidencia científica indica que el colesterol total y el colesterol LDL (lipoproteína de baja densidad), a menudo denominado 'colesterol malo', contribuyen a las enfermedades cardíacas;<ref>{{Cita publicación|url=http://dx.doi.org/10.1093/ajcn/nqaa322|título=The homeoviscous adaptation to dietary lipids (HADL) model explains controversies over saturated fat, cholesterol, and cardiovascular disease risk|apellidos=Zinöcker|nombre=Marit Kolby|apellidos2=Svendsen|nombre2=Karianne|fecha=2021-01-20|publicación=The American Journal of Clinical Nutrition|volumen=113|número=2|páginas=277–289|fechaacceso=2022-12-26|issn=0002-9165|doi=10.1093/ajcn/nqaa322|cita=At the core of the diet–heart hypothesis lies 3-step reasoning:
-Considerando estos aspectos, y teniendo en cuenta la revisión de los trabajos analizados en este artículo, entre los que se incluyen estudios del más alto rigor científico (metaanálisis y revisiones sistemáticas), se recomienda que se reconsidere en las guías dietéticas cubanas las limitaciones de la ingesta de grasa saturada para la población en general.|apellidos3=Lema|nombre3=J. M.}}</ref>
+A dietary intervention enriched in SFAs leads to increased total and LDL cholesterol concentrations.
+Elevated total and LDL cholesterol concentrations are associated with atherosclerotic cardiovascular disease (ASCVD).
+Ergo, a diet rich in SFAs promotes ASCVD.
+Viewed separately, Steps 1 and 2 are well documented in the literature, although there are inconsistent findings and large individual differences both with respect to the LDL cholesterol response and its association with disease (1, 2). However, causal evidence for Step 3 is lacking (1), despite the large and still-growing number of studies that have addressed this question (3–5).|apellidos3=Dankel|nombre3=Simon Nitter}}</ref><ref name=":0">{{Cita noticia|título=¿Realmente comer grasas saturadas aumenta el colesterol y el riesgo de enfermedades del corazón?|url=https://www.bbc.com/mundo/vert-fut-49229783|periódico=BBC News Mundo|fechaacceso=2022-12-26|idioma=es}}</ref> sin embargo, existencia evidencia que no encuentra relación de causalidad entre la ingesta de grasas saturadas y las enfermedades cardiovasculares; asimismo, hay estudios que evidencian una relación inversa entre la ingesta de grasa saturada y la salud cardiovascular; además la sustitución de grasas saturadas por grasas poliinsaturadas omega 6 no se traduce en una disminución del riesgo de padecer enfermedades cardiovasculares;<ref>{{Cita publicación|url=http://dx.doi.org/10.3989/gya.1993.v44.i4-5.1072|título=Eliminación de ácido clorogénico durante el procesado acuoso de las almendras de girasol|apellidos=Domínguez|nombre=H.|apellidos2=Núñez|nombre2=M. J.|fecha=1993-10-30|publicación=Grasas y Aceites|volumen=44|número=4-5|páginas=235–242|fechaacceso=2022-12-26|issn=1988-4214|doi=10.3989/gya.1993.v44.i4-5.1072|cita=En vista de la evidencia presentada se concluye que no se encuentra relación de causalidad entre la ingesta de grasas saturadas y las enfermedades cardiovasculares. Hay estudios que evidencian una relación inversa entre la ingesta de grasa saturada y la salud cardiovascular. La sustitución de grasas saturadas por grasas poliinsaturadas omega 6 no se traduce en una disminución del riesgo de padecer enfermedades cardiovasculares.
+Considerando estos aspectos, y teniendo en cuenta la revisión de los trabajos analizados en este artículo, entre los que se incluyen estudios del más alto rigor científico (metaanálisis y revisiones sistemáticas), se recomienda que se reconsidere en las guías dietéticas cubanas las limitaciones de la ingesta de grasa saturada para la población en general.|apellidos3=Lema|nombre3=J. M.}}</ref>en tal sentido, existen opiniones de que las pautas dietéticas globales deben reconsiderarse.<ref name=":3">{{Cita publicación|url=https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)32252-3/abstract|título=Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study|apellidos=Dehghan|nombre=Mahshid|apellidos2=Mente|nombre2=Andrew|fecha=2017-11-04|publicación=The Lancet|volumen=390|número=10107|páginas=2050–2062|fechaacceso=2022-12-26|idioma=English|issn=0140-6736|doi=10.1016/S0140-6736(17)32252-3|pmid=28864332|cita=High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality, whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.|apellidos3=Zhang|nombre3=Xiaohe|apellidos4=Swaminathan|nombre4=Sumathi|apellidos5=Li|nombre5=Wei|apellidos6=Mohan|nombre6=Viswanathan|apellidos7=Iqbal|nombre7=Romaina|apellidos8=Kumar|nombre8=Rajesh|apellidos9=Wentzel-Viljoen|nombre9=Edelweiss}}</ref>
 == Historia ==
 {{VT|Ancel Keys}}
 La hipótesis de que las grasas saturadas causan CVD surgió a fines de la década de 1950, cuando los científicos observaron que estas grasas tienden a elevar la concentración de colesterol sérico total, que a su vez se consideraba un potente factor de riesgo de enfermedad cardíaca.<ref>{{Cita publicación|url=https://www.mdpi.com/2072-6643/13/10/3305|título=Dietary Saturated Fats and Health: Are the U.S. Guidelines Evidence-Based?|apellidos=Astrup|nombre=Arne|apellidos2=Teicholz|nombre2=Nina|fecha=2021-10|publicación=Nutrients|volumen=13|número=10|páginas=3305|fechaacceso=2022-12-26|idioma=en|issn=2072-6643|doi=10.3390/nu13103305|cita=The hypothesis that saturated fats cause CVD emerged in the late 1950s, when scientists observed that these fats tend to raise the concentration of total serum cholesterol, which in turn was considered a potent risk factor for heart disease. Ancel Keys, a physiologist at the University of Minnesota, postulated that saturated fats along with dietary cholesterol were the principal causes of cardiovascular disease, and his “diet-heart hypothesis” was adopted by leading groups, including the American Heart Association.|apellidos3=Magkos|nombre3=Faidon|apellidos4=Bier|nombre4=Dennis M.|apellidos5=Brenna|nombre5=J. Thomas|apellidos6=King|nombre6=Janet C.|apellidos7=Mente|nombre7=Andrew|apellidos8=Ordovas|nombre8=José M.|apellidos9=Volek|nombre9=Jeff S.}}</ref>La hipótesis dieta-corazón ganó amplia aceptación en las décadas de 1970 y 1980.<ref>{{Cita publicación|url=https://www.mdpi.com/2072-6643/13/10/3305|título=Dietary Saturated Fats and Health: Are the U.S. Guidelines Evidence-Based?|apellidos=Astrup|nombre=Arne|apellidos2=Teicholz|nombre2=Nina|fecha=2021-10|publicación=Nutrients|volumen=13|número=10|páginas=3305|fechaacceso=2022-12-26|idioma=en|issn=2072-6643|doi=10.3390/nu13103305|cita=the diet-heart hypothesis gained widespread acceptance in the 1970s and 1980s, yet the results from the totality of these trials did not provide support for the hypothesis, as many critics at the time pointed out|apellidos3=Magkos|nombre3=Faidon|apellidos4=Bier|nombre4=Dennis M.|apellidos5=Brenna|nombre5=J. Thomas|apellidos6=King|nombre6=Janet C.|apellidos7=Mente|nombre7=Andrew|apellidos8=Ordovas|nombre8=José M.|apellidos9=Volek|nombre9=Jeff S.}}</ref>
+A pesar de que el público estadounidense sigue las recomendaciones para disminuir la ingesta absoluta de grasas en la dieta y específicamente disminuir la ingesta de grasas saturadas, se ha visto un aumento dramático en los últimos 40 años en las tasas de enfermedades cardiovasculares.<ref name=":2" />
+Numerosos metanálisis y revisiones sistemáticas de la literatura histórica y actual revelan que la hipótesis de la dieta y el corazón no estaba, y aún no está, respaldada por la evidencia.<ref>{{Cita publicación|url=https://doi.org/10.1007/s13668-018-0238-x|título=Saturated Fat: Part of a Healthy Diet|apellidos=Gershuni|nombre=Victoria M.|fecha=2018-09-01|publicación=Current Nutrition Reports|volumen=7|número=3|páginas=85–96|fechaacceso=2022-12-26|idioma=en|issn=2161-3311|doi=10.1007/s13668-018-0238-x|cita=Advances in understanding the role of various lipoprotein particles and their atherogenic risk have been helpful for understanding how different dietary components may impact CVD risk. Numerous meta-analyses and systematic reviews of both the historical and current literature reveals that the diet-heart hypothesis was not, and still is not, supported by the evidence. There appears to be no consistent benefit to all-cause or CVD mortality from the reduction of dietary saturated fat. Further, saturated fat has been shown in some cases to have an inverse relationship with obesity-related type 2 diabetes.}}</ref>
 == Recomendaciones ==
-Reino Unido recomienda, sobre las grasas saturadas, que no incluya más del 11% de nuestras calorías de alimentos y bebidas, mientras que Estados Unidos y la Organización Mundial de la Salud recomiendan menos del 10%.<ref name=":0" />
+Reino Unido recomienda, sobre las grasas saturadas, que no incluya más del 11% de nuestras calorías de alimentos y bebidas, mientras que Estados Unidos y la Organización Mundial de la Salud recomiendan menos del 10%.<ref>{{Cita publicación|url=https://www.jacc.org/doi/abs/10.1016/j.jacc.2020.05.077|título=Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations|apellidos=Astrup|nombre=Arne|apellidos2=Magkos|nombre2=Faidon|fecha=2020-08-18|publicación=Journal of the American College of Cardiology|volumen=76|número=7|páginas=844–857|fechaacceso=2022-12-26|doi=10.1016/j.jacc.2020.05.077|cita=•The U.S. Dietary Guidelines recommend the restriction of SFA intake to <10% of calories to reduce CVD.
+•Different SFAs have different biologic effects, which are further modified by the food matrix and the carbohydrate content of the diet.
+•Several foods relatively rich in SFAs, such as whole-fat dairy, dark chocolate, and unprocessed meat, are not associated with increased CVD or diabetes risk.
+•There is no robust evidence that current population-wide arbitrary upper limits on saturated fat consumption in the United States will prevent CVD or reduce mortality.|apellidos3=Bier|nombre3=Dennis M.|apellidos4=Brenna|nombre4=J. Thomas|apellidos5=de|nombre5=Oliveira Otto Marcia C.|apellidos6=Hill|nombre6=James O.|apellidos7=King|nombre7=Janet C.|apellidos8=Mente|nombre8=Andrew|apellidos9=Ordovas|nombre9=Jose M.}}</ref><ref name=":0" />
 == Fisiología ==
+{{Artículo principal|Ateroesclerosis}}
+Algunos estudios refieren que una mayor ingesta de grasas saturadas proporciona sustratos para la síntesis de colesterol en forma de acetil-CoA.<ref>{{Cita publicación|url=http://dx.doi.org/10.1093/ajcn/nqaa322|título=The homeoviscous adaptation to dietary lipids (HADL) model explains controversies over saturated fat, cholesterol, and cardiovascular disease risk|apellidos=Zinöcker|nombre=Marit Kolby|apellidos2=Svendsen|nombre2=Karianne|fecha=2021-01-20|publicación=The American Journal of Clinical Nutrition|volumen=113|número=2|páginas=277–289|fechaacceso=2022-12-26|issn=0002-9165|doi=10.1093/ajcn/nqaa322|cita=Studies have investigated whether increased SFA intake increases the endogenous synthesis of cholesterol: for example, by providing substrates for synthesis in the form of acetyl-CoA.|apellidos3=Dankel|nombre3=Simon Nitter}}</ref>
 Cuando existe un exceso de colesterol se deposita en nuestras arterias engrosando las paredes de éstas.<ref>{{Cita web|url=https://cardiavant.com/colesterol-por-que-es-un-factor-de-riesgo-cardiovascular/|título=Colesterol: ¿Por qué es un factor de riesgo cardiovascular?|fechaacceso=2022-12-26|apellido=Cardiavant|fecha=2022-03-18|sitioweb=Cardiavant|idioma=es}}</ref>
+Zinöcker, Svendsen y Nitter han propuesto el modelo de '''adaptación homeoviscosa a los lípidos dietéticos''' (HADL), que explica los cambios en el colesterol de lipoproteínas como ajustes homeostáticos adaptativos que sirven para mantener la fluidez de la membrana celular y, por lo tanto, una función celular óptima;<ref>{{Cita publicación|url=http://dx.doi.org/10.1093/ajcn/nqaa322|título=The homeoviscous adaptation to dietary lipids (HADL) model explains controversies over saturated fat, cholesterol, and cardiovascular disease risk|apellidos=Zinöcker|nombre=Marit Kolby|apellidos2=Svendsen|nombre2=Karianne|fecha=2021-01-20|publicación=The American Journal of Clinical Nutrition|volumen=113|número=2|páginas=277–289|fechaacceso=2022-12-26|issn=0002-9165|doi=10.1093/ajcn/nqaa322|cita=SFAs play the leading role in 1 of the greatest controversies in nutrition science. Relative to PUFAs, SFAs generally increase circulating concentrations of LDL cholesterol, a risk factor for atherosclerotic cardiovascular disease (ASCVD). However, the purpose of regulatory mechanisms that control the diet-induced lipoprotein cholesterol dynamics is rarely discussed in the context of human adaptive biology. We argue that better mechanistic explanations can help resolve lingering controversies, with the potential to redefine aspects of research, clinical practice, dietary advice, public health management, and food policy. In this paper we propose a novel model, the homeoviscous adaptation to dietary lipids (HADL) model, which explains changes in lipoprotein cholesterol as adaptive homeostatic adjustments that serve to maintain cell membrane fluidity and hence optimal cell function. Due to the highly variable intake of fatty acids in humans and other omnivore species, we propose that circulating lipoproteins serve as a buffer to enable the rapid redistribution of cholesterol molecules between specific cells and tissues that is necessary with changes in dietary fatty acid supply. Hence, circulating levels of LDL cholesterol may change for nonpathological reasons. Accordingly, an SFA-induced raise in LDL cholesterol in healthy individuals could represent a normal rather than a pathologic response. These regulatory mechanisms may become disrupted secondarily to pathogenic processes in association with insulin resistance and the presence of other ASCVD risk factors, as supported by evidence showing diverging lipoprotein responses in healthy individuals as opposed to those with metabolic disorders such as insulin resistance and obesity.|apellidos3=Dankel|nombre3=Simon Nitter}}</ref>asimiso, de acuerdo con el modelo, la desregulación de la captación de colesterol es causada por la endotoxemia, que provoca inflamación y, por lo tanto, impide la captación de colesterol a través de los receptores de colesterol LDL.<ref>{{Cita publicación|url=http://dx.doi.org/10.1093/ajcn/nqab230|título=Limitations in the “homeoviscous adaptation to dietary lipids” model|apellidos=Laila|nombre=Amar|fecha=2021-08|publicación=The American Journal of Clinical Nutrition|volumen=114|número=2|páginas=822–823|fechaacceso=2022-12-26|issn=0002-9165|doi=10.1093/ajcn/nqab230|cita=I read with interest the article by Zinöcker et al. (1), in which the authors proposed a model to explain the observed pathologic increase in LDL-cholesterol concentrations in response to higher SFA intake. The model de-emphasized the role of SFAs and suggested that dysregulation of cholesterol uptake is caused by endotoxemia, which causes inflammation and, therefore, prevents cholesterol uptake via LDL-cholesterol receptors. The authors’ conclusion was that, if the model is verified, recommendations should focus on reducing intake of refined carbohydrates, which increases the growth of LPS-containing gut bacteria, but not reducing intake of SFAs.}}</ref>
-== Evidencia contradictoria ==
+== Evidencia a favor ==
+El Minnesota Coronary Experiment (MCE), un ensayo controlado aleatorizado realizado entre 1968 y 1973, fue el ensayo dietético más grande y quizás el más rigurosamente ejecutado para reducir el colesterol mediante el reemplazo de grasas saturadas con aceite vegetal rico en ácido linoleico. SIn embargo, posteriores hallazgos de publicación incompleta sugieren una sobreestimación de los beneficios y  subestimación de los riesgos potenciales de reemplazar grasas saturadas con aceites vegetales ricos en ácido linoleico.<ref>{{Cita publicación|url=http://dx.doi.org/10.1136/bmj.i1246|título=Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)|apellidos=Ramsden|nombre=Christopher E|apellidos2=Zamora|nombre2=Daisy|fecha=2016-04-12|publicación=BMJ|páginas=i1246|fechaacceso=2022-12-26|issn=1756-1833|doi=10.1136/bmj.i1246|cita=The Minnesota Coronary Experiment (MCE), a randomized controlled trial conducted in 1968-73, was the largest (n=9570) and perhaps the most rigorously executed dietary trial of cholesterol lowering by replacement of saturated fat with vegetable oil rich in linoleic acid. The MCE is the only such randomized controlled trial to complete postmortem assessment of coronary, aortic, and cerebrovascular atherosclerosis grade and infarct status and the only one to test the clinical effects of increasing linoleic acid in large prespecified subgroups of women and older adults.|apellidos3=Majchrzak-Hong|nombre3=Sharon|apellidos4=Faurot|nombre4=Keturah R|apellidos5=Broste|nombre5=Steven K|apellidos6=Frantz|nombre6=Robert P|apellidos7=Davis|nombre7=John M|apellidos8=Ringel|nombre8=Amit|apellidos9=Suchindran|nombre9=Chirayath M}}</ref><ref>{{Cita publicación|url=http://dx.doi.org/10.1136/bmj.i1246|título=Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)|apellidos=Ramsden|nombre=Christopher E|apellidos2=Zamora|nombre2=Daisy|fecha=2016-04-12|publicación=BMJ|páginas=i1246|fechaacceso=2022-12-26|issn=1756-1833|doi=10.1136/bmj.i1246|cita=Available evidence from randomized controlled trials shows that replacement of saturated fat with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes. MCE findings add to growing evidence that incomplete publication has contributed to overestimation of benefits, and underestimation of potential risks, of replacing saturated fat with vegetable oils rich in linoleic acid.|apellidos3=Majchrzak-Hong|nombre3=Sharon|apellidos4=Faurot|nombre4=Keturah R|apellidos5=Broste|nombre5=Steven K|apellidos6=Frantz|nombre6=Robert P|apellidos7=Davis|nombre7=John M|apellidos8=Ringel|nombre8=Amit|apellidos9=Suchindran|nombre9=Chirayath M}}</ref>
+== Evidencia en contra ==
+De acuerdo con Ramsden, ningún ensayo controlado aleatorizado (ECA) ha demostrado que el reemplazo de grasas saturadas con ácido linoleico reduzca significativamente los eventos de enfermedad coronaria o las muertes.<ref name=":1" />
 Un metanálisis revisado de ECAs mostró que la sustitución de ácidos grasos (AG) saturados por AG ω6 sin aumentar simultáneamente AG ω3 no presenta indicios de beneficio e incluso es probable que aumente el riesgo de ECV<ref>{{Cita publicación|url=https://www.sciencedirect.com/science/article/pii/S095528631600005X|título=The relation of saturated fatty acids with low-grade inflammation and cardiovascular disease|apellidos=Ruiz-Núñez|nombre=Begoña|apellidos2=Dijck-Brouwer|nombre2=D. A. Janneke|fecha=2016-10-01|publicación=The Journal of Nutritional Biochemistry|volumen=36|páginas=1–20|fechaacceso=2022-12-26|idioma=en|issn=0955-2863|doi=10.1016/j.jnutbio.2015.12.007|apellidos3=Muskiet|nombre3=Frits A. J.}}</ref>
+Los hallazgos del estudio Prospective Urban Rural Epidemiology (PURE), un gran estudio epidemiológico de cohortes de personas de 35 a 70 años en 18 países con una mediana de seguimiento de 7·4 años, determinaron que La ingesta alta de carbohidratos se asoció con un mayor riesgo de mortalidad total, mientras que la grasa total y los tipos individuales de grasa se relacionaron con una mortalidad total más baja. La grasa total y los tipos de grasa no se asociaron con enfermedad cardiovascular, infarto de miocardio o mortalidad por enfermedad cardiovascular, mientras que la grasa saturada tuvo una asociación inversa con el accidente cerebrovascular.<ref>{{Cita publicación|url=https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)32252-3/abstract|título=Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study|apellidos=Dehghan|nombre=Mahshid|apellidos2=Mente|nombre2=Andrew|fecha=2017-11-04|publicación=The Lancet|volumen=390|número=10107|páginas=2050–2062|fechaacceso=2022-12-26|idioma=English|issn=0140-6736|doi=10.1016/S0140-6736(17)32252-3|pmid=28864332|cita=The Prospective Urban Rural Epidemiology (PURE) study is a large, epidemiological cohort study of individuals aged 35–70 years (enrolled between Jan 1, 2003, and March 31, 2013) in 18 countries with a median follow-up of 7·4 years (IQR 5·3–9·3). Dietary intake of 135 335 individuals was recorded using validated food frequency questionnaires. The primary outcomes were total mortality and major cardiovascular events (fatal cardiovascular disease, non-fatal myocardial infarction, stroke, and heart failure). Secondary outcomes were all myocardial infarctions, stroke, cardiovascular disease mortality, and non-cardiovascular disease mortality. Participants were categorised into quintiles of nutrient intake (carbohydrate, fats, and protein) based on percentage of energy provided by nutrients. We assessed the associations between consumption of carbohydrate, total fat, and each type of fat with cardiovascular disease and total mortality. We calculated hazard ratios (HRs) using a multivariable Cox frailty model with random intercepts to account for centre clustering.|apellidos3=Zhang|nombre3=Xiaohe|apellidos4=Swaminathan|nombre4=Sumathi|apellidos5=Li|nombre5=Wei|apellidos6=Mohan|nombre6=Viswanathan|apellidos7=Iqbal|nombre7=Romaina|apellidos8=Kumar|nombre8=Rajesh|apellidos9=Wentzel-Viljoen|nombre9=Edelweiss}}</ref><ref name=":3" />
 == Referencias ==