The dietary pattern that characterizes the Western diet is strongly associated with obesity and related metabolic diseases, but biological mechanisms supporting these associations remain largely unknown. We argue that the Western diet promotes inflammation that arises from both structural and behavioral changes in the resident microbiome. The environment created in the gut by ultra-processed foods, a hallmark of the Western diet, is an evolutionarily unique selection ground for microbes that can promote diverse forms of inflammatory disease. Recognizing the importance of the microbiome in the development of diet-related disease has implications for future research, public dietary advice as well as food production practices. Research into food patterns suggests that whole foods are a common denominator of diets associated with a low level of diet-related disease. Hence, by studying how ultra-processing changes the properties of whole foods and how these foods affect the gut microbiome, more useful dietary guidelines can be made. Innovations in food production should be focusing on enabling health in the super-organism of man and microbe, and stronger regulation of potentially hazardous components of food products is warranted.

The nutrition literature and authoritative reports increasingly recognise the concept of ultra-processed foods (UPF), as a descriptor of unhealthy diets. UPFs are now prevalent in diets worldwide. This review aims to identify and appraise the studies on healthy participants that investigated associations between levels of UPF consumption and health outcomes. This involved a systematic search for extant literature; integration and interpretation of findings from diverse study types, populations, health outcomes and dietary assessments; and quality appraisal. Of 43 studies reviewed, 37 found dietary UPF exposure associated with at least one adverse health outcome. Among adults, these included overweight, obesity and cardio-metabolic risks; cancer, type-2 diabetes and cardiovascular diseases; irritable bowel syndrome, depression and frailty conditions; and all-cause mortality. Among children and adolescents, these included cardio-metabolic risks and asthma. No study reported an association between UPF and beneficial health outcomes. Most findings were derived from observational studies and evidence of plausible biological mechanisms to increase confidence in the veracity of these observed associations is steadily evolving. There is now a considerable body of evidence supporting the use of UPFs as a scientific concept to assess the ‘healthiness’ of foods within the context of dietary patterns and to help inform the development of dietary guidelines and nutrition policy actions.

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. Corresponding with the model, we suggest alternative contributing factors to the association between elevated LDL cholesterol concentrations and ASCVD, involving dietary factors beyond SFAs, such as an increased endotoxin load from diet–gut microbiome interactions and subsequent chronic low-grade inflammation that interferes with fine-tuned signaling pathways.

Abstract:The dietary pattern that characterizes the Western diet is strongly associated with obesity and related metabolic diseases, but biological mechanisms supporting these associations remain largely unknown. We argue that the Western diet is promoting inflammation that arises from both structural and behavioral changes in the resident microbiome. The environment created in the gut by ultra-processed foods, a hallmark of the Western diet, is an evolutionarily unique selection ground for microbes that can promote diverse forms of inflammatory disease. Recognizing the importance of the microbiome in the development of diet-related disease has implications for future research, public dietary advice as well as food production practices. Research into food patterns suggest that whole foods is a common denominator of diets associated with a low level of diet-related disease. Hence, by studying how ultra-processing changes properties of whole foods and how these foods affect the gut microbiome, more useful dietary guidelines can be made. Innovations in food production should be focusing on enabling health in the super-organism of man and microbe, and stronger regulation of potentially hazardous components of food products is warranted.

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