Ultra-processed foods provide 58 % of energy intake and 89 % of added sugars in the American diet. Nevertheless, the association between ultra-processed foods and excess weight has not been investigated in a US sample. The present investigation therefore aims to examine the association between ultra-processed foods and excess weight in a nationally representative sample of US adults. We performed a cross-sectional analysis of anthropometric and dietary data from 15 977 adults (20–64 years) participating in the National Health and Nutrition Examination Survey 2005–2014. Dietary data were collected by 24-h recall. Height, weight and waist circumference (WC) were measured. Foods were classified as ultra-processed/non-ultra-processed according to the NOVA classification. Multivariable linear and logistic regression was used to evaluate the association between ultra-processed food consumption (% energy) and BMI, WC and odds of BMI≥25 kg/m², BMI≥30 kg/m² and abdominal obesity (men: WC≥102 cm, women: WC≥88 cm). Prevalence of BMI≥25 kg/m², BMI≥30 kg/m² and abdominal obesity was 69·2, 36·1 and 53·0 %, respectively. Consuming ≥74·2 v. ≤36·5 % of total energy from ultra-processed foods was associated with 1·61 units higher BMI (95 % CI 1·11, 2·10), 4·07 cm greater WC (95 % CI 2·94, 5·19) and 48, 53 and 62 % higher odds of BMI≥25 kg/m², BMI≥30 kg/m² and abdominal obesity, respectively (OR 1·48; 95 % CI 1·25, 1·76; OR 1·53; 95 % CI 1·29, 1·81; OR 1·62; 95 % CI 1·39, 1·89, respectively; P_{for trend}<0·001 for all). A significant interaction between being female and ultra-processed food consumption was found for BMI (F_4,79=4·89, P=0·002), WC (F_4,79=3·71, P=0·008) and BMI≥25 kg/m² (F_4,79=5·35, P<0·001). As the first study in a US population, our findings support that higher consumption of ultra-processed food is associated with excess weight, and that the association is more pronounced among women.

Accumulating evidence links ultra-processed foods to poor diet quality and chronic diseases. Understanding dietary trends is essential to inform priorities and policies to improve diet quality and prevent diet-related chronic diseases. Data are lacking, however, for trends in ultra-processed food intake. We examined US secular trends in food consumption according to processing level from 2001 to 2018. We analyzed dietary data collected by 24-h recalls from adult participants (aged >19 y; N = 40,937) in 9 cross-sectional waves of the NHANES (2001–2002 to 2017–2018). We calculated participants’ intake of minimally processed foods, processed culinary ingredients, processed foods, and ultra-processed foods as the relative contribution to daily energy intake (%kcal) using the NOVA framework. Trends analyses were performed using linear regression, testing for linear trends by modeling the 9 surveys as an ordinal independent variable. Models were adjusted for age, sex, race/ethnicity, education level, and income. Consumption trends were reported for the full sample and stratified by sex, age groups, race/ethnicity, education level, and income level. Adjusting for changes in population characteristics, the consumption of ultra-processed foods increased among all US adults from 2001–2002 to 2017–2018 (from 53.5 to 57.0 %kcal; P-trend < 0.001). The trend was consistent among all sociodemographic subgroups, except Hispanics, in stratified analyses. In contrast, the consumption of minimally processed foods decreased significantly over the study period (from 32.7 to 27.4 %kcal; P-trend < 0.001) and across all sociodemographic strata. The consumption of processed culinary ingredients increased from 3.9 to 5.4 %kcal (P-trend < 0.001), whereas the intake of processed foods remained stable at ∼10 %kcal throughout the study period (P-trend = 0.052). The current findings highlight the high consumption of ultra-processed foods in all parts of the US population and demonstrate that intake has continuously increased in the majority of the population in the past 2 decades.

Ultra-processed foods are industrially manufactured ready-to-eat or ready-to-heat formulations containing food additives and little or no whole foods, in contrast to processed foods, which are whole foods preserved by traditional techniques such as canning or pickling. Recent epidemiological studies suggest that higher consumption of ultra-processed food is associated with increased risk of cardiovascular disease (CVD). However, epidemiological evidence needs to be corroborated with criteria of biological plausibility. This review summarizes the current evidence on the putative biological mechanisms underlying the associations between ultra-processed foods and CVD. Research ranging from laboratory-based to prospective epidemiological studies and experimental evidence suggest that ultra-processed foods may affect cardiometabolic health through a myriad of mechanisms, beyond the traditionally recognized individual nutrients. Processing induces significant changes to the food matrix, for which ultra-processed foods may affect health outcomes differently than unrefined whole foods with similar nutritional composition. Notably, the highly degraded physical structure of ultra-processed foods may affect cardiometabolic health by influencing absorption kinetics, satiety, glycemic response, and the gut microbiota composition and function. Food additives and neo-formed contaminants produced during processing may also play a role in CVD risk. Key biological pathways include altered serum lipid concentrations, modified gut microbiota and host-microbiota interactions, obesity, inflammation, oxidative stress, dysglycemia, insulin resistance, and hypertension. Further research is warranted to clarify the proportional harm associated with the nutritional composition, food additives, physical structure, and other attributes of ultra-processed foods. Understanding how ultra-processing changes whole foods and through which pathways these foods affect health is a prerequisite for eliminating harmful processing techniques and ingredients.

Age-related macular degeneration (AMD) is a degenerative disease of the macula, the region of the retina that is responsible for central vision. It is the leading cause of irreversible vision loss as people age in the United States.¹ In its later stages, AMD affects about 7% of people between the ages of 75 and 84 years.² Early and intermediate stages of AMD, which increase the risk of developing advanced AMD,³ are even more common, affecting about one quarter of people older than 65 years.² Because there is no cure for this condition and limited treatment is available to slow its progression, and there are no established means of prevention, it is important to identify modifiable risk factors that may reduce disease occurrence or prevent progression to the late stages of AMD. The pathogenesis of AMD is likely to involve a complex interaction of cellular and vascular factors, which may be promoted by light damage,⁴ oxidative stress,⁵ and inflammation.⁶

Although obesity is a well-known risk factor for several cancers, its role on cancer survival is poorly understood. We conducted a systematic literature review to assess the current evidence evaluating the impact of body adiposity on the prognosis of the three most common obesity-related cancers: prostate, colorectal, and breast. We included 33 studies of breast cancer, six studies of prostate cancer, and eight studies of colo-rectal cancer. We note that the evidence overrepresents breast cancer survivorship research and is sparse for prostate and colorectal cancers. Overall, most studies support a relationship between body adiposity and site-specific mortality or cancer progression. However, most of the research was not specifically designed to study these outcomes and, therefore, several methodological issues should be considered before integrating their results to draw conclusions. Further research is urgently warranted to assess the long-term impact of obesity among the growing population of cancer survivors.