Past public health crises (e.g., tobacco, alcohol, opioids, cholera, human immunodeficiency virus (HIV), lead, pollution, venereal disease, even coronavirus (COVID-19) have been met with interventions targeted both at the individual and all of society. While the healthcare community is very aware that the global pandemic of non-communicable diseases (NCDs) has its origins in our Western ultraprocessed food diet, society has been slow to initiate any interventions other than public education, which has been ineffective, in part due to food industry interference. This article provides the rationale for such public health interventions, by compiling the evidence that added sugar, and by proxy the ultraprocessed food category, meets the four criteria set by the public health community as necessary and sufficient for regulation—abuse, toxicity, ubiquity, and externalities (How does your consumption affect me?). To their credit, some countries have recently heeded this science and have instituted sugar taxation policies to help ameliorate NCDs within their borders. This article also supplies scientific counters to food industry talking points, and sample intervention strategies, in order to guide both scientists and policy makers in instituting further appropriate public health measures to quell this pandemic.

Sugar intake, particularly fructose, is implicated as a factor contributing to insulin resistance via hepatic de novo lipogenesis (DNL). A nine-day fructose reduction trial, controlling for other dietary factors and weight, in children with obesity and metabolic syndrome, decreased DNL and mitigated cardiometabolic risk (CMR) biomarkers. Ceramides are bioactive sphingolipids whose dysregulated metabolism contribute to lipotoxicity, insulin resistance, and CMR. We evaluated the effect of fructose reduction on ceramides and correlations between changes observed and changes in traditional CMR biomarkers in this cohort. Analyses were completed on data from 43 participants. Mean weight decreased (−0.9 ± 1.1 kg). The majority of total and subspecies ceramide levels also decreased significantly, including dihydroceramides, deoxyceramides and ceramide-1-phoshates. Change in each primary ceramide species correlated negatively with composite insulin sensitivity index (CISI). Change in deoxyceramides positively correlated with change in DNL. These results suggest that ceramides decrease in response to dietary fructose restriction, negatively correlate with insulin sensitivity, and may represent an intermediary link between hepatic DNL, insulin resistance, and CMR.

Objective: The aim of the study is to analyze the impact of physical activity and eating behaviors on precursors of cardiovascular disease—including overweight/obesity, hypertension, low high‐density lipoprotein, and impaired glucose tolerance—in pediatric liver transplant (LT) recipients and matched controls.Method: Cross‐sectional study of pediatric LT recipients 8 to 30 years, matched to controls from the National Health and Nutrition Examination Survey. Dietary intake assessed with 24‐hour recall. Physical activity assessed by standardized questionnaires. LT recipients ≥12 years completed a confidential survey on alcohol consumption.Results: LT recipients (n = 90) were 0.9 to 24.7 years post‐transplant. LT recipients and controls were equally likely to consume excess carbohydrates (32% vs 34%) and sugar, per age‐ and gender‐specific recommended dietary intake guidelines. LT recipients spent more hours sedentary or on the computer daily and fewer days each week physically active for >60 minutes than controls. More overweight/obese LT recipients spent 3+ hours at the computer than non‐overweight LT recipients (49% vs 27%; P = 0.02). Normal weight LT recipients spent more days doing vigorous activity each week (median 5 days, interquartile range 2–6) than did the overweight/obese LT recipients (median 3 days, interquartile range 2–4; P = 0.01). Among LT recipients, neither dietary intake nor physical activity were consistently associated with measures of hypertension, glucose intolerance, or dyslipidemia. Among LT adolescents and young adults (n = 38), 36% reported ever consuming alcohol; 38% of these reported significant alcohol consumption by frequency or quantity.Conclusions: Additional counseling during routine post‐LT care on the importance of physical activity and healthy diet may be useful. However, it is unlikely that these factors alone explain the increased prevalence of metabolic syndrome components in pediatric LT recipients.

Perhaps the most unexpected development in pediatric endocrinology in the past 50 years has been the recognition of obesity as an endocrine/metabolic disorder rather than a life choice or moral failing. The history of obesity research is disjointed, having followed two separate paths in the 20th century, based on two independent yet overlapping paradigms. Proponents of the “Energy Storage” hypothesis point to data implicating monogenetic disorders, the ventromedial hypothalamus, insulin, cortisol, and the adipocyte itself in the pathogenesis of obesity. Alternatively, proponents of the “Energy Balance” hypothesis point to data implicating increased caloric intake, decreased caloric expenditure, gastrointestinal hormones, and microbiome changes as being critical for obesity. These two separate lines of research merged somewhat with the discovery of leptin in 1994, as leptin established a major hormonal role in weight control. Leptin has explained some of the dichotomy and has proved essential in understanding the importance of developmental programming and epigenetics. However, the mystery of leptin resistance remains unsolved. Despite all our collective knowledge, we appear no closer in solving the obesity puzzle today than we were 50 years ago.

The Journal of Insulin Resistance is a peer-reviewed, clinically oriented journal covering advances in disorders of insulin resistance. Articles focus on clinical care and advancing therapy for patients with insulin resistance-related disorders. Insulin resistance includes pathophysiology, management, patient education, and treatment considerations for different patient populations.

Despite decades of nutrition, obesity, and diabetes research, and worsening prevalences and severities of virtually every chronic metabolic disease, the scientific community remains divided over the existence and veracity of the concept of food addiction. There are numerous rationalizations — 1) you need food to survive, (of which “Food is Medicine” is the latest mantra); 2) people with obesity should not be stigmatized as “mentally ill”; 3) people with obesity should instead adhere to “personal responsibility”; 4) the data are incomplete and not strong enough; 5) it’s correlation but not causation; 6) everyone is exposed, but not everyone is addicted; 7) there is no “withdrawal” phenotype; and 8) it’s not “food addiction” but “eating addiction”. All are in play, yet more health care dollars are diverted to the treatment of food-related disease every year. While various ingestible chemicals (e.g. nicotine, cocaine, heroin, alcohol) are clearly addictive, it appears to be a stretch by some scientists to argue that individual substances found in food (e.g. sugar, caffeine), or the food itself (e.g. ultraprocessed food), rise to meet the same criteria. Symposia on food addiction proliferate and journal debates continue. The definition of addiction consists of numerous criteria, including public health demographics, biochemistry, imaging, animal trials, clinical trials, and economics. None of these have proven to be “slam dunks” to align a general consensus. But paramount for scientific acceptance is the delineation of mechanism. This article will review the history of the controversy, the data on which foods are most likely to be addictive, the two mechanisms involved in the pathogenesis of food addiction and relate it to the most likely culprits, and the role of the food industry in promulgating false narratives, in order to provide a rational way forward from this debate.