With more than sixty percent of U.S. adults struggling with at least one diet-related health condition, the relationship between nutrition and public health has never been clearer. Indeed, for the first time in over a century, food has a prominent place on the national political stage and is one of the exceedingly few issues that has garnered bipartisan support. The recent rise in popularity of “Food Is Medicine” initiatives, which seek to provide medically tailored or healthy meals to vulnerable populations, underscores the critical importance of food to public health. Yet, while “Food Is Medicine” is shifting the insurance, business, and nutritional landscape, the Food and Drug Administration (“FDA”) — the primary regulator in charge of both food and drug safety — treats food as anything but medicine. Known and unknown food additives, color dyes categorically banned in other countries, chemicals leaching from paper and plastic, and environmental toxins and pathogens all contaminate our food and sicken children and adults alike. All the while, the FDA acts as if it were powerless to fulfill its mission of protecting the public from unsafe food.

In a time when the political will to reform our food system and rid it of harmful chemicals and ingredients is high, this article offers a blueprint for how to do so in a scientifically grounded, legally consistent, and lasting manner. Starting from the basic premise that food can be medicine, the article explores ways to bring food safety review closer to the much more demanding safety process for pharmaceuticals. Part I defends the premise that food is every bit as important to human health as medicine — both for good and for ill — and posits that food safety should be regulated just as much as (even if not in identical ways to) the safety of medical drugs. Parts II and III offer a comparison between the rigors of drug safety review, albeit with its own set of problems, and the laxity and at times utter lack of food safety review. Finally, Part IV advances a comprehensive package of both legislative and regulatory reforms, all designed to shift the de facto burden of proving the safety of food ingredients from the overtaxed FDA and the overburdened consumers to food manufacturers.

Despite the increasing market share of commercial complementary foods, their nutritional characteristics and those associated with the price of products are still unknown in Japan. We compared the nutritional characteristics of commercially available complementary foods of different price levels in Japan. Data were obtained from the websites of Japanese brands of infant and young children’s food. Nutrient profiles (unit/100 g), ingredients and food additives were compared between low- and high-priced products by product type. Sixty-three dry meals, 425 soft meals, 187 snacks and sweets, and 60 drinks were analysed. One-fifth of meals and snacks exceeded the CODEX-defined limit (200 mg Na/100 g). Most products lacked content information on nutrients non-mandated to be indicated. High-priced soft meals contained more protein (2·5 v. 1·9 g/100 g) and less Na (0·18 v. 0·46 g/100 g), less frequently used ≥ 1 added sugar (23 % v. 82 %), and less frequently used food additives than low-priced products; however, they had a lower variety of ingredients. The prevalence of products containing ≥ 1 added sugar was higher in low-priced snacks and sweets (91 % v. 77 %) but lower in drinks (48 % v. 84 %) than in their high-priced counterparts. High Na content is a concern among commercial complementary foods in Japan. Nonetheless, the relationship between the price and nutritional profile of these foods differs by product type. High-priced soft meals might be more favourable regarding nutrient content but not the variety of ingredients than low-priced counterparts. These findings elucidate the nutritional characteristics of commercial complementary foods in Japan.

We used data from the Campinas Health Survey (ISACamp 2014/15) and the Food Consumption and Nutritional Status Survey (ISACamp-Nutri 2015/16) to estimate the prevalence of the consumption of foods and beverages that contain low-calorie sweeteners (LCS) by individuals ≥ 10 years to estimate the dietary exposure of the population to high levels of LCS. We first estimated the prevalence of consuming LCS-containing foods and beverages and identified the top sources of LCS consumption. We then verified whether the prevalence of consumption varied according to individual-level characteristics or the presence of obesity and diabetes. Finally, we estimated the population dietary exposure to high levels of LCS and compared it with the acceptable daily intake (ADI) levels. Over 40 % of the study population consumed at least one LCS-containing food or beverage. Sweetened beverages, tabletop sweeteners and dairy beverages were the top contributors to the consumption of LCS. Among all age groups, education levels, and income levels, the consumption of LCS-containing foods and beverages ranged from 35 % to 55 %. The prevalence was only slightly greater among higher income 40–59-year-olds than among other income groups and was not higher among individuals with obesity or diabetes. Although dietary exposure to LCS did not exceed the ADI levels, we identified several limitations in our ability to measure exposure to high levels of LCS. Because of these challenges and the unclear evidence linking LCS to better health outcomes, the consumption of LCS-containing foods and beverages should be closely monitored.

Overweight and obesity have become epidemic worldwide and are linked to sedentary lifestyle and the consumption of processed foods and drinks. Citrate is a metabolite that plays central roles in carbohydrate and lipid metabolism. In addition, citrate is the additive most commonly used by the food industry, and therefore is highly consumed. Extracellular citrate can freely enter the cells via the constitutively expressed plasma membrane citrate transporter. Within the cytosol, citrate is readily metabolised by ATP-citrate lyase into acetyl-CoA – the metabolic precursor of endogenously produced lipids and cholesterol. We therefore hypothesised that the citrate ingested from processed foods and drinks could contribute to increased postprandial fat production and weight gain. To test our hypothesis, we administered citrate to mice through their drinking water with or without sucrose and monitored their weight gain and other metabolic parameters. Our results showed that mice receiving citrate or citrate+sucrose did not show increased weight gain or an increase in the weight of the liver, skeletal muscles or adipose tissues (AT). Moreover, the plasma lipid profiles (TAG, total cholesterol, LDL and HDL) were similar across all groups. However, the group receiving citrate+sucrose showed augmented fasting glycaemia, glucose intolerance and the expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6 and IL-10) in their AT. Therefore, our results suggest that citrate consumption contributes to increased AT inflammation and altered glucose metabolism, which is indicative of initial insulin resistance. Thus, citrate consumption could be a previously unknown causative agent for the complications associated with obesity.

Food additives have been used throughout history to perform specific functions in foods. A comprehensive framework of legislation is in place within Europe to control the use of additives in the food supply and ensure they pose no risk to human health. Further to this, exposure assessments are regularly carried out to monitor population intakes and verify that intakes are not above acceptable levels (acceptable daily intakes). Young children may have a higher dietary exposure to chemicals than adults due to a combination of rapid growth rates and distinct food intake patterns. For this reason, exposure assessments are particularly important in this age group. The paper will review the use of additives and exposure assessment methods and examine factors that affect dietary exposure by young children. One of the most widely investigated unfavourable health effects associated with food additive intake in preschool-aged children are suggested adverse behavioural effects. Research that has examined this relationship has reported a variety of responses, with many noting an increase in hyperactivity as reported by parents but not when assessed using objective examiners. This review has examined the experimental approaches used in such studies and suggests that efforts are needed to standardise objective methods of measuring behaviour in preschool children. Further to this, a more holistic approach to examining food additive intakes by preschool children is advisable, where overall exposure is considered rather than focusing solely on behavioural effects and possibly examining intakes of food additives other than food colours.

The purpose of the present study was to evaluate the effect of fermented liquid food (FLF) and the addition of lactic acid to a diet based on wheat and barley on the development of swine dysentery in pigs experimentally infected with a Danish field isolate of Brachyspira hyodysenteriae. Furthermore, to confirm if low non-starch polysaccharide (NSP)-containing diets reduce swine dysentery the effect of different dietary levels of NSP and resistant starch (RS) was evaluated. These diets were based on cooked rice and animal protein, cooked rice and potato starch, cooked rice and wheat bran, or cooked rice and sugar-beet pulp. The experiment was designed as a randomized-block trial and was performed in triplicate including a total of 192 pigs. After feeding the diets for 2 weeks, six pigs in each group were challenged orally with B. hyodysenteriae and observed for another 4 weeks. After challenge, swine dysentery was observed in all feeding groups. The incidence of disease varied between 94% (rice/wheat bran) and 44% (FLF). The effect of diet on faecal shedding of B. hyodysenteriae was statistically significant (P < 0·05). Feeding a diet based on cooked rice with a low content of NSP and RS, did not prevent the development of swine dysentery upon experimental challenge, and increasing the level of NSP or RS did not result in a higher incidence of disease or faecal shedding of B. hyodysenteriae. The incidence of swine dysentery in the FLF group was significantly lower (P < 0·05) compared with all other feeding groups, except for the lactic acid group. In conclusion, a low level of NSP or RS in the diet did not prevent the development of swine dysentery. Furthermore, the lowest incidence of disease was observed in the FLF group, even though this diet has a high content of NSP. The addition of organic acids to the food was not able to reduce infection with B. hyodysenteriae.