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Introduction

The first prominent ultra-processed food (UPF) personal injury case was dismissed after the court found that a lengthy complaint said comparatively little about the plaintiff’s own exposure. The complaint did not adequately identify which products the plaintiff ate, how much and how often, or when relative to diagnosis. The court also emphasized that the alleged diseases have many possible causes. The plaintiff then proposed a substantially expanded complaint that identified 179 products and added rough consumption frequencies. On June 30, 2026, the court declined to allow the proposed amendment because the additional detail still did not adequately connect the alleged injuries to each product. In this blog, we examine a question that matters for both pleading and expert proof: are plaintiffs’ exposure allegations becoming more specific than the science offered to support them?

This sequence reflects an important shift. Plaintiffs are learning to plead exposure in more detail, identifying specific products and how often, how long, and when they were consumed. But the science has not necessarily kept pace. Most studies still look at total UPF intake, overall eating patterns, broad UPF categories, or selected ingredient types, not specific branded products. Plaintiffs’ exposure allegations may therefore be getting more specific faster than the supporting science.

A second strategy is also emerging. In December 2025, the San Francisco City Attorney filed a government action focused on alleged marketing practices, harm to the public at large, and public-health costs. Unlike an individual personal injury case, that action does not turn on whether a particular person’s consumption caused that person’s disease. The distinction matters because the same studies may be used to prove very different things.

“Ultra-Processed” Is a Broad and Disputed Category

The NOVA system, the classification most UPF studies use, sorts foods by how heavily they are industrially processed rather than by their nutritional content. This has prompted research into many possible explanations for health effects, including how foods are structured, how fast people eat them, how calorie-dense and appealing they are, and what additives or packaging chemicals they contain. But it creates a threshold problem for litigation: “ultra-processed” is not a single substance, ingredient, process, or dose. It is a broad label covering a wide variety of very different foods and beverages.

Moreover, even experts do not always agree on what counts as ultra-processed. Braesco et al. asked nutrition specialists to classify foods under NOVA and found low agreement, for both branded products and generic foods, even when ingredient lists were available. Critics also argue that lumping foods together by processing level can hide meaningful nutritional differences between them. A 2025 review concerning plant-based alternatives similarly concluded that findings about UPFs as a whole should not be assumed to apply to every type of UPF.

For attorneys, the point is not that NOVA is unusable. It is that classifying a product as ultra-processed can be a judgment call that an expert should document and be able to defend, including accounting for any recipe changes over time. If independent reviewers cannot consistently classify a product, or if the product’s formulation changed during the alleged exposure period, the plaintiff’s exposure evidence may be uncertain before causation is even considered. 

Associations Are Substantial, but Evidentiary Strength Varies

Lane and colleagues reviewed 45 pooled analyses covering nearly 10 million participants and found that higher UPF intake was associated with worse results for 32 health measures. However, when the researchers graded how much confidence the evidence deserved, none of the analyses was rated high quality: four were rated moderate, 22 low, and 19 very low. The link to type 2 diabetes was among the better-supported findings, rated moderate. The key takeaway is that a statistically consistent association is not the same as reliable evidence of cause and effect.

Newer studies continue to report positive associations. A 2025 analysis of 12 long-term studies found that people who ate the most UPFs had about a 48% higher risk (1.48 RR) of diabetes than those who ate the least. But the results differed by food type: processed meats were linked to higher risk, while certain cereals, breads, and packaged savory snacks were linked to lower risk. Kim and colleagues therefore strengthens the population-level diabetes link while also showing that different kinds of UPFs do not necessarily behave the same way.

A 2026 umbrella review of 26 systematic reviews and meta-analyses likewise reported associations  across multiple health outcomes but cautioned that the strength of the evidence varied. An updated 2026 narrative umbrella review found that higher UPF consumption was associated with increased risk for most outcomes examined, while noting that the evidence was mainly observational (tracking what people ate rather than testing it in controlled experiments) and that, for several outcomes, studies had not reliably shown that more consumption means more risk. These newer reviews are current, but none measures the effect of a specific manufacturer’s product.

Accounting for Other Risk Factors Changes the Results, and How Experts Do It Matters

Chen and colleagues followed three large U.S. cohorts and found that total UPF intake was linked to developing type 2 diabetes. People who ate the most UPFs had about 56% higher risk than those who ate the least, after accounting for factors such as age, lifestyle, and other aspects of diet. When the researchers also accounted for participants’ body weight (BMI), the increased risk dropped to about 1.28.

That drop is significant, but its meaning depends on assumptions. If excess weight is a separate risk factor that happens to travel with UPF consumption, accounting for it gives a more accurate picture of UPFs’ own effect. But if UPFs cause weight gain, which in turn causes diabetes, accounting for weight may strip out part of the very effect being studied. The same factor can play different roles depending on timing and the question asked. The lesson is not simply that “adjusting weakens the result,” but that any expert’s conclusion rests on assumptions about how the risk factors relate to one another, and those assumptions should be stated and tested. Observational studies may still miss other explanations, while over-adjusting can create its own distortions.

Different Types of UPFs Produce Different Results

Drawing conclusions about UPFs as a whole becomes harder when different types of UPFs point in different directions. In the U.S. cohorts analyzed by Chen and colleagues, some types of UPFs were linked to higher diabetes risk, while others were linked to lower risk. In a multinational study, Cordova and colleagues found that artificially and sugar-sweetened beverages and animal-based products were linked to higher risk of developing multiple chronic diseases, while ultra-processed breads and cereals and plant-based alternatives were not.

These findings do not prove that any particular type of UPF is always harmful or always harmless. They do show that the broad-UPF category does not behave consistently across studies. A claim about a specific product therefore requires an explanation of why evidence about UPFs generally, or about one type of UPF, applies to the specific product, amount consumed, plaintiff, and disease at issue.

What Controlled Feeding Establishes, and What It Does Not

A randomized trial by Hall and colleagues remains central because researchers controlled and measured what participants ate, rather than relying on participants’ own reports. Twenty adults lived in a research facility and ate an ultra-processed diet and an unprocessed diet for two weeks each, in random order. Participants ate about 500 more calories per day on the ultra-processed diet and gained weight during that period.

In other words, when allowed to eat as much as they wanted, participants on the ultra-processed diet ate more and gained weight over a short period. The study did not identify which feature of the diet caused the difference. Possible explanations include calorie density, how the foods were structured, how quickly people ate, how appealing the foods were, and additives. A 2026 review summarizes these theories, but they remain unproven explanations about overall diets, not established causes for every product.

This distinction matters in litigation. A two-week study of an entire diet does not show how much of any single product is harmful, does not show that chronic disease follows years of exposure, and does not divide responsibility among manufacturers. Long-term experiments testing one commercial product while holding the rest of a person’s diet constant would be extremely difficult, if not impossible, to run. Long-term observational studies can cover longer periods, but they depend on self-reported diets, statistical adjustments, and assumptions about how people’s eating and habits change over time.

More Detailed Exposure Allegations Improve the Story, Not Necessarily the Science

A detailed consumption history can identify a type of product, estimate servings per week, provide a starting year, and show that consumption came before diagnosis. Those details make the exposure allegations more complete. But how often and how long someone ate a product does not automatically translate into a harmful dose. Products differ in recipe, processing, portion size, and the theory of how they cause harm, and recipes can change over time.

The rest of the plaintiff’s diet also matters. Any one product was eaten alongside other UPFs, less-processed foods, restaurant and cafeteria meals, beverages, and an overall diet that changed over time. Exercise, weight, medications, other health conditions, socioeconomic circumstances, and genetics may all offer alternative explanations or affect how diet influences disease, which complicates any effort to attribute a plaintiff’s illness to a particular product.

The June 2026 ruling illustrates the difference between greater detail and stronger scientific proof. The proposed amended complaint added 179 products, rough frequencies, ingredients, and repeated assertions that the products could plausibly cause harm. The court nevertheless found that correlation, increased risk, and plausibility did not adequately connect each product to the alleged injuries. That was a legal ruling, not a scientific review of the UPF research. But it reflects a point the science supports: more exposure detail does not, by itself, bridge the gap between research on a broad food category and a claim that a specific product caused a specific person’s disease.

The Important Qualification

The lack of a study testing a specific commercial product does not, by itself, defeat a causation claim. Product-specific trials are not always feasible  or necessary. Experts may evaluate causation by showing that multiple lines of evidence, such as population studies, experiments, biological explanations, clinical data, and product-specific information, point in the same direction.

The real question is fit. The more the exposure studied differs from the plaintiff’s alleged exposure, the more an expert must explain and justify applying the research to the plaintiff. Evidence about an overall diet may support a theory of harm. It should not be presented as though it measured the effect of every product within that diet.

Conclusion

UPF litigation is developing along two tracks. Individual plaintiffs are adding product-level details about what they ate and when. Government actions rely on population-wide allegations focused on marketing practices, public health effects, and public costs. Both may cite the same studies, but they ask those studies to prove different things.

For individual claims, detailed exposure allegations are not the same as scientific proof. The research increasingly tells us about overall diets, broad food types, short-term experimental results, and possible explanations for harm. It says much less about specific products, how much of a given product is harmful, the long-term effect of one product apart from the rest of the diet, and whether a product caused a particular person’s disease.

For companies, counsel, and experts, the task is neither to dismiss the research nor to assume that more detailed consumption histories close the gap. It is to ask whether the exposure studied, the amount measured, the outcome observed, the proposed explanation, and the population studied actually match the claim being made. That disciplined inquiry clarifies what the evidence proves, what it suggests, and where significant uncertainty remains.