Metrics of sperm quality—such as sperm concentration and total sperm count—have declined substantially over recent decades. A large meta-analysis spanning more than 200 studies reported roughly a 50% drop in sperm concentration between 1973 and 2018, alongside an estimated 60% decline in total sperm count.1 While these measures are not synonymous with fertility itself, their downward trajectory has raised concern about population-level changes in male reproductive health and the modifiable factors that might be contributing to them.
Diet is an especially compelling candidate. Everyone eats, and few would dispute that the food environment has changed dramatically since the 1970s. Much of the current attention has focused on so-called ultra-processed foods (UPFs). Under the NOVA classification system, UPFs are defined as industrial formulations made largely from refined or synthesized ingredients—such as extracted fats, sugars, starches, protein isolates, and additives designed to enhance flavor, texture, or shelf life. In practical terms, this category includes many packaged meals, snack foods, breakfast cereals, and sugar-sweetened beverages that now dominate supermarket shelves.
It is easy to construct a plausible pathway linking these foods to poorer sperm quality: Calorie-dense diets promote excess energy intake and weight gain, which can lead to metabolic dysfunction—an established disruptor of reproductive hormones and spermatogenesis. The more important, and harder, question is whether ultra-processed foods exert effects on metabolic health and sperm quality independent of energy intake, or whether any observed effects are largely explained by differences in calories consumed and overall diet composition.
So we are left with this central question: Do specific features of the modern diet exert direct biological effects on reproductive function, or is their impact mediated primarily through energy intake, weight gain, and metabolic health? The distinction matters, because it determines whether “ultra-processed” is a causal mechanism or simply a label for dietary patterns that promote excess caloric intake and metabolic dysfunction.
A recent study2 attempted to address this question, and the results quickly attracted headlines—for example, The Washington Post, declared that an “ultra-processed diet decreases male sex hormones.”3 That framing implies a direct, calorie-independent effect of ultra-processed foods on reproductive biology. The question is whether the study actually demonstrates that.
Testing the hypothesis
Whether UPFs exert effects independent of total calorie intake is difficult to determine from observational data alone. People who eat more UPFs tend to differ in many ways from those who eat fewer of them, including total calorie intake, physical activity, and overall health status. Disentangling cause from correlation requires experimental control.
To address this, Preston et. al.conducted a randomized, crossover feeding study in 43 non-obese men aged 20–35 years old.2 Each participant was provided three weeks of either an ultra-processed diet or an unprocessed diet to consume at home. The unprocessed diet centered on whole foods such as eggs, vegetables, beans, fruit, fish, and whole grains, whereas the ultra-processed diet relied more heavily on packaged items such as pastries, sweetened cereals, chips, candy, chocolate milk, and white-bread sandwiches. Then, after a 12-week washout period, each participant was switched to the other diet, allowing them to serve as their own control. The intervention was further stratified into two calorie conditions—one designed to meet estimated energy needs and another providing excess calories (approximately 500–800 kcal/day higher)—with the explicit goal of separating the effects of food processing from those of energy intake itself.
On the surface, the results appear compelling. The ultra-processed diet led to rapid increases in body weight of roughly 1.3 to 1.4 kg over three weeks, driven largely by fat mass, and this occurred in both the adequate- and excess-calorie arms. Cardiometabolic markers shifted in parallel, including increases in total cholesterol, LDL:HDL ratio, and diastolic blood pressure. Taken at face value, these findings suggest a rapid deterioration in metabolic health under the ultra-processed dietary pattern.
Reproductive measures moved in the same general direction. In the excess-calorie condition, the ultra-processed diet was associated with a decline in follicle-stimulating hormone of about 0.5 IU/L, a hormone central to the regulation of spermatogenesis. In that same arm, total sperm motility fell by roughly 13% over the three-week intervention. Taken together, these shifts suggest that short-term exposure to an ultra-processed dietary pattern can influence both metabolic and reproductive signaling, leading the authors to conclude that UPFs indeed influence male reproductive health regardless of calories consumed.
When examined in full, however, the data tell a more uneven and internally inconsistent story.
A closer look
The first complication is that participants gained weight and fat mass on the ultra-processed diet regardless of calorie arm. Even under the condition intended to match estimated energy needs, the ultra-processed diet produced weight gain on the order of 1.3–1.4 kg, driven almost entirely by increases in fat mass. In a free-living study that relies on self-reported adherence, this makes it difficult to maintain that calories were truly held constant in practice. The observed increases in body weight and fat mass raise the possibility that actual energy intake differed between conditions despite the study’s design. Indeed, in a highly controlled metabolic ward setting, weight changes on a UPF diet closely track differences in caloric intake when every calorie is meticulously accounted for.4 In other words, the excess weight gain observed on ultra-processed diets appears to be driven largely by higher spontaneous energy intake rather than a uniquely fattening effect of processing itself.
A second issue is that the reproductive data themselves are more uneven than the headline framing suggests. Most semen parameters—including semen volume, sperm concentration, and morphology—did not meaningfully change. The lone signal in sperm motility did not reach statistical significance after correction, and hormonal effects were modest and inconsistent, with follicle-stimulating hormone declining only in the ultra-processed, excess-calorie condition. Taken together, these findings do not demonstrate a coherent or robust impairment of male reproductive health directly attributable to ultra-processed foods independent of energy balance and overall diet composition, nor do they establish a consistent biological signal across reproductive endpoints.
Finally, the contrast was not specifically limited to food processing alone. The ultra-processed diet was higher in saturated fat and refined carbohydrates and lower in fiber than the unprocessed diet. As a result, the intervention effectively compared a broadly metabolically unfavorable dietary pattern with a more favorable one. This makes it impossible to distinguish among several plausible drivers of the observed effects, including differences in total energy intake, saturated fat, refined carbohydrates, fiber content, and food texture or eating rate. In this context, food processing itself becomes a residual category rather than an isolated causal variable.
None of this is meant to dismiss the potential role of ultra-processed foods in promoting excess calorie intake and weight gain. A clear example comes from a tightly controlled inpatient feeding study led by Kevin Hall, PhD, in which 20 adults were randomized to consume either an ultra-processed or unprocessed diet for two weeks, followed by a crossover.4 Diets were matched for macronutrients, sugar, fiber, and sodium, though still differed in saturated fat content. Importantly, despite being matched for calories offered, participants eating the ultra-processed diet consumed roughly 500 additional calories per day and gained about 1 kg over the intervention period. The ultra-processed foods—such as packaged breads and meats, canned ravioli or chili, chips, and crackers with peanut butter—were eaten more quickly, likely because of their softer texture, a factor that may have encouraged higher energy intake.
Taken together with tightly controlled inpatient data, the evidence consistently supports a primary role for ultra-processed foods in driving excess energy intake and weight gain, while providing little support for a direct, calorie-independent effect on male reproductive health.
Our research team spends hundreds of hours each month vetting studies and distilling dense literature to deliver evidence-informed insights on health and longevity. If you find value in our work, consider becoming a premium member and supporting our mission.
The bottom line
Taken as a whole, the study reinforces a broader and already well-supported idea: Dietary patterns that impair metabolic health may also influence male reproductive physiology. Changes in body weight, fat mass, cardiometabolic markers, and select reproductive hormones all move in directions that are consistent with this link, even over relatively short time frames.
What the study does not do is isolate ultra-processing itself as an independent causal driver separate from differences in energy intake, diet composition, and metabolic effects. Despite the authors’ intentions, the intervention does not disentangle food processing from differences in energy balance, saturated fat intake, carbohydrate quality, or overall diet composition. As a result, the data cannot support a mechanistic claim that ultra-processed foods impair male reproductive health independent of their effects on energy intake, weight gain, and metabolic status.
In this context, “ultra-processed” functions less as a mechanism than as a label for a dietary pattern that is often calorie-dense, fiber-poor, and metabolically unfavorable. To be fair, this reflects how many people actually consume ultra-processed foods in the real world. But it does not necessarily mean that processing per se is the problem, or that avoiding foods based on classification alone is the most informative strategy.
The more defensible takeaway is not about policing food labels, but about understanding the hierarchy of effects. The strongest and most consistent signal in this and related studies is the impact of diet on energy intake, body weight, and metabolic health. Those factors, in turn, are well-established regulators of reproductive physiology. In contrast, the independent role of food processing remains unproven.
For practical purposes, the focus should shift away from classification systems and toward dietary patterns that reliably control energy intake, maintain healthy body composition, and support metabolic health, the variables most likely to determine reproductive outcomes.
For a list of all previous weekly emails, click here.
References
1. Levine H, Jørgensen N, Martino-Andrade A, et al. Temporal trends in sperm count: a systematic review and meta-regression analysis of samples collected globally in the 20th and 21st centuries. Hum Reprod Update. 2023;29(2):157-176. doi:10.1093/humupd/dmac035
2. Preston JM, Iversen J, Hufnagel A, et al. Effect of ultra-processed food consumption on male reproductive and metabolic health. Cell Metab. 2025;37(10):1950-1960.e2. doi:10.1016/j.cmet.2025.08.004
3. O’Connor A. Ultra-processed diet decreases male sex hormones, new study suggests. The Washington Post. https://www.washingtonpost.com/wellness/2025/08/28/ultra-processed-sperm-quality-male-fertility/. August 28, 2025. Accessed March 19, 2026.
4. Hall KD, Ayuketah A, Brychta R, et al. Ultra-processed diets cause excess calorie intake and weight gain: An inpatient randomized controlled trial of ad libitum food intake. Cell Metab. 2019;30(1):67-77.e3. doi:10.1016/j.cmet.2019.05.008
