What the Research Says About Ultra-Processed Food and Joint and Bone Health

We only cite studies published in peer-reviewed journals. We summarize findings without overstating conclusions.

This article summarizes a scoping review published on March 28, 2025, in the open-access journal Nutrients (MDPI), titled “Ultra-Processed Food and Its Impact on Bone Health and Joint Diseases: A Scoping Review.” The review was authored by Jacopo Ciaffi (corresponding author) and Francesco Ursini, both affiliated with the Medicine and Rheumatology Unit at the IRCCS Istituto Ortopedico Rizzoli and the Department of Biomedical and Neuromotor Sciences (DIBINEM) at the Alma Mater Studiorum University of Bologna in Italy, alongside colleagues Luana Mancarella, Claudio Ripamonti, Veronica Brusi, Federica Pignatti, and Lucia Lisi (Rizzoli Institute), and Andrea D’Amuri (General Medicine Unit, ASST Mantova, Ospedale Carlo Poma, Mantova). The review was conducted in accordance with the methodological guidelines of the Joanna Briggs Institute and followed PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analysis extension for Scoping Reviews) reporting standards. Its protocol was pre-registered on the Open Science Framework (OSF) registry before data collection began. The review synthesized 19 studies – 3 preclinical and 16 clinical, spanning populations from children to older adults, and from five continents – examining how ultra-processed food consumption relates to bone mineral density, osteoporosis, osteoarthritis, rheumatoid arthritis, gout, and spondyloarthritis. The full text is freely available at PubMed Central (PMC11990240).

The authors declare no conflicts of interest. This research received no external funding.

Background: What Are Ultra-Processed Foods, and Why Do They Matter for Joints?

The NOVA Classification System

The term “ultra-processed food” has a specific technical meaning in nutrition science. It comes from the NOVA food classification system, a framework developed by researchers at the University of São Paulo that categorizes all foods not by their nutrient content but by the extent and purpose of the industrial processing they have undergone. NOVA divides foods into four groups: unprocessed or minimally processed foods (fresh fruits, vegetables, eggs, plain meats, milk); processed culinary ingredients (oils, flours, sugars, salt used in cooking); processed foods (canned vegetables, fermented cheeses, cured meats – foods altered to improve preservation or palatability but still recognizable as derived from whole foods); and ultra-processed foods, the fourth and most heavily industrialized group.

Ultra-processed foods (UPFs) are defined as industrial formulations that contain little to no whole food ingredients, and which include a range of additives, preservatives, colorings, emulsifiers, artificial flavors, and other substances whose primary function is to enhance taste, texture, shelf life, or visual appeal – rather than to provide nutrition. Common examples include soft drinks and sweetened beverages, mass-produced packaged breads and baked goods, instant noodles, pre-packaged ready-to-heat meals, processed meat products such as hot dogs and reconstituted chicken nuggets, refined breakfast cereals, candy, chips, and commercial sauces and dressings. These products are engineered to be convenient, highly palatable, and inexpensive – and their global consumption has risen steeply over the past three decades, including in countries that have historically had more traditional food cultures.

Nutritionally, UPFs share a consistent profile: they tend to be energy-dense but nutrient-poor, high in refined sugars, saturated and trans fats, and sodium, while being low in dietary fiber, protein, and the micronutrients essential to musculoskeletal health – including calcium, vitamin D, magnesium, potassium, zinc, phosphorus, vitamin C, vitamin B12, niacin, and antioxidants. The broader health consequences of this nutritional profile are now well-documented. Prior research has associated high UPF consumption with a 39 percent higher risk of obesity, a 79 percent increased risk of metabolic syndrome, and a 31 percent greater risk of type 2 diabetes. UPFs are also linked to elevated cardiovascular disease risk, cognitive decline, inflammatory bowel disease, anxiety and depression, and an 11 to 49 percent increased risk of several cancers depending on type.

Despite this broad evidence base, the musculoskeletal consequences of UPF consumption – their effects on bones and joints specifically – had received relatively little systematic attention before this 2025 review. Most prior research on diet and bone health focused on individual nutrients (calcium, vitamin D, protein) or broad dietary patterns (the Mediterranean diet versus the Western diet), rather than examining UPF as a distinct and measurable dietary exposure. The Ciaffi et al. review was designed to map the existing evidence on this specific question and identify gaps requiring further research.

Why UPFs Are Mechanistically Plausible Joint and Bone Hazards

Several biological pathways connect the nutritional deficiencies and harmful components of UPFs to bone and joint tissue specifically. The review authors identify the following as the most relevant.

Systemic inflammation. UPF diets consistently elevate circulating markers of chronic low-grade inflammation – including C-reactive protein, interleukin-6, and tumor necrosis factor-alpha. These same inflammatory mediators play central roles in the pathogenesis of rheumatoid arthritis, gout, and osteoarthritis. In OA, for example, inflammatory cytokines activate the enzymes that degrade cartilage matrix and simultaneously suppress the activity of chondrocytes, the cells responsible for cartilage maintenance. In RA, systemic inflammation is the disease’s defining feature. Anything that chronically elevates baseline inflammation levels can therefore be expected to worsen the conditions of those with, or at genetic risk for, inflammatory joint disease.

Oxidative stress. UPFs are low in the antioxidant micronutrients – vitamin C, vitamin E, selenium, zinc, polyphenols – that normally protect cells against damage by reactive oxygen species (unstable molecules generated as byproducts of normal metabolism and amplified by inflammation). Oxidative stress contributes to both cartilage destruction in OA and bone loss in osteoporosis by damaging chondrocytes, osteoblasts (bone-forming cells), and the extracellular matrix scaffolding of both tissues.

Micronutrient displacement. Because UPFs occupy an outsized share of total caloric intake in heavy consumers, they displace the whole foods that would otherwise deliver bone- and joint-critical nutrients. Someone whose diet is 60 percent UPF by calories has correspondingly less room for the calcium-rich dairy, the magnesium-rich legumes and nuts, the vitamin D from oily fish, and the collagen-supporting vitamin C from fruits and vegetables that bone and connective tissue depend upon.

Metabolic syndrome and obesity. UPFs are strongly associated with obesity and metabolic syndrome – conditions that independently elevate OA risk through increased mechanical load on weight-bearing joints, altered adipokine signaling (adipose tissue produces inflammatory signaling molecules that affect cartilage), and insulin resistance. Hyperuricemia – the elevated blood uric acid level that predisposes to gout – is also worsened by fructose-heavy diets, and many UPFs contain abundant added fructose in the form of high-fructose corn syrup.

Disruption of bone remodeling. Bone is a dynamic tissue that undergoes continuous remodeling throughout life: osteoclasts dissolve old or damaged bone, and osteoblasts lay down new bone matrix that subsequently mineralizes. The high sodium content of many UPFs promotes urinary calcium excretion. Their high content of phosphoric acid (especially in cola-type beverages) may disturb the calcium-phosphorus ratio in ways unfavorable to bone mineralization. Excess refined sugar may promote insulin resistance in bone cells, impairing the anabolic (building) phase of remodeling.

Methodology: What a Scoping Review Is and How This One Was Conducted

Scoping Review Versus Systematic Review

A scoping review is a distinct type of evidence synthesis, and understanding its design is necessary to interpret its conclusions appropriately. Unlike a systematic review or meta-analysis, which attempts to answer a specific, narrow clinical question by pooling quantitative results from methodologically similar studies, a scoping review is explicitly designed to map the breadth and nature of evidence on a topic – particularly when that topic is emerging, heterogeneous, or when the research field is not yet mature enough to support quantitative pooling. A scoping review identifies what kinds of studies exist, what populations and outcomes have been examined, what the general direction of findings is, and where the most important knowledge gaps lie.

One methodological consequence of the scoping design is that it does not include formal risk-of-bias assessment of included studies – a standard component of systematic reviews. The Joanna Briggs Institute guidelines, under which this review was conducted, consider critical appraisal optional rather than mandatory for scoping reviews, because the goal is mapping rather than quality-filtered evidence synthesis. This means the reader cannot assume that all 19 included studies met a rigorous quality threshold; some were conference abstracts, some had methodological weaknesses the review itself acknowledges. This context is important for calibrating how strongly the review’s conclusions should be held.

Search Strategy and Study Selection

The authors searched three major biomedical databases – MEDLINE (via PubMed), Web of Science, and Embase – with no restrictions on publication date, up to February 14, 2025. Search terms combined vocabulary related to UPF exposure (including “ultra-processed food,” “highly processed food,” and “fast food,” acknowledging that older studies often used “fast food” as a proxy for what NOVA would classify as UPF) with vocabulary related to bone health (bone mineral density, osteoporosis, osteopenia, fracture, bone loss, bone growth) and joint diseases (osteoarthritis, rheumatoid arthritis, psoriatic arthritis, spondyloarthritis, ankylosing spondylitis, gout). Manual reference list screening supplemented the database searches.

The initial search returned 119 records. After removing 40 duplicates, 79 records were screened by title and abstract; 60 were excluded, leaving 19 studies that met the inclusion criteria for full-text inclusion in the qualitative synthesis. Eligible study designs included randomized controlled trials, cohort studies, case-control studies, cross-sectional studies, and qualitative reports. Both preclinical animal studies and human clinical studies were eligible.

The 19 included studies spanned publications from 2013 to 2025, originated from nine countries (the United States, China, Korea, Israel, Brazil, the United Kingdom, Portugal, Japan, and France), and ranged in size from 36 animal subjects in a preclinical study to 207,012 adults in the UK Biobank prospective cohort. Four of the 19 studies were conference abstracts or posters rather than peer-reviewed full-text publications, which the authors acknowledge as a limitation.

Results by Domain

Part One: Preclinical Studies – What Animal Models Reveal

Three studies examined the effects of UPF-type diets on bone health in rodent models, and all three found significant skeletal harm.

A 2021 Israeli study (Travinsky-Shmul et al.) fed young female mice a UPF-based diet containing food additives and compared them to mice on a standard control diet. Micro-CT scans revealed impaired bone morphology in the UPF-fed animals, and biomechanical testing showed inferior bone strength. An unexpected additional finding was a significant increase in marrow adiposity – the replacement of the red bone marrow (which produces blood cells and supports bone remodeling) with yellow fat-storing marrow. Elevated marrow adiposity is a recognized marker of impaired bone remodeling and is associated with osteoporosis in humans.

A companion 2021 Israeli study (Zaretsky et al.) fed young rats a UPF-based diet and found a different but overlapping pattern of harm: impaired bone microarchitecture and disrupted endochondral ossification – the developmental process by which cartilage templates are gradually replaced by bone during growth. RNA sequencing of bone tissue revealed disruptions in extracellular matrix formation and mineralization processes at the molecular level. Structural deterioration was found in both trabecular bone (the spongy inner lattice that provides compressive strength) and cortical bone (the dense outer shell). The authors concluded that UPF exposure during growth periods may produce lasting skeletal fragility.

A 2024 Japanese study (Saito et al.) examined a “cafeteria diet” – a research model that presents rats with a variety of palatable, calorie-dense processed foods (resembling the variety a human UPF consumer might encounter) – versus standard chow, in both sedentary and exercise-trained male rats. The cafeteria diet produced a significant increase in adipose tissue, reduced bone mineral density, and impaired biomechanical properties including stiffness and maximum load capacity. The most striking finding was that resistance exercise (ladder climbing training) did not prevent the bone quality deterioration caused by the diet. This suggests that physical activity, while beneficial in many contexts, may not be sufficient to compensate for the skeletal damage of a high-UPF diet – dietary modification appears necessary.

The preclinical evidence is mechanistically coherent: across different animal models, sexes, and dietary formulations, UPF consumption consistently impairs bone formation, reduces bone mass, weakens bone strength, and disrupts the structural integrity of skeletal tissue. While animal models do not perfectly predict human outcomes, their consistency across three independent studies strengthens the plausibility of similar effects in humans.

Part Two: UPF and Bone Health in Children and Adolescents

Four studies examined the relationship between UPF or fast-food intake and bone mineral density in young populations, with findings that were directionally consistent but statistically variable.

A 2018 Korean study (Lim et al.) of 161 college students found a significant negative association between frequent fast-food consumption and total body BMD in both males and females. The study also characterized the nutritional profile driving this association: frequent fast-food consumers had excess sodium and protein intake combined with deficiencies in vitamins A and C – a pattern that could impair bone mineralization through multiple pathways during the critical window of young adulthood when peak bone mass is still being consolidated.

A particularly creative 2016 UK study (Vogel et al.) in 1,107 children from the Southampton Women’s Survey took an environmental approach rather than an individual dietary assessment approach: it measured the density of fast-food outlets near each child’s home as a proxy for fast-food exposure. This ecological approach revealed that each additional fast-food outlet near a child’s home corresponded to a 0.23 standard deviation decrease in BMD – a meaningful effect at the population level. Conversely, greater access to healthy food stores was associated with higher BMD at ages 4 and 6. This finding is notable because it suggests that the food environment shapes skeletal development from early childhood onward, independent of individual choice or awareness.

A 2015 Portuguese longitudinal study (Monjardino et al.) followed 1,007 adolescents from ages 13 to 17 and examined how dietary patterns affected bone mineral accrual over that critical growth period. Although no significant association was found between a “fast food and sweets” dietary pattern and mean BMD at age 13, girls who consumed nutrient-poor diets (characterized by lower intake of nutrient-dense foods) showed significantly lower BMD accrual over the four-year follow-up, with an adjusted coefficient of −0.451 mg/cm²/year. This longitudinal result is particularly important: it suggests the harm may not be in lower baseline bone mass at adolescence, but in a slower rate of bone building during the years when rapid accumulation normally occurs – potentially setting individuals up for lower peak bone mass in adulthood, which is a major long-term risk factor for osteoporosis.

A 2013 Korean cross-sectional study (Shin et al.) of 196 adolescents found a trend toward lower BMD at the lumbar spine, femur, and total body in those with high fast-food intake, though the association did not reach statistical significance in the fast-food group specifically. The comparison was illuminating nonetheless: adolescents following a milk-and-cereal dietary pattern – high in calcium and other bone-supporting micronutrients – had a 64 percent lower likelihood of low BMD, reinforcing that the protective effect of nutrient-rich whole foods and the potential harm of UPF-dominant diets represent two sides of the same dietary coin.

Part Three: UPF and Bone Health in Adults

Five studies examined UPF consumption and bone outcomes in adult populations. The strongest and most recent evidence came from analyses of two large U.S. datasets.

A 2025 study (Greatorex Brooks et al.) used National Health and Nutrition Examination Survey (NHANES) data from U.S. adults aged 50 and older (n = 5,729) to examine the relationship between UPF intake and osteoporosis prevalence. NHANES is a nationally representative survey combining interviews, dietary recalls, and clinical examinations including bone density measurement. The study found that adults in the highest quintile of UPF consumption had a 52 percent greater likelihood of osteoporosis compared to those in the lowest quintile – a large and clinically significant association. Additionally, every 1 percent increase in UPF as a share of total caloric intake correlated with a 1.9 percent increase in self-reported fractures among women, directly linking the dietary pattern to the skeletal consequence that matters most clinically.

A 2024 Chinese-authored study (Wang et al.) also used NHANES data (n = 4,912 adults) and focused specifically on femoral neck BMD – the measurement site most predictive of hip fracture risk – and total femur BMD. Adults whose diets consisted of more than 57.5 percent UPF by caloric content had significantly lower femoral neck and total femur BMD, and high UPF intake was associated with 78.9 percent increased odds of developing osteoporosis. Importantly, this study found that physical activity partially mitigated the negative association between UPF and BMD – a finding with practical implications suggesting that exercise may buffer some skeletal harm from poor diet, even if it cannot fully eliminate it.

A 2023 conference poster (Noel et al.) examined a smaller but demographically specific population: Puerto Rican adults aged 47 to 79 years (n = 1,254). Higher UPF intake was significantly associated with increased odds of osteoporosis at both the femoral neck and lumbar spine, and the association remained statistically significant after adjusting for age, sex, BMI, and lifestyle habits – supporting UPF as an independent risk factor rather than a marker of a generally poor lifestyle.

Two studies provided more nuanced or null results within the adult evidence base. A 2015 Korean study (Shin et al.) of 3,573 adults found no direct significant association between a “fast food and soda” dietary pattern and BMD, though a fruit-milk-whole-grain pattern was positively correlated with BMD – again highlighting the protective power of nutrient-dense diets rather than clearly implicating UPF. A 2017 Framingham Third Generation cohort study (Mangano et al., n = 2,986) found that a dietary pattern characterized by fast food and full-fat dairy showed no significant association with BMD, but that higher total protein intake – even from processed sources – was associated with greater lean mass. This last finding introduces an important nuance: not all components of UPF-heavy diets are equally damaging, and adequate dietary protein (which many UPFs do provide, even if in lower quality forms) may preserve muscle mass independently of its bone effects.

Part Four: UPF and Osteoarthritis

Three studies examined UPF consumption and osteoarthritis, two of them drawing on the well-characterized Osteoarthritis Initiative (OAI) cohort discussed in the previous article in this series.

The largest and most methodologically robust OA study was a 2024 prospective cohort analysis by Wei et al. using UK Biobank data from 163,987 adults – one of the largest OA studies ever conducted. The UK Biobank is a prospective study of approximately 500,000 British adults with detailed genetic, lifestyle, and health data collected over many years, making it an exceptionally powerful resource for studying diet-disease relationships. The study found that adults in the highest quartile of UPF consumption had a 10 percent increased risk of developing knee OA compared to those in the lowest quartile, after adjustment for potential confounders. No significant association was found for hip OA, suggesting that the relationship is joint-specific rather than a general effect on all large joint OA. The study also performed a substitution analysis: replacing 20 percent of daily caloric intake from UPF with unprocessed or minimally processed food equivalents was associated with a 6 percent lower risk of knee OA. This substitution effect is clinically relevant because it frames the intervention not as radical dietary elimination but as a realistic partial shift toward whole foods.

A 2024 conference abstract by Akkaya et al. used OAI data from 4,330 OA patients to examine the relationship between UPF intake and knee cartilage thickness, measured using quantitative MRI – a more sensitive structural measure than X-ray-based joint space width. Higher UPF intake was significantly associated with thinner cartilage, with a particularly strong signal in women. In women, greater UPF consumption was linked to thinner cartilage in the medial tibia, medial femur, and lateral femur – all regions that bear the primary load in knee OA. In men, the association was weaker and mostly non-significant, suggesting a possible sex-specific vulnerability, the biological basis of which is not yet established.

A companion 2024 conference poster by Sims et al. also used OAI data (n = 4,796) and examined the relationship between UPF intake and OA-related pain and functional outcomes. After adjusting for confounders including BMI, women consuming higher UPF amounts reported greater knee OA-related pain, worse performance in activities of daily living, and lower physical performance scores than men. The sex difference in both the Akkaya and Sims analyses is a recurring and unexplained signal that warrants further investigation.

The mechanism connecting UPF to OA risk likely operates through several of the pathways already described: systemic inflammation, obesity and mechanical overloading of cartilage, oxidative stress in chondrocytes, and micronutrient depletion. The absence of a significant hip OA association is intriguing and may reflect differences in how mechanical loading interacts with inflammation at the hip joint versus the knee, or may simply reflect insufficient statistical power to detect a smaller association at the hip within the available studies.

Part Five: UPF and Inflammatory Arthritis

Four studies examined UPF consumption in relation to inflammatory arthritis – rheumatoid arthritis, spondyloarthritis, and gout – producing the most striking risk estimates in the entire review.

Rheumatoid Arthritis: A 2024 retrospective cohort study by Zhao et al. used UK Biobank data from 207,012 adults – the largest sample in this review – to examine UPF intake and incident RA. Participants were divided into quintiles of UPF consumption as a percentage of total dietary intake. Those in the highest quintile had a 17 percent increased risk of developing RA compared to those in the lowest quintile. The investigators then conducted mediation analyses to understand what biological mechanisms might account for this association. They found that inflammation (measured by systemic inflammatory markers), lipid profile changes, and liver enzyme alterations together partially explained the link, collectively accounting for 3 to 15 percent of the total association. This means that most of the UPF-to-RA relationship remains unexplained by the measured mediators, suggesting additional mechanisms – gut microbiome disruption, epigenetic modifications, hormonal effects of food additives – may be involved.

A 2020 Brazilian cross-sectional study by Smaira et al. examined 56 adults already diagnosed with RA and found that higher UPF intake was significantly associated with worsened metabolic and cardiovascular health profiles, including an elevated Framingham cardiovascular risk score and higher glycated hemoglobin levels. Patients with RA already face a significantly elevated cardiovascular risk due to the systemic inflammatory burden of their disease; UPF consumption appears to compound that risk further. Conversely, patients who consumed more unprocessed or minimally processed foods had lower cardiovascular risk. Though small (56 participants), this study is clinically important because it addresses not just disease incidence but the health consequences of UPF for people already living with inflammatory arthritis.

Gout: A 2024 prospective cohort study by Zhang et al. used UK Biobank data from 181,559 adults to examine the relationship between UPF consumption and incident gout, with the additional dimension of genetic predisposition. Higher UPF intake was associated with a 16 percent increased risk of developing gout. When the researchers stratified participants by genetic risk for gout (based on polygenic risk scores derived from known gout-associated genetic variants), the interaction was striking: individuals with both high genetic predisposition and high UPF intake had nearly twice the risk of developing gout compared to those with low genetic predisposition and low UPF intake. This gene-diet interaction suggests that UPF consumption may be particularly harmful for those with inherited vulnerability to uric acid dysregulation – a finding that could eventually inform personalized dietary guidance. A substitution analysis mirrored the OA finding: replacing 20 percent of daily UPF caloric intake with unprocessed or minimally processed foods was associated with a 13 percent lower gout risk.

Spondyloarthritis: A 2019 French conference abstract (Nguyen et al.) examined dietary profiles, including UPF intake, in 140 patients with spondyloarthritis (SpA) – an umbrella term for inflammatory arthritis conditions primarily affecting the spine, including ankylosing spondylitis and psoriatic arthritis. No significant difference in UPF consumption was found between patients with active versus inactive SpA. However, poor diet overall (not specifically UPF) was associated with worse quality of life in SpA patients. The authors of the scoping review characterize this as an inconclusive finding, noting that the study was small, available only as a conference abstract, and may not have been adequately powered to detect a relationship if one exists.

The Limitations: What This Review Cannot Tell Us

The authors devote substantial attention to the limitations of their conclusions, and these deserve careful elaboration.

The fundamental constraint of a scoping review is that it maps rather than adjudicates. It identifies what evidence exists without formally evaluating the quality of that evidence or statistically combining results. The 19 included studies are heterogeneous in design, population, sample size, exposure measurement, and outcome assessment – making them inappropriate to pool quantitatively and difficult to compare qualitatively with full confidence. The review itself does not attempt to generate a single summary estimate; its conclusions are directional and descriptive rather than precise.

The dominant study design across the clinical evidence is cross-sectional – a snapshot of dietary exposure and disease status measured at a single point in time. Cross-sectional studies cannot establish which came first: did heavy UPF consumption precede and contribute to poor bone or joint health, or did people with established joint disease change their dietary habits (perhaps toward more convenient UPF) as a consequence of their reduced mobility and function? This reverse causation problem is impossible to resolve without longitudinal data that captures diet before disease onset. Only the UK Biobank-based studies (Wei et al. on OA, Zhao et al. on RA, and Zhang et al. on gout) used prospective cohort designs that partially addressed this problem by measuring diet before disease occurrence.

Residual confounding is a persistent concern across all observational studies in this domain. People who consume large amounts of UPF tend to differ from lower consumers in many ways that also affect musculoskeletal health: they tend to have lower incomes, lower educational attainment, higher rates of sedentary behavior, higher rates of smoking and alcohol use, and a generally more disadvantaged social environment. Although most of the adult studies adjusted for some confounders – age, sex, BMI, and energy intake were common adjustments – fewer controlled for physical activity, smoking, alcohol consumption, socioeconomic status, corticosteroid use (important given its impact on bone density), or comorbid inflammatory conditions. The depth and range of confounder adjustment varied considerably across studies, making the independence of UPF as a risk factor uncertain in the studies with weaker adjustment.

The measurement of UPF exposure itself was highly inconsistent across studies. Some used NOVA-based classification applied to food frequency questionnaire data. Some used 24-hour dietary recall methods. Some used the percentage of total caloric intake from UPF as their exposure metric. Some – particularly the older studies – did not use the NOVA system at all and instead used “fast food consumption” or “dietary pattern clusters” as proxies for UPF, which may not capture the full range of ultra-processed products. The UK ecological study used fast-food outlet density near the home as its exposure measure – an indirect environmental proxy that cannot distinguish individual dietary choices. This methodological heterogeneity means that “UPF” is not being defined or measured consistently across the 19 studies, which limits comparability.

The evidence base for joint diseases is thin. Only seven of the 19 studies addressed chronic joint diseases specifically, and of those seven, three were conference abstracts or posters (the lowest form of published evidence, with no peer-reviewed full-text methodology or result detail). For osteoarthritis and inflammatory arthritis combined, the literature is at an early stage, and the review’s conclusions on these conditions are appropriately tentative.

Finally, no intervention studies – trials that actually reduce UPF intake and measure the effect on bone or joint outcomes – have been published in this space. The entire evidence base is observational, meaning no study has yet demonstrated that switching away from UPF improves bone density or joint health. The substitution analyses in the Wei et al. (OA) and Zhang et al. (gout) studies are statistical modeling exercises, not real-world interventions. Whether the associations are causal and reversible remains to be tested.

Why This Review Matters Despite Its Limitations

The limitations described above are real and important, and the authors are transparent about them throughout the paper. But the scoping review serves a valuable purpose in the scientific process: it establishes the current state of the field, identifies the most promising and consistent signals, and defines the research agenda. Several findings are notable enough to deserve emphasis even while awaiting stronger confirmatory evidence.

The consistency of the preclinical data – three independent animal studies in three different rodent models, using different UPF formulations, all finding significant skeletal harm – provides biological plausibility and mechanism that strengthens the interpretation of the human epidemiological associations. It is harder to dismiss a statistical association in human cohort data as mere confounding when animal models provide a mechanistic explanation for the same effect.

The UK Biobank studies on RA and gout risk (n = 207,012 and 181,559 respectively) are among the largest dietary cohort analyses in musculoskeletal research. At these sample sizes, even small associations are precisely estimated, and confounding, while never fully eliminable in observational data, is substantially reduced by the scale and richness of available covariates.

The substitution effect findings – 6 percent lower knee OA risk and 13 percent lower gout risk from replacing 20 percent of caloric UPF intake with minimally processed foods – are framed in a way that is immediately actionable. They do not ask people to adopt a radical dietary transformation but to make partial, gradual shifts. This framing aligns with realistic public health communication.

The sex-specific signal in the OA data – women showing stronger associations between UPF intake and both thinner cartilage and worse pain than men – is consistent with existing knowledge that postmenopausal women face accelerated cartilage loss and are disproportionately affected by knee OA. Whether UPF interacts with estrogen biology, body composition differences, or other sex-specific factors warrants dedicated investigation.

Summary of Key Takeaways

• This 2025 scoping review – the first to comprehensively map the evidence on ultra-processed food and musculoskeletal health – synthesized 19 studies across five disease areas (bone health/osteoporosis, osteoarthritis, rheumatoid arthritis, gout, and spondyloarthritis), published between 2013 and 2025 from nine countries.
• Three independent preclinical studies in rodents consistently found that UPF diets reduced bone mineral density, impaired trabecular and cortical bone microarchitecture, weakened biomechanical properties, increased marrow adiposity, and disrupted bone-forming cellular processes. In one study, resistance exercise training did not prevent these skeletal harms, suggesting dietary modification is necessary rather than optional.
• In children and adolescents, higher fast-food and UPF consumption was associated with lower BMD at multiple skeletal sites and slower bone mineral accrual during adolescence – a critical developmental window. An ecological study found that each additional fast-food outlet near a child’s home corresponded to a 0.23 standard deviation decrease in BMD.
• In adults, large NHANES-based analyses found that adults in the highest quintile of UPF consumption had a 52 percent greater likelihood of osteoporosis, and those with more than 57.5 percent of calories from UPF had 78.9 percent increased odds of osteoporosis and lower femoral neck BMD. Each 1 percent increase in UPF share of calories correlated with a 1.9 percent increase in fractures among women.
• In a UK Biobank prospective cohort of nearly 164,000 adults, those in the highest quartile of UPF intake had a 10 percent increased risk of developing knee OA (but not hip OA). Replacing 20 percent of UPF calories with minimally processed foods was associated with a 6 percent lower knee OA risk. OAI data further linked higher UPF intake to thinner knee cartilage (particularly in women) and worse OA pain and physical function.
• In a UK Biobank cohort of over 207,000 adults, those in the highest quintile of UPF intake had a 17 percent increased risk of developing rheumatoid arthritis. A separate Brazilian study found that RA patients consuming more UPF had significantly worse metabolic and cardiovascular risk profiles.
• In a UK Biobank cohort of nearly 182,000 adults, higher UPF intake was associated with a 16 percent increased risk of gout, and individuals with high UPF intake combined with high genetic predisposition to gout had nearly twice the gout risk of those with low UPF intake and low genetic risk. Replacing 20 percent of UPF caloric intake with minimally processed foods was associated with a 13 percent lower gout risk.
• The evidence base for UPF and joint disease is at an early stage: most studies are observational (limiting causal inference), UPF measurement was inconsistent across studies, key confounders were not always adequately controlled, and no intervention trials have yet tested whether reducing UPF intake improves bone or joint outcomes. The scoping review design itself does not include risk-of-bias appraisal of individual studies.
• Despite these limitations, the directional consistency across preclinical models, pediatric studies, adult cohorts, and multiple disease areas – combined with plausible mechanistic pathways through systemic inflammation, oxidative stress, micronutrient displacement, and metabolic dysfunction – strengthens the overall signal and supports dietary UPF reduction as a reasonable and evidence-consistent strategy for musculoskeletal health promotion.

Ciaffi, Jacopo, Luana Mancarella, Claudio Ripamonti, Andrea D’Amuri, Veronica Brusi, Federica Pignatti, Lucia Lisi, and Francesco Ursini. “Ultra-Processed Food and Its Impact on Bone Health and Joint Diseases: A Scoping Review.” Nutrients, vol. 17, no. 7, 2025, article 1188. https://doi.org/10.3390/nu17071188. Full text available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC11990240/.