6 februari 2023: Bron: The Lancet en CNN artikel

Uit de resultaten van een bevolkingsonderzoek onder meer dan 197.000 mensen in het VK - Verenigd Koninkrijk, waarvan meer dan de helft vrouw (54 procent was vrouw in dit bevolkingsondeerzoek), verhoogt het eten van meer sterk bewerkte voedingsmiddelen het risico op het ontwikkelen van en overlijden aan kanker. Met name het ontwikkelen en overlijden aan eierstokkanker, borstkanker en hersenkanker blijken gekoppeld te zijn aan een dagelijks eetpatroon / dieet van sterk bewerkte voedingsproducten.

Overmatig bewerkte voedingsmiddelen zijn onder meer voorverpakte soepen, sauzen, diepvriespizza's en kant-en-klare maaltijden, maar ook hotdogs, worstjes, frites, frisdrank, koekjes uit de winkel, cakes, snoepjes, donuts, ijs enz. 

De hoeveelheid sterk bewerkt voedsel die door mensen in het onderzoek werd geconsumeerd, varieerde van een minimum van 9,1% tot een maximum van 41,4% van hun dagelijkse dieet, zo bleek uit de studie.
Eetpatronen werden vervolgens vergeleken met medische dossiers waarin zowel diagnoses als sterfgevallen door kanker werden vermeld.
Elke toename van 10% in de consumptie van sterk bewerkt voedsel werd geassocieerd met een toename van 2% in het ontwikkelen van kanker en een verhoogd risico van 19% om de diagnose eierstokkanker te krijgen.

Sterfgevallen door kanker namen ook toe, zo bleek uit de studie. Voor elke extra toename van 10% in de consumptie van overmatig bewerkt voedsel, nam het risico om te overlijden aan welke vorm van kanker dan ook toe met 6%, terwijl het risico om te overlijden aan eierstokkanker met 30% toenam, aldus een verklaring van de onderzoekers verbonden aan het Imperial College London.

"Ultrabewerkte voedingsmiddelen worden geproduceerd met industrieel afgeleide ingrediënten en gebruiken vaak voedseladditieven om de kleur, smaak, consistentie, textuur aan te passen of de houdbaarheid te verlengen", zegt eerste auteur Dr. Kiara Chang, een National Institute for Health and Care Research fellow bij Imperial College London's School of Public Health, in een verklaring.
"Ons lichaam reageert mogelijk niet op dezelfde manier op deze ultraverwerkte ingrediënten en additieven als op vers en voedzaam, minimaal verwerkt voedsel," zei Chang.

"Mensen die meer ultrabewerkt voedsel eten, hebben echter ook de neiging om meer koolzuurhoudende dranken en minder thee en koffie te drinken, evenals minder groenten en andere voedingsmiddelen die verband houden met een gezond voedingspatroon", zegt Duane Mellor, een geregistreerde diëtist en senior docent fellow aan de Aston Medical School in Birmingham, VK, in een e-mail.
"Dit zou kunnen betekenen dat het misschien niet specifiek een effect is van de sterk bewerkte voedingsmiddelen zelf, maar in plaats daarvan de impact weerspiegelt van een lagere inname van gezonder voedsel", zei Duana Mellor, die niet bij het onderzoek betrokken was.

"Mensen die het meest sterk bewerkt voedsel aten waren jonger en hadden minder kans op een familiegeschiedenis van kanker", schreven Chang en haar collega's.
Grote consumenten van sterk bewerkte voedingsmiddelen waren minder geneigd om aan lichaamsbeweging te doen en werden eerder als zwaarlijvig geclassificeerd. Deze mensen hadden waarschijnlijk ook een lager gezinsinkomen en opleiding en leven in de meest kansarme gemeenschappen, zo bleek uit de studie.

"Deze studie draagt bij aan het groeiende bewijs dat overmatig bewerkte voedingsmiddelen waarschijnlijk een negatieve invloed hebben op onze gezondheid, inclusief ons risico op kanker," zei Dr. Eszter Vamos, de hoofdauteur van de studie en een klinische hoofddocent aan de Imperial College London's School of Public Health in een verklaring.

De onderzoekers stellen: 

Onze studie biedt de eerste meest uitgebreide beoordeling voor preventieve associaties tussen sterk bewerkte voedselconsumptie en risico van algemene mortaliteit en 34 vormen van plaatsspecifieke kankerincidentie en bijbehorende mortaliteit.
Onze bevindingen tonen aan dat een hoger verbruik van sterk bewerkte voedingsproducten wordt geassocieerd met een groter risico op algehele kanker en met name eierstokkanker en hersenkanker, evenals toegenomen risico op algemene sterfte en eierstokkanker en borstkanker geassocieerde sterfte. Deze associaties bleven bestaan na correctie voor een reeks van sociaal-demografische factoren, rookstatus, fysieke activiteit en belangrijke voedingsfactoren.

Het volledige studierapport is via the Lancet of een PDF in te zien of te downloaden. Klik daarvoor op de titel van de studie:

Ultra-processed food consumption, cancer risk and cancer mortality: a large-scale prospective analysis within the UK Biobank

Open AccessPublished:January 31, 2023DOI:https://doi.org/10.1016/j.eclinm.2023.101840

Summary

Background

Global dietary patterns are increasingly dominated by relatively cheap, highly palatable, and ready-to-eat ultra-processed foods (UPFs). However, prospective evidence is limited on cancer development and mortality in relation to UPF consumption. This study examines associations between UPF consumption and risk of cancer and associated mortality for 34 site-specific cancers in a large cohort of British adults.

Methods

This study included a prospective cohort of UK Biobank participants (aged 40–69 years) who completed 24-h dietary recalls between 2009 and 2012 (N = 197426, 54.6% women) and were followed up until Jan 31, 2021. Food items consumed were categorised according to their degree of food processing using the NOVA food classification system. Individuals’ UPF consumption was expressed as a percentage of total food intake (g/day). Prospective associations were assessed using multivariable Cox proportional hazards models adjusted for baseline socio-demographic characteristics, smoking status, physical activity, body mass index, alcohol and total energy intake.

Findings

The mean UPF consumption was 22.9% (SD 13.3%) in the total diet. During a median follow-up time of 9.8 years, 15,921 individuals developed cancer and 4009 cancer-related deaths occurred. Every 10 percentage points increment in UPF consumption was associated with an increased incidence of overall (hazard ratio, 1.02; 95% CI, 1.01–1.04) and specifically ovarian (1.19; 1.08–1.30) cancer. Furthermore, every 10 percentage points increment in UPF consumption was associated with an increased risk of overall (1.06; 1.03–1.09), ovarian (1.30; 1.13–1.50), and breast (1.16; 1.02–1.32) cancer-related mortality.

Interpretation

Our UK-based cohort study suggests that higher UPF consumption may be linked to an increased burden and mortality for overall and certain site-specific cancers especially ovarian cancer in women.

Funding

The Cancer Research UK and World Cancer Research Fund.

Research in context

Evidence before this study

We searched PubMed using combinations of search terms such as “ultra”, “industrial”, “processed”, “food”, “drink”, and “cancer” on 10 September 2022 with no date or language restrictions. Our search results showed limited prospective evidence for the association between ultra-processed consumption and cancer outcomes. To date, only incidence of the most common cancer sites including colorectal, breast, and prostate cancer has been examined and the cohort studies that assessed total cancer mortality may be potentially limited by small sample size. No previously published cohort study has assessed incidence and mortality for a comprehensive range of site-specific cancers in relation to ultra-processed food consumption, and there is currently no data from the UK despite it is one of the world's leading consumers of ultra-processed foods.

Added value of this study

Our study provides the first most comprehensive assessment for the prospective associations between ultra-processed food consumption and risk of overall and 34 site-specific cancer incidence and associated mortality. Our findings show that higher consumption of ultra-processed foods is associated with a greater risk of overall cancer and specifically ovarian and brain cancer, as well as increased risk of overall, ovarian, and breast cancer-associated mortality. These associations persisted after adjustment for a range of socio-demographic, smoking status, physical activity, and key dietary factors.

Implications of all the available evidence

Cancer has surpassed cardiovascular disease as the leading cause of premature death in many high-income countries while cancer burden is rising most rapidly in low and middle-income countries. Our study adds important prospective evidence linking ultra-processed food to an increased risk of adverse cancer outcomes. Lowering consumption of ultra-processed foods in dietary patterns may be beneficial for the prevention and risk reduction of overall and certain site-specific cancers.

Discussion

This large prospective cohort analysis conducted within the UK Biobank provides a comprehensive assessment of associations between UPF consumption and risk of many site-specific cancer outcomes for the first time to our knowledge. There are three particularly noteworthy findings: First, every 10% increment in UPF content of diet was associated with an increased incidence of overall cancer by 2% and ovarian cancer by 19%. Second, participants with the highest compared with lowest UPF consumption quartile had higher incidence of overall and brain cancer, and a lower incidence of head and neck cancer. Finally, every 10% increment in UPF consumption was associated with increased mortality of overall cancer by 6%, breast cancer by 16%, and ovarian cancer by 30%. These associations persisted after adjustment for a range of key socio-economic, behavioural and dietary factors.
No previously published study has assessed the incidence and mortality comprehensively for site-specific cancers in relation to UPF consumption. Only two previously published studies assessed incidence of common cancer sites.  The French NutriNet-Santé study showed a 12% and 11% increase in risk of overall and breast cancer per 10% increment in UPF consumption (g/day), and no evidence of association for prostate and colorectal cancer.  A recent study from the US found a 29% increase in the risk of colorectal cancer among men in the highest quintile of UPF consumers compared with the lowest (based on servings/day).  Our findings are more aligned with the NutriNet-Santé study for overall, prostate, and colorectal cancer incidence, but not for breast cancer incidence. While we used the same measure of UPF consumption (weight ratio) as the NutriNet-Santé study, the US study had a much longer follow-up time (24–28 years compared with 5 years in the NutriNet-Santé and 10 years in this study). Moreover, our study cohort had a larger proportion of never smokers than in previous studies and these differences in characteristics, design and setting may all contribute to the differences in findings. Mortality of site-specific cancers have not been previously assessed, but overall cancer mortality has been examined in three cohort studies conducted in Spain, Italy, and North America with similar lengths of follow-up to this study.      None of the three studies, however, have identified any significant association with cancer mortality. Our study cohort is more than two-folds larger than previous studies and comparatively older due to the recruitment of middle-aged adults. Moreover, our study cohort was originated from a population with a substantially greater consumption of UPFs. Importantly, our study presents findings for many less common cancers not examined before, and our findings of the positive associations between UPF consumption and risks and associated mortality of overall and ovarian cancer were consistent among weight and energy ratio measures of UPF consumption.
Various mechanisms may explain the positive associations found between UPF consumption and the risk of adverse cancer outcomes. Recommendations for cancer prevention emphasise the importance of nutritionally balanced diets involving greater consumption of vegetables and fruit, lower consumption of unprocessed red meat and avoidance of processed meat, besides other behavioural factors including alcohol consumption and smoking. ,  However, dietary patterns with a high UPF content are generally nutritionally inferior and are higher in energy, total and saturated fats, salt, and free sugars, and lower in fibre and several micronutrients.  Alteration of food matrices by ultra-processing results in degradation of food health potential and deterioration of nutrient bioavailability and bioaccessibility.  Furthermore, evidence has been accumulating on the strong obesity and T2D-promoting potential of UPFs,  both of which are risk factors for many cancers including those of the digestive tract and some hormone-related cancers in women. , ,
Emerging research has suggested other common properties of UPFs that may contribute to adverse cancer outcomes, including through the use of controversial food additives, neoformed contaminants during ultra-processing, and toxic contaminants migrated from food packaging. Recent evidence from the NutriNet-Santé cohort showed higher intake of artificial sweeteners associated with increased risk of overall, breast, and obesity-related cancers,  while higher intake of nitrate and nitrite from food additives was associated with increased risk of breast and prostate cancer, respectively.  Higher dietary exposure of acrylamide, an industrial chemical formed during high-temperature cooking procedures, was found associated with an increased risk of ovarian and endometrial cancers.  Phthalates and bisphenols are endocrine-disrupting chemicals commonly found in food storage, packaging and contacting materials, and higher urinary concentration of phthalates and bisphenols-F (analogue of the more regulated bisphenol-A) have been detected in individuals with higher UPF consumption.  Available data on bisphenols are predominantly experimental but have consistently shown many toxic effects including for human breast cancer and damage to DNA, nervous and immune systems.  Epidemiological studies have suggested a positive association between phthalates and T2D and insulin resistance. ,  Recent animal models have shown that phthalates may induce neuroinflammation and disruption of the blood–brain barrier.  No previous studies have assessed the link between UPF consumption and brain cancer, but human studies have demonstrated associations with potential harmful effects on brain functions. ,
This study has many strengths. The large sample size and long prospective follow-up has enabled the investigation into outcomes of many anatomical cancer sites, especially site-specific cancer mortality. Also, the date and type of cancer incidence and mortality were ascertained through national cancer and death registries. The use of validated 24-h recalls allowed for more detailed dietary data being captured than many food frequency questionnaires, crucial for food processing classifications.
Our study has important limitations. First, the study cohort was not nationally representative and may over-represent populations with white ethnicity and those living in a less socio-economically deprived areas, and the mean UPF consumption and prevalence of obesity were lower than the UK average.  However, this study has reported important associations comparing cancer risk and mortality by levels of UPF consumption which may still be generalisable to the wider population or similar cohorts in other contexts. Second, misclassification of a few food items may occur owing to limited food processing information and we assigned them to the most probable food group based on published findings of common foods and drinks consumed in the UK.  Third, while we considered the average of multiple 24-h recalls the best representation of usual dietary intake, 39.7% of the cohort had only one 24-h recall and may be prone to measurement error owing to its limited ability to fully capture individuals’ variation in diet. Fourth, the associations for head and neck cancer incidence may be partly due to the complex interrelationships between UPF consumption, alcohol intake and smoking. However, we could not explore these further due to limited sample size shown in exploratory analysis. Finally, although we adjusted the analyses for a wide range of potential confounders including key lifestyle and nutritional factors, residual confounding may have affected the findings due to observational nature of the study.
In summary, this large contemporary prospective study of middle-aged UK adults found that higher UPF consumption was associated with a greater incidence and mortality of overall and certain site-specific cancers. Although causality may not be implied owing to the observational nature of the study, these findings highlight the importance of considering degrees of food processing in diets. In particular, the associations were found most consistent for overall cancer and ovarian cancer outcomes in women. These findings suggest that limiting UPF consumption may be beneficial to prevent and reduce the modifiable burdens of cancer.

Contributors

KC, CM, and EPV conceptualised the study and all authors contributed to the study design. KC compiled the data and performed statistical analyses with supervisory input from EPV. KC and EPV had access and verified the underlying data used in this study. All authors contributed to the finalisation of statistical models and interpretation of findings. KC and EPV wrote the first draft of the manuscript, and MJG, FR, RBL, IH, NK, and CM critically reviewed and edited the manuscript. All authors had full access to all the data in the study, approved the final manuscript, and accept responsibility for the decision to submit for publication.

Data sharing statement

UK Biobank data are available through application to the database https://www.ukbiobank.ac.uk/.

Declaration of interests

All authors declare no conflict of interest.

Acknowledgements

This work was supported by Cancer Research UK C33493/A29678. Funding IIG_FULL_2020_033 was obtained from World Cancer Research Fund (WCRF UK), as part of the World Cancer Research Fund International grant programme. Where authors are identified as personnel of the International Agency for Research on Cancer / World Health Organization, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy or views of the International Agency for Research on Cancer / World Health Organization. FR declares funding from The São Paulo Research Foundation (FAPESP) 16/14302-7 and 18/19820-1. This research has been conducted using the UK Biobank Resource under Application Number 29239. The authors would like to thank the participants of the UK Biobank study.

Appendix A. Supplementary data


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Figures

  • Figure thumbnail gr1
    Fig. 1Sources of NOVA subgroups in the total diet by quartile of ultra-proces

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