---
title: "Low-fat dietary pattern reduced dietary advanced glycation end-products in the Women’s Health Init"
id: "british-journal-of-cancer-0-low-fat-dietary-pattern-and-dietary-advanced-glycation-end-products-intake-a"
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content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "British Journal of Cancer"
source_url: "https://www.nature.com/articles/s41416-026-03514-x"
published_at: "2026-07-28T09:16:05.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Low-fat dietary pattern reduced dietary advanced glycation end-products in the Women’s Health Init
## Provenance & Clinical Metadata
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- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** British Journal of Cancer
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41416-026-03514-x)
- **Published At:** 2026-07-28T09:16:05.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The Women’s Health Initiative (WHI) Dietary Modification randomized trial enrolled 48,835 postmenopausal women to evaluate a **low-fat dietary pattern** versus a usual diet; randomization was 40:60 (intervention:comparison). - The WHI intervention aimed to reduce fat to 20% of total energy and increase fruits, vegetables, and grains; sessions included 18 group visits in year one and quarterly maintenance thereafter. - Dietary intake was assessed with food frequency questionnaires (FFQs) at baseline, year 1, and annually in a rotating one-third subgroup through 5–7 years; anthropometrics were measured annually. - Dietary advanced glycation end-products (**dAGE**) were estimated by matching FFQ items to CML-AGE values from the Uribarri et al. database (ELISA-derived CML values for 540 foods), expressed as kilo Units per 1000 kcal (kU/1000 kcal). - Baseline mean dAGE scores were similar between groups (intervention 7542 kU/1000 kcal, SD 912; comparison 7514 kU/1000 kcal, SD 917). - Across 5–7 years, dAGE scores were persistently and significantly lower in the intervention group versus comparison (intervention mean range 5361–6236 kU/1000 kcal; comparison mean range 7159–7669 kU/1000 kcal; P < 0.0001). - The WHI low-fat intervention previously demonstrated reduced incidence of specific breast cancer subtypes and a reduction in **breast cancer mortality** (HR 0.79, 95% CI 0.64–0.97, P = 0.02) and improved metabolic syndrome components. - Foods of animal origin, red and processed meats, high-fat spreads, and fried/baked foods are high contributors to dietary AGEs, while fruits, vegetables, whole grains and legumes are generally lower in AGE content; the intervention targeted these food groups. - The analysis supports that the WHI dietary modification substantially reduced estimated **dAGE consumption**, consistent with the intervention’s food targets and prior mechanistic hypotheses linking diet, metabolic health, and cancer outcomes.
## Clinical Analysis & Structured Key Points
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[nature](https://www.nature.com/) 2. [british journal of cancer](https://www.nature.com/bjc) 3. [articles](https://www.nature.com/bjc/articles?type=article) 4. article Low-fat dietary pattern and dietary advanced glycation end-products intake: a secondary analysis of the Women’s Health Initiative randomized trial [ Download PDF ](https://www.nature.com/articles/s41416-026-03514-x.pdf) [ Download PDF ](https://www.nature.com/articles/s41416-026-03514-x.pdf) * Article * [Open access](https://www.springernature.com/gp/open-science/about/the-fundamentals-of-open-access-and-open-research) * Published: 28 July 2026 Clinical Study # Low-fat dietary pattern and dietary advanced glycation end-products intake: a secondary analysis of the Women’s Health Initiative randomized trial * [Margaret S. Pichardo](https://www.nature.com/articles/s41416-026-03514-x#auth-Margaret_S_-Pichardo-Aff1) [ORCID: orcid.org/0000-0002-9132-4400](https://orcid.org/0000-0002-9132-4400)[1](https://www.nature.com/articles/s41416-026-03514-x#Aff1), * [Rebecca P. Hunt](https://www.nature.com/articles/s41416-026-03514-x#auth-Rebecca_P_-Hunt-Aff2)[2](https://www.nature.com/articles/s41416-026-03514-x#Aff2), * [Lindsay L. Peterson](https://www.nature.com/articles/s41416-026-03514-x#auth-Lindsay_L_-Peterson-Aff3)[3](https://www.nature.com/articles/s41416-026-03514-x#Aff3), * [Kathy Pan](https://www.nature.com/articles/s41416-026-03514-x#auth-Kathy-Pan-Aff4) [ORCID: orcid.org/0000-0003-3546-2566](https://orcid.org/0000-0003-3546-2566)[4](https://www.nature.com/articles/s41416-026-03514-x#Aff4), * [Mace Coday](https://www.nature.com/articles/s41416-026-03514-x#auth-Mace-Coday-Aff5)[5](https://www.nature.com/articles/s41416-026-03514-x#Aff5), * [Su Yon Jung](https://www.nature.com/articles/s41416-026-03514-x#auth-Su_Yon-Jung-Aff6) [ORCID: orcid.org/0000-0002-0513-1830](https://orcid.org/0000-0002-0513-1830)[6](https://www.nature.com/articles/s41416-026-03514-x#Aff6), * [Linda Snetselaar](https://www.nature.com/articles/s41416-026-03514-x#auth-Linda-Snetselaar-Aff7)[7](https://www.nature.com/articles/s41416-026-03514-x#Aff7), * [Marian L. Neuhouser](https://www.nature.com/articles/s41416-026-03514-x#auth-Marian_L_-Neuhouser-Aff2)[2](https://www.nature.com/articles/s41416-026-03514-x#Aff2), * [Susan E. Steck](https://www.nature.com/articles/s41416-026-03514-x#auth-Susan_E_-Steck-Aff8) [ORCID: orcid.org/0000-0002-3201-9537](https://orcid.org/0000-0002-3201-9537)[8](https://www.nature.com/articles/s41416-026-03514-x#Aff8), * [Fred K. Tabung](https://www.nature.com/articles/s41416-026-03514-x#auth-Fred_K_-Tabung-Aff9) [ORCID: orcid.org/0000-0001-8193-7150](https://orcid.org/0000-0001-8193-7150)[9](https://www.nature.com/articles/s41416-026-03514-x#Aff9), * [Nazmus Saquib](https://www.nature.com/articles/s41416-026-03514-x#auth-Nazmus-Saquib-Aff10)[10](https://www.nature.com/articles/s41416-026-03514-x#Aff10), * [JoAnn E. Manson](https://www.nature.com/articles/s41416-026-03514-x#auth-JoAnn_E_-Manson-Aff11) [ORCID: orcid.org/0000-0002-9426-7595](https://orcid.org/0000-0002-9426-7595)[11](https://www.nature.com/articles/s41416-026-03514-x#Aff11) & * … * [Rowan T. Chlebowski](https://www.nature.com/articles/s41416-026-03514-x#auth-Rowan_T_-Chlebowski-Aff12)[12](https://www.nature.com/articles/s41416-026-03514-x#Aff12) Show authors [_British Journal of Cancer_](https://www.nature.com/bjc) (2026) [Cite this article](https://www.nature.com/articles/s41416-026-03514-x#citeas) [ Save article ](https://www.nature.com/articles/s41416-026-03514-x/save-research?_csrf=93wDSHWaOX3C5P1rVQEMeFIKJPAexYeN) [ View saved research ](https://www.nature.com/saved-research) ## Abstract ### Background In the Women’s Health Initiative (WHI) Dietary Modification (DM) randomized trial, a low-fat dietary pattern intervention reduced breast cancer mortality (_P_ = 0.02). Higher dietary advanced glycation end-products (dAGE) may be associated with higher breast cancer incidence. In this report, we examined whether the WHI dietary intervention influenced dAGE consumption. ### Methods Of 48,835 postmenopausal women randomized (40:60) to dietary intervention versus usual diet comparison, 40,209 had food frequency questionnaires at baseline, and serially through 5–7 years, which were used to estimate dAGE scores (kilo Unit/1000 kilocalories [kU/1000 kcal]) using a commonly referenced database. Multivariate regressions with repeated dAGE measures were examined by randomization group. ### Results Baseline mean dAGE scores were similar for intervention (7542 kU/1000 kcal, standard deviation (SD) = 912) and comparison (7514 kU/1000 kcal, SD = 917) groups. Through 5–7 years, dAGE scores were persistently lower in intervention versus comparison groups (mean range 5361–6236 kU/1000 kcal versus 7159–7669 kU/1000 kcal (_P_ < 0.0001). ### Conclusions The WHI low-fat dietary pattern intervention substantially reduced dAGE consumption. ### Clinical trial registration NCT00000611; Date: 10/28/1999. ## Introduction In the Women’s Health Initiative (WHI) Dietary Modification (DM) randomized trial involving 48,835 postmenopausal women, a low-fat dietary pattern intervention compared with a usual diet, reduced fat intake and increased consumption of fruits, vegetables and grains [[1](https://www.nature.com/articles/s41416-026-03514-x#ref-CR1 "Prentice RL. Dietary assessment and the reliability of nutritional epidemiology reports. Lancet. 2003;362:182–3.")]. Over 20 years of follow-up, the intervention was associated with a statistically significant early and sustained reduction in the incidence of estrogen receptor-positive, progesterone receptor-negative, breast cancers (HR, 0.77; 95% CI, 0.64–0.94) as well as a reduction in breast cancer mortality (hazard ratio [HR] 0.79, 95% confidence interval [CI] 0.64–0.97, _P_ = 0.02) [[2](https://www.nature.com/articles/s41416-026-03514-x#ref-CR2 "Chlebowski RT, Aragaki AK, Anderson GL, Pan K, Neuhouser ML, Manson JE, et al. Dietary modification and breast cancer mortality: long-term follow-up of the Women’s Health Initiative randomized trial. J Clin Oncol. 2020;38:1419–28.")]. Efforts to understand the mechanisms underlying this mortality benefit have focused in part on metabolic pathways. The WHI dietary intervention was shown to reduce the number of metabolic syndrome components, including central obesity, hypertension, dyslipidemia, and diabetes history [[3](https://www.nature.com/articles/s41416-026-03514-x#ref-CR3 "Neuhouser ML, Howard B, Lu J, Tinker LF, Van Horn L, Caan B, et al. A low-fat dietary pattern and risk of metabolic syndrome in postmenopausal women: the Women’s Health Initiative. Metabolism. 2012;61:1572–81.")], leading to the hypothesis that metabolic health may influence breast cancer outcomes. Supporting this, Pan et al. reported that among women in the intervention group, those with three or four components at baseline experienced a 69% reduction in breast cancer mortality compared with those with no components (HR 0.31 95% CI 0.14–0.69, interaction _P_ = 0.01) [[4](https://www.nature.com/articles/s41416-026-03514-x#ref-CR4 "Pan K, Aragaki AK, Neuhouser ML, Simon MS, Luo J, Caan B, et al. Low-fat dietary pattern and breast cancer mortality by metabolic syndrome components: a secondary analysis of the Women’s Health Initiative \(WHI\) randomised trial. Br J Cancer. 2021;125:372–9.")]. Advanced glycation end products (AGEs) are reactive metabolites formed endogenously and consumed through the diet, particularly in foods high in fat and processing [[5](https://www.nature.com/articles/s41416-026-03514-x#ref-CR5 "Uribarri J, Woodruff S, Goodman S, Cai W, Chen X, Pyzik R, et al. Advanced glycation end products in foods and a practical guide to their reduction in the diet. J Am Diet Assoc. 2010;110:911–16 e12.")]. Dietary AGEs have been implicated in metabolic dysfunction [[6](https://www.nature.com/articles/s41416-026-03514-x#ref-CR6 "Sergi D, Boulestin H, Campbell FM, Williams LM. The role of dietary advanced glycation end products in metabolic dysfunction. Mol Nutr Food Res. 2021;65:e1900934.")], obesity [[5](https://www.nature.com/articles/s41416-026-03514-x#ref-CR5 "Uribarri J, Woodruff S, Goodman S, Cai W, Chen X, Pyzik R, et al. Advanced glycation end products in foods and a practical guide to their reduction in the diet. J Am Diet Assoc. 2010;110:911–16 e12.")], chronic inflammation [[7](https://www.nature.com/articles/s41416-026-03514-x#ref-CR7 "Garay-Sevilla ME, Beeri MS, de la Maza MP, Rojas A, Salazar-Villanea S, Uribarri J. The potential role of dietary advanced glycation endproducts in the development of chronic non-infectious diseases: a narrative review. Nutr Res Rev. 2020;33:298–311."), [8](https://www.nature.com/articles/s41416-026-03514-x#ref-CR8 "Sharifi-Zahabi E, Sharafabad FH, Abdollahzad H, Malekahmadi M, Rad NB. Circulating advanced glycation end products and their soluble receptors in relation to all-cause and cardiovascular mortality: a systematic review and meta-analysis of prospective observational studies. Adv Nutr. 2021;12:2157–71.")] and cancer [[9](https://www.nature.com/articles/s41416-026-03514-x#ref-CR9 "Chen L, Duan Z, Tinker L, Sangi-Haghpeykar H, Strickler H, Ho GY, et al. A prospective study of soluble receptor for advanced glycation end-products and colorectal cancer risk in postmenopausal women. Cancer Epidemiol. 2016;42:115–23."),[10](https://www.nature.com/articles/s41416-026-03514-x#ref-CR10 "White DL, Hoogeveen RC, Chen L, Richardson P, Ravishankar M, Shah P, et al. A prospective study of soluble receptor for advanced glycation end products and adipokines in association with pancreatic cancer in postmenopausal women. Cancer Med. 2018;7:2180–91."),[11](https://www.nature.com/articles/s41416-026-03514-x#ref-CR11 "Wada K, Nakashima Y, Yamakawa M, Hori A, Seishima M, Tanabashi S, et al. Dietary advanced glycation end products and cancer risk in Japan: from the Takayama study. Cancer Sci. 2022;113:2839–48.")], including higher breast cancer incidence [[12](https://www.nature.com/articles/s41416-026-03514-x#ref-CR12 "Omofuma OO, Turner DP, Peterson LL, Merchant AT, Zhang J, Steck SE. Dietary advanced glycation end-products \(AGE\) and risk of breast cancer in the prostate, lung, colorectal and ovarian cancer screening trial \(PLCO\). Cancer Prev Res. 2020;13:601–10."), [13](https://www.nature.com/articles/s41416-026-03514-x#ref-CR13 "Peterson LL, Park S, Park Y, Colditz GA, Anbardar N, Turner DP. Dietary advanced glycation end products and the risk of postmenopausal breast cancer in the National Institutes of Health-AARP Diet and Health Study. Cancer. 2020;126:2648–57.")]. Experimental and observational evidence indicate that foods of animal origin, particularly red and processed meats, high-fat spreads and baked or fried foods, are among the highest contributors to dietary AGE intake, especially when prepared using dry heat methods, whereas fruits, vegetables, whole grains and legumes are generally lower in AGE content [[5](https://www.nature.com/articles/s41416-026-03514-x#ref-CR5 "Uribarri J, Woodruff S, Goodman S, Cai W, Chen X, Pyzik R, et al. Advanced glycation end products in foods and a practical guide to their reduction in the diet. J Am Diet Assoc. 2010;110:911–16 e12.")]. Given that the WHI dietary intervention reduced intake of foods expected to be high in AGE and increased intake of foods expected to be lower in AGE, we examined whether a low-fat dietary intervention, compared with a usual diet, was associated with changes in dietary AGE (dAGE) intake over time in a large randomized clinical trial. ## Materials and methods The WHI DM trial design and conduct have been described [[14](https://www.nature.com/articles/s41416-026-03514-x#ref-CR14 "Anderson GL, Manson J, Wallace R, Lund B, Hall D, Davis S, et al. Implementation of the Women’s Health Initiative study design. Ann Epidemiol. 2003;13:S5–17."), [15](https://www.nature.com/articles/s41416-026-03514-x#ref-CR15 "Prentice RL, Caan B, Chlebowski RT, Patterson R, Kuller LH, Ockene JK, et al. Low-fat dietary pattern and risk of invasive breast cancer: the Women’s Health Initiative randomized controlled dietary modification trial. JAMA. 2006;295:629–42.")], 48,835 postmenopausal women, aged 50–79 years, were enrolled at 40 US clinical centers from 1993 through 1998 and followed for a primary endpoint of incidence of breast cancer and colorectal cancer. The study was approved at participating clinical centers and all participants gave written informed consent. The randomization algorithm was implemented by the WHI Clinical Coordinating Center (Seattle, WA) and assigned women in a 40:60 ratio to a low-fat dietary pattern (_n_ = 19,541) or usual diet comparison (_n_ = 29,294) group. The Trial Registration # NCT00000611 [[16](https://www.nature.com/articles/s41416-026-03514-x#ref-CR16 "ClinicalTrials.gov. Women’s Health Initiative \(WHI\) \[Available from: https://clinicaltrials.gov/study/NCT00000611 ")]. This report follows the Consolidated Standard of Reporting Trials (CONSORT). Baseline characteristics were collected through interviews for medication use and by self-report questionnaires for other variables. Dietary intake was monitored using food frequency questionnaires at baseline, 1-year, and thereafter annually in a rotating subgroup of about a third of participants throughout the 7-year intervention period. Annual measurements were obtained for body weight and height, with body mass index (BMI) calculated by blinded trained clinical staff [[15](https://www.nature.com/articles/s41416-026-03514-x#ref-CR15 "Prentice RL, Caan B, Chlebowski RT, Patterson R, Kuller LH, Ockene JK, et al. Low-fat dietary pattern and risk of invasive breast cancer: the Women’s Health Initiative randomized controlled dietary modification trial. JAMA. 2006;295:629–42.")]. The dietary intervention goal was to reduce fat intake to 20% of total energy and increase consumption of fruits, vegetables, and grains. Intervention goals did not include caloric restriction or weight loss. The dietary intervention involved 18 group sessions led by centrally trained registered dietitians and nutritionists in year one and quarterly maintenance sessions that lasted through the intervention period. Comparison group women received written health-related materials only. In a previous report, the NƐ-carboxymethyl-lysine (CML)-AGE content of 540 selected foods was determined using an enzyme-linked immunosorbent assay (ELISA) based on monoclonal anti-CML antibody (detailed in Uribarri 2010 [[5](https://www.nature.com/articles/s41416-026-03514-x#ref-CR5 "Uribarri J, Woodruff S, Goodman S, Cai W, Chen X, Pyzik R, et al. Advanced glycation end products in foods and a practical guide to their reduction in the diet. J Am Diet Assoc. 2010;110:911–16 e12.")]). The CML-AGE values from the database of Uribarri et al. were matched to each food item on food frequency questionnaires (FFQ) [[17](https://www.nature.com/articles/s41416-026-03514-x#ref-CR17 "Patterson RE, Kristal AR, Tinker LF, Carter RA, Bolton MP, Agurs-Collins T. Measurement characteristics of the Women’s Health Initiative food frequency questionnaire. Ann Epidemiol. 1999;9:178–87.")] and used as a dAGE measure in studies evaluating dAGE intake [[12](https://www.nature.com/articles/s41416-026-03514-x#ref-CR12 "Omofuma OO, Turner DP, Peterson LL, Merchant AT, Zhang J, Steck SE. Dietary advanced glycation end-products \(AGE\) and risk of breast cancer in the prostate, lung, colorectal and ovarian cancer screening trial \(PLCO\). Cancer Prev Res. 2020;13:601–10."), [13](https://www.nature.com/articles/s41416-026-03514-x#ref-CR13 "Peterson LL, Park S, Park Y, Colditz GA, Anbardar N, Turner DP. Dietary advanced glycation end products and the risk of postmenopausal breast cancer in the National Institutes of Health-AARP Diet and Health Study. Cancer. 2020;126:2648–57."), [18](https://www.nature.com/articles/s41416-026-03514-x#ref-CR18 "Jiao L, Chen L, Wh
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