# Time-restricted feeding and breast cancer

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN DIEGO · 2024 · $301,592

## Abstract

There is abundant evidence that obesity confers increased risk for at least 13 forms of cancer. The
incidence of breast, colon, and liver cancer are all increased in obese populations, and the epidemiologic
evidence for the obesity-breast cancer connection is particularly strong. One in eight women will be diagnosed
with breast cancer during their lifetime. Breast cancer incidence increases approximately 10-fold for women
over the of age 60, compared to age 50 or younger. This increase in breast cancer risk is associated with an
increase in obesity. Indeed, obesity increases the risk of triple-negative breast cancer in premenopausal women
and estrogen receptor positive breast cancer in postmenopausal women. A rarer form of inflammatory breast
cancer is dramatically increased (up to 5-fold) in both groups. More importantly, obesity shortens disease-free
survival in both pre- and postmenopausal women. Patient mortality in breast cancer is primarily caused by distant
metastases. Obesity at the time of diagnosis is associated with increased risk of distant metastasis and mortality.
 Studies in rodents have confirmed these relationships, showing that dietary-induced obesity and high-fat
diets lead to increased incidence and growth of tumors in oncogene and carcinogen-induced breast cancers.
Despite this body of correlative evidence, the mechanisms of obesity-induced breast cancer risk remain poorly
understood. One possibility is that the obesity causes insulin resistance in the liver and compensatory elevation
in circulating insulin to control glucose levels. At the same time, other tissues, including tumors, may not be
insulin resistant and so are exposed to increased insulin signaling. Indeed, we have shown that reducing insulin
resistance by treating with omega-3 fatty acids reduces breast cancer growth in mice. We have also shown that
time-restricted feeding (TRF) versus unrestricted feeding of a high-fat diet improves insulin resistance despite
sustained obesity and equal caloric intake. Furthermore, we showed that TRF inhibited obesity-driven breast
tumor growth and corrected tumor circadian rhythms, and that the TRF impact on tumor growth was mediated
by reducing insulin levels. A number of important questions remain unanswered. Firstly, how does insulin drive
tumor growth? Is it a direct effect on the tumor cell, or on the microenvironment? Secondly, does correction of
the circadian rhythms in the tumor cell by TRF contribute to the reduced tumor growth? Thirdly, how do nutrients
and insulin entrain the circadian clock in tumors? Due to the link between obesity, insulin resistance and breast
cancer in pre- and postmenopausal women, and the translational potential of time-restricted feeding, we will
investigate the effect of deleting the insulin receptor, mTORC1 signaling, or components of the circadian clock
in tumor cells to test whether loss of these signals alters tumor growth in vivo and the response to TRF. We will
also test whether TRF e...

## Key facts

- **NIH application ID:** 10892243
- **Project number:** 5R01CA196853-08
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN DIEGO
- **Principal Investigator:** NICHOLAS J WEBSTER
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $301,592
- **Award type:** 5
- **Project period:** 2016-04-01 → 2027-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10892243

## Citation

> US National Institutes of Health, RePORTER application 10892243, Time-restricted feeding and breast cancer (5R01CA196853-08). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10892243. Licensed CC0.

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