# Role of High Omega-6 Diet as a Risk Factor for Pain Through Increased TRPV1 and TRPA1 Activity

> **NIH NIH F30** · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · 2020 · $34,140

## Abstract

Abstract
 Physicians recommend dietary interventions for management of cardiovascular disease,
diabetes and many autoimmune diseases; however, there is a large gap in knowledge on the role of
diet as a risk factor or potential therapy for chronic pain. Management of pain remains a substantial
medical problem, in part, because of an incomplete understanding of the physiologic mechanisms for
transduction and processing of noxious stimuli. Moreover, current analgesics are often limited by
incomplete efficacy, unacceptable side effects or risk of dependency. New discoveries for both the
treatment and prevention of chronic pain are essential, and investigating the relationship between diet
and pain allows for the potential development of new therapies along with a better understanding of the
mechanisms of persistent pain.
 Multiple studies have demonstrated that oxidized metabolites of linoleic acid (LA) or arachidonic
acid (AA) have potent biological actions in activating transient receptor potential (TRP) channels,
including TRPV1 and TRPA1, that are expressed on nociceptive neurons. Since LA and AA are
essential omega-6 polyunsaturated fatty acids (PUFA), their physiologic levels are a function of dietary
intake. Preliminary data presented in this application demonstrate that mice fed a 15-week high
omega-6 diet exhibit changes in basal thermal and mechanical nociceptive thresholds and increased
responses to noxious stimuli. However, there is still a large gap in knowledge as the mechanisms by
which dietary omega-6 lipid intake modulate pain is not understood. Based on recent studies and our
preliminary data, we propose to test the central hypothesis that increased dietary omega-6 PUFA leads
to increased thermal hyperalgesia and mechanical allodynia via increased TRPV1 and TRPA1
activities.
 Diet-induced increased TRPV1 and TRPA1 activity could be a common mechanism among
multiple chronic pain conditions and play a role in the transition from acute to chronic pain. The
following aims will test the hypothesis:
Specific Aim #1: Assess cellular lipid composition change following a 15-week high omega-6 diet and
determine the role of the lipids in thermal and mechanical nociception.
Specific Aims #2: Investigate the role of TRPV1 and TRPA1 in increased thermal and mechanical
nociception following a high omega-6 diet.
Specific Aim #3: Determine whether high lipid diet alters nociception in a sex-specific manner.
This study is innovative in its rationale and potential for identifying an environmental factor that could
predispose and possibly predict pain response. This project may also lead to novel therapeutic
approaches for treatment and prevention of chronic pain conditions. Moreover, the techniques and
research methods provide an ideal training vehicle for my career as an academic physician-scientist.

## Key facts

- **NIH application ID:** 9922871
- **Project number:** 5F30AT009949-03
- **Recipient organization:** UNIVERSITY OF TEXAS HLTH SCIENCE CENTER
- **Principal Investigator:** JACOB TYLER BOYD
- **Activity code:** F30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $34,140
- **Award type:** 5
- **Project period:** 2018-06-01 → 2023-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9922871

## Citation

> US National Institutes of Health, RePORTER application 9922871, Role of High Omega-6 Diet as a Risk Factor for Pain Through Increased TRPV1 and TRPA1 Activity (5F30AT009949-03). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/9922871. Licensed CC0.

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