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Dr. Sanjoy Ghosh's research group examined the role of n-6 PUFA consumption in physical inactivity and insulin resistance in female mice. Mice fed corn oil experienced reduced spontaneous locomotor activity after 6 weeks of diet, hyperinsulinemia, and increased insulin resistance.

In summary, Dr. Ghosh's results continue to add to the evidence on the potential negative effects associated with diets that are high in n-6 PUFAs, which are present in many current diets. In connection with Dr. Mercola to obtain the optimal nutritional value of PUFAs, research suggests that 1% of total daily energy intake is sufficient.

To underline the importance of this research, Dr. Ghosh was awarded a Michael Smith Foundation Academic Award for Health Research in British Columbia for 5 years, from 2014 to 2019. He also received a new grant to continue his research on the core mechanisms that explain how excess n-6 PUFA can affect fibrosis.

https://www.researchgate.net/profile/Sanjoy-Ghosh-2/publication/305846599_Excess_Omega-6_Polyunsaturated_Fatty_Acid_Intake_Is_Associated_with_Negative_Cardiovascular_Intestinal_and_Metabolic_Outcomes_in_Mice/links/6190c8d307be5f31b77bd 3ba/Excess-Omega-6-Polyunsaturated-Fatty-Acid-Intake-Is-Associated-with-Negative- Cardiovascular-Intestinal-and-Metabolic-Outcomes-in-Mice.pdf (2016).—

The hearts of rats fed omega-6 experienced loss of Mn superoxide dismutase and increased levels of mitochondrial nitrotyrosine. In these hearts, oxidative damage to mitochondrial DNA was demonstrated by 8-hydroxyguanosine immunopositivity, overexpression of DNA repair enzymes, and a decrease in respiratory subunit mRNA expression. The study, for the first time, reports that a diet rich in omega-6 PUFAs for only 4 weeks instigates mitochondrial nitrosative damage and causes cardiac dysfunction.

https://pubmed.ncbi.nlm.nih.gov/17023268/ (2006).—

The results of this study present evidence supporting a cardiac muscle-specific effect of n-6 PUFAs with aggravation of the collagen I/III ratio and cardiac stiffening by excess n-6 PUFAs representing a new pathway of cardiac lipotoxicity. caused by diets rich in n-6 PUFA.

https://www.jbc.org/article/S0021-9258(20)44783-0/fulltext (2015).--

As reported by Dr. Mercola, linoleic acid (LA) is converted to oxidized linoleic acid metabolites (OXLAM) by lipoxygenase (LOX). This thesis investigated how OXLAMs such as 13-hydroperoxyoctadecadienoic acid (13-HpODE), 13-hydroxyoctadecadienoic acid (13-HODE), 9-hydroperoxyoctadecadienoic acid (9-HpODE), and 9-hydroxyoctadecadenoic acid (9-HODE) They affect mitochondrial redox status and fibrotic pathways. 13-HpODE could be responsible for the drop in mitochondrial redox state and increased production of “stiff” collagen within fibroblasts, contributing to subsequent fibrosis and heart failure.

https://open.library.ubc.ca/soa/cIRcle/collections/ubctheses/24/items/1.0442002 (2024).--

Omega-6 PUFAs can promote the absorption of Lead (Pb). We report an investigation into the gene expression of several antioxidant genes and Pb-transporting membrane proteins, which may play a critical role in oxidative stress and fibrosis. Both exposure to heavy metals, such as lead (Pb), and excessive consumption of omega-6 polyunsaturated fatty acids (PUFAs) have separately been linked to increased oxidative stress and fibrosis. The results seem to indicate that omega-6 PUFAs can promote Pb absorption.

https://open.library.ubc.ca/soa/cIRcle/collections/ubctheses/24/items/1.0443977 (2024).--

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