INDUSTRIAL TRANS-FATTY ACIDS INCREASE THE RISK OF BRAIN DISEASE

S. Qin¹ and M. Di Emidio^2*

¹ Beijing MicroKpro Medical Instrument Co., Ltd., Daxing district, Beijing, China;
² Medical School, University of L’Aquila, Italy.

*Correspondence to:
Martina Di Emidio,
Medical School,
University of L’Aquila,
L’Aquila, Italy.
e-mail: Martina.diemidio1@gmail.com

Received: 03 March, 2025 Accepted: 09 April, 2025

ISSN 2279-5855 print ISSN 2974-6345 online. Copyright © by BIOLIFE 2025 This publication and/or article is for individual use only and may not be further reproduced without written permission from the copyright holder. Unauthorized reproduction may result in financial and other penalties. Disclosure: All authors report no conflicts of interest relevant to this article.

ABSTRACT

Trans-fatty acids (TFAs) consumed through diet are very dangerous for public health. TFAs should constitute less than 1% of the diet, as they bind to membrane phospholipids and alter the natural cis conformation. TFAs cause dysfunction of receptors and ion channels, signal transduction, endothelial function, and can clog arteries, resulting in ischemic stroke or cerebral ischemia. TFAs increase the risk vascular damage and attract immune cells, promoting inflammation. TFA-induced plaques contain cellular and noncellular components, such as free cholesterol, cholesterol esters, phospholipids, and cellular debris. Additionally, TFAs mediate oxidative stress, with damaging systemic effects that also affect the brain. Neuroinflammation and neuronal damage caused by TFAs are implicated in neurodegenerative diseases such as Alzheimer’s Disease and Parkinson’s Disease.

KEYWORDS: Trans-fatty acid, vascular damage, inflammation, neurodegeneration, unsaturated fat

INTRODUCTION

Trans-fatty acids (TFAs) from the diet are mainly produced industrially and are very harmful for public health and for the health of the brain (1). The World Health Organization (WHO) recommends completely eliminating TFAs from the diet, or at least they should represent less than 1% of daily energy intake (2). Omega-3 fatty acids are brain-protective fats and therefore have an opposite effect to TFAs. Damage from TFAs is a key issue in cardiovascular pathophysiology (3). In many European countries, the use of industrial TFAs has been severely limited since 2021 (<2 g per 100 g of total fat) (4).

TFAs are unsaturated fats derived from the partial hydrogenation of vegetable oils with at least one double bond in the trans configuration, which alters the natural cis conformation and causes cellular and molecular effects on blood circulation (5). They are found in small amounts in processed foods, as well as in milk and meat. TFAs bind to membrane phospholipids, endothelial cells, platelets, erythrocytes, macrophages, and other cells, subsequently altering the cell membrane to become more rigid (6). This effect alters receptors and ion channels, signal transduction, and endothelial function (7).

Eliminating as much saturated and trans fats as possible from the diet improves the physiology of the body and brain. TFAs can cause clogged arteries that increases the risk of heart attacks and blocks cerebral blood flow, which could result in ischemic stroke or cerebral ischemia (8).

DISCUSSION                                                                                                                                                                                          

Diets high in industrial TFAs, such as those found in some industrially produced hydrogenated foods, promote arterial clogging and increase the risk of cardiovascular disease and brain damage (9).  TFAs increase LDL cholesterol and decrease HDL, which can cause vascular disease that can be fatal (10).

TFAs promote vascular inflammation, promoting the formation of atherosclerotic plaques, chronic lesions in the arterial wall that form during atherosclerosis (11). Atherosclerotic plaques are composed of various cellular and noncellular components, which together determine their appearance and degree of risk for the body. The main composition of an atherosclerotic plaque is damaged endothelial cells that promote the adhesion of lipids and inflammatory cells (6). The cellular components of the plaque include smooth muscle cells that produce extracellular matrix such as collagen, elastin, and proteoglycans, and the inflammatory cells of the atherosclerotic plaque are primarily macrophages that phagocytose lipids and become foam cells (12,13).

Other immune cells found in atherosclerotic plaques include lymphocytes, neutrophils, and mast cells (MCs) (14). Lymphocytes modulate the immune and inflammatory response, neutrophils are activators and amplifiers of inflammation in the plaque, while MCs release chemokines, such as CXCL1, and other inflammatory compounds that drive neutrophil recruitment in atherosclerotic lesions (6).

MCs have been identified in the arterial wall, both in the intima and in the adventitia, and in regions of the atherosclerotic plaque. Their activation occurs through various stimuli: neuropeptide factors, complement system (C5a), IgE, and immune complexes (15).  They release biochemical mediators including proteases such as tryptase and chymase, which activate metalloproteinases (MMPs) that degrade the extracellular matrix. Furthermore, MCs generate prostaglandins (PGD2), leukotrienes, and pro-inflammatory cytokines that amplify local inflammation (16).

Plaques also contains noncellular components, such as the lipid core that consists of free cholesterol, cholesterol esters, phospholipids, and cellular debris (17).  The extracellular matrix is ​​composed of structural proteins that hold the plaque together. Calcium deposits accumulate as the plaque persists and calcifies (18). All of this increases the risk not only of cardiovascular disease, but also of stroke and other brain diseases.

In addition to the cardiovascular system, there is evidence that TFAs may also have negative effects on the brain (19). Inflammation and oxidative stress can be caused by industrial TFAs which can act systemically (20).  These effects can extend to the brain, contributing to neuroinflammation and oxidative stress, two factors implicated in neurodegenerative diseases such as Alzheimer’s Disease and Parkinson’s Disease (21).

TFAs can cause neuronal and cell membrane damage due to inflammation. They insert themselves into cell membranes, altering their fluidity and functionality. Neuronal membranes are very rich in lipids and TFAs can cause them to be less efficient in synaptic transmission, reducing cognitive function (22). Excessive TFA consumption can affect memory and learning, increasing the risk of cognitive decline (23). These symptoms can also be accompanied by mood changes and an elevated risk of depression (24). Elevated plasma levels of TFA can increase the risk of neurodegenerative diseases (25).  In addition to chronic inflammation due to TFAs, there may be impairment of the blood-brain barrier, which could contribute to brain damage (26).

CONCLUSIONS

TFAs are primarily produced industrially and when they are consumed through the diet for an extended period of time, they become harmful for the brain. They can cause clogged arteries to increase the risk of heart attacks and block cerebral blood flow, which can cause ischemic stroke or cerebral ischemia. Furthermore, TFAs can stimulate immune cells and induce local and systemic inflammation. The most common industrial trans fats consumed by humans are margarines and hydrogenated vegetable fats, packaged snacks, fast foods, and repeatedly used frying oils. The use of unsaturated fats such as omega-3, which have a protective effect on the brain, can be a healthy alternative (27).

Conflict of interest

The authors declare that they have no conflict of interest.

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