Does Acrylamide Increase the Risk of Neurodegenerative and Cardiovascular Disease?

Background

Acrylamide forms in foods rich in starch when cooked/processed at temperature >120°C (e.g., roasting, frying, grilling) in absence of moisture. Acrylamide may also form in foods from acrolein during the degradation of amino acids, carbohydrates, lipids, and organic acids. Of note, the content of acrylamide in diet may vary strongly depending on the food matrix and processing methods (home and restaurants cooking and/or industrial processing). Acrylamide is prevalent in a wide-range of commonly consumed foods (e.g. coffee, biscuits, breakfast cereals, bread especially crispy bread, potato products and vegetables crisps) - some of these are also part of a healthy diet. Acrylamide is also produced in heated tobacco.

Acrylamide-induced neurotoxic adverse effects have been well-documented in animal and occupational studies. From its inception, acrylamide is a chemical compound used in the industry to produce plastics (polyacrylamides). However, its occupational exposure is considered of low concern due to successful intervention and preventive measures. Cumulative exposure to acrylamide in workers via inhalation and/or dermal absorption have been observed to give rise central and peripheral neurotoxicity, supporting the concern related to cumulative dietary acrylamide exposure in the development of neurodegenerative disorders in the general population. Yet, to date, no epidemiological studies have investigated whether dietary acrylamide exposure associates to neurodegenerative diseases including dementia, Alzheimer´s, and Parkinson´s diseases.

Growing body of evidence also indicate that acrylamide´s mode of action might lead to cardiometabolic alteration which in turn, play a critical role in atherosclerosis and CVD development. Still, epidemiological evidence investigating dietary acrylamide and incidence of CVD including myocardial infarction are lacking.

In theory, acrylamide can exert toxicity in all the human organs. In vivo and vitro studies show that acrylamide-induced toxicity may be evident at low doses. However, it is proposed that the detrimental effects will exacerbate at high doses or most likely at prolonged/cumulative exposure such the dietary exposure resulting in the clinical manifestation of the diseases here investigated. There is substantial evidence showing that toxicity of acrylamide is mediated by glycidamide, a highly reactive compound and the main metabolite of acrylamide, via the formation of DNA adducts. Also, production of oxidative stress and formation of adducts with protein (especially alkylation) are considered plausible molecular initiating events to trigger cumulative neurotoxicity. For the acrylamide-induced neurotoxicity, acrylamide is suspected to promote neuroinflammation, induce neurite degeneration, inhibit axonal transport, alter the level and turnover of neurotransmitters (e.g., enhanced activity of acetylcholinesterase and dopamine depletion) and directly inhibit neurotransmission which ultimately may result in learning and memory impairment, anxiogenic responses, and disturbed motor coordination. Consequently, this can give rise to neurodegenerative disease.