Many food science and nutritional researchers continue to reassure us of the 'safety’of polyunsaturated fatty acid (PUFA)-rich, vegetable-derived cooking oils employed for standard frying practices, and have generally reported that molecular indices commonly utilised for their safety evaluation are within permissible limits. However, although the peroxidative deterioration of unsaturated fatty acids (UFAs) during such practices remains still largely unreported or even considered, there is now a steadily increasing number of scientists, and members of the general public, who appreciate the importance of circumventing the use of PUFA-rich culinary oils for frying purposes, domestically or otherwise. Exposure of such oils to high temperatures associated with such frying practices gives rise to the generation of lipid oxidation products (LOPs), particularly but not exclusively so cytotoxic, mutagenic and genotoxic aldehydes, from thermally-promoted, O2-powered, sequential UFA peroxidation processes, which recycle when frying episodes are repeated and the oils reused. These toxins penetrate into and hence are 'carried' by fried foods available for human consumption.
Although the above data provide powerful evidence that markedly challenges reports focused on the negligible or limited health risk status of such oils when employed for these purposes, and that foods fried therein are 'safe' for human consumption, to date they have not adequately considered public health threats posed by the ingestion of high concentrations of highly toxic LOPs detectable therein. Evidence available indicates that if sufficiently absorbed from the gastrointestinal (GI) system into the systemic circulation, such dietary LOPs may significantly contribute to enhanced risks of the development and/or perpetuation of chronic non-communicable diseases (NCDs) in humans, for example cancer, and cardiovascular, inflammatory and neurodegenerative diseases, as may higher frequencies of fried food consumption. Therefore, the major theme of this Research Topic is based on the very wide range of potential public health threats presented by the human ingestion of primary LOPs (lipid hydroperoxides, and epoxy-fatty acids such as leukotoxin, etc.) and their secondary fragmentation products (e.g., a,ß-unsaturated aldehydes).
List of Sub-Topics and Article Contributions:
(1) Availabilities of dietary sources of LOP toxins, with special emphasis on cooking oils and fried foods.
(2) Mechanisms for the generation of LOPs in culinary oils during high-temperature frying episodes, and for their transference to fried foods available for human consumption.
(3) Fate of both primary and secondary LOPs in the human body, including evaluations of their interactions in the GI system, in vivo absorption into the systemic circulation, biodistribution and metabolism; potential LOP toxin biomarkers.
(4) Toxicological and risk assessments of dietary LOPs, including potential associations between the frequencies and levels of their intakes and the incidence/severity of NCDs in humans; mechanisms available for the toxicities and associated adverse health effects of dietary LOPs, along with a critical consideration of the concentrations of these agents available in the GI system, the systemic circulation and elsewhere in vivo will also be featured.
(5) Population-based epidemiological and cohort meta-analysis explorations of linkages between NCD prevalence in humans, their fried food intakes and the unsaturation status of frying oils employed.
(6) Full evaluation and scrutiny of analytical/bioanalytical methods available for the determinations of LOPs in cooking oils and foods, and human biofluids and tissues (the selectivity and reliability of some conventional/traditional methods available for these purposes remains highly questionable).
(7) Assessments of the adverse public health risk threats engendered by inhaled aldehyde-containing cooking oil fumes.
(8) Targeted nutrition and potential interventional strategies for reducing the quantities of LOPs available in the human diet, which may effectively challenge and combat health risks posed by their ingestion (these include ‘anti-aldehyde’ prophylactic or therapeutic strategies such as endogenous thiol compounds).
Many food science and nutritional researchers continue to reassure us of the 'safety’of polyunsaturated fatty acid (PUFA)-rich, vegetable-derived cooking oils employed for standard frying practices, and have generally reported that molecular indices commonly utilised for their safety evaluation are within permissible limits. However, although the peroxidative deterioration of unsaturated fatty acids (UFAs) during such practices remains still largely unreported or even considered, there is now a steadily increasing number of scientists, and members of the general public, who appreciate the importance of circumventing the use of PUFA-rich culinary oils for frying purposes, domestically or otherwise. Exposure of such oils to high temperatures associated with such frying practices gives rise to the generation of lipid oxidation products (LOPs), particularly but not exclusively so cytotoxic, mutagenic and genotoxic aldehydes, from thermally-promoted, O2-powered, sequential UFA peroxidation processes, which recycle when frying episodes are repeated and the oils reused. These toxins penetrate into and hence are 'carried' by fried foods available for human consumption.
Although the above data provide powerful evidence that markedly challenges reports focused on the negligible or limited health risk status of such oils when employed for these purposes, and that foods fried therein are 'safe' for human consumption, to date they have not adequately considered public health threats posed by the ingestion of high concentrations of highly toxic LOPs detectable therein. Evidence available indicates that if sufficiently absorbed from the gastrointestinal (GI) system into the systemic circulation, such dietary LOPs may significantly contribute to enhanced risks of the development and/or perpetuation of chronic non-communicable diseases (NCDs) in humans, for example cancer, and cardiovascular, inflammatory and neurodegenerative diseases, as may higher frequencies of fried food consumption. Therefore, the major theme of this Research Topic is based on the very wide range of potential public health threats presented by the human ingestion of primary LOPs (lipid hydroperoxides, and epoxy-fatty acids such as leukotoxin, etc.) and their secondary fragmentation products (e.g., a,ß-unsaturated aldehydes).
List of Sub-Topics and Article Contributions:
(1) Availabilities of dietary sources of LOP toxins, with special emphasis on cooking oils and fried foods.
(2) Mechanisms for the generation of LOPs in culinary oils during high-temperature frying episodes, and for their transference to fried foods available for human consumption.
(3) Fate of both primary and secondary LOPs in the human body, including evaluations of their interactions in the GI system, in vivo absorption into the systemic circulation, biodistribution and metabolism; potential LOP toxin biomarkers.
(4) Toxicological and risk assessments of dietary LOPs, including potential associations between the frequencies and levels of their intakes and the incidence/severity of NCDs in humans; mechanisms available for the toxicities and associated adverse health effects of dietary LOPs, along with a critical consideration of the concentrations of these agents available in the GI system, the systemic circulation and elsewhere in vivo will also be featured.
(5) Population-based epidemiological and cohort meta-analysis explorations of linkages between NCD prevalence in humans, their fried food intakes and the unsaturation status of frying oils employed.
(6) Full evaluation and scrutiny of analytical/bioanalytical methods available for the determinations of LOPs in cooking oils and foods, and human biofluids and tissues (the selectivity and reliability of some conventional/traditional methods available for these purposes remains highly questionable).
(7) Assessments of the adverse public health risk threats engendered by inhaled aldehyde-containing cooking oil fumes.
(8) Targeted nutrition and potential interventional strategies for reducing the quantities of LOPs available in the human diet, which may effectively challenge and combat health risks posed by their ingestion (these include ‘anti-aldehyde’ prophylactic or therapeutic strategies such as endogenous thiol compounds).
