Why Fried Food is Unhealthy: Heat Induced Food Toxicants and Associated Health Risks

Abstract

Frying is a widespread process used in food preparation and manufacturing as reflected in a large spectrum of products. Fried foods such as potato chips, French fries, expanded snacks, roasted nuts, extruded noodles, doughnuts and fried fish and chicken have gained worldwide popularity due to their unique organoleptic characteristics like distinctive flavour, aroma, appearance, and crunchy texture. During frying, as several physical and chemical changes occur in foods that impart desirable characteristics, heat induced food toxicants such as acrylamide, hydroxymethylfurfural, heterocyclic amine, nitrosamines and polyaromatic hydrocarbons could also be produced. However, these toxicants and the oil used for frying can cause non-communicable diseases such as coronary heart diseases, diabetes, cancer, overweight obesity and hypertension. Diet and nutrition play a key role in the promotion and maintenance of good health. Therefore, use of antioxidants, frying time and temperature control, recipe optimization, use of saturated oil, and vacuum frying are some of the techniques used to reduce the formation of heat generated food toxicants. In addition, increasing consumer awareness of the relationship between nutrition and health and fried food consumption is also crucial.

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©2019 Pearl Research Journals
Why Fried Food is Unhealthy: Heat Induced Food Toxicants
and Associated Health Risks
Fikiru Dasa1,2* and Tilahun Abera3
Accepted 10 April 2019
1Ethiopian Institute of Agricultural Research, Melkassa Agricultural Research Center, Ethiopia.
2Can Tho University, Faculty of Food Technology, Vietnam.
3Jimma University College of Agriculture & Veterinary Medicine, Department of Postharvest Management, Ethiopia.
ABSTRACT
Frying is a widespread process used in food preparation and manufacturing as reflected in a large spectrum
of products. Fried foods such as potato chips, French fries, expanded snacks, roasted nuts, extruded noodles,
doughnuts and fried fish and chicken have gained worldwide popularity due to their unique organoleptic
characteristics like distinctive flavour, aroma, appearance, and crunchy texture. During frying, as several
physical and chemical changes occur in foods that impart desirable characteristics, heat induced food
toxicants such as acrylamide, hydroxymethylfurfural, heterocyclic amine, nitrosamines and polyaromatic
hydrocarbons could also be produced. However, these toxicants and the oil used for frying can cause non-
communicable diseases such as coronary heart diseases, diabetes, cancer, overweight obesity and
hypertension. Diet and nutrition play a key role in the promotion and maintenance of good health. Therefore,
use of antioxidants, frying time and temperature control, recipe optimization, use of saturated oil, and vacuum
frying are some of the techniques used to reduce the formation of heat generated food toxicants. In addition,
increasing consumer awareness of the relationship between nutrition and health and fried food consumption
is also crucial.
Keywords: Frying, Fried food, Thermal degradation, Heat-induced food toxicants, Health effects.
Corresponding author.Email: fikiru.dasa@gmail.com
INTRODUCTION
Frying is one of the most popular thermal processing
methods for food preparation and manufacturing
worldwide. It is a cheap and fast process of simultaneous
heat and mass transfer that imparts unique sensory
characteristics to food (Ngadi and Xue, 2016) and
changes the nutritional characteristics as a result of
complex interactions between food and oil (Ziaiifar et al.,
2008). In addition, food frying has benefits in reducing
risk of microbial spoilage and extends product shelf-life
by thermal destruction of microorganisms, enzymes, and
reduction of water activity on the surface of the food
(Fellows, 2009). Frying of food is widely used in the food
industry in food manufacturing, at home and street with
a significant impact on the final quality of foods. Deep
frying, shallow or pan frying, stir-frying and sautéing are
all standard frying techniques. Fried foods such as potato
chips, French fries, expanded snacks, roasted nuts,
extruded noodles, doughnuts and fried fish and chicken
have gained worldwide popularity. Heat generated food
toxicants such as acrylamide (Figure 1),
hydroxymethylfurfural (HMF), heterocyclic amine (2-2-
amino-1-methyl-6-phenylimidazo-pyridine), nitrosamines
and polyaromatic hydrocarbons such as benzoapyrene
and chloropropanols (for example, 3-
monochloropropane-1-diol, 3-MCPD) are produced
during food frying (Stadler, 2012). Such compounds
cause different types of DNA damage like nucleotide
alterations and gross chromosomal aberrations. Most
genotoxic compounds begin their action at the DNA level
by forming carcinogen–DNA adducts, which result from
the covalent binding of a carcinogen or part of a
carcinogen to a nucleotide (Jägerstad and Skog, 2005).
The major pathway for acrylamide formation in foods is
Maillard reaction with free asparagine as main precursor
(Mottram et al., 2002; Stadler et al., 2002; Zyzak et al.,
2003; Stadler et al., 2004). Furan also forms as an
intermediate in the Maillard Reaction (Ames,1992) and
from direct dehydration of sugars under acidic conditions
(caramelisation) during thermal treatments applied to
foods (Kroh, 1994). 3-MCPD is formed from glycerol
Journal of Agricultural Science and Food Technology
Vol. 5 (3), pp. 32-41, May, 2019
ISSN: 2465-7522
Review
http://pearlresearchjournals.org/journals/jasft/index.html

Fikiru and Tilahun 33
Figure 1. The structure of Acrylamide (Friedman,
2003).
or acylglycerols and chloride ions in heat-processed
foodstuffs that contain fat with low water activity (Calta et
al., 2004). Diet and nutrition play a key role in the
promotion and maintenance of good health, as they are
important modifiable risk factors for chronic diseases
(Mozaffarian et al., 2015). World Health Organization
recommends limiting the consumption of saturated and
trans-fats (hydrogenated fats), sugars and salt in the diet,
which are often found in snacks, processed foods and
drinks (Nishida et al., 2004). Evidence suggests that
regular and excessive consumption of energy-dense
foods high in fat, particularly saturated fat, and in refined
carbohydrates can lead to weight gain, obesity and pose
an increased risk for non-communicable diseases
(NCDs) (Mozaffarian et al., 2015). NCDs are the leading
causes of death globally, killing more people each year
than all other causes combined (Nishida et al., 2004). Of
56.4 million global deaths in 2015, 39.5 million, or 70%,
were due to non-communicable diseases.
The four main NCDs are cardiovascular diseases,
cancers, diabetes and chronic lung diseases (WHO,
1998). The burden of these diseases is rising
disproportionately among lower and middle-income
countries and populations. In addition, of the 57 million
deaths that occurred globally in 2008, 36 million almost
two-thirds were due to NCDs, comprising mainly
cardiovascular diseases, cancers, diabetes and chronic
lung diseases (Alwan et al., 2010). The association
between dietary fats and chronic diseases has been
extensively studied with evidence indicating that dietary
fats play an important role in the development of
coronary heart diseases, obesity, stroke, cancer and
diabetes. Improving population diets play an important
role in preventing chronic NCDs. According to estimates
by (WHO, 2009), without preventative measures, the
number of deaths by NCDs will increase by 17% on a
global scale over the next ten years. Therefore, it is
necessary to understand the fat absorption, mechanism
of formation and mitigation of heat generated foods
toxicants during food frying and the associated health
risks of fried food consumption on long-term. Thus, this
paper reviews the existing evidence on the generation of
heat-induced food toxicants, mitigation mechanisms and
the relation of fried food consumption with the major non-
communicable diseases. In this review article, all
relevant evidence from different sources such as
Scopus, ProQuest, SpringerLink, Taylor and Francis,
ACS, Wiley Online, and ScienceDirect were
systematically reviewed based on some important
questions and using key words related to the title and the
collected informations were compiled for interpretation.
FRYING GENERATED FOOD TOXICANTS
During frying, a variety of reactions cause a spectrum of
physical and chemical changes. In the presence of
oxygen, food moisture and high temperature, the oil
undergo different deleterious reactions particularly
hydrolysis caused by water, oxidation, and thermal
alteration caused by oxygen and heat. These are
tremendously complex reactions that cause the
formation of numerous polymerization products, of which
over 400 have been identified (Paul and Mittal, 1997).
Acrylamide
Acrylamide is a white odorless crystalline solid, soluble
in water, ethanol, ether, and chloroform. Formerly,
acrylamide was known only as a constituent of cigarette
smoke and products of plastics and water treatment
chemicals. In early 2002, acrylamide was detected in a
range of foods heated during production or preparation
(Tareke et al., 2002; Rosén and Hellenäs, 2002). It is one
of the chemicals known as Maillard reaction
products, which formed when foods are heated at high
temperatures (Mottram et al., 2002; Stadler et al., 2002;
Becalski et al., 2003). Particularly high concentrations
were found in products of plant origin heated to high
temperatures, such as potato chips, French fries, pan-
fried potato products, or crisp bread, whereas the
contents in foods rich in protein were low (Tareke et al.,

2002). The primary pathway for the formation of
acrylamide in foods is via Strecker degradation of
asparagine with dicarbonyls by the reaction between an
amino acid called asparagines and reducing sugars such
as glucose and fructose (Mottram et al., 2002). Strecker
degradation is a chemical reaction which converts α-
amino acid into an aldehyde containing the side chain,
by way of an imine intermediate. This reaction generally
occurs at higher temperatures (Biedermann et al., 2002)
and in low moisture conditions and it is part of the
Maillard reaction that provides color, flavor, and aroma in
cooked foods. Alternatively, it can be produced from
precursors such as 3-aminopropionamide, acrylic acid,
and acrolein, and reactions between other amino acids
such as alanine, arginine, cysteine and other sugars like
galactose, lactose, and sucrose. In addition, it has been
reported that acrylamide could be directly generated
from N-glycosides formed from sugars and amino acids
during an early stage of the Maillard reaction (Stadler et
al., 2002) (Stadler et al., 2002). The water content is one
of the most important factors in the formation of
acrylamide, besides the reaction temperature and time
(Slayne and Lineback, 2005; Gertz and Klostermann,
2002).
The minimum of acrylamide formation was observed at
the water content between 25 and 40%; outside of this
range, the acrylamide concentration was higher.
Fructose was more effective for the acrylamide formation
in comparison with glucose (Yaylayan et al., 2003). In
general, carbohydrate degradation products are
necessary to form acrylamide, activating asparagine by
forming a Schiff base, which subsequently
decarboxylates upon heating. The decarboxylated Schiff
base can form acrylamide directly or degrade into 3-
aminopropionamide (3-APA), which in turn yields
acrylamide by the elimination of ammonia.
In the past years many methods have been developed to
quantitatively analyse the acrylamide content in food.
The majority are classical methods based on LC-MS/MS
or GC technique. However, because of the complexity of
food matrices, these methods do not suffice for the
analysis of acrylamide in heat-treated foods at trace
levels. Particularly, they lack selectivity and the
additional degree of analyte certainty required to confirm
the presence of a small molecule, such as acrylamide in
a complex food matrix.
Gas chromatography (GC) - mass spectrometry (MS)
and HPLC analysis are both acknowledged as the major
useful and authoritative methods for the acrylamide
determination. A simple and rapid method was
developed and validated for the determination of
acrylamide in potato and cereal-based foods by using a
single quadrupole LC-MS interfaced
with positive atmospheric pressure chemical ionization
(APCI+) (Kim et al., 2010). In addition, a reverse phase
LC-MS based on stable isotope dilution assay was used
for acrylamide analysis.
Furthermore, a new Volta metric biosensor was
developed to detect acrylamide in food sample.
J.Agric. Sci. Food Technol. 34
Mitigation Mechanisms of Acylamide Formation
In 2011, the food and drink Europe (FDE) identified the
main measures that may lead to a reduction of
acrylamide in French fries, breakfast cereals, biscuits
and bakery wares. The mitigation strategies include
agronomical techniques (control of reducing sugars in
potato, control of tuber storage temperature, use of
sprout suppressants to prevent sweetening during
storage, maintaining sulphur levels for cereal cultivation),
recipes formulations techniques (selection of potato
varieties and cereal varieties low in acrylamide
precursors, addition of proteins, glycine, cysteine and
other amino acids, organic acids and acidulants, calcium
ions, cyclodextrin, natural antioxidants or antioxidant
extracts etc., replacement of reducing sugars with
sucrose and of ammonium bicarbonate with sodium
bicarbonate) and during preparation and processing (use
of asparaginase enzyme, optimization of time-
temperature of frying or baking, changing in the type of
oven, prolonged fermentation) (Palermo et al., 2016;
Torres and Parreño, 2009). Moreover, Anese et al.
(2009) proposed the removal of acrylamide after
formation by means of vacuum but its impact on
manufacturing practices and food quality has not yet
been clearly established.
FURAN AND 2-METHYLFURAN
Furan (C4H4O) is volatile with the boiling point of 310C
and colorless liquid and is classified as a possible human
carcinogen by the International Agency for Research on
Cancer. Similar to acrylamide, furan in food could
potentially become a serious problem due to its
widespread presence in many types of products. It has
been reported to occur in a number of foods that undergo
heat treatment, such as canned and jarred foods (US
FDA, 2004). There are multiple pathways underlying
furan formation, such as thermal degradation or
rearrangement of carbohydrates alone or in the presence
of amino acids, thermal degradation of certain amino
acids, oxidation of ascorbic acid under high
temperatures, and oxidation of polyunsaturated fatty
acids and carotenoids. According to Maga and Katz
(1979), the primary source of furans in food is thermal
degradation of carbohydrates such as glucose, lactose,
and fructose. Becalski and Seaman (2005) also reported
the formation of furan from ascorbic acid and its
derivatives. In addition, they demonstrated that furan
can be formed from the oxidation of
polyunsaturated fatty acids at elevated temperatures and
that the addition of commercially available antioxidants
(such as tocopherol acetate) reduced the formation of
furan by up to 70%. More recently, Perez Locas and
Yaylayan (2004) studied the formation of furan from
model systems using pyrolysis-GC-MS analysis and
13C3-labelled sugars, amino acids and ascorbic acid.
They observed that certain amino acids, such as serine

and cysteine, can degrade to form furan, but that other
amino acids, such as aspartic acid, threonine and -
alanine, require the presence of sugar to form furan. 2-
Methylfuran and 3-methylfuran, have been found
concurrently with furan, and apparently, are also formed
during thermal processing and are likely to undergo a
similar metabolic fate to furan. 3-methylfuran is the
analogue of 2-methylfuran. Like furan and 2-methylfuran,
3-methylfuran is also aromatic in nature. It can be
supposed that its chemical properties are similar, but
information is scarce.
Mitigation Strategies to Reduce Furan Concentration
in Foods
No available mitigation strategies specifically addressed
to reduce furan content in foods because of the nature of
its precursors and formation pathways. HMF forms
through Maillard reaction and caramelisation, which
mostly contribute to desired colour, taste and aroma of
heated foodstuffs. Unfortunately, HMF formation follows
the same pathways leading to brown and flavour
compounds. For instance, a high correlation between
HMF content and browning development has been
repeatedly reported (Capuano et al., 2009; Capuano and
Fogliano, 2011) so that modelling the time-temperature
profile by reducing heating times and/or temperatures is
likely to reduce HMF concentrations in the same time
resulting in a reduction of browning development which
can potentially compromise the quality and acceptability
of final products. The same happens when mitigation
strategies based on changes in recipes are applied, for
example by replacing reducing sugars with non-reducing
sugars or polyalcohols. Currently, no official standard
methods are available for the analysis of furan and
methylfurans in foods. Three analytical approaches are
used most often for the determination of furan and
methylfuran in foods. All of them are based on a mass-
spectrometric (MS) detection and quantification using
stable isotope dilution assays with d4-furan and d3-2-
methylfuran. Separation is accomplished by capillary gas
chromatography.
HETEROCYCLIC AMINES AND POLYCYCLIC
AROMATIC HYDROCARBONS
Heterocyclic amines (HCAs) and polycyclic aromatic
hydrocarbons (PAHs) are chemicals formed when meat,
including beef, pork, fish, muscle or poultry is cooked or
fried using high-temperature methods, such as pan frying
or grilling directly over an open flame (Cross and Sinha,
2004). Polycyclic aromatic hydrocarbons (PAHs) are
organic compounds containing only carbon and
hydrogen that are composed of multiple aromatic rings.
Heterocyclic amines (HCAs) are chemical compounds
containing at least one heterocyclic ring, which has
atoms of at least two different elements, as well as at
least one amine group. HCAs are formed when amino
Fikiru and Tilahun 35
acids, sugars, and creatine (a substance found in
muscle) react at high temperatures and long cooking
times. Amino-imidazo-azaarenes (AIA) and amino
carbolines are the two common toxic compounds formed
during frying of meat. PAHs are produced through
incomplete combustion of organic matter. They are
formed when fat and juices from meat grilled directly over
an open fire drip onto the fire, causing flames. PAHs can
also be formed during other food preparation processes,
such as smoking of meats (Cross and Sinha, 2004).
Cooking methods that expose meat to smoke or charring
contribute to PAH formation (Jägerstad and Skog, 2005).
The major contributors to PAH intake in the average diet
are oils and fats, cereals, and vegetables (Moret and
Conte, 2000). Purcaro et al., (2006) has set a maximum
level of 2 ppb for benzo[a]pyrene (BaP) in oils and fats
intended for direct consumption or for use as an
ingredient in foods. The amount and variety of AIAs and
carbolines formed in fried meat products primarily
depend on processing conditions, of which temperature,
time, and method of frying are the most important (Chiu
et al., 2016; Chen et al., 2016). A large variety of AIAs
and carbolines often occur in cooked meat products
under drastic conditions such as frying 200 or 3000C for
10 min. Liquid chromatography-mass spectrometry (LC-
MS) is a technique used to quantify the number of HCAs
and PAHs in foods.
Ways to Reduce HCA And PAH Formation
Even though no specific guidelines for HCA/PAH
consumption exist, concerned individuals can reduce
their exposure by using several cooking or frying
methods like avoiding direct exposure of meat to an open
flame or a hot metal surface and avoiding prolonged
cooking times (especially at high temperatures) can help
reduce HCA and PAH formation. Using a microwave
oven to cook meat prior to exposure to high temperatures
can also substantially reduce HCA formation by reducing
the time that meat must be in contact with high heat to
finish cooking. Furthermore, continuously turning the
meat over on a high heat source can substantially reduce
HCA formation compared with just leaving the meat on
the heat source without flipping it often and removing
charred portions of meat and refraining from using gravy
made from meat drippings can also reduce HCA and
PAH exposure (Knize and Felton, 2005).
HEALTH RISKS ASSOCIATED WITH CONSUMPTION
OF FRIED FOODS
Many of the Maillard reaction produce compounds that
contribute to the flavors and aromas of food during food
frying or cooking. However, compounds having adverse
physiological effects or potential health risks are also
formed. Nowadays, the consumption of deep-fried food
has gained popularity which may cause increased risk of
non-communicable diseases. To reduce the expenses,

the oil tends to be used repeatedly for frying. When
heated repeatedly, changes in physical appearance of
the oil will occur such as increased viscosity and
darkening in color, which may alter the fatty acid
composition of the oil. With each reuse, oil becomes
more degraded, and more gets absorbed into food,
which can contribute to weight gain, higher cholesterol,
and higher blood pressure all risk factors for type 2
diabetes and heart disease (Cahill et al., 2014).
Human Dietary Exposure Rate to Toxicants in Fried-
Foods
Fried foods particularly, potato chips and French fries are
among the food items that contain the highest levels of
acrylamide, furan, HCAs and PAHs, although
concentrations may vary significantly from one item to
the other. An individual’s exposure to these toxicants
reflects the combined intake from diet, smoking, second-
hand smoke, drinking water, occupational sources,
toiletries and household items. Acrylamide absorption
through dermal exposure is much lower because the skin
provides a barrier that reduces acrylamide uptake
(Fennell et al., 2005).
However, oral exposure is critical in determining the
amount of acrylamide and its metabolites that circulate in
the body. Becalski et al. (2003) documented
concentrations of acrylamide in commercial potato chips
and French fries ranging from 530 to 3700 ng/g and 200
to 1900 ng/g, respectively. Dietary acrylamide exposure
estimates are mainly available for the general adult
population to have been documented to range from 0.3
to 0.8 μg/kg of body weight per day (WHO, 2002). Mean
intake of acrylamide in adults averages 0.5 μg/kg body
weight per day across populations in several countries.
In Sweden, coffee intake is the major contributor to
intake, whereas, in U.S. populations, potato crisps and
chips are responsible for the majority of intake (Mucci,
2006).
Dietary acrylamide intake in children, youngsters and
adolescents has been suggested to be significantly
higher than that of adults (Dybing et al., 2005).
Similarly, WHO (2002) reported that acrylamide intake in
children is generally two to threefold higher than that of
adults when expressed on a body weight basis. In
addition to having a higher average food intake per kg
body weight than adults, children and adolescents also
consume acrylamide rich-food, such as potato chips and
French fries, on a more regular basis than the rest of the
population (Dybing et al., 2005). In 2004, the European
Food Safety Authority (EFSA) reported the dietary furan
exposures of 33.5 μg day-1 and 1.1 μg day-1 for adults (15
to 75 years old) and children (4 to 6 years old),
respectively. Additionally, children were the group
which contributed the most to the intake of furan through
breakfast cereals. The highest degree of furan inhalation
resulted from the frying of chipped potatoes in an open
chip pan (between 5 and 35 ng L-1) (Fromberg et al.,
2009).
J.Agric. Sci. Food Technol. 36
Overweight and Obesity as Resulting from
Consuming Fried Foods
Obesity is a chronic disease characterized by the
accumulation of excess adipose tissue. Worldwide, 2.8
million people die each year as a result of being
overweight and obesity (Resnikoff et al., 2004) and an
estimated 35.8 million (2.3%) of global disability-adjusted
life year (DALYs) are caused by overweight or obesity
(WHO, 2009). In addition, it is estimated that one in 13
annual deaths in the EU is likely to be related to excess
weight (Banegas et al., 2003).The risks of coronary heart
disease, ischemic stroke and type 2 diabetes mellitus
increase steadily with increasing body mass index (BMI),
a measure of weight relative to height (WHO, 2002).
Raised BMI also increases the risk of cancer of the
breast, colon/rectum, endometrium, kidney, esophagus
(adenocarcinoma) and pancreas (World Cancer
Research Fund/American Institute for Cancer Research.,
2007; WHO, 2002). The consumption of high levels of
high-energy foods, such as processed foods that are
high in fats and sugars, promotes obesity compared to
low-energy foods such as fruits and vegetables (WHO,
2003). Fried foods are crunchy, aromatic, highly
palatable, and rich in fats. As a consequence, eating fried
food in ad libitum conditions may result in higher absolute
intake of foods with high energy density and low satiety
index. The relatively low satiety index of fats (Blundell,
2002) may be related to their low ability to stimulate
insulin and leptin production (Havel et al., 1999). High
energy density diet, increased portion size, low physical
activity and adoption of a sedentary lifestyle as well as
eating disorders are considered as important risk factors
for the development of obesity (James, 2008).
Several studies reported a positive association between
fried food intake and being overweight (Srivastava et al.,
2009), waist circumference (Krachler et al., 2006) or
weight gain among pregnant women (Stuebe et al.,
2009). The European Prospective study showed a
positive association of fried food consumption with
central and general obesity (adjusted odds ratios for
general obesity in the highest versus the lowest quintile
of fried food intake: 1.26 (95% CI: 1.09 to 1.45, p for trend
<0.001) in men and 1.25 (95% CI: 1.11 to 1.41, p for
trend <0.001) in women) (Guallar-Castillón et al., 2007).
The prevalence of general obesity was 27.6% (out of
12,905) in men and 27.7% (out of 20,637) in women; the
prevalence of central obesity was 34.5 and 42.6%,
respectively. This study reported that the prevalence of
general and central obesity increased with increasing
intake of energy from fried food. General obesity is
defined as BMI > or = 30 kg/m2 and central obesity as
waist circumstance, WC > or = 88 cm. According to this
study, fried meat, fish, potatoes, and eggs were the 4
groups of fried food most frequently consumed by study
participants, with >75% of men and women consuming
each of those groups of food. The energy intake in men
and women, respectively, ranged from to 2.0 and 1.5%
for fried eggs to 5.0 and 3.6% for fried meat.

Consumption of fried meat was positively associated with
general obesity in men, and the intake of fried fish was
associated with general obesity in women. The same
pattern was observed for central obesity. In addition,
consumption of fried egg was associated with central
obesity in men. In gene-diet interaction analysis in three
US cohort studies revealed that the association between
total fried food consumption and BMI was stronger in
participants with a higher genetic risk score than in those
with a lower genetic risk score in both the Nurses’ Health
Study and Health Professionals Follow-up Study
(P=0.005 and 0.02, respectively, for interaction) (Qi et al.,
2014). Pereira et al., (2004) revealed that greater
consumption of fried food away from home was
associated with a higher BMI and weight gain in US
children and adolescents. In this study, 30.3% (out of
6212 children and adolescents 4 to 19 years old) of study
participants ate fast food on any given day, these foods
seem to contribute an additional 57 kcal (187 kcal ×
30.3%) to the daily diet of the average child in the United
States.
Coronary Heart Disease as Related with
Consumption of Fried Foods
Laboratory investigations show that fried foods may act
through many mechanisms, such that the resulting effect
on coronary heart disease is difficult to anticipate. Frying
can specifically increase the amount of trans-fatty acids
in foods (Litin and Sacks, 1993). Fried foods have been
associated with various cardiovascular risk factors in
cross-sectional studies. However, only a few studies
have evaluated the effect of fried foods on the risk of
cardiovascular disease. In a case-control study from
India, including 165 patients with coronary heart disease
and 199 matched controls, patients with coronary heart
disease when compared to controls reported a greater
intake of both shallow fried food (24.0 ± 60.4 versus 2.7
± 17.2 g/day; p < 0.01) and deep-fried food (15.2 ± 25.0
versus 1.0 ± 5.1 g/day; p < 0.01) (Panwar et al., 2011).
Similarly, Djoussé et al. (2015) showed a positive and
graded association between fried food consumption and
the incidence of heart failure in a prospective cohort
study; compared to subjects who reported fried food
consumption of <1 per week, the adjusted hazards ratios
(95% CI) for heart failure were 1.24 (1.04 to 1.48), 1.28
(1.00 to 1.63) and 2.03 (1.37 to 3.02) for fried food intake
of 1 to 3/week, 4 to 6/week and 7+/week, respectively (p
for linear trend: 0.0002). In addition, Belin et al. (2011)
found that fried fish consumption (>1 serving per week at
baseline) was associated with a 48% higher risk of heart
failure (HR, 1.48 (95% CI: 1.19 to 1.84). On the contrary,
the analysis of the Spanish cohort of the European
Prospective Investigation into Cancer and Nutrition found
no association between consumption of fried food and
the risk of coronary heart disease or cause mortality
(Guallar-Castillón et al., 2012). While the existing
evidence proposes a higher risk of heart failure in people
with frequent fried food consumption, underlying biologic
Fikiru and Tilahun 37
mechanisms remain to be elucidated.
Diabetes as Related with Consumption of Fried
Foods
Diabetes is the leading cause of renal failure in many
populations in both developed and developing countries.
Several studies have shown a positive association
between a high glycemic diet and the risk of type 2
diabetes (T2D) (Schulze et al., 2004). Consumption of
potatoes, red meat and other processed meats have
been positively associated with the risk of T2D (Ylönen
et al., 2007; Halton et al., 2006; Fung et al., 2004; Pan et
al., 2011; Khosravi-Boroujeni et al., 2012). According to
Halton et al. (2006), the intakes of potatoes and French
fries were positively associated with the incidence of type
2 diabetes in a large prospective cohort of women. The
increased risk was more pronounced when potatoes
replaced whole-grain products in the diet. This
association was independent of known risk factors for
type 2 diabetes, including family history, age, BMI,
physical activity, smoking status, postmenopausal
hormone use, and dietary factors. As expected, the
positive association between potato consumption and
the risk of type 2 diabetes was seen primarily in obese
and sedentary women.
In addition, fried foods from restaurants and fast food
consumption were positively associated with T2D
(Krishnan et al., 2010; Odegaard et al., 2012; Pereira et
al., 2005). Similarly, data from the Nurses' Health
Study/Health Professionals Follow-Up Study revealed a
strong association between the frequency of fried food
consumption and the risk of type 2 diabetes with adjusted
RRs (95% CIs) for individuals who consumed fried foods
<1, 1 to 3, 4 to 6 or ≥7 times/week of 1.00 (reference),
1.15 (0.97 to 1.35), 1.39 (1.30 to 1.49) and 1.55 (1.32 to
1.83), respectively (Cahill et al., 2014). The frequency of
fried food consumption was also associated with the
incidence of gestational diabetes (adjusted RR = 2.18
(95% CI: 1.53 to 3.09) comparing fried food intake of 7+
to that of <1 time per week) (Bao et al., 2014). However,
a study from Italy demonstrated that in obese (not in
lean), insulin-resistant women, consumption of foods
fried in extra-virgin olive oil significantly reduced both
insulin and C-peptide responses after a meal (Farnetti et
al., 2011). Thus, it’s possible to conclude as there is
strong evidence for a positive association between fried
food consumption and the risk of T2D.
Carcinogenic Effects Frying-Induced Food Toxicants
It has been postulated that acrylamide is carcinogenic
through a genotoxic pathway (Dybing et al., 2005), after
conversion to glycidamide, a DNA-reactive epoxide.
According to IARC, (1994) acrylamide concentrations
exceeded 1000 μg/k classified as Group 2A probably
carcinogenic to humans. Studies have shown that
exposure to HCAs and PAHs can cause cancer in animal
models (Sugimura et al., 2004). In many experiments,

rodents fed a diet supplemented with HCAs developed
tumors of the breast, colon, liver, skin, lung, prostate, and
other organs (Kato et al., 1989; Shirai et al., 2002). In
laboratory experiments, HCAs and PAHs have been
found to be mutagenic that is, they cause changes in
DNA that may increase the risk of cancer. HCAs and
PAHs become capable of damaging DNA only after they
are metabolized by specific enzymes in the body, a
process called bioactivation. Studies have found that the
activity of these enzymes, which can differ among
people, may be relevant to cancer risks associated with
exposure to these compounds (Moonen et al., 2005).
Population studies have not well established a definitive
link between HCA and PAH exposure from fried or
cooked foods and cancer in humans.
One difficulty with conducting such studies is that it can
be difficult to determine the exact level of HCA and/or
PAH exposure a person gets from meats. However,
researchers found that high consumption of well-done,
fried, or barbecued meats was associated with increased
risks of colorectal (Cross et al., 2010), pancreatic
(Anderson et al., 2002; Stolzenberg-Solomon et al.,
2007), and prostate cancer (Cross et al., 2005; Sinha et
al., 2009). Because many of PAHs are carcinogenic in
experimental animals, they are widely believed to make
a significant contribution to the burden of cancer in
humans. Several epidemiological studies conducted in
Taiwan and China revealed that Asian women ranked
highest in the world for lung cancer, probably because of
the exposure to fumes from cooking oil (Wu Williams et
al., 1990). Ko et al. (1997) reported that the risk of lung
cancer was higher from stir-frying than from deep frying.
Some authors suggested that the increased cancer risk
observed among people exposed to oil fumes is
correlated with the presence of PAHs in the fumes of
heated oils (Chen and Chen, 2001; Chiang et al., 1997).
Mutagenic Effects Frying-Induced Food Toxicants
High-temperature frying of protein-rich foods generates
volatile and non-volatile compounds with mutagenic and
carcinogenic properties (Straif et al., 2006). A variety of
volatile carcinogens and toxicants have been detected in
the fumes from high-temperature frying, including
acetaldehyde, acrolein, benzene, 1,3-butadiene,
ethylene oxide, heterocyclic amines and polycyclic
aromatic hydrocarbons and have been suggested to be
responsible for the mutagenic properties of the fumes
from cooking oils (Shields et al., 1995). The highest
levels of mutagenic activity from fried meat are detected
in the pan residue and meat crust, compared with lower
levels detected in the cooking fumes (Felton et al.,
1980). These mutagenic activity levels in the cooked
meat and surrounding air are driven primarily by the
cooking temperature rather than cooking duration (Berg
et al., 1990).
Genotoxicity Effects of Frying-Induced Food
Toxicants
J.Agric. Sci. Food Technol. 38
Genotoxicity of furan has been reported in many animal
studies. Furan appears to be mutagenic to mouse
lymphoma cells, independent of S9 activation. S9 is a
crude liver enzyme extract that can, under certain
conditions, convert materials without any genotoxic
activity to active genotoxic entities.
High doses of furan caused structural chromosome
abnormalities but did not affect chromatid exchange in
mouse bone marrow cells.
According to a study Mariotti et al. (2013), with a single
oral dose of 200 or 100 mg/kg body weight, furan did not
cause uncontrolled DNA synthesis in mouse or rat
hepatocytes in vivo. Mutagens such as cis-2-butene-1,4-
dial are similar to unsaturated compounds that react with
DNA. This was directly mutagenic at non-toxic
concentrations in a Salmonella enterica Typhimurium
strain (TA104) that was sensitive to aldehydes, but not to
some other strains (Perez Locas and Yaylayan, 2004). It
is possible that furan or cis2-butene-1,4-dial reacts with
DNA in target cells and can play a major role in furan-
induced tumors. After bioactivation into its metabolites,
furan induces loss of ATP, which causes an inevitable
uncoupling of hepatic mitochondrial oxidative
phosphorylation. This would activate cytotoxic enzymes,
including endonucleases that produce DNA double-
strand cleavage, leading to cell death (Perez Locas and
Yaylayan, 2004).
Hypertension Effects of Frying-Induced Food
Toxicants
So far, there is limited and inconsistent epidemiological
evidence directly relating fried food consumption and
hypertension. A cross-sectional study from Spain
reported that consumption of fried foods was associated
with a higher prevalence of hypertension (Soriguer et al.,
2003). The SUN (Seguimiento Universidad de Navarra)
Mediterranean cohort study reported that frequent
consumption of fried foods at baseline was associated
with a higher risk of hypertension (adjusted hazards
ratios = 1.18 (95% CI: 1.03 to 1.36) and 1.21 (95% CI:
1.04 to 1.41) for those consuming fried foods 2 to 4 and
>4 times/week, respectively, compared to those
consuming fried foods <2 times/week (p for trend =
0.009) (Sayon-Orea et al., 2014). Similarly, Kang and
Kim (2016) found that fried food consumption was
strongly associated with hypertension among Korean
women. However, a significant association was found
between the frequency of fried food consumption and
hypertension in men. The oxidation process during food
frying increases the amount of trans-fatty acids in food
and is positively associated with the risk of hypertension
(Wang et al., 2010). In addition, this study reported a
positive association between dietary intake of trans-fatty
acids and the risk of hypertension (adjusted RR in the
highest quintile: 1.08; 95% CI: 1.01 to 1.15). However,
more evidence is required to further clarify the
mechanism and association between fried food
consumption and hypertension.

Conclusion and recommendation
Frying is a common and popular process utilized in the
food industry and street due to its significant sales and a
vast quantity of products. From the consumers' point of
view fried food palatability is related to unique sensory
characteristics such as flavor, texture and appearance.
At the same time, heat generated food toxicants such as
acrylamide, hydroxymethylfurfural, heterocyclic amine,
nitrosamines and polyaromatic hydrocarbons can be
formed. These toxicants and the oil used for frying cause
a disease like cancer, diabetes, heart, obesity and DNA
complications. To minimize those health risks associated
with fried consumption, use of varieties that are low in
sugar and an amino acid asparagines, controlling frying
temperature (fry foods in the range of 145 to 170ºC),
frying in closed system not in open air due to oxidation,
frying French fries to a golden yellow rather than a golden
brown color, toasting bread to the lightest color, soaking
raw potato slices in water for 15 to 30 min before frying
or roasting and not storing raw potatoes in the
refrigerator are some of the techniques helps to reduce
those toxicants during frying process.
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