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Trans fatty acids and lipid profile: A serious risk factor to cardiovascular disease, cancer and diabetes


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Trans Fatty acids (TFAs) have long been used in food manufacturing due in part to their melting point at room temperature between saturated and unsaturated fats. However, increasing epidemiologic and biochemical evidence suggests that excessive trans fats in the diet are a significant risk factor for cardiovascular events as well as a risk factor for cancer and diabetes. A 2% absolute increase in energy intake from trans-fat has been associated with a 23% increase in cardiovascular risk. They increase the levels of low-density lipoprotein which is bad for health. Moreover, several epidemiological studies have been demonstrated that a high intake of TFAs increases the incidence of cancer and diabetes. On the other hand, total elimination of TFAs is not possible in a balanced diet due to their natural presence in dairy and meat products. Many products with almost 0.5 g trans-fat, if consumed over the course of a day, may approximate or exceed the 2 g maximum as recommended by the American Heart Association. The objective of the review to demonstrate the causal association between trans fatty acid intake and increase the risk of coronary heart disease through their influence on lipoprotein, association with atherosclerosis, stroke, diabetes and cancer.
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Trans fatty acids and lipid prole: A serious risk factor to
cardiovascular disease, cancer and diabetes
Md. Ashraful Islam
, Mohammad Nurul Amin
, Shafayet Ahmed Siddiqui
Md. Parvez Hossain
, Farhana Sultana
, Md. Ruhul Kabir
Department of Food Technology and Nutrition Science, Noakhali Science and Technology University, Noakhali, 3814, Bangladesh
Department of Pharmacy, Atish Dipankar University of Science and Technology, Dhaka, 1230, Bangladesh
article info
Article history:
Received 26 February 2019
Accepted 14 March 2019
Trans fatty acid
Trans Fatty acids (TFAs) have long been used in food manufacturing due in part to their melting point at
room temperature between saturated and unsaturated fats. However, increasing epidemiologic and
biochemical evidence suggests that excessive trans fats in the diet are a signicant risk factor for car-
diovascular events as well as a risk factor for cancer and diabetes. A 2% absolute increase in energy intake
from trans-fat has been associated with a 23% increase in cardiovascular risk. They increase the levels of
low-density lipoprotein which is bad for health. Moreover, several epidemiological studies have been
demonstrated that a high intake of TFAs increases the incidence of cancer and diabetes. On the other
hand, total elimination of TFAs is not possible in a balanced diet due to their natural presence in dairy and
meat products. Many products with almost 0.5 g trans-fat, if consumed over the course of a day, may
approximate or exceed the 2 g maximum as recommended by the American Heart Association. The
objective of the review to demonstrate the causal association between trans fatty acid intake and in-
crease the risk of coronary heart disease through their inuence on lipoprotein, association with
atherosclerosis, stroke, diabetes and cancer.
©2019 Published by Elsevier Ltd on behalf of Diabetes India.
1. Introduction
Trans-fatty acids (TFAs) are unsaturated fatty acids which
contain leastwise one double bond in the trans conguration. TFAs
are manufactured through industrial processes referred as indus-
trial trans fatty acids (iTFA) by partial hydrogenation and deodor-
ization of vegetable oils, and heating oil at very high temperature
[1]. Elaidic acid is the prime TFA often found in partially hydroge-
nated vegetable oil [2]. Low levels of naturally occurring TFAs are
obtained from the milk and meat of ruminant animals those are
referred as ruminant trans fatty acid (rTFA) e.g., cattle and sheep
[3]. The most predominant trans-isomer in ruminant TFA is vac-
cenic acid. Another TFA namely conjugated linoleic acid can be
formed from vaccenic acid [4]. In general, there is wide evidence
that all isomeric cis and trans fatty acids in ruminant fats and
partially hydrogenated vegetables oils are efciently absorbed and
incorporated into chylomicrons with the possible exceptions of
fatty acids with double bonds in the 2 to 7 positions. Once they
reach the liver, chylomicron remnant triacylglycerol is taken up,
repackaged and exported into the circulation in the form of low
density lipoproteins [5]. Following incorporation into lipoprotein
fractions, triacylglycerol is transported to the peripheral tissues,
where they are hydrolyzed by enzyme lipoprotein lipase and taken
up into cells. Though trans fats are edible, consumption of trans fats
has been showed to increase the risk of Coronary heart disease
(CHD) in part by increasing the level of low-density lipoprotein
(LDL) referred as bad cholesteroland decreases the level of high-
density lipoprotein (HDL) referred as good cholesteroland raising
Triglycerides (TG) in the bloodstream thus promoting systemic
inammation [6] (see Table 1).
Trans fatty acids are needed generally for commercial motives in
the food industries to yield semi fat foods and increase the shelf life
of products like margarine, crackers, deep-fried fast foods, pan-
cakes, omelets, etc. and can also be found in restaurants [7]. The
contents of TFAs differ from one food item to another, it is tough to
account their consumption in different countries. In USA it is
calculated to be 2e3 energy percent, whereas some countries in
Middle East and South Asia, it can be as aerial as 7 energy percent
*Corresponding author.
E-mail addresses: (M.N. Amin), research.noory@ (Md.R. Kabir).
Contents lists available at ScienceDirect
Diabetes &Metabolic Syndrome: Clinical Research &Reviews
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1871-4021/©2019 Published by Elsevier Ltd on behalf of Diabetes India.
Diabetes &Metabolic Syndrome: Clinical Research &Reviews 13 (2019) 1643e1647
[8]. In South Asian region, Vanaspati ghee is the principal source of
TFA. For instance, in India, Vanaspati ghee used to contain as high as
40e50% TFA [9]. In Iran, 33% fatty acids in partially hydrogenated oil
were TFA [10]. Around the world, different levels of TFA intake have
been accomplished due to dietary habit and varying quantities of
iTFA in processed foods [1].
High intake of dietary trans fatty acids (TFA) have a strong as-
sociation in increasing the risk of coronary heart disease [11 ].
Coronary heart disease (CHD) is commenced as a procurement of
atheromatous plaque in the arteries which inict oxygen and blood
to the working heart. Development of plaque in the arteries is a
consequence of abundant risk factors including infection, diabetes,
smoking, physical activity, increased BMI, and high triglyceride
levels [12]. Various epidemiological studies have demonstrated a
potent denitive adherence between the consumption of TFA and
risk of CHD [13]. It has been estimated that a 2% raise in energy
consumption from TFA is linked with a 23% increase risk of CHD [7].
Due to the adverse health effects, the WHO recommends less than
1% TFA intake of total energy percent [14]. In Europe, trans fat are
nearly bannedin Denmark (less than 2%), Australia, Austria,
Hungary, Iceland, Norway and Switzerland [15].
The objective of this paper is to review the causal association
between trans fatty acid intake and increase risk of coronary heart
disease through their inuence on lipoprotein, association with
atherosclerosis, stroke, diabetes and cancer. This review aims to
provide a critical and up-to-date overview of current information
on existing condition on trans-fat intake and risk of cardiovascular
disease, blood lipid prole, diabetes and cancer.
2. Potential mechanism of trans fats metabolism
Trans fats seem to affect lipid metabolism by diverse pathways.
In vitro, trans fatty acids alter the secretion, lipid composition, and
size of Apo lipoprotein B-100 (apoB-100) particles produced by
hepatic cells [16]. This alteration is assimilated in studies in humans
by reduced rates of LDL apoB-100 catabolism [17], losses in the size
of LDL cholesterol particles [18], increased rates of apoA-I catabo-
lism [17], and alter in serum lipid levels [19 ]. In humans, the
structure of trans fat increases plasma mobility of cholesteryl ester
transfer protein [20], the key enzyme for the transfer of cholesterol
esters from HDL to LDL and very low-density lipoprotein (VLDL)
cholesterol. Such increased mobility may set out reduces in the
levels of HDL and rises in the levels of LDL and VLDL cholesterol
noticed with consumption of trans fatty acids [19].
The cellular mechanisms uttering trans fats to inammatory
pathways and other non-lipid pathways are not well recognized.
Monocytes and macrophages, endothelial cells, and adipocytes may
each perform a role. Trans fatty acids accord monocyte and
macrophage reactions in humans, rising the production through
monocytes of tumor necrosis factor-
) and interleukin-6
(ILd6) [21] and probably also levels of monocyte chemo-
attractant protein (MCP) [22]. Trans fats also interfere in vascular
function. Trans fats have been demonstrated to raise circulating
biomarkers of endothelial dysfunction [23] and to weak nitric
oxideedependent arterial dilatation [24]. Trans fatty acids also
affect fatty acid metabolism of adipocytes, resulting in decreased
triglyceride elevation, decreased esterication of recently synthe-
sized cholesterol, and increased formulation of free fatty acids [25].
The effects of adiposity on the connection between consumption of
trans fat and circulating interleukin-6 and C-reactive protein levels
suspect that the inammatory effects of trans fats may be partly
negotiated by adipose tissue [22].
The contents of TFAs differ from one food item to another; it is
tough to account their health effects and mechanism of metabolism
and consumption in different countries. Trans fat content in various
foods, ordered in g per 100g.
3. Trans fat, inammation and atherosclerosis
There is competing evidence about the effect of trans fats on
systemic inammation: in an interventional study, trans fat raised
markers of inammation [27] but in other one did not [28]. There is
another conict in observational studies in two reviews of the
NursesHealth Study; two different groups of researchers have
found different markers of inammation [23].
One considerable reason of atherosclerosis is disorders of lipid
metabolism and positive interrelation between plasma cholesterol
and atherosclerosis is now amply certied. So, the potential for
dietary TFAs to promote this.
Concern was a feasible mechanism for harmful effects of TFAs on
the cardiovascular system [29]. Bassett and colleagues demon-
strated that supplementation of the diet of LDL receptor deleted
mice with an industrial trans-fat, elaidic acid, resulted in the
distinct and denite incitement of atherosclerosis. Moreover, they
also exhibited that coupling of elaidic acid to a cholesterol-
supplemented diet did not persuade an additive payoff [30].
Abruptly, in the study conducted in the same model of empirical
atherosclerosis an amazing anti-atherogenic act by the ruminant
TFA, the vaccenic acid was unrolled. A momentous reduction in the
area of the atherosclerotic plaques veiled in the aortas from LDL
receptor deleted mice was observed, when diets were supple-
mented with cholesterol and vaccenic acid in comparison to diets
supplemented with both cholesterol and elaidic acid, or just
cholesterol alone [31].
4. Trans fatty acids increasing risk of coronary heart disease
and stroke
Individuals with higher dietary TFA intake possess increased
low-density lipoprotein (LDL) levels and lowering high-density li-
poprotein (HDL) levels [17]. Replacing just 2% of energy with un-
hydrogenated unsaturated fat instead of TFA reduce the risk of
CHD by 53% [32]. Leth and colleagues found a 60% decrease in CVD
risk in Denmark after the Danish Government implemented the
legislation to reduce the iTFA intake (Depending on calorie basis,
risk of CHD increases about 1e3% with TFA intake) [33]. A more
crucial proof found from NursesHealth Study in which CHD risk
roughly doubled for each 2% increase in trans-fat calories consumed
Table 1
Contents of TFAs in different food types.
Food type TFA content Food type TFA content
Shortenings 10e33g Salty snacks 0e4g
Margarine/spreads 0.2e26g Cake frostings and sweets 0.1e7g
Butter 2e7g Animal fat 0e5g
Whole milk 0.07e0.1g Ground beef 1g
Breads/cake products 0.1e10g Vanaspati ghee (vegetable ghee) 3.5e28g
Source: [26], American Nutrition Association, The Heart Foundation.
Md.A. Islam et al. / Diabetes &Metabolic Syndrome: Clinical Research &Reviews 13 (2019) 1643e1647164 4
[32]. Epidemiological data have provided believing proof that the
inclusion of TFAs in our diet is related with an adoption of cardio-
vascular disease. Dietary TFAs have been associated with CHD and
an increased incidence of myocardial infarction [34]. According to
systemic review in 2009, there is convincing proof that intake of
trans fats increases the risk of CHD [35].
Regarding South Asia, it has been concluded that about 39% of
CHD cases in Iran can be reduced by replacing TFA with cis-unsat-
urated fats [10]. Indian Government has taken an attempt to pre-
vent TFA related health problems plans to reduce TFA content in
Vanaspati oil to 5% in 2013 [36]. In Pakistan there is no such
legislation in reducing TFAs intake. Therefore, an alarming rise of
CVD risk in Pakistan [37].
5. Trans fats adversely affect lipid prole &lipoproteins
There is a positive correlation between plasma LDL and
atherosclerosis and/or CHD [38]. Although epidemiological evi-
dence suggests that there is a positive association between TFA
intake and elevated plasma LDL [17] [as well as triglycerides [39], a
clear mechanism has not been established. In the human hepato-
blastoma (HepG2) cell line, TFAs have been associated with
increased LDL: high-density lipoprotein (HDL) ratios, increased Apo
lipoprotein B: Apo lipoprotein A (apoB: apoA) ratio and increased
cholesterol content in both LDL and HDL particles in comparison to
saturated fats [16]. All of these outcomes have been associated with
a higher risk of atherosclerosis and CHD. Similar outcomes reported
by Mitmesser et al. who suggested that TFAs altered the size and
composition of apoB-100 containing lipoproteins. These studies
provide a basic mechanism whereby TFAs deposit cholesterol in
arteries. However, itis important to recognize that these studies are
primarily correlative and more concrete evidence is necessary.
Furthermore, there is no distinction in these studies between rTFAs
and iTFAs. These two types of TFAs are structurally different and
therefore, their biological effects may also be very different [16].
Epidemiological evidence has generated conicting results with
respect to an association of TFAs with serum lipid levels. In an ev-
idence based analysis observing the effects of isocaloric replace-
ment of polyunsaturated fatty acids (PUFAs), saturated fatty acids
(SFAs) or monounsaturated fatty acids (MUFAs) with TFAs, a sig-
nicant increase in low-density lipoprotein cholesterol (LDL-C)
levels, total cholesterol: high-density lipoprotein cholesterol (HDL-
C) ratio and the ratio of Apo B: Apo A was observed as well as a
decrease in HDL-C levels [33]. Others have shown a decrease in
LDL-C particle size with consumption of TFAs as opposed to un-
saturated fatty acids [18]. It is important to recognize that these
studies investigated a particular isomer of TFAs associated with the
hydrogenation of vegetable oils (such as the trans isomer of oleic
acid); therefore, more investigation with a wider variety of TFAs
may be necessary to fully understand the effect of TFAs on
6. Can trans fatty acids effect on cancer?
There are very few epidemiological studies that have investi-
gated the association of intake of vaccenic acid (VA) [40] and
conjugated linolenic acid (CLA) [41] and risk of cancer. A prospec-
tive study on women (1989e2002) revealed that trans-fat intake
supposedly associated with increased risk of breast cancer [42].
Some of the epidemiological studies that have been reported a
direct association with VA concentrations in serum or erythrocytes
and risk of breast cancer [40,43] or prostate cancer [44]. In
Netherlands a Cohort Study, energy-adjusted intake of VA was
associated with an increased risk of breast cancer [45]. There have
been 4 case-control studies that have investigated CLA intake and
cancer. Of these, one study has reported an inverse association with
dietary intake of CLA and risk of colorectal cancer [41], and one
study found signicantly lower dietary intake and serum concen-
trations of CLA in individuals with breast cancer compared to those
without breast cancer among postmenopausal women [46]. In
women in the highest quartile of CLA intake, there was a 29%
reduction in the risk of colorectal cancer compared to those in the
lowest [41]. In the other 2 case-control studies, there was no sig-
nicant association of CLA [either as dietary intake [47] or con-
centration of CLA incorporated into adipose tissue [48] and the risk
of breast cancer]. However, in one of the studies, there was a
diminished risk of having an estrogen receptor (ER)-negative tu-
mor, in premenopausal women, when comparing the maximum
quartile of CLA intake and the minimum [47]. A prospective cohort
study has been demonstrated that intake of CLA is weakly related
with breast cancer incidence when comparing the maximum and
minimum quintiles of consumption [45].
7. Even trans fatty acid associates with diabetes
Three prospective studies have investigated the relationship
between the consumption of trans fatty acids and the occurrence of
diabetes. Consumption of trans fat was not signicantly associated
with the risk of diabetes in two of these studies - among male
health professionals [49] and among women in Iowa [50]. However,
the ingestion of trans fatty acids signicantly related to the risk of
diabetes among 84,941 female nurses who were observed for 16
years and in whom self-reported diabetes was afrmed and report
on dietary intake was periodically updated [51]. After adjustment
for other risk factors, trans fat consumption was positively linked
with the incidence of diabetes with a risk 39% points greater in the
upper quintile than in the lower quintile [13]. In the Iowa cohort, a
validation study supposed that the self-reported diagnosis of dia-
betes was incorrect in 36% of subjects, and diet was assessed onlyat
baseline and may have changed over time [50]. Molecular mecha-
nisms that might account for an effect of trans fatty acids on the
incidence of diabetes are not well established, but evidence of ef-
fects of trans fatty acids on metabolism in adipocytes [52].
8. Discussion
Trans fats are suspected to be nutritionally unnecessary.
Epidemiologic evidence has demonstrated that they are a signi-
cant risk factor for cardiovascular disease; several studies demon-
strated that a 2% increase in daily energy intake from TFAs is
associated with a 23% increase in cardiovascular disease risk [53].
Trans fats have also been exhibited to have an adverse impact on
serum lipids and lipoproteins, increasing cardiovascular disease
risk to a greater extent [19]. A number of mechanisms for the effects
of trans fats have been proposed, including increased activity of
cholesteryl-ester transfer protein and increased levels of inam-
matory marker [27], positive correlation with atherosclerosis [30],
increased risk of CHD [33], and positive association between TFAs
and elevated level of plasma LDL [17]. In case of diabetes there are
both inverse [49] and positive [51] association whereas epidemio-
logical studies demonstrated signicant association between TFAs
intake and risk of cancer [40,48]. In review of NursesHealth Study,
researchers have found different markers of inammation [23].
Specic epidemiological studies demonstrated that 2% increase
intake of TFAs causes two times more risk of CHD [32]. Excess
intake vaccenic acid and conjugated linoleic acid the risk of cancer
[41]. TFA intake is positively linked with the incidence of diabetes
with a risk 39% points greater the upper quintile than in the lower
quintile [13]. It is clear from several trans-fat related studies that
dietary trans fats should be minimized. However, the presence of
Md.A. Islam et al. / Diabetes &Metabolic Syndrome: Clinical Research &Reviews 13 (2019) 1643e1647 16 45
trans fats in dairy and meat products will make complete elimi-
nation from a balanced diet impossible.
Food manufacturers and the food industry want alternatives to
trans fats but barriers comprise supply of ingredients and unknown
health sequel of new processes. Trans fats gained popularity as a
means of replacing saturated fats in the diet. Nevertheless, we now
know that trans fats have greater adverse health implications than
the saturated fats they wanted to replace. Eradicating trans fats by
returning to a high-saturated-fat diet is inappropriate. Consumers
are not fully conscious of the well-established health complications
of trans fats. Actually, many are disconcerted as to what fats they
should or should not be eating. Many are likely consuming trans
fats in excess of the maximum intake recommended by the
American Heart Association [54]. The present FDA labeling re-
quirements are a better rst step in giving consumers with infor-
mation on trans fats. However, given the recommendation that
trans-fat intake be as low as possible, allowing all products with
<0.5 g trans fats to claim 0 g trans fats can be misleading to many
consumers. Eating four or ve daily servings of foods with close to
0.5 g trans-fat can mean an individual who believes he/she is
consuming a healthful, balanced diet is actually exceeding 1% total
energy from trans fats. Greater transparency is required to allow
consumers to restrict dietary trans fats more effectively. Average
consumers do not understand the Nutrition Facts label, or its
relation to actual portion size [55,56]. Consumer education is
extremely important. In the interim, educational programs targeted
at these consumers must be developed to help them determine
which foods likely contain trans fats based on the presence of hy-
drogenated or partially hydrogenated oils in the ingredient list, as
well as to more accurately estimate their portion size relative to
standardized values on the Nutrition Facts panel.
9. Recommendations
Public awareness about the adverse health effects of TFAs should
be increased. More study and survey should be implemented about
the health hazards of TFAs, especially in South Asian countries and
developing countries because of the high prevalence of CVD. Na-
tional and international agencies can perform vital role in this
perspective. Media can also be focusing the bad health effects of
TFAs to the root level. Several plan and policies can be implemented
to eliminate the available use of TFAs. The legislations of FDA and
World Health Organization on TFAs consumption should be fol-
lowed. Daily consumption of TFAs should be less than 1% of total
energy intake. Industrial manufacturers should take measures to
use alternatives of TFA in their produce food products. They should
label the contents of TFAs in the packet of their products.
In South Asian countries, there should be conducted epidemi-
ological studies on TFAs consumption and health hazards. Rules and
legislations should be implemented based on the ndings of the
study. In Bangladesh, people are less concern about the health
hazards of TFAs. So epidemiological studies should be implemented
and public awareness should be increased on adverse effect of high
intake of TFAs.
10. Conclusion
There is now overwhelming evidence based upon several
studies, TFAs have deleterious effects on our cardiovascular health,
cancer and diabetes when included in the diet in high amounts. The
synergistic effect of TFAs and other dietary components, drugs and
environmental factors also still needs to be investigated in order to
better understand TFAs and CHD and other health hazards. The
direct action of TFAs on cardio myocyte function is also unclear and
may represent yet another important mechanism for the
deleterious effects of TFAs. Due to the impressive preliminary
outcome documented in Denmark, many other countries across the
world are following their lead and creating legislation to limit the
amount of iTFAs available for public consumption. However,
restricting all TFA consumption may not be realistic or possible.
Finding novel ways to block the atherogenic action of TFAs may be a
more reasonable approach. Supplementation of the diet with ax
seed, for example, can prevent the atherogenic effects of dietary
iTFAs in animal models. Other dietary approaches remain to be
discovered. It is also important to recognize that many of our
concepts regarding TFAs do not consider other TFA isomers beyond
iTFAs. Because of the intriguing positive effects of vaccenic acid
consumption, the picture of the effects of TFAs as risk factors for
atherosclerosis may require further study to fully reveal the effects
of trans fats on cardiovascular disease. Ultimately, this may result in
some changes in the enacted public legislation.
Conicts of interest
None of the authors declare a conict of interest.
Sources of nancial support
There is no funding to be disclosed.
The authors Md. Ashraful Islama, and Mohammad Nurul Aminb
contributed equally to this work.
Appendix A. Supplementary data
Supplementary data to this article can be found online at
TFAs Trans fatty acids
iTFA industrial Trans fatty acids
rTFA ruminant Trans fatty acid
CHD Coronary heart disease
TG Triglycerides
LDL Low-density lipoprotein
HDL High-density lipoprotein
VLDL Very low-density lipoprotein
Tumor necrosis factor-
ILd6 Interleukin-6
MCP Monocyte chemoattractant protein
PUFAs Polyunsaturated fatty acids
SFAs Saturated fatty acids
MUFAs Monounsaturated fatty acids
LDL-C Low-density lipoprotein cholesterol
HDL-C High-density lipoprotein cholesterol
VA Vaccenic acid
CLA Conjugated linolenic acid
ER Estrogen receptor
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Md.A. Islam et al. / Diabetes &Metabolic Syndrome: Clinical Research &Reviews 13 (2019) 1643e1647 16 47
... Polyunsaturated fats like n-3 and n-6 fatty acids show a positive effect on cardiovascular disease [9,10]. Whereas it has been seen that a 2% increase in energy intake from trans-fat consumption increases the risk of heart disease by 23% [11]. ...
... However, the amount of trans fats consumed from natural sources such as dairy is minor and it is not practically possible to extract transfat from meat and dairy [11]. While partially hydrogenated vegetable oils contain upto 50% of trans fat, dairy contains only 5% which is almost negligible, making it hard to calculate. ...
... Following De Vito et al. (2022), we selected 53 nutrients that best represent the overall diet for Hispanics/Latinos. We expanded the fat profile for better identifying cardiovasculardisease-related dietary habits (Islam et al., 2019;Lichtenstein, 2003). In particular, we constructed four variables: 1-SCSFA short-chain saturated fatty acids (i.e., butyric acid), 2-MCSFA medium-chain saturated fatty acids (i.e., the sum of caproic acid, caprylic acid, capric acid, and lauric acid), 3-LCSFA long-chain saturated fatty acids (i.e., the sum of myristic acid, palmitic acid, margaric acid, stearic acid and arachidic acid), 4-LCSFA long-chain monounsaturated fatty acids (i.e., the sum of myristoleic acid, palmitoleic acid, oleic acid, and gadoleic acid). ...
Full-text available
Diet is a risk factor for many diseases. In nutritional epidemiology, studying reproducible dietary patterns is critical to reveal important associations with health. However, it is challenging: diverse cultural and ethnic backgrounds may critically impact eating patterns, showing heterogeneity, leading to incorrect dietary patterns and obscuring the components shared across different groups or populations. Moreover, covariate effects generated from observed variables, such as demographics and other confounders, can further bias these dietary patterns. Identifying the shared and group-specific dietary components and covariate effects is essential to drive accurate conclusions. To address these issues, we introduce a new modeling factor regression, the Multi-Study Factor Regression (MSFR) model. The MSFR model analyzes different populations simultaneously, achieving three goals: capturing shared component(s) across populations, identifying group-specific structures, and correcting for covariate effects. We use this novel method to derive common and ethnic-specific dietary patterns in a multi-center epidemiological study in Hispanic/Latinos community. Our model improves the accuracy of common and group dietary signals and yields better prediction than other techniques, revealing significant associations with health. In summary, we provide a tool to integrate different groups, giving accurate dietary signals crucial to inform public health policy.
... Some of the metabolic impacts of TFA include an increase in obesity, and insulin resistance, inflammation, and a reduction in endothelial function. TG and lipoprotein (a) levels are increased, whereas total cholesterol (TC):HDL ratio, apoB: apoA ratio, and TC: HDL ratio are all decreased by TFAs [55,56]. TFA inhibits the antilipolytic impact of insulin in adipose tissue and insulin-mediated glucose transport in animal models. ...
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Abstract Type 2 diabetes mellitus (T2DM), one of the main types of Noncommunicable diseases (NCDs), is a systemic inflammatory disease characterized by dysfunctional pancreatic β-cells and/or peripheral insulin resistance, resulting in impaired glucose and lipid metabolism. Genetic, metabolic, multiple lifestyle, and sociodemographic factors are known as related to high T2DM risk. Dietary lipids and lipid metabolism are significant metabolic modulators in T2DM and T2DM-related complications. Besides, accumulated evidence suggests that altered gut microbiota which plays an important role in the metabolic health of the host contributes significantly to T2DM involving impaired or improved glucose and lipid metabolism. At this point, dietary lipids may affect host physiology and health via interaction with the gut microbiota. Besides, increasing evidence in the literature suggests that lipidomics as novel parameters detected with holistic analytical techniques have important roles in the pathogenesis and progression of T2DM, through various mechanisms of action including gut-brain axis modulation. A better understanding of the roles of some nutrients and lipidomics in T2DM through gut microbiota interactions will help develop new strategies for the prevention and treatment of T2DM. However, this issue has not yet been entirely discussed in the literature. The present review provides up-to-date knowledge on the roles of dietary lipids and lipidomics in gut-brain axis in T2DM and some nutritional strategies in T2DM considering lipids- lipidomics and gut microbiota interactions are given.
During recent years, the applicability of bi-, oleo- and emulgels has been widely studied, proving several advantages as compared to conventional fats, such as increasing the unsaturated fat content of products and being more sustainable for temperate regions as compared to tropical fats. Moreover, these alternative fat systems improve the nutritional profile, increase the bioavailability of bioactive compounds, and can be used as preservation films and markers for the inactivation of pathogens, while in 3D printing facilitate the obtaining of superior food products. Furthermore, bi-, oleo- and emulgels offer food industries efficient, innovative, and sustainable alternatives to animal fats, shortenings, margarine, palm and coconut oil due to the nutritional improvements. According to recent studies, gels can be used as ingredients for the total or partial replacement of saturated and trans fats in the meat, bakery and pastry industry. The evaluation of the oxidative quality of this gelled systems is significant because the production process involves the use of heat treatments and continuous stirring where large amounts of air can be incorporated. The aim of this literature review is to provide a synthesis of studies to better understand the interaction of components and to identify future improvements that can be applied in oil gelling technology. Generally, higher temperatures used in obtaining polymeric gels, lead to more oxidation compounds, while a higher concentration of structuring agents leads to a better protection against oxidation. Due to the gel network ability to function as a barrier against oxidation factors, gelled matrices are able to provide superior protection for the bioactive compounds. The release percentage of bioactive molecules can be regulated by formulating the gel matrix (type and concentration of structuring agents and type of oil). In terms of food products, future research may include the use of antioxidants to improve the oxidative stability of the reformulated products.
Frying is one of the most common methods of preparing foods. However, it may lead to the formation of potentially hazardous substances, such as acrylamide, heterocyclic amines, trans fatty acids, advanced glycation end products, hydroxymethyl furfural and polycyclic aromatic hydrocarbons, and adversely alter the desirable sensory attributes of foods, thereby reducing the safety and quality of fried foods. Currently, the formation of toxic substances is usually reduced by pretreatment of the raw materials, optimization of process parameters, and the use of coatings. However, many of these strategies are not highly effective at inhibiting the formation of these undesirable reaction products. Plant extracts can be used for this purpose because of their abundance, safety, and beneficial functional attributes. In this article, we focus on the potential of using plant extracts to inhibit the formation of hazardous substances, so as to improve the safety of fried food. In addition, we also summarized the effects of plant extracts, which inhibit the production of hazardous substances, on food sensory aspects (flavor, color, texture, and taste). Finally, we highlight areas where further research is required.
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High-density lipoprotein cholesterol (HDL-C) is a strong and independent predictor of major cardiovascular events in a wide range of patients. The relationship between HDL-C cholesterol and cardiovascular risk appears to be linear, continuous, negative and independent of other risk factors such as blood pressure, smoking and BMI. In addition, the inverse relationship between HDL-C and cardiovascular events does not depend on low-density lipoprotein cholesterol (LDL-C) levels, so a substantial residual cardiovascular risk is maintained also in individuals with LDL-C levels below the target recommended by scientific guidelines. Furthermore, a strong relationship among HDL-C levels, progression of atherosclerosis and risk of cardiovascular diseases has been also demonstrated. Treatments that increase HDL-C levels have been shown to be effective in reducing incidence of cardiovascular diseases both in primary and secondary prevention settings. However, proof that increasing HDL-C levels by pharmacological treatment is able to confer a reduction in major cardiovascular outcomes independent of changes in LDL-C or triglycerides levels is not completely defined. Among currently available compounds, statins do not seems to have a sufficient effect on HDL-C profile. Studies on fibrates have shown inconclusive results. Although niacin has been demonstrated to reduce the incidence of major cardiovascular events paralleling the regression of atherosclerosis, significant side-effects still limit its use. The potential benefit of cholesterol ester transfer protein inhibition is still under investigation. The combination therapy of fibrates with statins is also controversial. Thus, despite the potentially favorable effect of raising HDL-C levels, the available guidelines still do not consider HDL-C levels as a specific target for therapy. Further studies are needed to assess the role of new compounds to raise HDL-C levels or modify HDL composition and functionality.
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The consumption of high-fat hamburger enriched with SFA and trans-fatty acids may increase risk factors for coronary vascular disease, whereas hamburger enriched with MUFA may have the opposite effect. Ten mildly hypercholesterolaemic men consumed five, 114 g hamburger patties per week for two consecutive phases. Participants consumed high-SFA hamburger (MUFA:SFA = 0.95; produced from pasture-fed cattle) for 5 weeks, consumed their habitual diets for 3 weeks and then consumed high-MUFA hamburger (MUFA:SFA = 1.31; produced from grain-fed cattle) for 5 weeks. These MUFA:SFA ratios were typical of ranges observed for retail ground beef. Relative to habitual levels and levels during the high-MUFA phase, the high-SFA hamburger: increased plasma palmitic acid, palmitoleic acid and TAG (P < 0.01); decreased HDL cholesterol (HDL-C) and LDL particle diameter percentile distributions (P < 0.05); and had no effect on LDL cholesterol or plasma glucose (P>0.10). Plasma palmitoleic acid was positively correlated with TAG (r 0.90), VLDL cholesterol (r 0.73) and the LDL:HDL ratio (r 0.45), and was negatively correlated with plasma HDL-C (r - 0.58), whereas plasma palmitic, stearic and oleic acids were negatively correlated with LDL particle diameter (all P <or= 0.05). Because plasma palmitoleic acid was derived from Delta9 desaturation of palmitic acid in liver, we conclude that alterations in hepatic stearoyl-CoA desaturase activity may have been responsible the variation in HDL-C and TAG caused by the high-SFA and high-MUFA hamburgers.
Partially hydrogenated oils are the main dietary source of trans fatty acids. They entered the food supply in the early 1900s and quickly became a key ingredient in processed foods given their long shelf life and low cost. Trans fatty acid consumption from partially hydrogenated oils adversely affect lipid metabolism, and has been linked with an increased risk of coronary heart disease. In addition, there is evidence to suggest that high intakes may be associated with visceral adiposity, insulin resistance and type 2 diabetes. In order to reduce intakes of trans fatty acids, countries, cities and states worldwide have adopted trans fat labeling and bans. Accumulating evidence suggest these initiatives have resulted in the gradual reduction of trans fat levels in processed foods, which have coincided with reductions in intakes. Despite on-going policy efforts to lower trans fat levels in the food supply, global intakes of trans fatty acids remain high, and exceeds recommended upper limits of intake in many countries. Further implementation of policies and continued monitoring is needed to ensure progress towards elimination of harmful partially hydrogenated oil derived trans fatty acids from the food supply. Moreover, continued global monitoring of TFA levels in foods, as well as population intakes, is essential.
Objective The goal of this article was to review the causal link between trans fatty acids (TFA) produced from partially hydrogenated vegetable oil (PHVO) and cardiovascular disease (CVD) risk and its likely mechanisms. The potential risk of TFA from ruminant dairy and meats, which are currently the major sources of dietary TFA, is also discussed. Methods Evidence was derived from observational studies of large cohorts followed up prospectively; from randomized controlled trials of clinical interventions; and from specific case-control studies that investigated biomarkers in tissues. Searches included PubMed and Medline from 1990 to 2013. Results Despite TFA from PHVO being associated more strongly with CVD risk than even saturated fats, it may prove difficult to totally eliminate PHVO from all foods. This raises the issue of the lower limit of TFA consumption below which CVD risk is not increased. Limits of <1% of total energy have been suggested. The major mechanism underlying the increased CVD risk from TFA is an increase in LDL-C and Lp(a) lipoproteins and a decrease in HDL-C; increased inflammation and adverse effects on vascular function have also been shown. Both PHVO and ruminant TFA comprise a range of isomers, some specific to each source but including a substantial commonality that supports findings of similar adverse effects at equivalent intakes of TFA. However, the amount of TFA in ruminant fat is relatively small; this limits the CVD risk from eating ruminant products, an inference supported by analysis of prospective cohort studies. Conclusions Two key challenges to the health industry arise from this evidence. They must first determine whether a small intake of TFA from PHVO is safe and what constitutes a safe amount. They must also determine whether TFA from ruminant fat in currently consumed amounts represent limited cardiovascular risk that is balanced by the nutritional benefits of dairy products.
Consumption of industrial trans fatty acids (iTFA) increases LDL cholesterol, decreases HDL cholesterol, and is strongly associated with a higher risk of cardiovascular disease (CVD). However, changes in circulating cholesterol cannot explain the entire effect. Therefore, we studied whether iTFA and conjugated linoleic acid (CLA) affect markers of inflammation and oxidative stress. Sixty-one healthy adults consumed each of 3 diets for 3 wk, in random order. Diets were identical except for 7% of energy provided by oleic acid (control diet), iTFA, or CLA. At the end of the 3 wk, we measured plasma inflammatory markers IL-6, C-reactive protein, tumor necrosis factor receptors I and II (TNF-RI and -RII), monocyte chemotactic protein-1 and E-selectin, and urinary 8-iso-PGF(2α), a marker of lipid peroxidation. Consumption of iTFA caused 4% lower TNF-RI concentrations and 6% higher E-selectin concentrations compared with oleic acid (control) and had no significant effect on other inflammatory markers. CLA did not significantly affect inflammatory markers. The urine concentration of 8-iso-PGF(2α) [geometric mean (95% CI)] was greater after the iTFA [0.54 (0.48, 0.60) nmol/mmol creatinine] and the CLA [1.2 (1.1, 1.3) nmol/mmol creatinine] diet periods than after the control period [0.45 (0.41, 0.50) nmol/mmol creatinine; P < 0.05]. In conclusion, high intakes of iTFA and CLA did not substantially affect plasma concentrations of inflammatory markers, but they increased the urine 8-iso-PGF(2α) concentration. However, it is unlikely this plays a major role in the mechanism by which iTFA increase the risk of CVD. However, more research is needed to fully understand the implications of these findings.
The aim of this systematic review and meta-analysis was to summarize the evidence from observational studies assessing the association between intake of trans fatty acids (TFA) and the risk of coronary heart disease (CHD), with a specific emphasis on distinguishing between TFA of industrial and ruminant origin. By searching five bibliographic databases, analyses from six published and two unpublished prospective cohort studies, assessing the association of intake of TFA with fatal and/or non-fatal CHD, were identified. Four and three studies reported separate associations for intake of ruminant or industrial-TFA, respectively. The pooled relative risk estimates for comparison of extreme quintiles of total-TFA intake (corresponding to intake increments ranging from 2.8 to ∼10 g/day) were 1.22 (95% confidence interval: 1.08-1.38; P=0.002) for CHD events and 1.24 (1.07-1.43; P=0.003) for fatal CHD. Ruminant-TFA intake (increments ranging from 0.5 to 1.9 g/day) was not significantly associated with risk of CHD (risk ratio (RR)=0.92 (0.76-1.11); P=0.36), and neither was industrial-TFA intake, although there was a trend towards a positive association (RR=1.21 (0.97-1.50); P=0.09). In conclusion, our analysis suggests that industrial-TFA may be positively related to CHD, whereas ruminant-TFA is not, but the limited number of available studies prohibits any firm conclusions concerning whether the source of TFA is important. The null association of ruminant-TFA with CHD risk may be due to lower intake levels.
Epidemiological evidence has associated dietary trans fatty acids (TFA) with heart disease. TFA are primarily from hydrogenated fats rich in elaidic acid, but dairy products also contain naturally occurring TFA such as vaccenic acid. Our purpose in this study was to compare the effects of consuming a commercially hydrogenated vegetable shortening rich in elaidic TFA (18:1t9) or a butter rich in vaccenic TFA (18:1t11) in the absence and presence of dietary cholesterol on atherosclerosis. LDL receptor deficient (LDLr(-/-)) mice were fed 1 of 8 experimental diets for 14 wk with the fat content replaced by: regular (pork/soy) fat (RG), elaidic shortening (ES), regular butter (RB), vaccenic butter (VB), or an atherogenic diet containing 2% cholesterol with RG (CH+RG), ES (CH+ES), RB (CH+RB), or VB (CH+VB). Serum cholesterol levels were elevated with cholesterol feeding (P < 0.001), whereas serum triglyceride levels were higher only in the CH+RB (P < 0.001) and CH+VB (P < 0.001) groups compared with the other 6 groups. Serum cholesterol and triglyceride levels were significantly lower in the CH+VB group than in the CH+RB group (P < 0.001). Atherosclerosis was stimulated by dietary ES compared with RG (P = 0.021), but CH+ES did not stimulate atherosclerosis beyond CH+RG alone. In contrast, VB did not induce an increase in atherosclerotic plaque formation compared with the RG and RB diets and the CH+VB diet reduced atherosclerosis compared with the other diets containing cholesterol (P < 0.01). In summary, consuming a hydrogenated elaidic acid-rich diet stimulates atherosclerosis, whereas a vaccenic acid-rich butter protects against atherosclerosis in this animal model.
Consumption of industrially produced trans fatty acids (TFA) remains high in many populations, particularly in developing nations where partially hydrogenated vegetable oils are frequently used for home cooking and among individuals in developed countries having high intakes of bakery or processed foods. Well-controlled observational studies and randomized trials indicate that TFA consumption adversely affects multiple risk factors for chronic diseases, including numerous blood lipids and lipoproteins, systemic inflammation, endothelial dysfunction, and possibly insulin resistance, diabetes, and adiposity. Growing evidence for the latter effects is particularly concerning given the worldwide obesity pandemic and high contents of industrially produced TFA in many foods marketed toward children. Consistent evidence from prospective observational studies of habitual TFA consumption and retrospective observational studies using TFA biomarkers indicates that TFA consumption increases risk of clinical coronary heart disease (CHD). Based on the adverse effects of risk factors and consistent relationships with clinical endpoints, the evidence that TFA consumption increases CHD risk is convincing. Some evidence suggests that TFA consumption may also increase other disease outcomes, but further investigation is needed to confirm the presence and magnitude of such effects. More research is also needed to understand how specific TFA isomers of varying chain length and double bond location may affect different biologic pathways of disease. Both individual- and policy-level initiatives to decrease TFA consumption should continue, particularly in population subgroups and in developing nations with high consumption of partially hydrogenated vegetable oils.
Epidemiological evidence has associated dietary trans-fatty acids (TFAs) with coronary heart disease. It is assumed that TFAs stimulate atherosclerosis, but this has not been proven. The purpose of this study was to determine the effects of consuming 2 concentrations of TFAs obtained from commercially hydrogenated vegetable shortening on atherosclerotic development in the presence or absence of elevated dietary cholesterol. Low-density lipoprotein receptor-deficient mice were fed 1 of 7 experimental diets for 14 weeks: low regular fat (LR), low trans-fat (LT), regular high fat, high trans-fat (HT), or a diet containing 2% cholesterol with low regular fat (C + LR), low trans-fat (C + LT), or high trans-fat (C + HT). The extent of lesion development was quantified by en face examination of the dissected aortae. Dietary cholesterol supplementation significantly elevated serum cholesterol levels. Surprisingly, this rise was partially attenuated by the addition of TFAs (C + LT and C + HT) in the diet. Serum triglyceride levels were elevated with the higher-fat diets and with the combination of trans-fat and cholesterol. Animals consuming TFAs in the absence of dietary cholesterol developed a significantly greater extent of aortic atherosclerotic lesions as compared with control animals (LT > LR and HT > regular high fat). Atherosclerotic lesions were more extensive after cholesterol feeding, but the addition of TFAs to this atherogenic diet did not advance atherosclerotic development further. In summary, TFAs are atherogenic on their own; but they do not stimulate further effects beyond the strongly atherogenic effects of dietary cholesterol.