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| Is dietary fats cause CVD or CHD |
According to the authors(Oguzhan Yildiz, Melik Seyrek and Kemal Gokhan Ulusoy),here is brief description of foods that really cause cardiovascular/coronary heart diseases or not.
Total fat
Since the beginning of the concern about diet and CVD risk assessment,
dietary fat, especially the total fat, is the main point of interest.
Till the beginning of the 1990s, the recommendations for the public
health was focused on limiting the total fat intake, especially to
reduce CVD.
As part of the Dietary Approaches to Stop Hypertension (DASH) diet,
low-fat dairy intake has been shown to lower blood pressure . However,
lowering total cholesterol by replacing dietary total fat with
carbohydrate may contrarily increase serum triglyceride concentration .
Moreover, in a meta-analysis of prospective cohort studies, intake of
total fat was not found significantly associated with CHD mortality or
CHD events .
One of the key studies about total fat intake was the Women’s
Health Initiative Dietary Modification Trial. In this study, dietary
intervention that reduced total fat intake did not significantly reduce
the risk of CHD or CVD in postmenopausal women and only modest effects
on CVD risk factors were achieved . According to the 2006 AHA Diet and
Lifestyle recommendations, for decreasing the CVD risk, the
recommendations are much about limitations of intake of each type of
fat, instead of reducing the total fat intake. Specifically, the AHA
recommends to supply 7% of energy from saturated fat and 1% of energy
from trans fat . And also, according to the Dietary Guidelines for
Americans 2010, lowering the percentage of calories from dietary
saturated fatty acids to 7% of calories and replacing them with
monounsaturated and/or polyunsaturated fatty acids can further reduce
the risk of CVD .
Saturated Fatty Acids (SFA)
The primary SFA sources are animal fat such as meat, milk, and dairy
products, some plant oils such as palm and coconut oils, and the
industrially-prepared food (cookies, cakes, and pies). Several
meta-analyses showed that SFA intake was not significantly associated
with risk of CAD or CVD . Recent data from meta-analyses of cohort
studies and randomized control trials suggest that SFA consumption on
CVD risk depends on the replacement nutrient. The latest epidemiologic
studies and clinical trials suggest that differing effects depending on
the replacement nutrient scenario such as replacing saturated fat with
polyunsaturated fat in the diet is more beneficial for CAD risk than
with carbohydrates .
In a pooled analysis of 11 prospective cohort studies, Jakobsen et al.
revealed that consumption of polyunsaturated fatty acid (PUFA) in place
of SFA was associated with reduced CAD risk . In another study,
Mozaffarian et al. indicated as the result of 8 randomised clinical
trials that changing the energy intake from SFA to PUFA by 5% reduced
the CAD risk by 10% . Additionally, in the Cochrane Collaboration
meta-analysis of 48 RCTs, Hooper et al. revealed that reducing saturated
fat by reducing and/or modifying dietary fat reduced the risk of
cardiovascular events by 14%. And this study also suggested that the
beneficial effects occurred in the case of fat modification rather than
reduction of fat intake and in a two-year period. Also, males and
population who have moderate or high risk of CVD are more prone to have
benefits from dietary fat modification. However, dietary fat
modification was not found to be beneficial on CVD mortality . Based on
recent evidence, both the AHA and the European Society of Cardiology
advise to limit saturated fat intake to <10% and <7% of total
daily calories, respectively .
According to the 2013 AHA/ACC Guideline on Lifestyle Management to
Reduce Cardiovascular Risk, for adults to benefit from LDL cholesterol
lowering, only 5%-6% of calories should come from saturated fat (through
replacement of PUFA > monounsaturated fat (MUFA) > whole grains
> refined carbohydrates).
Monounsaturated Fatty Acids (MUFA)
The main dietary MUFA is oleic acid, which is abundant in nuts,
sunflower oil, olive oil, canola oil, high oleic safflower oil, and
avocado. Because olive oil is the essential part of the Mediterranean
diet, the role of MUFA in the prevention of CAD has a close interest,
especially after Mattson and Grundy showed that high SFA diets increase
the LDL cholesterol/HDL cholesterol ratio and changing SFA with MUFA
reduces LDL cholesterol levels but not HDL cholesterol. Replacing MUFA
with carbohydrates in the diet causes several alterations in the lipid
profile, such as TG and VLDL cholesterol decrease and HDL cholesterol
and apoA1 increase . However, the epidemiologic data about oleic acid
and CAD prevention is controversial. While the Nurses' Health Study
(NHS) found remarkable protection, in the Zutphen and Puerto Rico Heart
Health Program studies there were no beneficial effects reported between
controls and CAD cases . In a recent study, Schwingshackl and Hoffmann
recapped the most available data about MUFA and CVD risk in which they
found no accepted rationale for MUFA recommendation, although there are
no significant side effects of diets with rich MUFA up to date . Also,
according to the Cochrane meta-analysis by Hooper et al., reduction of
SFA intake and replacement with unsaturated fat is advised for the
population under risk of CVD .
Trans Fatty Acids (TFA)
Trans fatty acids (TFA) are a type of unsaturated fat that became
commonly produced industrially from vegetable fats for use in margarine,
snack food, packaged baked goods, and frying fast food. TFA has at
least one carbon-carbon double bond in the trans, rather than the
typical cis configuration. Early in the 20th century, TFA was invented
for increasing the shelf life of oils and consumption of these fats, as
margarine increased all over the world. Recently, it has been recognized
that it causes elevated cholesterol levels and has a major role in the
risk of CAD. Beyond their energy value, TFA does not have any known
health benefits and there is an apparent association between TFA
consumption and the risk of heart disease. In a meta-analysis of 28
cohort studies, there has been found a highly significant positive
association between TFA intake and CAD morbidity and mortality [68].
Energy replacement of TFA with SFA, MUFA, or PUFA 1% resulted in the
decrease of the TC: HDL ratio in controlled trials and each 2%
replacement would lower CAD risk in prospective cohort studies.
Because of this CVD risk increase, the Food and Drug Administration
(FDA) and the other Health Regulatory Agencies required food
manufacturers to list TFA on the Nutrition Facts and some Supplement
Facts sections on the package of food, although TFA levels of less than
0.5 g per serving can be listed as 0 g.
N-3 fatty acids
Because of the low rates of ischemic heart disease in Greenland
Eskimos, there was close attention to their diet. This protection was
thought to be caused by long-chained PUFA’s anti-thrombotic effects,
which is an important part of their diet . Prospective cohorts revealed
the protective effects of intake of n-3 fatty acids on CAD, and since
then evidence suggests that n-3 fatty acid intake may be effective for
secondary prevention. The possible effects were thought to be prevention
of arrhythmias, as well as lowering of heart rate and blood pressure,
decreasing platelet aggregation, and lowering triglyceride concentration
.
The n-3 fatty acids also decrease hepatic TG secretion and increase
clearance from plasma. In diabetic patients, n-3 PUFA are found to
reduce TG levels by 25% and VLDL levels by 36%; however, LDL
concentrations increased slightly by 5.7% [73].
Since then, several meta-analysis and RCTs have been published about
the role of seafood n-3 fatty acids on CVD and CVD mortality. Some of
them suggested that n-3 fatty acid intake lowers the CVD risk, but some
of them found no significant effect on CVD risk and/or mortality. In the
last US guidelines on patients with CAD, fish and/or fish oil
supplement is indicated only in the control of a patient’s lipid profile
(class IIB, level of evidence B).
But in the latest European Society of Cardiology (ESC) guidelines, the
protective effects of fish on CVD is associated with n-3 PUFA. Moreover,
it is suggested that eating fish at least once a week reduces the CAD
risk by 15% . There are controversies between epidemiologic studies and
clinical trials, probably due to the different study groups.
Epidemiologic observational studies usually evaluate the disease-free
population, but clinical trials are often conducted in a population at
risk of CVD.
Plant-based fatty acids
α-linolenic acid (ALA) is a short chain n-3 PUFA found in plant sources
such as soybeans, walnuts, rapeseed oil, and flaxseed. It could be an
alternative to fish n-3 PUFA because it can be converted to
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are
n-3 PUFAs that are found in fish. But this conversion is limited and the
evidence for ALA in CVD protection is limited. In a systematic review
of 14 human studies, at least four weeks of supplementation of ALA has
no significant effect on the lipid profile . However, since no current
specific recommendations for ALA for CAD risk reduction is present,
epidemiologic studies suggest a protective role, the diet including ALA
(2 to 3 g per day) has been recommended for both primary and secondary
prevention of CAD . Further studies need to strengthen the evidence for
the effects of ALA on CVD.
B Vitamins
The main role of B vitamins is principally for energy production, cell
metabolism, and nerve function. Beside these, vitamins B12, B6, and
folic acid are known to have homocysteine lowering effect. Several
studies suggested that high homocysteine levels are associated with
increased risk of MI and/or stroke. Because folic acid, B12, and B6
decreased the blood homocysteine level in 20%-40%, from baseline, it has
been assumed that these supplements can subsequently reduce CVD risk.
The studies about the effects of folic acid and B vitamin
supplementation failed to prove that reducing homocysteine level by
folic acid and vitamin B supplements decreases CVD incidence. Most of
the epidemiologic studies suggested protective effects of B vitamins on
CAD but the randomized clinical trials did not show the same beneficial
effects.
A meta-analysis of 12 randomized trials that has 16,958
participants with pre-existing vascular disease revealed that folic acid
supplementation had no effect on CAD risk . After 1996, the US FDA made
a regulation for the fortification of grain products (flour, breads,
rice, pasta, cornmeal, etc.) with folic acid. Since then, the prevalence
of low plasma folate concentrations has decreased . The role of B
vitamins and folate are plausible in the prevention of CVD and more
studies are needed.
I hope you will like this article'' Is Dietary fats really trigger cardiovascular/coronary heart diseases?''.
I hope you will like this article'' Is Dietary fats really trigger cardiovascular/coronary heart diseases?''.
